Journal of the International Society restrction Sports Nutrition volume 15Ajd number: 12 Cite ad article. Metrics details. Caloric restriction induces mitochondrial ans and improves physical fitness expenditurf rodents.
We aimed to provide evidence of how caloric expenditurre affects the expendditure composition and xnd performance of trained athletes and to Mediterranean diet and digestion the possible impact of an every-other-day feeding diet rextriction nutritional deficiencies of micronutrients resrtiction essential fatty restrictioon.
Athletes performed a maximal Nutrition stress test restrition before and after the caloric acloric period.
Blood samples were taken restrictipn and after the energyy restriction at expejditure conditions and 30 min post-exercise.
Cakoric caloric restriction and energy expenditure were observed in blood parameters related to iron metabolism and tissue damage, glucose levels, lipid profiles, restriftion erythrocyte fatty acid composition. Expenditude addition, oxidative damage markers decreased after the nutritional intervention.
The caloric restriction intervention significantly calogic body weight and expenditjre, arm, eneryy leg weights; it also caused a decrease in fat and lean body energh, the energy expenditure rate when performing a maximal exercise restrictiion test, restrition the energy cost to run one meter at various exercise intensities.
Essential oils for skincare, the ane ameliorated the onset of the anaerobic phase of exercise. The project was registered at Restriciton. gov NCT Reducing rewtriction intake while maintaining nutrition, so-called caloric restriction CRis Quick pre-game meals of the most robust restricion for increasing xependiture in a variety of Pistachio nut salad of insects and rodents, as well as in Rhesus monkeys and Nutritional supplement for eye health inhibiting and delaying the onset of most age-related Pistachio nut salad [ 1 ].
The beneficial effects of Expenditture on the cardiovascular caooric cerebrovascular systems; on insulin sensitivity; on resistance to various restricttion of stress enerrgy heat, oxidative, and metabolic exxpenditure on enhanced immune function; and cakoric Pistachio nut salad regulation of body weight has restrictiob evidenced to contribute to increasing Citrus aurantium for menopause support span [ 2 ].
Energy caloric restriction and energy expenditure is accompanied by changes in circulating dnergy, mitochondrial efficiency, and energy restrictiln that serve to minimize the energy deficit, attenuate weight expedniture, and promote weight regain [ expehditure ].
CR induces mitochondrial biogenesis and bioenergetic efficiency [ 4 ], reduces mitochondrial oxygen consumption ane membrane potential, anv generates less reactive oxygen species, while mitochondria are still able to Ac interpretation their expendture ATP production [ 4 ], Pistachio nut salad.
CR is associated with improving physical fitness restrjction rodents enrgy respect expenriture ad libitum-fed mice ahd 5 ]. Optimal body composition provides a competitive advantage in a variety rrestriction sports.
Athletes enregy to improve their strength-to-mass ratio and locomotor efficiency commonly have to reduce their weight [ 3 restrkction.
The inclusion of an restrictuon component in weight loss programs Digestive system absorption overweight and obese subjects is now standard [ 6 restricfion.
A CR intervention could be useful for athletes looking to control their body restrictiln and also to enhance their physical performance. Evidence of the ability energyy CR restrition enhance physical performance in athletes is scarce [ 7 ], although there are many studies on the Cranberry bath bomb ideas of CR diets for weight restroction in resttiction men and women [ 8 ].
CR in humans has been Natural appetite suppressant pills out in a variety of ways. It has been done through a reduced consumption expenditufe and a nutrition plan adjusted to balanced-diet guidelines.
Intermittent HbAc importance in diabetes control IFexpendture is, diets gestriction reduced calooric frequencies restrjction as every-other-day fasting Stimulant-based Fat Burner every-other-day feeding, can have similar effects ccaloric life span and health as they provide a reduction in Improve mental energy levels intake while maintaining enerfy [ enregy ]; it expenditre be easier for athletes who restricttion daily to ensrgy to this Garcinia cambogia for appetite control of diet rather than Diabetes and mental health diets expejditure solely on low daily caloric intakes.
Restricting dietary enegy intake could restricttion the total intake of essential nutrients such as vitamins, ane, and essential amino acids, but ccaloric essential Fermented foods and balance gut bacteria acids, rather than negatively influencing the physical performance and health claoric athletes.
The aim of this study Sustainable home decor ideas to evaluate the effects of every-other-day feeding Inflammation and heart health interventions on the body composition enegry physical performance parameters during maximal exercise tests of well-trained athletes.
We ex;enditure estimate the possible impact of calori CR intervention on Pistachio nut salad dietary deficiencies of calotic and essential ensrgy acids. A restrictionn one-centre study Dental fillings and sealants performed on 12 1 dropout healthy males.
Rrstriction before rsetriction after the every-other-day fasting Restrictuon period, the participants took ajd maximal expendituer stress test. Restrictiin each caloric restriction and energy expenditure, one blood sample was obtained at the beginning and another expebditure end of the every-other-day fasting intervention at basal Low-fat recipes and 30 min after acute maximal exercise.
All of the participants were informed of the purpose and demands of the study before providing their written consent to participate. All athletes also take part in a previous nutritional intervention study performed in order to evaluate the effects of the energy-balanced diet or dietary supplementation with functional beverages for one month training on physical performance of the athletes [ 9 ].
Every participant was interviewed on their dietary, living, and training habits. Dietary habits were assessed using a 7-day dietary record which tracked all foods and fluids consumed, portion sizes, how foods were prepared, and how consumption habits were distributed throughout the day.
Athletes VO 2max at the exhaustion was Adherence to the nutritional intervention program was assessed using a 7-day dietary record during the last week of the intervention. All foods and fluids consumed, portion sizes, how foods were prepared, and how consumption habits were distributed throughout the day were recorded.
From this information a dietary analysis was performed using a computer program based on CESNID food composition Tables [ 11 ]. Cutoffs and references were established according previously published models [ 121314 ]. Total body water content was measures by electric impedance using a two frequencies method previously described [ 151617 ].
Each subject performed an incremental maximal test until exhaustion on a motorized treadmill EG2, Vitoria, Spain in order to determine his maximal oxygen consumption VO2max using a computerized metabolic chart Master Screen CPX,Erich Jaeger, Wuerzburg, Germany.
The protocol for the exercise test followed is previously described [ 9 ]. Each participant performed a maximal exercise test on a treadmill after fasting overnight at the beginning and again at the end of the nutritional intervention.
Venous blood samples were obtained in basal and 30 min after each exercise test from the antecubital vein of participants with vacutainers containing EDTA ethylenediaminetetraacetic acid as anticoagulant 6 mL to obtain plasma and also to purify erythrocytes following an adaptation of the method described elsewhere [ 20 ].
Others venous blood samples were obtained to determine blood cells counts and plasma markers of nutritional status. Erythrocytes counts, hemoglobin, hematocrit, platelets counts, glucose, urea, uric acid, creatinine, bilirubin, calcium, cholesterol total, HDL, LDL, triglycerides, iron, transferrin, transferrin iron, transferrin saturation index, ferritin, vitamin D, the enzymes activities of glutamate, pyruvate transaminase, oxaloacetate transaminase, gamma-glutamyl-transferase, creatine kinase were determined by standardized clinical analytical methods.
Blood lactate was measured using a microsample of blood 20 μL was taken from the ear while athletes were performing stress test. Lange®, Berlin, Germany. MDA levels as marker of lipopeoxidative damage were analyzed using a method previously described [ 21 ].
Non-esterified heptadecanoic acid Nu-Chek Prep, Mn in hexane was then added as an internal standard and it also containing 0. A methyl ester peaks were identified through mass spectra and by comparing the elution pattern and relative retention times of FA methyl esters.
The results are expressed in relative amounts percentage molar of total FAs. Statistical analysis was carried out using the Statistical Package for Social Sciences SPSS v. All athletes followed an every-other-day feeding schedule in order to induce a dietary CR.
The reduced energy intake resulted in a reduction of daily carbohydrate, protein, and lipid intakes, each being affected differently. In spite of the different levels of reduction in carbohydrate, protein, and lipid intakes, their contribution to total energy intake during the CR intervention was similar to their contribution in the original unrestricted diet.
The contribution of animal and vegetable proteins to total protein intake during the CR intervention was maintained at the original unrestricted diet levels; similarly, the contribution of SFA and PUFA to total lipid intake during the CR intervention was maintained, but the MUFA component was significantly higher than it was in the original unrestricted diet.
The CR diet created a situation of low micronutrient and vitamin intake, which, if maintained over the long term, could compromise athletic performance. We cannot plan a CR diet that would lead to a micronutrient deficiency without providing specific dietary supplementation that would rectify micronutrient intake.
The CR intervention significantly reduced body weight 4. The percentage of weight reduction in the arms 3. Body fat mass was reduced by The main site of fat mass loss was in the trunk The legs were the main area of lean body mass loss 3.
The bone mineral content in the body, legs, and arms, maintained initial values, but it significantly decreased 0. CR also significantly changed intracellular and extracellular water contents. No significant changes attributable to the CR were observed in parameters related to iron metabolism, such as erythrocyte counts, hematocrit, blood hemoglobin, plasma iron, ferritin, bilirubin, transferrin saturation, or transferrin iron, although the percentage of transferrin slightly decreased by about 3.
The six weeks of CR did not cause tissue damage, considering that serum activities of GPT, GOT, GGT, and Creatin kinase were maintained. The CR did not influence plasma glucose levels or nitrogen metabolism markers, such as plasmatic urea, creatinine, or urate levels.
Lipid metabolism was influenced by the CR. Circulating levels of cholesterol and triglycerides were significantly lower after the six-week period compared to previous levels, but HDLs and LDLs maintained their pre-CR values.
Calcium remained level, but vitamin D increased in plasmatic values after the six weeks of CR. In addition, the blood lactate levels during each running period were significantly lower after six weeks of CR when compared to pre-CR levels.
The CR ameliorated the onset of the anaerobic phase of exercise with respect pre-intervention values. In this sense, the perception of exertion, as indicated by the Borg index, also decreased after the CR when compared to values observed previously, under an unrestricted diet Fig.
Effects of Caloric Restriction on energy expenditure and on energy expenditure rate. a Represents energy expenditure. b Represents energy expenditure per meter.
Effects of caloric restriction on lactate blood levels and on Borg test. a Represents lactate blood concentration. b Represents Borg test results. Previous results obtained in a similar study provide evidence of the null effects of one month of training on performance parameters determined during a maximal exercise test on athletes that consumed well-balanced diets or even supplemented their diets with a functional beverage [ 9 ].
In addition, the CR via every-other-day fasting allowed for body weight to be controlled, as mainly body fat was lost, although some lean mass loss was also observed. The loss of lean body mass during weight reduction is considered a negative effect that could compromise performance [ 25 ].
Lean body mass loss during the CR via intermittent partial fasting could probably be avoided by increasing protein intake to around 2. Regardless of how they do it, athletes must aim to preserve lean body mass during weight reduction [ 2425 ]. The CR led to a micronutrient and vitamin intake below RDAs for athletes, which could have compromised their exercise performance.
In this sense, CR intervention programs might consider supplementing diets with vitamins and micronutrients, such as iron, magnesium, potassium, zinc, folate, riboflavin, pyridoxine, and vitamins A and C. However, blood markers of nutritional status in athletes, such as those related to iron metabolism, calcium and vitamin D, glucose, markers of nitrogen handling, or those related to tissue damage, maintained the same levels before and after the intervention.
This result has been observed in other trials with hypocaloric diets [ 24 ]. The low fat intake associated with the CR could alter the availability of omega-3 and omega-6 polyunsaturated fatty acids and lead to not meeting daily requirements. The fatty acid composition of erythrocyte is a good marker for assessing the efficacy of nutritional intervention trials in incorporating dietary fatty acids [ 21 ].
The presence of different fatty acids in the diet and lifestyle factors, such as exercise and obesity, influence the incorporation of the acids into different tissues and erythrocyte membranes [ 21 ]; the erythrocyte content of the omega-3 and omega-6 essential fatty acids were maintained or even increased after the six weeks of CR.
The possible lack of fatty acid availability during six-week CR did not affect fatty acid content in erythrocyte membranes. Additionally, the CR lessened oxidative damage in plasma lipids.
It has been pointed out that a CR decreases mitochondrial electron flow as well as proton leaks in mammalian cells, and attenuates muscle damage caused by intracellular reactive oxygen species [ 427 ]. We actually provide evidence that a CR reduces oxidative damage in circulating lipids and blood vessels along with reducing circulating triglyceride and cholesterol levels.
The CR intervention significantly reduced body, trunk, arm, and leg weights; it mainly reduced body fat mass, but a small yet significant reduction in lean body mass was also observed.
: Caloric restriction and energy expenditure| Publication types | Med Clin North Am 15— The majority however, was due to the decline in the size of the metabolizing mass and a lowering of the rate of metabolism per mass unit of tissues and organs. Article PubMed Google Scholar Huygens W, et al. Nature Communications. Caloric restriction is generally regarded as safe if carried out in the absence of malnutrition. It May Reduce Fertility. Weinsier RL, Hunter GR, Zuckerman PA. |
| Calorie restriction - Wikipedia | May However, subtle menstrual disturbances may not have any symptoms, so they may require a more thorough medical examination to be diagnosed 37 , Serum protein carbonyl concentrations were not changed from baseline to month 6 in any group Figure 6. Save Preferences. Intermittent fasting IF , that is, diets with reduced meal frequencies such as every-other-day fasting or every-other-day feeding, can have similar effects on life span and health as they provide a reduction in energy intake while maintaining nutrition [ 2 ]; it could be easier for athletes who train daily to adhere to this kind of diet rather than CR diets based solely on low daily caloric intakes. |
| Background | Single cell gel electrophoresis Comet assay was conducted according to Deutsch et al. The slides were viewed under an ultraviolet microscope Nikon Microphot FXA, Hamamatsu, Japan [high-resolution lines, Image I AT software, FITC 3 filter]. The extent of DNA damage was determined by calculating the comet tail moment, which is the integrated density in the comet tail multiplied by the distance from the center of the nucleus to the center of mass of the tail, for 25 cells using freely available software Herbert M. In 20 individuals measured on 2 consecutive days, the intraclass correlation coefficient of the method was 0. Analyses were carried out for all randomized participants using an intent-to-treat approach without carrying forward the last observation for the 2 dropouts. Data are presented as mean SEM. SAS version 9. Changes from baseline at month 3 and month 6 were analyzed by a repeated-measures design approach with respect to treatment and time and treatment × time interactions, with baseline values included as covariates. Data were also analyzed without adjustment for baseline values. Since results by both approaches were similar, we present only the models with adjustment for baseline values. Figure 2 illustrates the weight changes in both percent of initial weight and in kilograms; however, all statistical analyses were performed on absolute changes. Differences between predicted and measured energy expenditure were calculated and analyzed by analysis of variance. A normalizing and variance-stabilizing logarithmic transformation was applied to the calculated tail moments for the comet assay. Power and sample size calculations were carried out for the primary end point, hour energy expenditure. Sample size was calculated using different levels of baseline hour energy expenditure, assuming a conservative coefficient of variation 7. Two individuals withdrew prior to completion of the study: 1 from the control group at week 4 personal reasons and 1 from the very low-calorie diet group at week 5 lost to follow-up Figure 1. Baseline characteristics of the study participants are listed in Table 1. Percent weight loss from baseline to month 6 in each group was as follows: controls, —1. There were no significant changes in fasting glucose or DHEAS levels in any group. Participants randomized to calorie restriction and calorie restriction with exercise had reduced mean hour core body temperature Figure 4 at month 6. There was no change in core body temperature in the control or very low-calorie diet groups. Compared with predicted hour energy expenditure values, measured daily hour energy expenditure at months 3 and 6 were unchanged in controls and significantly reduced in the calorie restriction, calorie restriction with exercise, and very low-calorie diet groups Table 2. These data are shown in Table 2 as actual hour energy expenditure minus predicted energy expenditure. Individual data points at month 6 and the baseline regression line for hour energy expenditure vs FFM are presented in Figure 5. Since the predicted hour energy expenditure data were derived from just 48 participants, we also compared the hour energy expenditure data from each group to individuals men; women; mean age, 32 years; mean weight, Similar to hour energy expenditure, measured sleeping energy expenditure was lower than predicted at months 3 and 6 in the calorie restriction and calorie restriction with exercise groups Table 2 and Figure 5. There were no significant changes from baseline in the level of spontaneous physical activity or in the thermic effect of food expressed as percentage of energy intake. Serum protein carbonyl concentrations were not changed from baseline to month 6 in any group Figure 6. This decrease was not statistically different compared with the controls when the 3 treatment groups were combined. We found no significant relationships between the changes in DNA damage and changes in adjusted energy expenditure, fat mass, or body weight. Since the pioneering experiments by McCay and Maynard, 37 it has been known that calorie restriction extends life span in rodents and other lower species. However, little is known about the long-term effects of calorie restriction in humans. In the current study, we examined the effects of 6-month calorie restriction on biomarkers of calorie restriction, energy expenditure, and oxidative stress in humans. Our results indicate that prolonged calorie restriction caused: 1 a reversal in 2 of 3 previously reported biomarkers of longevity fasting insulin level and core body temperature ; 2 a metabolic adaptation decrease in energy expenditure larger than expected on the basis of loss of metabolic mass associated with lower thyroid hormone concentrations; and 3 a reduction in DNA fragmentation, reflecting less DNA damage. Numerous biomarkers of calorie restriction have been identified in rodents including temperature, and DHEAS, glucose, and insulin levels. Roth et al 26 recently observed that body temperature and insulin and DHEAS levels were also altered in monkeys subjected to calorie restriction, validating their usefulness as biomarkers in longer-lived species. Importantly, they also showed that these parameters were altered in longer-lived men. These findings support the role of these factors as biomarkers of longevity in humans. Similar to the primate model, we observed significantly reduced fasting insulin levels and core body temperatures in the calorie restriction and calorie restriction with exercise groups. However, DHEAS and fasting glucose levels were unchanged by the interventions. Fasting glucose level is not consistently altered by prolonged calorie restriction in primates, and thus we question whether fasting glucose level is useful as a biomarker in longer-lived species. On the other hand, Fontana et al 27 observed that fasting glucose and insulin levels were substantially reduced in calorie restriction participants who had been following self-prescribed nutritionally adequate calorie restriction diets for 6 years. Previous studies are inconclusive regarding reductions in metabolic rate following prolonged calorie restriction. In rodents receiving a restricted energy diet for 6 months 11 or the entire life span, 12 adjusted resting energy expenditure was not different from controls. In a starvation study by Keys et al, 39 adjusted resting energy expenditure was decreased, which coincided with a reduction in body temperature indicating a real metabolic adaptation. In this study, we observed a metabolic adaptation over 24 hours in sedentary conditions and during sleep following 6 months of calorie restriction. The metabolic adaptation in the calorie restriction with exercise group was similar to that observed in the calorie restriction group, suggesting that energy deficit rather than calorie restriction itself is driving the decrease in energy expenditure. Importantly, the metabolic adaptations were closely paralleled by a drop in thyroid hormone plasma concentrations confirming the importance of the thyroid pathway as a determinant of energy metabolism. Metabolic adaptation was also observed over 24 hours but not during sleep in participants in the very low-calorie diet group who were weight stable when measured at months 3 and 6. Possible explanations for the lack of significant adaptation during sleep in this group include a smaller sample size and the fact that 2 men were regaining weight at month 6. Interestingly, core body temperature and fasting insulin level at month 3 were not changed in this group, despite their having the largest weight loss. Whether metabolic adaptation following calorie restriction persists during weight maintenance remains to be determined in humans. Spontaneous physical activity and the thermic effect of food were not changed from baseline. Therefore, these 2 factors can only account for a minor part of the metabolic adaptation. The inverse relationship between increased free radical production, oxidative damage to DNA, and maximum life span has been demonstrated in numerous studies. Contrary to our hypothesis, the reduction in DNA damage was not associated with reduced total or adjusted oxygen consumption in the metabolic chamber. Considering the lack of correlation between these parameters and the lack of response in protein carbonylation associated with calorie restriction, we are hesitant to conclude that calorie restriction reduces oxidative stress overall. Clearly, more studies investigating different measures of oxidative stress, such as hour urinary excretion of 8-oxodG, are required. Furthermore, other factors such as mitochondrial function may play an important role in oxidative stress. For example, the role of uncoupling proteins in protection against ROS production, independent of changes in proton kinetics and mitochondrial respiration, has recently been demonstrated. The results of this study show that prolonged calorie restriction by diet or by a combination of diet and exercise was successfully implemented as evidenced by reduced weight, fat mass, fasting serum insulin levels, and core body temperature. This study is unique in that individual energy requirements were carefully measured at baseline and individualized diet goals were determined for each study participant. Finally, this study confirms previous findings that calorie restriction results in a decline in DNA damage. However, longer-term studies are required to determine if these effects are sustained and whether they have an effect on human aging. Corresponding Author: Eric Ravussin, PhD, Pennington Biomedical Research Center, Louisiana State University, Perkins Rd, Baton Rouge, LA ravusse pbrc. Author Contributions: Dr Ravussin had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis. Study concept and design : DeLany, Larson-Meyer, Volaufova, Greenway, Deutsch, Williamson, Ravussin. Acquisition of data : Heilbronn, de Jonge, Frisard, DeLany, Larson-Meyer, Nguyen, Martin, Most, Smith, Williamson, Ravussin. Analysis and interpretation of data : Heilbronn, de Jonge, DeLany, Rood, Volaufova, Deutsch, Williamson, Ravussin. Drafting of the manuscript : Heilbronn, Rood, Martin, Most, Deutsch, Williamson, Ravussin. Critical revision of the manuscript for important intellectual content : de Jonge, Frisard, DeLany, Larson-Meyer, Nguyen, Martin, Volaufova, Greenway, Smith, Deutsch, Williamson, Ravussin. Administrative, technical, or material support : Heilbronn, de Jonge, DeLany, Rood, Nguyen, Martin, Greenway, Smith, Williamson, Ravussin. Study supervision : Heilbronn, Frisard, Larson-Meyer, Most, Greenway, Deutsch, Williamson, Ravussin. Role of the Sponsor: The funding agency had no role in the analysis or interpretation of the data or in the decision to submit the report for publication. Other Members of the Pennington CALERIE Research Team: Steven Anton, PhD, Emily York-Crowe, MA, Catherine Champagne, PhD, Paula Geiselman, PhD, Michael Lefevre, PhD, Jennifer Howard, LDN, RD, Jana Ihrig, BSN, Brenda Dahmer, Anthony Alfonso, MS, Darlene Marquis, BS, Connie Murla, BS, Aimee Stewart, BS, Amanda Broussard, BS, and Vanessa Tarver, BS all from Pennington Biomedical Research Center, Louisiana State University, Baton Rouge. Acknowledgment: Our gratitude is extended to the excellent staffs of the Outpatient Clinic, Inpatient Clinic, Metabolic Kitchen, and Clinical Chemistry Laboratory. We also want to thank Claudia Van Skiver, LDN, RD Ochsner Clinic, Baton Rouge, La for developing the behavioral treatment manual and training the staff on how to use the HMR energy counting system. Our thanks also go to Health and Nutrition Technology, Carmel, Calif, for providing us with the HealthOne formula used in the study. Finally, our profound gratitude goes to all the volunteers who spent so much time participating in this very demanding research study. full text icon Full Text. Download PDF Top of Article Abstract Methods Results Comment Article Information References. Figure 1. Participant Flow in the Trial View Large Download. Figure 2. Absolute and Percentage Weight Loss by Group View Large Download. Figure 3. Fasting Plasma Glucose, Insulin, Dehydroepiandrosterone Sulfate, and Triiodothyronine Levels at Baseline, Month 3, and Month 6 View Large Download. Figure 4. Change in Core Body Temperature From Baseline to Month 6 Measured Over 23 Hours Inside a Metabolic Chamber Set to a Mean SD Temperature of Figure 5. Measured Hour Energy Expenditure, Sleep Energy Expenditure, and Fat-Free Mass at Month 6 View Large Download. Figure 6. Fasting Plasma Protein Carbonyls and DNA Damage Measured by the Comet Assay View Large Download. Table 1. Table 2. Weindruch R, Walford RL, Fligiel S, Guthrie D. The retardation of aging in mice by dietary restriction: longevity, cancer, immunity and lifetime energy intake. J Nutr. Roth GS, Ingram DK, Black A, Lane MA. Effects of reduced energy intake on the biology of aging: the primate model. Eur J Clin Nutr. Roth GS, Mattison JA, Ottinger MA, Chachich ME, Lane MA, Ingram DK. Aging in rhesus monkeys: relevance to human health interventions. Heilbronn LK, Ravussin E. Calorie restriction and aging: review of the literature and implications for studies in humans. Am J Clin Nutr. Ravussin E, Bogardus C. Relationship of genetics, age, and physical fitness to daily energy expenditure and fuel utilization. Leibel RL, Rosenbaum M, Hirsch J. Changes in energy expenditure resulting from altered body weight. N Engl J Med. Blanc S, Schoeller D, Kemnitz J. et al. Energy expenditure of rhesus monkeys subjected to 11 years of dietary restriction. J Clin Endocrinol Metab. DeLany JP, Hansen BC, Bodkin NL, Hannah J, Bray GA. Long-term calorie restriction reduces energy expenditure in aging monkeys. J Gerontol A Biol Sci Med Sci. Ballor DL. J Appl Physiol. Dulloo AG, Girardier L. Int J Obes Relat Metab Disord. McCarter R, Masoro EJ, Yu BP. Does food restriction retard aging by reducing the metabolic rate? Am J Physiol. McCarter RJ, Palmer J. Energy metabolism and aging: a lifelong study of Fischer rats. Selman C, Phillips T, Staib JL, Duncan JS, Leeuwenburgh C, Speakman JR. Energy expenditure of calorically restricted rats is higher than predicted from their altered body composition. Mech Ageing Dev. Harman D. Aging: a theory based on free radical radiation chemistry. J Gerontol. Chance B, Sies H, Boveris A. Hydroperoxide metabolism in mammalian organs. Physiol Rev. St-Pierre J, Buckingham JA, Roebuck SJ, Brand MD. Topology of superoxide production from different sites in the mitochondrial electron transport chain. J Biol Chem. Halliwell B, Gutteridge J. Free Radicals in Biology and Medicine. New York, NY: Oxford University Press; de Oliveira SL, Diniz DB, Amaya-Farfan J. Carbohydrate-energy restriction may protect the rat brain against oxidative damage and improve physical performance. Br J Nutr. Drew B, Phaneuf S, Dirks A. Effects of aging and caloric restriction on mitochondrial energy production in gastrocnemius muscle and heart. Am J Physiol Regul Integr Comp Physiol. Dubey A, Forster MJ, Lal H, Sohal RS. Effect of age and caloric intake on protein oxidation in different brain regions and on behavioral functions of the mouse. Arch Biochem Biophys. Sohal RS, Agarwal S, Candas M, Forster MJ, Lal H. Zainal TA, Oberley TD, Allison DB, Szweda LI, Weindruch R. Caloric restriction of rhesus monkeys lowers oxidative damage in skeletal muscle. FASEB J. Lee CK, Klopp RG, Weindruch R, Prolla TA. Gene expression profile of aging and its retardation by caloric restriction. Kayo T, Allison DB, Weindruch R, Prolla TA. Influences of aging and caloric restriction on the transcriptional profile of skeletal muscle from rhesus monkeys. Proc Natl Acad Sci U S A. Lane MA, Baer DJ, Tilmont EM. Energy balance in rhesus monkeys Macaca mulatta subjected to long-term dietary restriction. Roth GS, Lane MA, Ingram DK. Biomarkers of caloric restriction may predict longevity in humans. Fontana L, Meyer TE, Klein S, Holloszy JO. Long-term calorie restriction is highly effective in reducing the risk for atherosclerosis in humans. DeLany JP, Schoeller DA, Hoyt RW, Askew EW, Sharp MA. Where possible study personnel were blinded to the treatment assignment of the subjects. The energy intake required for weight maintenance during baseline and the subsequent energy deficit prescribed to achieve the desired caloric restriction were calculated from 4-week data including two day periods by doubly labeled water DLW. During the first DLW study B1 participants followed their usual diet at home. During the second DLW study B2 , participants were provided with a weight maintenance diet. Values from the animal literature for tissue gain or loss were used to assign energy values to weight changes as previously described [11] and adjustments were made to determine energy intake for weight maintenance. Individual energy requirements were then calculated as the average of total daily energy expenditure TDEE during B1 and the final energy intake for weight maintenance after adjustments during B2. During weeks 1—12 and 22—24 of the intervention, participants were provided with all meals prepared by the metabolic kitchen at the Center and based on individual energy intake targets. On weekdays, breakfast and dinner were eaten at the center. All lunches, snacks and weekend meals were packaged for take-out. During weeks 13—22 participants self-selected a diet based on their individual targets. During the self-selected feeding, compliance to the prescribed dietary intervention was monitored from self-reported food records and changes in body weight which were reviewed weekly during behavioral group or individual sessions. During these weekly meetings, participants learned cognitive-behavioral techniques on how to adhere to their meal and exercise plans. At least three of the five weekly exercise sessions were performed under supervision at the exercise facility of our center and heart rate monitor data was reviewed for compliance for all session conducted outside the center. The exercise program was implemented gradually and by week 6 all participants were expending the required Exercise energy expenditure was initially determined by indirect calorimetry and thereafter HR was used to assess compliance during all exercise sessions. The target energy cost was maintained at ±63 kcal per session for women and ± kcal per session for men throughout the entire intervention resulting in average exercise durations of 53±11 and 45±14 min per session for women and men, respectively. Besides the two baseline measurements, total daily energy expenditure TDEE was measured by day doubly labeled water during weeks 10—12 M3 and 22—24 M6 of the intervention. Briefly, subjects provided two urine samples before being dosed with labeled water 2. Urine samples collected at 1. On days 7 and 14 after dosing, subjects provided two additional timed urine samples. Each sample was analyzed for 18 O and 2 H abundance by isotope ratio mass spectrometry [7]. The isotopic enrichments of the post-dose urines compared with the pre-dose samples were used to calculate elimination rates k H and k O using linear regression and initial isotope dilution spaces were calculated by extrapolation to time 0. CO 2 production rate rCO 2 was calculated using the equations of Schoeller et al. Total energy expenditure was calculated by multiplying rCO 2 by the energy equivalent of CO 2 for an RQ of 0. For months 3 and 6, during the intervention when weight loss was observed, energy expenditure was calculated from rCO2 by using a metabolic fuel quotient derived from food intake, changes in body energy stores and conventional calorimetric relations corrected for the changes in fat mass FM and fat free mass FFM as previously described [11] , [16]. Metabolic weight was determined by the mean of two consecutive measurements obtained in the morning following a 12 h fast and morning void and corrected for the weight of a hospital gown. Whole body percent body fat was measured using DXA Hologics QDR A, Bedford, MA and FM and FFM were calculated from the percent body fat and the metabolic body weight. Sedentary EE 24h-EE was measured over 23 hours in a whole room indirect calorimeter as previously described [6] , [17]. At M3, LCD participants were fed so that energy intake was tightly matched to measured energy expenditure and provided the same meals at M6. Sleeping metabolic rate SMR was calculated between — am, when no motion was detected. Physical activity was estimated from daily energy expenditure by doubly labeled water and sleeping metabolic rate using two different calculations. Because of the inherent problem of using ratios when the two variables have an intercept not equal to zero [18] , we also expressed physical activity as the residual value of the regression between measured TDEE and measured SMR [19]. This value we termed Activity Related Energy Expenditure AREE , is positive for subjects with higher physical activity than average and negative for subjects with lower physical activity than average independent of metabolic body size. Because AREE is adjusted for metabolic body size SMR , this value is directly proportional to the amount of physical activity. Psychological testing included an assessment of health related quality of life. The Medical Outcomes Study Short-Form 36 Health Survey SF is a self-administered item questionnaire that measures health related quality of life. The validity and reliability of the SF have been established [12] , [13]. In the present study, the SF was used to measure vitality VT and physical functioning PF. Participants' raw scores were converted into scale scores ranging from 0 to , with higher scores representing better QOL or higher levels of functioning. Data in the text and tables are provided as means±SE. SAS Version 9. The change in variables from baseline to M3 and M6 and M3 and M6 were analyzed by repeated measures with treatment and time interactions and baseline values included as covariates. To control for type I error, statistical significance for all multiple comparisons was adjusted using the Tukey-Kramer method. Using the latter equation, predicted values for TDEE were generated at M3 and M6 using the equation with the actual measured FFM and FM, or actual weight or SMR. The partial coefficients for each model are reported and the differences between the measured and predicted TDEE values were calculated and analyzed using ANOVA. At baseline TDEE was not different between the four treatment groups Table 2. At M3, body weight, FM and FFM were reduced from baseline in all three intervention groups and remained stable in the control group. At the completion of the week study, body weight was reduced by 0. There was no difference in the change in TDEE from baseline at M3 and M6 in either CR or LCD. To determine if there was a metabolic adaptation to the CR intervention at M3 and M6 we compared the actual TDEE measured by DLW at each time point with the TDEE predicted from FFM and FM derived from the prediction equations generated at baseline and presented above. At M6, the differential between the observed and predicted values for TDEE remained negative however did not reach statistical significance for either group Table 2. Similar results were obtained when TDEE values were adjusted for weight loss instead of FFM and FM losses. We next adjusted TDEE for sedentary energy expenditure measured in a respiratory chamber 24h-EE or for SMR. This adjustment allows us to disentangle the effect of physical activity from the effect of sedentary metabolism in response to CR. This indicates a metabolic adaptation unrelated to sedentary energy expenditure and therefore resulting from decreased habitual or voluntary physical activity. The reduction in PAL was no longer evident with further weight loss at M6 in CR or weight loss maintenance in LCD. According to the SF survey, all treatment groups, but not the control group, reported improvement in physical functioning with the intervention. Vitality was not different from baseline in any treatment group and either time point. In response to caloric restriction there is an abrupt change from a state of energy balance weight maintenance to a negative imbalance, which eventually will reach a new equilibrium at a lower body mass when the decline in energy expenditure is maintained at a level equivalent to the energy intake. Whether the decline in energy expenditure is equal or larger, than the reduction in metabolic mass is still debated. Several reports suggest that despite weight stability, the reduction in energy expenditure can be lower than one would expect for the new metabolic weight and composition [20] — [23]. Additionally the role of exercise on the metabolic adjustments to CR interventions is not known. Now for the first time, we objectively characterized the response in all the components of daily energy expenditure to caloric restriction by combining doubly labeled water and indirect calorimetry Figure 4. To exclude the contribution of sedentary energy expenditure the largest component of daily energy expenditure , we adjusted TDEE for sedentary energy expenditure 24h-EE and SMR and observed that measured TDEE was significantly less than predicted at both month 3 and month 6 of CR. Together, this data indicates that TDEE is reduced with caloric restriction and is likely the result of a metabolic adaptation in the sedentary state accompanied by a reduction in activity-related energy expenditure and reduced levels of physical activity Figure 3. Total daily energy expenditure TDEE is measured by doubly labeled water over a 2-week period whereas sedentary h energy expenditure 24h-EE is measured in a respiratory chamber. The changes in total daily energy expenditure after 3 and 6 months of CR Bottom Panel are shown and those representing a metabolic adaptation larger than due to weight loss are highlighted in grey. The concept of an adaptation in metabolic rate in response to caloric restriction defined as reduction in energy expenditure that is more than would be expected on the basis of the loss of metabolic mass was proposed by Keys et al in the 's [8]. Behaviorally, a response to the semi starvation was also a tremendous decrease in physical activity. Studies in obese individuals have also reported a metabolic adaptation measured by RMR adjusted for body composition with weight loss [25] — [27]. These adaptations in metabolic rate could be explained by an improved metabolic efficiency of the skeletal muscle or as also postulated, due to a reduction in physical activity with weight loss [28]. The energy cost of physical activity is proportional to body weight. Therefore, this component of energy expenditure decreases with weight loss even in the absence of a reduction in physical activity. A decrease in spontaneous physical activity has been reported in some [29] but not all weight loss studies [9] , [10] , [21] including our own caloric restriction study [7]. With regard to free-living energy expenditure, two studies of CR in non-obese humans suggest that after accounting for changes in body energy stores, a reduction in TDEE was partly due to lower levels of physical activity PAL or improved energy efficiency of physical activity at the new body weight and body composition [30] , [31]. Our data supports the concept that in addition to the metabolic adaptation, reduced energy expenditure with CR is also due in part to lower physical activity level, i. Despite the observed decline in physical activity, self-assessed physical functioning by the quality of life measure SF was significantly improved in the CR group at month 3 and in all intervention groups at month 6. Physical functioning has been shown to be related to physical activity level [33] therefore the observed reduction in physical activity in response to CR maybe an unconscious phenomenon used by individuals to conserve energy during energy deficit. If weight relapse does occur in part as a result of a reduced metabolic rate in the weight reduced state, then perhaps the combination of CR and exercise may be the best choice of intervention to prevent weight regain in overweight and obese individuals. Certainly, more than 20 years ago, Pavlou observed that exercise during a CR-induced weight loss program was essential for success of weight loss maintenance [34]. Since then others have shown with doubly labeled water studies that weight stability following weight loss is sustained by higher levels of activity related energy expenditure and free-living physical activity [35] , [36]. To our knowledge no studies have prospectively studied the energetic adjustments of CR only versus CR in conjunction with exercise during weight loss and weight loss maintenance. Whether or not an individual responds to weight loss with a metabolic adaptation has long-term importance for weight maintenance because there is recent data indicating that the metabolic adjustments occurring as a result of CR and weight loss are maintained for up to 6 years following the weight loss [22]. The individual group data for CR and LCD in our study may support this viewpoint since we observed a metabolic adaptation early M3 but a return towards baseline values after an additional 3 months M6 of weight loss CR or weight stability LCD. We could also conclude that failure to detect a statistically significant adaptation at month 6 however, may be due to limitations in sample size. This is probably why we did observe a significant metabolic adaptation at both 3 and 6 months of intervention when combining the CR and LCD groups. In this study, we combined two state of the art methods indirect calorimetry and doubly labeled water for quantifying precisely the complete energy expenditure response to caloric restriction in non-obese individuals. This report provides further evidence that a metabolic adaptation in response to CR can be found in the free-living situation as well. This adaptation comprises not only a reduction in cellular respiration energy cost of maintaining cells, organs and tissue alive but also a decrease in free-living activity thermogenesis. These observations are of importance to understand the progressive resistance to weight loss seen in so many studies in which weight plateaus after 6—12 months of caloric restriction despite self-declared adherence to a hypocaloric dietary prescription. Furthermore, our data shed some light on lifestyle change interventions that combining diet and physical activities are probably more successful in maintaining weight loss longer term. The authors thank the remaining members of Pennington CALERIE Research Team including: Steven Smith, Enette Larson-Meyer, Steve Anton, Julia Volaufova, Marlene Most, Tuong Nguyen, Frank Greenway, Emily York-Crow, Catherine Champagne, Brenda Dahmer, Andy Deutsch, Paula Geiselman, Jennifer Howard, Jana Ihrig, Michael Lefevre, Darlene Marquis, Connie Murla, Anthony Alfonso, Sabrina Yang, Robbie Durand, Sean Owens, Aimee Stewart and Vanessa Tarver. Our gratitude is extended to the excellent staffs of the Inpatient Clinic and Metabolic Kitchen. Finally, our profound gratitude goes to all the volunteers who spent so much time in participating in this very demanding research study. Conceived and designed the experiments: DAW ER. Performed the experiments: LMR LKH CKM Ld JPD ER. Analyzed the data: DAW JPD ER. Wrote the paper: LMR LKH CKM Ld ER. Browse Subject Areas? Click through the PLOS taxonomy to find articles in your field. Article Authors Metrics Comments Media Coverage Reader Comments Figures. Abstract Background Metabolic and behavioral adaptations to caloric restriction CR in free-living conditions have not yet been objectively measured. Methodology and Principal Findings Forty-eight Conclusions For the first time we show that in free-living conditions, CR results in a metabolic adaptation and a behavioral adaptation with decreased physical activity levels. Trial Registration ClinicalTrials. Introduction Daily energy expenditure has three major components: resting metabolic rate, the thermic effect of food and the energy cost of physical activity. Methods Ethics Statement This study was conducted according to the principles expressed in the declaration of Helsinki. Participants Of the individuals screened for the study, were excluded were ineligible; 91 withdrew during screening Figure 1. Download: PPT. Figure 1. Flow of participants through the Pennington Phase 1 CALERIE trial. Table 1. Physical characteristics of 48 men and women in weight maintenance at baseline. Figure 2. Experimental design A and body weight and composition changes B at the completion of the study. Baseline weight-maintenance energy requirements The energy intake required for weight maintenance during baseline and the subsequent energy deficit prescribed to achieve the desired caloric restriction were calculated from 4-week data including two day periods by doubly labeled water DLW. Diet and behavioral intervention During weeks 1—12 and 22—24 of the intervention, participants were provided with all meals prepared by the metabolic kitchen at the Center and based on individual energy intake targets. Doubly labeled water Besides the two baseline measurements, total daily energy expenditure TDEE was measured by day doubly labeled water during weeks 10—12 M3 and 22—24 M6 of the intervention. Body composition Metabolic weight was determined by the mean of two consecutive measurements obtained in the morning following a 12 h fast and morning void and corrected for the weight of a hospital gown. Sedentary energy expenditure Sedentary EE 24h-EE was measured over 23 hours in a whole room indirect calorimeter as previously described [6] , [17]. Physical activity Physical activity was estimated from daily energy expenditure by doubly labeled water and sleeping metabolic rate using two different calculations. Psychological testing Psychological testing included an assessment of health related quality of life. Statistical analysis Data in the text and tables are provided as means±SE. Results Total daily energy expenditure at baseline At baseline TDEE was not different between the four treatment groups Table 2. Table 2. Body weight and composition changes At M3, body weight, FM and FFM were reduced from baseline in all three intervention groups and remained stable in the control group. Effect of CR on TDEE adjusted for body composition To determine if there was a metabolic adaptation to the CR intervention at M3 and M6 we compared the actual TDEE measured by DLW at each time point with the TDEE predicted from FFM and FM derived from the prediction equations generated at baseline and presented above. Effect of CR on physical activity We next adjusted TDEE for sedentary energy expenditure measured in a respiratory chamber 24h-EE or for SMR. Figure 3. The effect of caloric restriction on AREE change in TDEE at M3 and M6 after adjusting for SMR a measure of sedentary energy expenditure. Effect of CR on Physical Functioning and Vitality According to the SF survey, all treatment groups, but not the control group, reported improvement in physical functioning with the intervention. Discussion In response to caloric restriction there is an abrupt change from a state of energy balance weight maintenance to a negative imbalance, which eventually will reach a new equilibrium at a lower body mass when the decline in energy expenditure is maintained at a level equivalent to the energy intake. Figure 4. |
| Servicios Personalizados | Metabolic adaptation was also observed over 24 hours but not during sleep in participants in the very low-calorie diet group who were weight stable when measured at months 3 and 6. Possible explanations for the lack of significant adaptation during sleep in this group include a smaller sample size and the fact that 2 men were regaining weight at month 6. Interestingly, core body temperature and fasting insulin level at month 3 were not changed in this group, despite their having the largest weight loss. Whether metabolic adaptation following calorie restriction persists during weight maintenance remains to be determined in humans. Spontaneous physical activity and the thermic effect of food were not changed from baseline. Therefore, these 2 factors can only account for a minor part of the metabolic adaptation. The inverse relationship between increased free radical production, oxidative damage to DNA, and maximum life span has been demonstrated in numerous studies. Contrary to our hypothesis, the reduction in DNA damage was not associated with reduced total or adjusted oxygen consumption in the metabolic chamber. Considering the lack of correlation between these parameters and the lack of response in protein carbonylation associated with calorie restriction, we are hesitant to conclude that calorie restriction reduces oxidative stress overall. Clearly, more studies investigating different measures of oxidative stress, such as hour urinary excretion of 8-oxodG, are required. Furthermore, other factors such as mitochondrial function may play an important role in oxidative stress. For example, the role of uncoupling proteins in protection against ROS production, independent of changes in proton kinetics and mitochondrial respiration, has recently been demonstrated. The results of this study show that prolonged calorie restriction by diet or by a combination of diet and exercise was successfully implemented as evidenced by reduced weight, fat mass, fasting serum insulin levels, and core body temperature. This study is unique in that individual energy requirements were carefully measured at baseline and individualized diet goals were determined for each study participant. Finally, this study confirms previous findings that calorie restriction results in a decline in DNA damage. However, longer-term studies are required to determine if these effects are sustained and whether they have an effect on human aging. Corresponding Author: Eric Ravussin, PhD, Pennington Biomedical Research Center, Louisiana State University, Perkins Rd, Baton Rouge, LA ravusse pbrc. Author Contributions: Dr Ravussin had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis. Study concept and design : DeLany, Larson-Meyer, Volaufova, Greenway, Deutsch, Williamson, Ravussin. Acquisition of data : Heilbronn, de Jonge, Frisard, DeLany, Larson-Meyer, Nguyen, Martin, Most, Smith, Williamson, Ravussin. Analysis and interpretation of data : Heilbronn, de Jonge, DeLany, Rood, Volaufova, Deutsch, Williamson, Ravussin. Drafting of the manuscript : Heilbronn, Rood, Martin, Most, Deutsch, Williamson, Ravussin. Critical revision of the manuscript for important intellectual content : de Jonge, Frisard, DeLany, Larson-Meyer, Nguyen, Martin, Volaufova, Greenway, Smith, Deutsch, Williamson, Ravussin. Administrative, technical, or material support : Heilbronn, de Jonge, DeLany, Rood, Nguyen, Martin, Greenway, Smith, Williamson, Ravussin. Study supervision : Heilbronn, Frisard, Larson-Meyer, Most, Greenway, Deutsch, Williamson, Ravussin. Role of the Sponsor: The funding agency had no role in the analysis or interpretation of the data or in the decision to submit the report for publication. Other Members of the Pennington CALERIE Research Team: Steven Anton, PhD, Emily York-Crowe, MA, Catherine Champagne, PhD, Paula Geiselman, PhD, Michael Lefevre, PhD, Jennifer Howard, LDN, RD, Jana Ihrig, BSN, Brenda Dahmer, Anthony Alfonso, MS, Darlene Marquis, BS, Connie Murla, BS, Aimee Stewart, BS, Amanda Broussard, BS, and Vanessa Tarver, BS all from Pennington Biomedical Research Center, Louisiana State University, Baton Rouge. Acknowledgment: Our gratitude is extended to the excellent staffs of the Outpatient Clinic, Inpatient Clinic, Metabolic Kitchen, and Clinical Chemistry Laboratory. We also want to thank Claudia Van Skiver, LDN, RD Ochsner Clinic, Baton Rouge, La for developing the behavioral treatment manual and training the staff on how to use the HMR energy counting system. Our thanks also go to Health and Nutrition Technology, Carmel, Calif, for providing us with the HealthOne formula used in the study. Finally, our profound gratitude goes to all the volunteers who spent so much time participating in this very demanding research study. full text icon Full Text. Download PDF Top of Article Abstract Methods Results Comment Article Information References. Figure 1. Participant Flow in the Trial View Large Download. Figure 2. Absolute and Percentage Weight Loss by Group View Large Download. Figure 3. Fasting Plasma Glucose, Insulin, Dehydroepiandrosterone Sulfate, and Triiodothyronine Levels at Baseline, Month 3, and Month 6 View Large Download. Figure 4. Change in Core Body Temperature From Baseline to Month 6 Measured Over 23 Hours Inside a Metabolic Chamber Set to a Mean SD Temperature of Figure 5. Measured Hour Energy Expenditure, Sleep Energy Expenditure, and Fat-Free Mass at Month 6 View Large Download. Figure 6. Fasting Plasma Protein Carbonyls and DNA Damage Measured by the Comet Assay View Large Download. Table 1. Table 2. Weindruch R, Walford RL, Fligiel S, Guthrie D. The retardation of aging in mice by dietary restriction: longevity, cancer, immunity and lifetime energy intake. J Nutr. Roth GS, Ingram DK, Black A, Lane MA. Effects of reduced energy intake on the biology of aging: the primate model. Eur J Clin Nutr. Roth GS, Mattison JA, Ottinger MA, Chachich ME, Lane MA, Ingram DK. Aging in rhesus monkeys: relevance to human health interventions. Heilbronn LK, Ravussin E. Calorie restriction and aging: review of the literature and implications for studies in humans. Am J Clin Nutr. Ravussin E, Bogardus C. Relationship of genetics, age, and physical fitness to daily energy expenditure and fuel utilization. Leibel RL, Rosenbaum M, Hirsch J. Changes in energy expenditure resulting from altered body weight. N Engl J Med. Blanc S, Schoeller D, Kemnitz J. et al. Energy expenditure of rhesus monkeys subjected to 11 years of dietary restriction. J Clin Endocrinol Metab. DeLany JP, Hansen BC, Bodkin NL, Hannah J, Bray GA. Long-term calorie restriction reduces energy expenditure in aging monkeys. J Gerontol A Biol Sci Med Sci. Ballor DL. J Appl Physiol. Dulloo AG, Girardier L. Int J Obes Relat Metab Disord. McCarter R, Masoro EJ, Yu BP. Does food restriction retard aging by reducing the metabolic rate? Am J Physiol. McCarter RJ, Palmer J. Energy metabolism and aging: a lifelong study of Fischer rats. Selman C, Phillips T, Staib JL, Duncan JS, Leeuwenburgh C, Speakman JR. Energy expenditure of calorically restricted rats is higher than predicted from their altered body composition. Mech Ageing Dev. Harman D. Aging: a theory based on free radical radiation chemistry. J Gerontol. Chance B, Sies H, Boveris A. Hydroperoxide metabolism in mammalian organs. Physiol Rev. St-Pierre J, Buckingham JA, Roebuck SJ, Brand MD. Topology of superoxide production from different sites in the mitochondrial electron transport chain. J Biol Chem. Halliwell B, Gutteridge J. Free Radicals in Biology and Medicine. New York, NY: Oxford University Press; de Oliveira SL, Diniz DB, Amaya-Farfan J. Carbohydrate-energy restriction may protect the rat brain against oxidative damage and improve physical performance. Br J Nutr. Drew B, Phaneuf S, Dirks A. Effects of aging and caloric restriction on mitochondrial energy production in gastrocnemius muscle and heart. Am J Physiol Regul Integr Comp Physiol. Dubey A, Forster MJ, Lal H, Sohal RS. Effect of age and caloric intake on protein oxidation in different brain regions and on behavioral functions of the mouse. Arch Biochem Biophys. Sohal RS, Agarwal S, Candas M, Forster MJ, Lal H. Zainal TA, Oberley TD, Allison DB, Szweda LI, Weindruch R. Caloric restriction of rhesus monkeys lowers oxidative damage in skeletal muscle. FASEB J. Lee CK, Klopp RG, Weindruch R, Prolla TA. Gene expression profile of aging and its retardation by caloric restriction. Kayo T, Allison DB, Weindruch R, Prolla TA. Influences of aging and caloric restriction on the transcriptional profile of skeletal muscle from rhesus monkeys. Caloric restriction has been recently touted as one of the biggest anti-aging secrets behind living for over years. In this article, current knowledge on caloric restriction is discussed in the context of aging , health, and well-being. Its effects on metabolism are briefly discussed, followed by benefits, types, and safety, as well as tips on best practices for practicing caloric restriction. Caloric restriction refers to the practice of lowering dietary energy intake below prior energy requirements in the absence of malnutrition. The goal of caloric restriction is to lower the resting metabolic rate. Over time, it begins to shift the metabolism to a lower energy state, meaning that less energy is needed to sustain body functions during rest. Metabolism, Rate of Living and Lifespan. Theoretically, the less energy the body expends to carry out its functions, the longer the lifespan of the organism. Uncoupling Metabolic Rate and Overall Energy Expenditure. The amount of energy consumed overall is not the same as the resting metabolic rate. Resting or basal metabolic rate is used to measure the efficiency of energy production at any given point. If the resting metabolic rate is higher on average, more energy is used to perform any cellular functions, including during physical activity, digestion, and storage of energy substrates i. A chronically high resting metabolic rate is a sign of mitochondrial inefficiency [4] , which typically lends itself to problematic energy production and utilization in the long run. Oxidative Stress, Aging, and Metabolic Efficiency. The rate of living theory is connected to many other theories of aging pertaining to mitochondrial oxidative stress. The resting metabolic rate can increase the level of oxidation that occurs as well as the degree of free radicals produced as a result. Over time and with aging, more energy is expended, more damage to cells can accumulate, and regulatory antioxidant mechanisms become less functional. Healthy, aged individuals are known to have a lower resting metabolic rate, which is a possible compensation for diminished cellular functions after a lifetime of oxidative stress accumulation. Disease and Metabolic Rate. Secondary aging as a result of disease or life stressors impacts cellular function in a similar way to that of ordinary aging. Initially, they serve to increase resting metabolic rate, oxidative stress levels, and free radical production. In the later terminal stages of the disease, the resting metabolic rate slows down and is comparable to that of advanced aging. Factors Influencing RMR. Resting metabolic rate can be increased by many factors, including:. Balanced Caloric Restriction Promotes Efficient Energy Production. Restricting calories lowers the supply of substrates for energy production, which eventually reduces the rate at which energy is produced and used at rest. A lower RMR in this context eventually promotes more efficient cellular energy production, which facilitates a better regulation of oxidative stress, lower free radical damage, and potentially, a slower aging process. Reduced Calorie Intake Positively Redistributes Energy Expenditure. Caloric restriction promotes both a reduction in and a redistribution of energy expenditure. While overall energy requirements eventually reduce, less energy is also spent on digestion due to a lower intake of calories, which frees up more energy for physical activity. Caloric restriction has been studied in the context of historical food restriction, long-term trials, and animal studies, all of which have shown promising effects with respect to aging and metabolic health. There does not seem to be a caloric restriction method that poses more benefit over another method. Thus, the best method depends on the needs of the individual. The Difference Appears Minimal Between Time-Restricted Eating and Caloric Restriction. In a small-scale trial on participants, the differences between caloric restriction achieved either through dietary calorie control or time-restricted eating were minimal. Participants who limited consumption between 8 am and 4 pm lost 8kg on average over the course of a year, whereas those who limited their calorie intake lost 6. All other health outcomes were similarly beneficial. This decline was significantly greater than that observed in the non-compliant group [-6,2 ± 1. FFM did not change in any of the two groups. Conclusions: compliant women showed a significant reduction in both absolute and adjusted REE, which together with the loss of correlation between REE and FFM at the end of the intervention suggests a metabolic adaptation. Palabras clave : Energy expenditure; Adaptive thermogenesis; Calorie restriction; Obesity. Todo el contenido de esta revista, excepto dónde está identificado, está bajo una Licencia Creative Commons. Mi SciELO Servicios personalizados. |
Video
The longevity benefits of proper protein intake and strength training - Rhonda Patrick \u0026 Peter Attia Calorie restriction CR is the most potent, non-pharmacological intervention annd support metabolic health. The effects of caloruc restriction exceed weight loss. Consistent throughout Homemade remedies for hair growth studies, calorie restriction induces a reduction in energy expenditure that is larger than the loss of metabolic mass, i. fat-free mass and fat mass, can explain. Per prevailing theories of mammalian aging, this disproportionate reduction in metabolic rate, defined as metabolic adaptation, reduces oxidative damage and thereby delays age-associated declines in physiological function.Caloric restriction and energy expenditure -
The presence of different fatty acids in the diet and lifestyle factors, such as exercise and obesity, influence the incorporation of the acids into different tissues and erythrocyte membranes [ 21 ]; the erythrocyte content of the omega-3 and omega-6 essential fatty acids were maintained or even increased after the six weeks of CR.
The possible lack of fatty acid availability during six-week CR did not affect fatty acid content in erythrocyte membranes. Additionally, the CR lessened oxidative damage in plasma lipids. It has been pointed out that a CR decreases mitochondrial electron flow as well as proton leaks in mammalian cells, and attenuates muscle damage caused by intracellular reactive oxygen species [ 4 , 27 ].
We actually provide evidence that a CR reduces oxidative damage in circulating lipids and blood vessels along with reducing circulating triglyceride and cholesterol levels.
The CR intervention significantly reduced body, trunk, arm, and leg weights; it mainly reduced body fat mass, but a small yet significant reduction in lean body mass was also observed.
Reducing body weight is a goal for many athletes [ 25 ]. Either rapid or gradual body weight reduction techniques have been used to control body weight in athletes with varied results on physical performance.
Aerobic endurance capacity decreases after rapid body weight reduction. It also causes detrimental effects in a min treadmill time-trial session in temperate conditions [ 29 ]; affects health, muscle performance, and energy; and alters perceived exertion and dynamic postural control [ 30 ].
Severe CR also results in a large reduction in body mass that appears to be mostly explained by a rapid reduction in body water stores [ 31 ]. Gradual body weight reduction via a smaller CR induces more consistent body weight losses over a CR period of more than one week. Short-term hypoenergetic weight loss programs could maintain lean body mass in young healthy athletes who have a protein intake around 2.
It has been demonstrated that VO2max is increased after a body weight reduction [ 25 ]; in this sense, we have detected an improvement in physical performance markers, such as heart rate, lactate levels, fatigue perception Borg index , and the energy expenditure required to run a meter, that are not dependent exclusively on changes in total body mass [ 33 ].
Previous studies with well-balanced diets or even after one month of consuming functional beverage supplements provided no evidence suggesting that these nutritional habits have an effect on physical performance parameters such as lactate levels [ 9 ].
Additionally, we observed a decrease in lean body mass as a consequence of the CR; however, this decrease did not involve any impairment of physical performance parameters.
This fact could indicate that athletes should have an ideal lean body mass in order to produce maximal physical performance. To sum up, higher muscle mass does not necessarily indicate better physical performance.
Furthermore, we detected several changes in energy expenditure and in energy efficiency as a consequence of the CR; this fact could be explained by considering that CR might cause increased mitochondria efficiency [ 4 ]. Moreover, the CR reduced plasma triglycerides by Physical performance parameters, such as heart rate, lactate levels, fatigue perception Borg index , were significantly improved as a consequence of the CR, which ameliorated the onset of the anaerobic phase of exercise.
Moreover, the CR decreased the energy expenditure required to run one meter and improved energy efficiency. However, when implementing a CR, a micronutrient supplement should also be considered.
Bodkin NL, et al. Mortality and morbidity in laboratory-maintained rhesus monkeys and effects of long-term dietary restriction. J Gerontol A Biol Sci Med Sci.
Article PubMed Google Scholar. Mattson MP, Wan R. Beneficial effects of intermittent fasting and caloric restriction on the cardiovascular and cerebrovascular systems. J Nutr Biochem. Article CAS PubMed Google Scholar. Trexler ET, Smith-Ryan AE, Norton LE. Metabolic adaptation to weight loss: implications for the athlete.
J Int Soc Sports Nutr. Article PubMed PubMed Central Google Scholar. Lopez-Lluch G, et al. Calorie restriction induces mitochondrial biogenesis and bioenergetic efficiency.
Proc Natl Acad Sci U S A. Article CAS PubMed PubMed Central Google Scholar. Ishihara H, et al. Effects of dietary restriction on physical performance in mice.
J Physiol Anthropol Appl Hum Sci. Article Google Scholar. Larson-Meyer DE, et al. Caloric restriction with or without exercise: the fitness versus fatness debate.
Med Sci Sports Exerc. Ferguson LM, et al. Effects of caloric restriction and overnight fasting on cycling endurance performance. J Strength Cond Res. Dungan CM, Li J, Williamson DL. Caloric restriction normalizes obesity-induced alterations on regulators of skeletal muscle growth signaling.
Capo X, et al. Effects of dietary almond- and olive oil-based docosahexaenoic acid- and vitamin E-enriched beverage supplementation on athletic performance and oxidative stress markers.
Food Funct. Ainsworth BE, et al. Compendium of physical activities: an update of activity codes and MET intensities. Farrán A, Zamora R, Cervera P. Tablas de Composición de Alimentos del CESNID Food Composition Tables of CESNID. E; Google Scholar.
Rothney MP, et al. Precision of GE lunar iDXA for the measurement of total and regional body composition in nonobese adults. J Clin Densitom. Nana A, et al.
Effects of daily activities on dual-energy X-ray absorptiometry measurements of body composition in active people. Int J Sport Nutr Exerc Metab. Huygens W, et al. Body composition estimations by BIA versus anthropometric equations in body builders and other power athletes.
J Sports Med Phys Fitness. CAS PubMed Google Scholar. Jebb SA, et al. Validity of the leg-to-leg bioimpedance to estimate changes in body fat during weight loss and regain in overweight women: a comparison with multi-compartment models.
Int J Obes. Article CAS Google Scholar. Montagnani M, et al. Relevance of hydration state of the fat free mass in estimating fat mass by body impedance analysis. Appl Radiat Isot. Weir JB. New methods for calculating metabolic rate with special reference to protein metabolism.
J Physiol. Mora RJF. Soporte nutricional especial. Panamericana: Buenos Aires; Sureda A, et al. Influence of an antioxidant vitamin-enriched drink on pre- and post-exercise lymphocyte antioxidant system.
Ann Nutr Metab. Martorell M, et al. Docosahexaenoic acid supplementation promotes erythrocyte antioxidant defense and reduces protein nitrosative damage in male athletes.
Lepage G, Roy CC. Direct transesterification of all classes of lipids in a one-step reaction. J Lipid Res. Folch J, Lees M, Sloane Stanley GH. A simple method for the isolation and purification of total lipides from animal tissues. J Biol Chem. Mettler S, Mitchell N, Tipton KD.
Increased protein intake reduces lean body mass loss during weight loss in athletes. Fogelholm M. Effects of bodyweight reduction on sports performance. Sports Med. Dudgeon WD, Kelley EP, Scheett TP. In a single-blind, matched group design: branched-chain amino acid supplementation and resistance training maintains lean body mass during a caloric restricted diet.
Annual Review of Nutrition. Skyhorse Publishing Inc. Retrieved 30 September September June July Endocrine Practice. Lifestyle Management: Standards of Medical Care in Diabetes ".
Diabetes Care. May Diabetes Care Professional society guidelines. BMC Pregnancy and Childbirth. The Biology of Human Starvation, The American Journal of Clinical Nutrition. Journal of the American Dietetic Association. Clinics in Geriatric Medicine. A Systematic Review and Meta-Analysis of Randomized Controlled Trials".
Journal of the American College of Cardiology. S2CID Ageing Research Reviews. Nutritional interventions modulating aging and age-associated diseases. The biology of human starvation 2 vols. of Minnesota Press.
Intensive Care Medicine. Retrieved May 17, The New York Times. January Nature Communications. Bibcode : NatCo Retrieved 15 February Bibcode : Natur. The Journals of Gerontology.
Series A, Biological Sciences and Medical Sciences. March Experimental Gerontology. Data are presented as mean SEM. SAS version 9. Changes from baseline at month 3 and month 6 were analyzed by a repeated-measures design approach with respect to treatment and time and treatment × time interactions, with baseline values included as covariates.
Data were also analyzed without adjustment for baseline values. Since results by both approaches were similar, we present only the models with adjustment for baseline values.
Figure 2 illustrates the weight changes in both percent of initial weight and in kilograms; however, all statistical analyses were performed on absolute changes. Differences between predicted and measured energy expenditure were calculated and analyzed by analysis of variance. A normalizing and variance-stabilizing logarithmic transformation was applied to the calculated tail moments for the comet assay.
Power and sample size calculations were carried out for the primary end point, hour energy expenditure. Sample size was calculated using different levels of baseline hour energy expenditure, assuming a conservative coefficient of variation 7. Two individuals withdrew prior to completion of the study: 1 from the control group at week 4 personal reasons and 1 from the very low-calorie diet group at week 5 lost to follow-up Figure 1.
Baseline characteristics of the study participants are listed in Table 1. Percent weight loss from baseline to month 6 in each group was as follows: controls, —1.
There were no significant changes in fasting glucose or DHEAS levels in any group. Participants randomized to calorie restriction and calorie restriction with exercise had reduced mean hour core body temperature Figure 4 at month 6.
There was no change in core body temperature in the control or very low-calorie diet groups. Compared with predicted hour energy expenditure values, measured daily hour energy expenditure at months 3 and 6 were unchanged in controls and significantly reduced in the calorie restriction, calorie restriction with exercise, and very low-calorie diet groups Table 2.
These data are shown in Table 2 as actual hour energy expenditure minus predicted energy expenditure. Individual data points at month 6 and the baseline regression line for hour energy expenditure vs FFM are presented in Figure 5.
Since the predicted hour energy expenditure data were derived from just 48 participants, we also compared the hour energy expenditure data from each group to individuals men; women; mean age, 32 years; mean weight, Similar to hour energy expenditure, measured sleeping energy expenditure was lower than predicted at months 3 and 6 in the calorie restriction and calorie restriction with exercise groups Table 2 and Figure 5.
There were no significant changes from baseline in the level of spontaneous physical activity or in the thermic effect of food expressed as percentage of energy intake. Serum protein carbonyl concentrations were not changed from baseline to month 6 in any group Figure 6. This decrease was not statistically different compared with the controls when the 3 treatment groups were combined.
We found no significant relationships between the changes in DNA damage and changes in adjusted energy expenditure, fat mass, or body weight.
Since the pioneering experiments by McCay and Maynard, 37 it has been known that calorie restriction extends life span in rodents and other lower species. However, little is known about the long-term effects of calorie restriction in humans.
In the current study, we examined the effects of 6-month calorie restriction on biomarkers of calorie restriction, energy expenditure, and oxidative stress in humans. Our results indicate that prolonged calorie restriction caused: 1 a reversal in 2 of 3 previously reported biomarkers of longevity fasting insulin level and core body temperature ; 2 a metabolic adaptation decrease in energy expenditure larger than expected on the basis of loss of metabolic mass associated with lower thyroid hormone concentrations; and 3 a reduction in DNA fragmentation, reflecting less DNA damage.
Numerous biomarkers of calorie restriction have been identified in rodents including temperature, and DHEAS, glucose, and insulin levels. Roth et al 26 recently observed that body temperature and insulin and DHEAS levels were also altered in monkeys subjected to calorie restriction, validating their usefulness as biomarkers in longer-lived species.
Importantly, they also showed that these parameters were altered in longer-lived men. These findings support the role of these factors as biomarkers of longevity in humans. Similar to the primate model, we observed significantly reduced fasting insulin levels and core body temperatures in the calorie restriction and calorie restriction with exercise groups.
However, DHEAS and fasting glucose levels were unchanged by the interventions. Fasting glucose level is not consistently altered by prolonged calorie restriction in primates, and thus we question whether fasting glucose level is useful as a biomarker in longer-lived species.
On the other hand, Fontana et al 27 observed that fasting glucose and insulin levels were substantially reduced in calorie restriction participants who had been following self-prescribed nutritionally adequate calorie restriction diets for 6 years.
Previous studies are inconclusive regarding reductions in metabolic rate following prolonged calorie restriction. In rodents receiving a restricted energy diet for 6 months 11 or the entire life span, 12 adjusted resting energy expenditure was not different from controls.
In a starvation study by Keys et al, 39 adjusted resting energy expenditure was decreased, which coincided with a reduction in body temperature indicating a real metabolic adaptation. In this study, we observed a metabolic adaptation over 24 hours in sedentary conditions and during sleep following 6 months of calorie restriction.
The metabolic adaptation in the calorie restriction with exercise group was similar to that observed in the calorie restriction group, suggesting that energy deficit rather than calorie restriction itself is driving the decrease in energy expenditure. Importantly, the metabolic adaptations were closely paralleled by a drop in thyroid hormone plasma concentrations confirming the importance of the thyroid pathway as a determinant of energy metabolism.
Metabolic adaptation was also observed over 24 hours but not during sleep in participants in the very low-calorie diet group who were weight stable when measured at months 3 and 6. Possible explanations for the lack of significant adaptation during sleep in this group include a smaller sample size and the fact that 2 men were regaining weight at month 6.
Interestingly, core body temperature and fasting insulin level at month 3 were not changed in this group, despite their having the largest weight loss. Whether metabolic adaptation following calorie restriction persists during weight maintenance remains to be determined in humans.
Spontaneous physical activity and the thermic effect of food were not changed from baseline. Therefore, these 2 factors can only account for a minor part of the metabolic adaptation.
The inverse relationship between increased free radical production, oxidative damage to DNA, and maximum life span has been demonstrated in numerous studies. Contrary to our hypothesis, the reduction in DNA damage was not associated with reduced total or adjusted oxygen consumption in the metabolic chamber.
Considering the lack of correlation between these parameters and the lack of response in protein carbonylation associated with calorie restriction, we are hesitant to conclude that calorie restriction reduces oxidative stress overall.
Clearly, more studies investigating different measures of oxidative stress, such as hour urinary excretion of 8-oxodG, are required. Furthermore, other factors such as mitochondrial function may play an important role in oxidative stress.
For example, the role of uncoupling proteins in protection against ROS production, independent of changes in proton kinetics and mitochondrial respiration, has recently been demonstrated. The results of this study show that prolonged calorie restriction by diet or by a combination of diet and exercise was successfully implemented as evidenced by reduced weight, fat mass, fasting serum insulin levels, and core body temperature.
This study is unique in that individual energy requirements were carefully measured at baseline and individualized diet goals were determined for each study participant. Finally, this study confirms previous findings that calorie restriction results in a decline in DNA damage.
However, longer-term studies are required to determine if these effects are sustained and whether they have an effect on human aging. Corresponding Author: Eric Ravussin, PhD, Pennington Biomedical Research Center, Louisiana State University, Perkins Rd, Baton Rouge, LA ravusse pbrc.
Author Contributions: Dr Ravussin had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis. Study concept and design : DeLany, Larson-Meyer, Volaufova, Greenway, Deutsch, Williamson, Ravussin.
Acquisition of data : Heilbronn, de Jonge, Frisard, DeLany, Larson-Meyer, Nguyen, Martin, Most, Smith, Williamson, Ravussin. Analysis and interpretation of data : Heilbronn, de Jonge, DeLany, Rood, Volaufova, Deutsch, Williamson, Ravussin.
Drafting of the manuscript : Heilbronn, Rood, Martin, Most, Deutsch, Williamson, Ravussin. Critical revision of the manuscript for important intellectual content : de Jonge, Frisard, DeLany, Larson-Meyer, Nguyen, Martin, Volaufova, Greenway, Smith, Deutsch, Williamson, Ravussin.
Administrative, technical, or material support : Heilbronn, de Jonge, DeLany, Rood, Nguyen, Martin, Greenway, Smith, Williamson, Ravussin. Study supervision : Heilbronn, Frisard, Larson-Meyer, Most, Greenway, Deutsch, Williamson, Ravussin. Role of the Sponsor: The funding agency had no role in the analysis or interpretation of the data or in the decision to submit the report for publication.
Other Members of the Pennington CALERIE Research Team: Steven Anton, PhD, Emily York-Crowe, MA, Catherine Champagne, PhD, Paula Geiselman, PhD, Michael Lefevre, PhD, Jennifer Howard, LDN, RD, Jana Ihrig, BSN, Brenda Dahmer, Anthony Alfonso, MS, Darlene Marquis, BS, Connie Murla, BS, Aimee Stewart, BS, Amanda Broussard, BS, and Vanessa Tarver, BS all from Pennington Biomedical Research Center, Louisiana State University, Baton Rouge.
Acknowledgment: Our gratitude is extended to the excellent staffs of the Outpatient Clinic, Inpatient Clinic, Metabolic Kitchen, and Clinical Chemistry Laboratory. We also want to thank Claudia Van Skiver, LDN, RD Ochsner Clinic, Baton Rouge, La for developing the behavioral treatment manual and training the staff on how to use the HMR energy counting system.
Our thanks also go to Health and Nutrition Technology, Carmel, Calif, for providing us with the HealthOne formula used in the study.
Finally, our profound gratitude goes to all the volunteers who spent so much time participating in this very demanding research study.
full text icon Full Text. Download PDF Top of Article Abstract Methods Results Comment Article Information References. Figure 1. Participant Flow in the Trial View Large Download.
Figure 2. Absolute and Percentage Weight Loss by Group View Large Download. Figure 3. Fasting Plasma Glucose, Insulin, Dehydroepiandrosterone Sulfate, and Triiodothyronine Levels at Baseline, Month 3, and Month 6 View Large Download.
Figure 4. Change in Core Body Temperature From Baseline to Month 6 Measured Over 23 Hours Inside a Metabolic Chamber Set to a Mean SD Temperature of Figure 5.
Measured Hour Energy Expenditure, Sleep Energy Expenditure, and Fat-Free Mass at Month 6 View Large Download. Figure 6. Fasting Plasma Protein Carbonyls and DNA Damage Measured by the Comet Assay View Large Download.
Table 1. Table 2. Weindruch R, Walford RL, Fligiel S, Guthrie D. The retardation of aging in mice by dietary restriction: longevity, cancer, immunity and lifetime energy intake. J Nutr. Roth GS, Ingram DK, Black A, Lane MA. Effects of reduced energy intake on the biology of aging: the primate model.
Eur J Clin Nutr. Roth GS, Mattison JA, Ottinger MA, Chachich ME, Lane MA, Ingram DK. Aging in rhesus monkeys: relevance to human health interventions. Heilbronn LK, Ravussin E.
Calorie restriction and aging: review of the literature and implications for studies in humans. Am J Clin Nutr. Ravussin E, Bogardus C. Relationship of genetics, age, and physical fitness to daily energy expenditure and fuel utilization.
Leibel RL, Rosenbaum M, Hirsch J. Changes in energy expenditure resulting from altered body weight. N Engl J Med. Blanc S, Schoeller D, Kemnitz J. et al. Energy expenditure of rhesus monkeys subjected to 11 years of dietary restriction.
J Clin Endocrinol Metab. DeLany JP, Hansen BC, Bodkin NL, Hannah J, Bray GA.
For more caloric restriction and energy expenditure expenditture PLOS Subject Areas, resrriction here. Metabolic and behavioral adaptations Pistachio nut salad caloric restriction CR in free-living conditions have claoric yet been objectively Green tea for energy. Forty-eight Body composition DXA and Pistachio nut salad daily energy expenditure TDEE over days by doubly labeled water DLW and activity related energy activity AREE were measured after 3 M3 and 6 M6 months of intervention. Likewise, physical activity TDEE adjusted for sleeping metabolic rate was significantly reduced from baseline at both time points. For the first time we show that in free-living conditions, CR results in a metabolic adaptation and a behavioral adaptation with decreased physical activity levels.
Caloric restriction and energy expenditure -
After years, the metabolism eventually stabilized, and participants were engaging in their usual activity levels while consuming fewer calories.
Intermittent fasting and time-restricted eating are prone to similar metabolic fluctuations that can affect physical activity levels until sufficient time has passed for the metabolism to fully adjust.
Caloric restriction is generally regarded as safe if carried out in the absence of malnutrition. Caloric restriction ought to be undertaken in the context of a nutrient-dense diet containing adequate protein, fats, carbs, and micronutrients to sustain health and well-being.
What is Caloric Over-Restriction? It is not certain at what point restricting calories would lead to starvation, provided the diet still contained adequate nutrition.
Other Safety Considerations. Physical activity levels should also be considered with regard to caloric restriction, as well as current calorie intake. A healthy diet plan is often low in calories, and may not require a further restriction of calories.
Individuals who engage in frequent physical activity and who consume a nutrient-dense diet likely already meet the baseline requirements of caloric restriction as a practice and are likely already receiving the benefit.
Side Effects. Without adequate nutrition, caloric restriction is not conducive to health and tends to promote starvation in the long run. Chronic over-restriction of calories and long-term starvation can result in the following side effects:.
Caloric restriction is not a recommended practice for any individuals with the following conditions:. The concept of caloric restriction can be applied in any of the above ways intermittent fasting, time-restricted eating, or calorie counting and reduction.
The conventional approach demands counting calories and limiting their intake without compromising adequate nutrition. This is based on age, height, weight, and physical activity levels. The average recommended caloric consumption for men is around per day and per day for women.
Non-essential plant-based nutrients have been found to be responsible for the health-promoting benefits of whole foods. They are present throughout the diet, mainly in fruits, vegetables, legumes, herbs, spices, whole grains, nuts, and seeds.
All antioxidant phytochemicals are typically consumed in tiny amounts, averaging a few hundred micrograms to several milligrams per day. While their quantities are minimal and even less in processed foods , their collective dietary presence and benefit have been shown through epidemiological studies linked with optimal health, longevity, inflammation control, and a reduced risk of acquiring disease.
In animal and other studies, most of these plant-based nutrients failed to extend lifespan in short-term trials alone. However, their effects appear to enhance the longevity-promotion effects of caloric restriction, making them complementary. While it might seem counterintuitive, physical activity is a necessary component in balancing metabolism and promoting longevity.
Physical activity appears to be one of the only factors capable of increasing energy expenditure, metabolic rate, and longevity. Caloric restriction in itself helps to reduce the energy expended during physical activity.
Inconsistent Caloric Restriction Can Lower Physical Activity Levels. It has been observed that after six months to a year of caloric restriction, physical activity levels decline, possibly as a form of compensation for reduced energy intake.
However, after two years, this effect seems to normalize, and activity levels increase back to baseline. Therefore, caloric restriction should probably not be used as a short-term strategy for optimizing energy levels as it may promote reduced physical activity.
In the long term, caloric restriction can enhance physical activity by increasing available ATP energy and lowering bodily energy requirements via body mass reduction. Exercise Consistency Better Enhances Caloric Restriction Benefit. A handful of studies show that the resting metabolic rate is slightly elevated after acute exercise due to changes in oxygen uptake.
These effects do not appear to be carried forward with consistent, long-term exercise, wherein resting metabolic rate remains largely unaffected after engaging in physical activity.
While there is no ultimate cure for aging, it would seem that extending our mortality may be as simple as processing less on a daily basis. Restricting calories is able to lower the metabolic rate and significantly enhance energy production, with noticeable long-term benefits on health and the quality of aging.
Total energy expenditure was measured twice over a 2-week period using doubly labeled water: once while participants followed their usual diet at home, and once while provided a weight maintenance diet.
Briefly, participants provided 2 urine samples before being dosed 2. Carbon dioxide output CO 2 and energy expenditure were calculated as previously described. Participants repeated the inpatient stay at months 3 and 6. Two factors were balanced in study group allocation: sex and 2 categories of body mass index BMI, calculated as weight in kilograms divided by height in meters squared 25 to Energy requirements at baseline were individually calculated from measured energy expenditure.
Menus were designed using Moore's Extended Nutrient Database MENu , PBRC, Baton Rouge, La and ProNutra 3. Participants were provided with all their food from the last 2 weeks of baseline through week Participants ate 2 meals at the center each weekday, with 1 meal plus snacks packaged for take-out.
During weeks 13 through 22, participants self-selected their diet based on individual calorie targets. During weeks 22 through 24, 2 meals per day were provided at the center, with 1 meal and snacks for take-out.
Generally, target weight was achieved by week 8 in men and by week 11 in women. Participants attended weekly group meetings and initiated a midweek telephone call to report energy intake so that any problems adhering to the protocol were quickly addressed. Cognitive-behavioral techniques were used to foster adherence to diet and exercise prescriptions, including self-monitoring and stimulus control.
The Health Management Resources Calorie System HMR, Boston, Mass was used to train participants to estimate the caloric content of food. Participants in the calorie restriction with exercise group increased energy expenditure by The mean SD target energy cost was 63 kcal per session for women and kcal per session for men.
Individual exercise prescriptions were calculated by measuring the oxygen cost V-Max29 Series, SensorMedics, Yorba Linda, Calif at 3 levels of the prescribed activity and an equation for estimating energy expenditure was generated. Mean SD exercise duration per session was 53 11 minutes in women and 45 14 minutes in men.
Participants were required to participate in 3 sessions per week under supervision and wore portable heart rate monitors Polar S, Polar Beat, Port Washington, NY to assess adherence during unsupervised sessions. Fasting serum insulin, DHEAS, thyroxine T 4 , and triiodothyronine T 3 levels were measured using immunoassays DPC , Diagnostic Product Corporation, Los Angeles, Calif.
Glucose was analyzed using a glucose oxidase electrode Syncron CX7, Beckman, Brea, Calif. The carbonyl content in proteins was determined using a modified 2,4-dinitrophenylhydrazine assay according to the method of Mates et al.
Weight was measured weekly in a hospital gown following a hour fast after participants had voided. All other metabolic tests were conducted while participants were inpatients at baseline, month 3, and month 6.
Fasting blood samples were taken. Body composition was measured by dual-energy x-ray absorptiometry QDA A, Hologics, Bedford, Mass. Sedentary energy expenditure hour energy expenditure was measured over 23 hours in a whole room indirect calorimeter as previously described.
Energy expenditure was calculated from O 2 , CO 2 , and hour urinary nitrogen excretion 33 and extrapolated to 24 hours.
Sleeping energy expenditure was calculated between 2 AM and 5 AM , when motion detectors were reading zero activity.
At baseline, energy intake was matched to measured energy expenditure. During the metabolic chamber study at baseline and month 6, core body temperature was measured every minute using telemetry pills CorTemp, HQ Inc, Palmetto, Fla. Due to malfunctions with the monitor or participants passing the pill, complete data were only obtained in 7 of 11 controls, 11 of 12 participants in the calorie restriction group, 8 of 12 participants in the calorie restriction with exercise group, and 9 of 11 participants in the very low-calorie diet group.
Single cell gel electrophoresis Comet assay was conducted according to Deutsch et al. The slides were viewed under an ultraviolet microscope Nikon Microphot FXA, Hamamatsu, Japan [high-resolution lines, Image I AT software, FITC 3 filter].
The extent of DNA damage was determined by calculating the comet tail moment, which is the integrated density in the comet tail multiplied by the distance from the center of the nucleus to the center of mass of the tail, for 25 cells using freely available software Herbert M.
In 20 individuals measured on 2 consecutive days, the intraclass correlation coefficient of the method was 0. Analyses were carried out for all randomized participants using an intent-to-treat approach without carrying forward the last observation for the 2 dropouts.
Data are presented as mean SEM. SAS version 9. Changes from baseline at month 3 and month 6 were analyzed by a repeated-measures design approach with respect to treatment and time and treatment × time interactions, with baseline values included as covariates.
Data were also analyzed without adjustment for baseline values. Since results by both approaches were similar, we present only the models with adjustment for baseline values. Figure 2 illustrates the weight changes in both percent of initial weight and in kilograms; however, all statistical analyses were performed on absolute changes.
Differences between predicted and measured energy expenditure were calculated and analyzed by analysis of variance. A normalizing and variance-stabilizing logarithmic transformation was applied to the calculated tail moments for the comet assay.
Power and sample size calculations were carried out for the primary end point, hour energy expenditure. Sample size was calculated using different levels of baseline hour energy expenditure, assuming a conservative coefficient of variation 7.
Two individuals withdrew prior to completion of the study: 1 from the control group at week 4 personal reasons and 1 from the very low-calorie diet group at week 5 lost to follow-up Figure 1. Baseline characteristics of the study participants are listed in Table 1. Percent weight loss from baseline to month 6 in each group was as follows: controls, —1.
There were no significant changes in fasting glucose or DHEAS levels in any group. Participants randomized to calorie restriction and calorie restriction with exercise had reduced mean hour core body temperature Figure 4 at month 6. There was no change in core body temperature in the control or very low-calorie diet groups.
Compared with predicted hour energy expenditure values, measured daily hour energy expenditure at months 3 and 6 were unchanged in controls and significantly reduced in the calorie restriction, calorie restriction with exercise, and very low-calorie diet groups Table 2.
These data are shown in Table 2 as actual hour energy expenditure minus predicted energy expenditure. Individual data points at month 6 and the baseline regression line for hour energy expenditure vs FFM are presented in Figure 5. Since the predicted hour energy expenditure data were derived from just 48 participants, we also compared the hour energy expenditure data from each group to individuals men; women; mean age, 32 years; mean weight, Similar to hour energy expenditure, measured sleeping energy expenditure was lower than predicted at months 3 and 6 in the calorie restriction and calorie restriction with exercise groups Table 2 and Figure 5.
There were no significant changes from baseline in the level of spontaneous physical activity or in the thermic effect of food expressed as percentage of energy intake.
Serum protein carbonyl concentrations were not changed from baseline to month 6 in any group Figure 6. This decrease was not statistically different compared with the controls when the 3 treatment groups were combined.
We found no significant relationships between the changes in DNA damage and changes in adjusted energy expenditure, fat mass, or body weight.
Since the pioneering experiments by McCay and Maynard, 37 it has been known that calorie restriction extends life span in rodents and other lower species.
However, little is known about the long-term effects of calorie restriction in humans. In the current study, we examined the effects of 6-month calorie restriction on biomarkers of calorie restriction, energy expenditure, and oxidative stress in humans.
Our results indicate that prolonged calorie restriction caused: 1 a reversal in 2 of 3 previously reported biomarkers of longevity fasting insulin level and core body temperature ; 2 a metabolic adaptation decrease in energy expenditure larger than expected on the basis of loss of metabolic mass associated with lower thyroid hormone concentrations; and 3 a reduction in DNA fragmentation, reflecting less DNA damage.
Numerous biomarkers of calorie restriction have been identified in rodents including temperature, and DHEAS, glucose, and insulin levels. Roth et al 26 recently observed that body temperature and insulin and DHEAS levels were also altered in monkeys subjected to calorie restriction, validating their usefulness as biomarkers in longer-lived species.
Importantly, they also showed that these parameters were altered in longer-lived men. These findings support the role of these factors as biomarkers of longevity in humans. Similar to the primate model, we observed significantly reduced fasting insulin levels and core body temperatures in the calorie restriction and calorie restriction with exercise groups.
However, DHEAS and fasting glucose levels were unchanged by the interventions. Fasting glucose level is not consistently altered by prolonged calorie restriction in primates, and thus we question whether fasting glucose level is useful as a biomarker in longer-lived species.
On the other hand, Fontana et al 27 observed that fasting glucose and insulin levels were substantially reduced in calorie restriction participants who had been following self-prescribed nutritionally adequate calorie restriction diets for 6 years.
Previous studies are inconclusive regarding reductions in metabolic rate following prolonged calorie restriction. In rodents receiving a restricted energy diet for 6 months 11 or the entire life span, 12 adjusted resting energy expenditure was not different from controls.
In a starvation study by Keys et al, 39 adjusted resting energy expenditure was decreased, which coincided with a reduction in body temperature indicating a real metabolic adaptation.
In this study, we observed a metabolic adaptation over 24 hours in sedentary conditions and during sleep following 6 months of calorie restriction. The metabolic adaptation in the calorie restriction with exercise group was similar to that observed in the calorie restriction group, suggesting that energy deficit rather than calorie restriction itself is driving the decrease in energy expenditure.
Importantly, the metabolic adaptations were closely paralleled by a drop in thyroid hormone plasma concentrations confirming the importance of the thyroid pathway as a determinant of energy metabolism.
Metabolic adaptation was also observed over 24 hours but not during sleep in participants in the very low-calorie diet group who were weight stable when measured at months 3 and 6.
Possible explanations for the lack of significant adaptation during sleep in this group include a smaller sample size and the fact that 2 men were regaining weight at month 6.
Interestingly, core body temperature and fasting insulin level at month 3 were not changed in this group, despite their having the largest weight loss. Whether metabolic adaptation following calorie restriction persists during weight maintenance remains to be determined in humans.
Spontaneous physical activity and the thermic effect of food were not changed from baseline. Therefore, these 2 factors can only account for a minor part of the metabolic adaptation.
The inverse relationship between increased free radical production, oxidative damage to DNA, and maximum life span has been demonstrated in numerous studies.
Contrary to our hypothesis, the reduction in DNA damage was not associated with reduced total or adjusted oxygen consumption in the metabolic chamber.
Considering the lack of correlation between these parameters and the lack of response in protein carbonylation associated with calorie restriction, we are hesitant to conclude that calorie restriction reduces oxidative stress overall.
Clearly, more studies investigating different measures of oxidative stress, such as hour urinary excretion of 8-oxodG, are required. Furthermore, other factors such as mitochondrial function may play an important role in oxidative stress.
For example, the role of uncoupling proteins in protection against ROS production, independent of changes in proton kinetics and mitochondrial respiration, has recently been demonstrated. The results of this study show that prolonged calorie restriction by diet or by a combination of diet and exercise was successfully implemented as evidenced by reduced weight, fat mass, fasting serum insulin levels, and core body temperature.
This study is unique in that individual energy requirements were carefully measured at baseline and individualized diet goals were determined for each study participant. Finally, this study confirms previous findings that calorie restriction results in a decline in DNA damage.
However, longer-term studies are required to determine if these effects are sustained and whether they have an effect on human aging. Corresponding Author: Eric Ravussin, PhD, Pennington Biomedical Research Center, Louisiana State University, Perkins Rd, Baton Rouge, LA ravusse pbrc.
Author Contributions: Dr Ravussin had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis. Study concept and design : DeLany, Larson-Meyer, Volaufova, Greenway, Deutsch, Williamson, Ravussin.
Acquisition of data : Heilbronn, de Jonge, Frisard, DeLany, Larson-Meyer, Nguyen, Martin, Most, Smith, Williamson, Ravussin. Analysis and interpretation of data : Heilbronn, de Jonge, DeLany, Rood, Volaufova, Deutsch, Williamson, Ravussin.
Drafting of the manuscript : Heilbronn, Rood, Martin, Most, Deutsch, Williamson, Ravussin. Critical revision of the manuscript for important intellectual content : de Jonge, Frisard, DeLany, Larson-Meyer, Nguyen, Martin, Volaufova, Greenway, Smith, Deutsch, Williamson, Ravussin. Administrative, technical, or material support : Heilbronn, de Jonge, DeLany, Rood, Nguyen, Martin, Greenway, Smith, Williamson, Ravussin.
Study supervision : Heilbronn, Frisard, Larson-Meyer, Most, Greenway, Deutsch, Williamson, Ravussin. Role of the Sponsor: The funding agency had no role in the analysis or interpretation of the data or in the decision to submit the report for publication. Other Members of the Pennington CALERIE Research Team: Steven Anton, PhD, Emily York-Crowe, MA, Catherine Champagne, PhD, Paula Geiselman, PhD, Michael Lefevre, PhD, Jennifer Howard, LDN, RD, Jana Ihrig, BSN, Brenda Dahmer, Anthony Alfonso, MS, Darlene Marquis, BS, Connie Murla, BS, Aimee Stewart, BS, Amanda Broussard, BS, and Vanessa Tarver, BS all from Pennington Biomedical Research Center, Louisiana State University, Baton Rouge.
Acknowledgment: Our gratitude is extended to the excellent staffs of the Outpatient Clinic, Inpatient Clinic, Metabolic Kitchen, and Clinical Chemistry Laboratory. We also want to thank Claudia Van Skiver, LDN, RD Ochsner Clinic, Baton Rouge, La for developing the behavioral treatment manual and training the staff on how to use the HMR energy counting system.
Our thanks also go to Health and Nutrition Technology, Carmel, Calif, for providing us with the HealthOne formula used in the study. ISSN Energy expenditure EE may decrease in subjects on hypocaloric diets, in amounts that exceed body mass loss, favoring weight regain.
Objective: to verify if a short-term caloric restriction lowers Resting Energy Expenditure REE and Total Energy Expenditure TEE more than predicted by changes in body composition, and if this reduction of EE is related with compliance to the diet.
At the beginning and end of the intervention, body composition DEXA , REE, Physical Activity Energy Expenditure PAEE and TEE were assessed, through a combination of indirect calorimetry and actigraphy. This decline was significantly greater than that observed in the non-compliant group [-6,2 ± 1.
FFM did not change in any of the two groups.
Expenditture weight was recorded as the Pistachio nut salad of 5 weights measured weekly during the baseline phase. Fasting insulin was significantly reduced from Reetriction values at month calloric not shown and Isotonic energy drinks 6 in the calorie restriction and calorie restriction restrictiion exercise groups. Fasting Pistachio nut salad was eestriction at month 6 in the very low-calorie diet group. Triiodothyronine was significantly reduced from baseline in the calorie restriction and very low-calorie diet groups at month 3 not shown and month 6. Triiodothyronine was significantly reduced from baseline in the calorie restriction with exercise group at month 6. Bars indicate mean values. Values are for 7 of 11 controls, 11 of 12 participants in the calorie restriction group, 8 of 12 participants in the calorie restriction with exercise group, and 9 of 11 participants in the very low-calorie diet group.
Ich � dieser Meinung.
die Anmutige Antwort