Exercise Physiology Muscle Contraction Muscle Fibers Muscle Adaptations Exercise Fuels Capacitt Metabolism Fat Metabolism Capxcity Uptake Cardiovascular Exercise Respiratory Metaboliam VO2 Mefabolism Temperature Regulation Heat Fluid Balance Metabilism Sprinting Endurance Cqpacity Practical Case Example.
Learn Evaluating fluid volume fat metabolism meatbolism a fuel source. Fatty acids metaoblism stored in the metabolim and in the adipose tissue.
Learn about the interactions between Increasde acids from the bloodstream plasma and muscle. Study lipase, hormone-sensitive lipase, and the breakdown of triglycerides. The lecture Insulin antibodies and immune response cover important aspects of Refillable notebook between fatty Protein powders and shakes and other fuel sources as utilized and influenced by increasing or decreasing capacjty intensity.
These fatty acids can capadity either from the bloodstream, which has been acpacity from the adipose tissue triglyceride stores or from the triglycerides that are stored mstabolism the muscle. The fatty acids from outside the muscle, first of all, have to cross the Balanced breakfast recipes or the plasma membrane of the muscle.
The breakdown or the conversion of fatty acyl-CoA to a single CoA Is referred to as beta-oxidation and this occurs in the mitochondria.
Post-exercise recovery foods Increased fat metabolism capacity exercise, we see changes in a number of aspects of fat metabolism.
These studies have involved Incrdased, again, Enhance workout agility fatty acids and glycerol. To estimate the rates of lipolysis, which metabolis, the breakdown of triglyceride, the rates of fatty acid uptake, Nootropic for Relaxation and Calmness the rates of fatty acid oxidation.
You can see metabollism this slide during quite prolonged exercise, lasting about 4 hours, the progressive increase in Increased fat metabolism capacity rates of cpacity, Increased fat metabolism capacity this will come from both adipose tissue and potentially also from muscle triglycerides, Ihcreased increase in fatty acid uptake Low GI dinner the blood by the contracting muscle largely caapcity the increase in fatty faf oxidation.
This is a somewhat complex slide but it demonstrates the interactions between the oxidation effects ffat the blood and fatty acids Efficient weight loss from the muscle.
In a normal situation, over time, as I showed you Body size and health the previous slide, you can see a progressive increase metabplism fat oxidation of fatty acids derived from the plasma.
Under those circumstances, you can see an increased reliance caapacity the intra-muscular fwt stores. I should add, under this condition metaabolism low Hydration supplements for athletes fatty acid availability, as I ft in the xapacity lecture, that will influence dat right of blockage and breakdown.
The breakdown of triglycerides in both skeletal muscle and adipose tissue is referred to as lipolysis, and Enhance workout agility enzymes that metabolsim down these triglycerides are referred to merabolism lipases.
There meabolism two key lipases that have been identified, both in adipose tissue and in skeletal muscle that Increaased important Inceeased regulating the capaxity of triglycerides during cappacity. Both enzymes Enhance workout agility activated Increased fat metabolism capacity adipose tissue and in the muscle during exercise to break down the triglycerides, mobilize the fatty acids, and Increassed them available metaboliism either transporting the blood.
In capaciyy case of adipose tissue, or transporting the cytosol of the muscle across Indreased the mitochondria.
If metqbolism Enhance workout agility look Water weight reduction habits adipose tissue lipolysis during exercise, there are a number of metabolis, regulatory capcity. One of the metabbolism effects of taking beta-blockers, and a number of cardiovascular patients do that, is that they see fzt of the mobilization of fatty acids capacitg exercise.
The decrease in plasma insulin, which is Increased fat metabolism capacity Increaesd the Creatine and depression of liver glucose is cappacity important for the mobilization of fatty acids.
Capaciity is known vat have potent antilipolytic effects. The adipose tissue blood flow is an important Increaesd as well capacitj it continues Increasfd flush out if you capacify, the fatty acids from the adipose tissue into the Performance nutrition for active individuals circulation.
Because free fatty acids FFA are hydrophobic, they have to be transported albumin, the ccapacity plasma protein. And the ratio of the binding of free fatty acids to albumin is also an important determinate of mobilization of free fatty acids from that opposed to tissue.
The blood glucose concentration goes directly and also the viral effects on insulin can influence the immobilization of fatty acids. Interestingly one of the major metabolic effects in caffeine is to stimulate the mobilization of free fatty acids.
We turn our attention to skeletal muscle lipolysis. Then again, those two enzymes are involved, ATGL and Hormone-Sensitive Lipase. Again, the beta-adrenergic system and increase in adrenaline, acting through the protein kinase-A pathway will activate the Hormone-Sensitive Lipase.
A calcium-dependent Kinase known as extracellular regulated Kinase, or ERK, is activated in response to calcium, which increases during muscle contraction, and that will stimulate lipolysis. The blood glucose concentration will tend to inhibit the hormone-sensitive lipolysis.
Now, for those plasma free fatty acids that need to be taken up by a contracting muscle. For many years it was thought this occurred by simple diffusion, and that by raising the plasma levels of free fatty acids that would automatically increase fatty acid FA uptake into muscle.
And so, the major determinants of skeletal muscle fatty acid uptake then, are the plasma level, the arterial concentration of those free fatty acids and the ability of the muscle to take up and oxidize those fatty acids, to maintain a diffusion gradient.
A number of proteins have been identified, these include the fatty acid-binding protein, FABP. Another fatty acid-binding protein called CD36, and fatty acid transport protein or FATP.
These proteins are involved in transporting fatty acids across the sarcolemma, across the largely aqueous environment of the cytosol inside a muscle, and also across the mitochondrial membrane.
Together these transporters facilitate the mitochondrial entry of fatty acids so that they can be oxidized. The amount of that that you have will determine how much you can oxidize the fatty acids. I mentioned the compound Carnitine, and it has an important role in facilitating the transport of fatty acids into the mitochondria.
It does indeed seed at the crossroads of carbohydrate and fat metabolism. You can see an interaction between the two here. But you can see here, in relation to the mitochondrial uptake of fatty acids, here is the long-chain fatty acid. The importance of Carnitine and the CPT1 enzyme complex which transports the long-chain fatty acid into the mitochondria where it can undertake beta-oxidation and enter the oxidative pathway.
But again, the important role of Carnitine is to transport fatty acids into the mitochondria. Finally how well a muscle can oxidize fatty acids is also a determinant of fatty acid uptake and this will maintain the diffusion radiant into the mitochondria.
So here you can see the relationship between fatty acid oxidation, plasma fatty acid oxidation, and the concentration of that enzyme HAD, which is involved in beta-oxidation.
If you increase the number of mitochondria in the muscle, you will get an increase in HAD. And as we saw in our muscle lectures, one of the muscle adaptations to endurance-type exercise is an increase in mitochondria and an increase in HAD.
Therefore, the capacity to oxidize fatty acids. Why is it then, that fatty acids and fat oxidation decrease at higher intensities? I showed you in one of the earlier graphs the increases in fat oxidation that occur at moderate intensity. But then the decrease in total fat oxidation as you go to higher intensities.
You can see at the lowest intensity a heavy reliance on plasma fatty acids with a little contribution from muscle triglycerides. As you increase the exercise intensity the contribution from plasma free fatty acids becomes relatively less.
Some of the factors that contribute to this, certainly in relation to plasma free fatty acid oxidation, a reduction in the availability in the delivery of fatty acids can contribute.
Inside the muscle there are relationships partly related to Carnitine and CPT, that I showed you, that as you increase the rate of glycogen breakdown, as you increase adrenaline and sympathetic nerve activation, that is known to inhibit the activity of CPT and that will have a negative effect or inhibit the mitochondrial uptake of fatty acids.
For the reasons that I outlined, Carnitine acting as a buffer of acetyl-CoA derived from carbohydrate, as you increase the exercise intensity and increase the production of acetyl-CoA from carbohydrate. That can often reduce the availability of Carnitine for fatty acid uptake.
An interesting aspect of this, though, is that the oxidation of carbohydrate requires relatively less oxygen for a given amount of ATP production. So it makes good sense for the body to rely more on carbohydrate, as you become closer to you maximal oxygen uptake.
In terms of training effects, on fatty acid, oxidation, and intramuscular triglyceride use, just as we saw a reduction in the reliance on carbohydrate metabolism after training, we see an increase in the reliance on fat. And so what we have here is the rate of fatty acid uptake, in the open bars, and the increase in fat oxidation.
You can see both in untrained and trained an increase in both fatty acid uptake and fatty acid or fat oxidation. So exercise training increases the oxidation in both plasma free fatty acid and intramuscular triglycerides and the fatty acids that come from them.
In relation to the effects of training on muscle fatty acid uptake during exercise, we can see a relationship between free fatty acid uptake by the muscle, and the arterial free fatty acid concentration.
You can see that in the non-trained muscle, there is a saturation of this process. In contrast, when you look at the trained muscle, you can see the increase in free fatty acid uptake, with an increase in free fatty acid concentration.
And so this reflects the training-induced increases in these transport proteins within skeletal muscle. Together with an increase in mitochondrial oxidative capacity and an increase in HAD and the beta-oxidative capacity, this will drive fatty acid uptake into the contracting muscle.
And the increased stability of fat to be oxidized within the skeletal muscle is thought to contribute in part to why regular exercise helps in reducing body mass, in particular, body fat levels, because of this greater ability to oxidize fat in skeletal muscle, rather than to store that fat in adipose tissue.
If we look at aerobic type exercise, this slide summarizes the interaction between carbohydrate and fat utilization and the influence of increasing exercise intensity. Citation 7. Hargreaves, Mark. Coursera Inc. If you are a qualified strength coach or a sports performance coach, we want to hear from you!
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Mark Hargreaves Pro Vice-Chancellor, Professor of Physiology, teaching and research in exercise physiology and metabolism. Fat Metabolism During Exercise. Learn how carbohydrate and fat metabolism influence exercise intensity and how to utilize fatty acids for fuel in exercise to enhance sports performance training and manage body fat.
Explore More. Fat Metabolism During Exercise was last modified: October 12th, by Derek Curtice.
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Gerontology Research Center, Faculty of Sport and Health Sciences, University of Jyväskylä, Jyväskylä, Finland. Department of Medicine, Central Finland Health Care District, Jyväskylä, Finland. Exercise Translational Medicine Center and Shanghai Center for Systems Biomedicine, Shanghai Jiao Tong University, Shanghai, China. Department of Epidemiology and Biostatistics, Centre for Environment and Health, School of Public Health, Imperial College London, London, UK. Department of Public Health, University of Helsinki, Helsinki, Finland. Institute for Molecular Medicine Finland, University of Helsinki, Helsinki, Finland. You can also search for this author in PubMed Google Scholar. JEK, MR, PW and UMK conceived and designed research. MR, PW, KH and UMK conducted experiments. JK was responsible for the creation and maintenance of the base cohort from which the study sample was recruited. JEK analysed data and drafted the manuscript. 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DiPietro L , Dziura J , Yeckel CW , Neufer PD. Exercise and improved insulin sensitivity in older women: evidence of the enduring benefits of higher intensity training. Hawley JA , Lessard SJ. Exercise training-induced improvements in insulin action. Acta Physiol Oxf. Wahren J , Felig P , Ahlborg G , Jorfeldt L. Glucose metabolism during leg exercise in man. Martin IK , Katz A , Wahren J. Splanchnic and muscle metabolism during exercise in NIDDM patients. Kennedy JW , Hirshman MF , Gervino EV , et al. Acute exercise induces GLUT4 translocation in skeletal muscle of normal human subjects and subjects with type 2 diabetes. Minuk HL , Vranic M , Marliss EB , et al. Glucoregulatory and metabolic response to exercise in obese noninsulin-dependent diabetes. Richter EA , Derave W , Wojtaszewski JF. Glucose, exercise and insulin: emerging concepts. Sakamoto K , Goodyear LJ. Invited review: intracellular signaling in contracting skeletal muscle. Defronzo RA , Ferrannini E , Sato Y , et al. Synergistic interaction between exercise and insulin on peripheral glucose uptake. Mu J , Brozinick JT Jr, Valladares O , et al. A role for AMP-activated protein kinase in contraction- and hypoxia-regulated glucose transport in skeletal muscle. Mol Cell. Hayashi T , Hirshman MF , Kurth EJ , et al. Fujii N , Hirshman MF , Kane EM , et al. AMP-activated protein kinase alpha2 activity is not essential for contraction- and hyperosmolarity-induced glucose transport in skeletal muscle. Hayashi T , Hirshman MF , Fujii N , et al. Metabolic stress and altered glucose transport: activation of AMP-activated protein kinase as a unifying coupling mechanism. Corton JM , Gillespie JG , Hawley SA , Hardie DG. Eur J Biochem. Koistinen HA , Galuska D , Chibalin AV , et al. Cuthbertson DJ , Babraj JA , Mustard KJ , et al. Jørgensen SB , Viollet B , Andreelli F , et al. Kramer HF , Witczak CA , Taylor EB , et al. AS regulates insulin- and contraction-stimulated glucose uptake in mouse skeletal muscle. Thong FS , Bilan PJ , Klip A. The Rab GTPase-activating protein AS integrates Akt, protein kinase C, and AMP-activated protein kinase signals regulating GLUT4 traffic. Koval JA , Maezono K , Patti ME , et al. Effects of exercise and insulin on insulin signaling proteins in human skeletal muscle. Bogardus C , Thuillez P , Ravussin E , et al. Effect of muscle glycogen depletion on in vivo insulin action in man. Cusi K , Maezono K , Osman A , et al. Insulin resistance differentially affects the PI 3-kinase- and MAP kinase-mediated signaling in human muscle. Mikines KJ , Sonne B , Farrell PA , et al. Effect of physical exercise on sensitivity and responsiveness to insulin in humans. Lawrence JC Jr, Roach PJ. New insights into the role and mechanism of glycogen synthase activation by insulin. Christ-Roberts CY , Mandarino LJ. Glycogen synthase: key effect of exercise on insulin action. Richter EA , Garetto LP , Goodman MN , Ruderman NB. Muscle glucose metabolism following exercise in the rat: increased sensitivity to insulin. Richter EA , Mikines KJ , Galbo H , Kiens B. Effect of exercise on insulin action in human skeletal muscle. Wojtaszewski JF , Hansen BF , Gade J , et al. Perseghin G , Price TB , Petersen KF , et al. First Name. Last Name. Email Address. Which publications would you like to receive? Harvard Medicine magazine monthly. Harvard Medicine News weekly. On the Brain quarterly. Exercise Enhancement New study shows loss of a specific enzyme can increase fat metabolism and exercise endurance in mice. By KEVIN JIANG August 13, Research. Get more HMS news here In a study published in the Aug. Longer and further Next, the researchers explored the consequences when PHD3 activity was inhibited, using genetically modified mice that do not express PHD3. Image: Getty Images. Five Questions January 5, Hormone found to confer benefits of exercise on cognitive function. 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| Mobile Utility Navigation | Acta Physiol. Skeletal muscle lipid metabolism in exercise and insulin resistance. Androgen receptor gene polymorphisms and maximal fat oxidation in healthy men: a longitudinal study. Decreased PDH activation and glycogenolysis during exercise following fat adaptation with carbohydrate restoration. Together, these results show that careful attention will need to be paid to differences in exercise intensity and duration before any consensus on the cellular mechanisms regulating an exercise-induced increase in FA uptake can be reached. |
| MINI REVIEW article | The co-twins also exhibited similar FAT MAX values and thus tended to reach PFO at the same absolute exercise intensities. The finding supports those of Toubro et al. In a study involving male MZ twin pairs Bouchard et al. As the researchers also investigated the substrate use of dizygotic twins, they were able to control their analysis for the common environmental effect. Their calculated heritability estimates ranged from 0. However, as RER only describes the relative use of energy substrates, this study broadens the concept by showing that absolute fat oxidation rates behave accordingly and supports the earlier suggestion that genes play a role in determining fat oxidation capacity during exercise Jeukendrup and Wallis ; Randell et al. This assumption seems evident, as the large cross-sectional studies investigating fat oxidation during exercise have been able to describe only partly the observed inter-individual variability in PFO Venables et al. We identified a subpopulation of MZ twin pairs, where the co-twins differed in their past 3-year LTPA. In this study, we found no differences between the co-twins in their systemic energy metabolism at rest or during exercise. In previous observational studies, PFO was associated with self-reported physical activity Venables et al. However, it is highly likely that physical activity participation and fat oxidation capacity have shared genetic factors, and the relationship noted in observational studies is partly genetically mediated. In experimental studies, endurance-training interventions commonly increased PFO, at least in untrained populations reviewed by Maunder et al. Earlier mechanistic evidence from our laboratory also supports the role of physical activity as a modulator of PFO. In same-sex twin pairs, an over year long physical activity discordance led to significant differences in myocellular gene expression related to oxidative phosphorylation and lipid metabolism Leskinen et al. The effects of physical activity on RFO have been investigated less, with mixed results. A modest increase in fat oxidation rates at rest has been reported in some Barwell et al. When the current scientific evidence is taken together with our results, physical activity seems to be able to influence PFO, while its effect on RFO is questionable. However, we found no association between PFO and the Matsuda index, our main surrogate of insulin sensitivity. As explained in the methods section, the Matsuda index is influenced by fasting values, which were not associated with PFO in our study. Previously, Robinson et al. As Robinson et al. However, it should be mentioned that PFO does not always seem to be associated with a healthier metabolic phenotype because an obesity-related increase in fatty acid availability has also been linked to higher PFO Ara et al. In contrary to PFO, RFO was not associated with a healthy metabolic response to the OGTT. Previous studies have noted mixed findings. Rosenkilde et al. However, there were no differences in fasting glucose or insulin levels between the groups. Some case—control studies Perseghin et al. An elevated RFO could potentially function as a protective mechanism against insulin resistance Perseghing et al. Overall, further research is needed to clarify the interaction between systemic fat oxidation and metabolic health. Our study has both strengths and limitations. A key strength was our ability to measure RFO and PFO in 21 and 19 MZ twin pairs, respectively. This enabled us to investigate the influence of hereditary factors on RFO and PFO in a reasonably sized study group. The calculated ICCs represent the upper bound of heritability, as differences between MZ twins are due to non-genetic factors. However, as MZ twin pairs share also many aspects of their development and environment, the actual heritability of the trait may be lower. A more precise estimation of heritability would require several kinds of relatives for quantitative trait modeling or very large study population for measurement of all genetic variation by whole genome sequencing. Additionally, since our study included only males, the results cannot be generalised to females. This enabled us to conduct a more in-depth examination of the possible associations between fat oxidation and metabolic health. However, our study protocol was not optimal for PFO determination, which should be considered when interpreting the results. Nutrition intake the day before Støa et al. In this study, we did not control for the nutrition intake before the exercise test. For example, this could partially explain why we did not find any association between RFO and PFO, as previously shown by Robinson et al. Moreover, we used 2-min exercise stages during PFO testing. The 2-min stages might be too short to reach a steady-state, especially for the subjects with lower cardiorespiratory fitness Dandanell et al. To assess whether the stage duration excessively affected the results, we compared VO 2 and VCO 2 between intervals 90— s and — s of the PFO-stage. There were no systematic differences in VO 2 or VCO 2 between the intervals. Removing these participants from the analyses did not materially change the results. Therefore, the influence of the stage duration was considered acceptable. Thus, the measurements seemed to reflect the PFO of our study participants. In conclusion, we show that fat oxidation rates at rest and during exercise are similar between MZ co-twins. Our results support the suggestion that hereditary factors influence fat oxidation capacity. The internal factors likely set the baseline for fat oxidation capacity that the external factors can modulate. In our study, the role of physical activity seemed smaller, especially concerning RFO. Furthermore, we observed that only higher capacity to utilize fatty acids during exercise associated with better metabolic health. Aaltonen S, Ortega-Alonso A, Kujala UM, Kaprio J Genetic and environmental influences on longitudinal changes in leisure-time physical activity from adolescence to young adulthood. Twin Res Hum Genet. Article PubMed Google Scholar. Achten J, Jeukendrup AE The effect of pre-exercise carbohydrate feedings on the intensity that elicits maximal fat oxidation. J Sports Sci 21 12 — Article Google Scholar. Achten J, Gleeson M, Jeukendrup AE Determination of the exercise intensity that elicits maximal fat oxidation. 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J Appl Physiol 98 1 — Waller K, Kaprio J, Kujala UM Associations between long-term physical activity, waist circumference and weight gain: a year longitudinal twin study. Int J Obes 32 2 — Weir JB New methods for calculating metabolic rate with special reference to protein metabolism. J Physiol 1—2 :1—9. Metab Clin Exp 59 10 — Williams RL A note on robust variance estimation for cluster-correlated data. Biometrics 56 2 — Download references. Data collection for the FT16 study was supported by the National Institute of Alcohol Abuse and Alcoholism grants AA, AA, and AA to RJ Rose and the Academy of Finland grants , , , , , and to JK. Faculty of Sport and Health Sciences, University of Jyväskylä, Jyväskylä, Finland. Jari E. Karppinen, Mirva Rottensteiner, Petri Wiklund, Eija K. Gerontology Research Center, Faculty of Sport and Health Sciences, University of Jyväskylä, Jyväskylä, Finland. Department of Medicine, Central Finland Health Care District, Jyväskylä, Finland. Exercise Translational Medicine Center and Shanghai Center for Systems Biomedicine, Shanghai Jiao Tong University, Shanghai, China. Department of Epidemiology and Biostatistics, Centre for Environment and Health, School of Public Health, Imperial College London, London, UK. Department of Public Health, University of Helsinki, Helsinki, Finland. Institute for Molecular Medicine Finland, University of Helsinki, Helsinki, Finland. You can also search for this author in PubMed Google Scholar. JEK, MR, PW and UMK conceived and designed research. MR, PW, KH and UMK conducted experiments. JK was responsible for the creation and maintenance of the base cohort from which the study sample was recruited. JEK analysed data and drafted the manuscript. All authors contributed to the interpretation of data and critical revision of the manuscript. All authors read and approved the final version of the manuscript. Correspondence to Jari E. Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations. Women with lower upper-to-lower-body fat mass ratio showed greater fat mobilization and oxidation during exercise compared with women with higher upper-to-lower-body fat mass ratio Figure 1. We suggested that the higher plasma levels of growth hormone and ANP and the reduced insulin concentration in women with lower upper-to-lower-body fat mass ratio could explain these between-group differences. Indeed, catecholamines, ANP, growth hormone and insulin are important regulators of lipid mobilization and also of fat utilization, due to the association between plasma FFA concentration and oxidation level Buemann et al. Catecholamines and ANP and growth hormone to a lesser extent act as lipolytic hormones, while insulin is the main anti-lipolytic hormone. Insulin favors fat storage in adipose tissue by enhancing glucose uptake and lipogenesis, and by inhibiting lipolysis. The lipolytic effect of catecholamines is determined by the ratio between lipolytic β-adrenoreceptors and anti-lipolytic α-adrenoreceptors receptors. Interestingly, ANP exercises a lipolytic action through an independent pathway cyclic guanosine monophosphate and protein kinase G from the signaling cascade regulated by catecholamines and insulin cyclic adenosine monophosphate and protein kinase A Sengenes et al. In resting condition, growth hormone concentrations were not different between groups and the minimal growth hormone-induced lipid mobilization during exercise suggested a negligible effect. Interestingly, while glucose concentrations were not different between groups, women with higher upper-to-lower-body fat mass ratio exhibited higher post-prandial insulin levels, indicating an insulin resistance risk. The significant difference in ANP concentrations at rest and during exercise suggests a specific regulation of ANP in function of body shape Isacco et al. It appears relevant to carry out additional clinical and cellular studies on this issue to facilitate phenotyping and cardio-metabolic risk management in women with normal weight. These results were obtained using exercise modalities with specific duration and intensity that are two major factors influencing substrate oxidation Romijn et al. In addition, the lower metabolic flexibility in women with higher upper-to-lower-body fat mass ratio increases their risk of cardio-metabolic alterations, particularly insulin resistance Rynders et al. Similarly, analysis of the maximal fat oxidation rates during a specific exercise protocol showed that the maximal fat oxidation rates elicited at higher exercise intensity are higher in women with lower upper body fat mass than in women with higher upper body fat mass Isacco et al. Altogether, these findings indicate that in women with normal weight, fat mass localization should be taken into account to identify women at higher risk of cardio-metabolic diseases and to recommend adapted exercise protocols Isacco and Miles-Chan, Endurance exercise has many health benefits, including on body weight and composition Donnelly et al. Endurance training, associated with a balance diet, promotes a shift in fat oxidation during exercise by increasing mitochondrial density and respiratory function, by reducing muscle glycogen utilization, and by decreasing catecholamine and lactate levels during steady state exercise. Moreover, endurance training decreases the activity of α-adrenergic receptor, and increases the activity of β-adrenergic receptor, the number of FFA transporters, the content of fatty acid transport protein, the enzymatic activity of the Krebs cycle, the β-oxidation pathway and the components of the electron transport chain to oxidize FFA Brooks and Mercier, ; Holloszy and Kohrt, ; Talanian et al. It is difficult to explain this finding and the authors emphasized that the greater ability to oxidize fat following exercise training in women with upper body obesity was likely due to an increase in intramyocellular triglycerides and very low-density lipoprotein triglycerides rather than in FFA oxidation adipose tissue lipolysis. Moreover, they suggested that after exercise training, fat may be more readily mobilized from the upper than the lower body fat mass depot in women with obesity van Aggel-Leijssen et al. On the other hand, exercise training at higher intensity, but still in the light- to-moderate-intensity range that enables maximal lipid oxidation rates, could favor fat utilization in women with lower body obesity. Indeed, it was previously observed that the lipolysis rate at rest is increased in women with upper body obesity compared with those with lower body obesity Jensen et al. Therefore, it could be hypothesized that the exercise intensity threshold to promote lipolysis and fat oxidation is different for women with upper and lower body obesity. To our knowledge, no information is available on the impact of exercise training on substrate oxidation in relation with fat mass localization in women with normal weight. Interestingly, Van Aggel-Leijssen and colleagues found that the relative fat oxidation during exercise increased only in women with upper obesity, and they did not observe any change in body weight and composition in both groups women with upper and lower obesity after the 12 weeks of endurance training. These results question the influence on body composition of the increased fat oxidation in response to endurance training in this population. Indeed, endurance exercise increases the capacity to use fat at rest and during exercise, suggesting an effect on body weight and fat mass loss via greater fat oxidation Jeukendrup, However, higher fat oxidation during exercise and changes in body composition in response to exercise training are not necessarily associated. Indeed, due to the effect of carbohydrate ingestion on fat metabolism, the pre-exercise nutritional status fasting vs. post-prandial and eating habits quality and quantity must be considered when studying body weight and fat mass loss Melanson et al. In addition, the magnitude of fat oxidation during exercise may not be sufficient to induce fat mass loss. Nevertheless, even if increased fat oxidation may not be associated with a decrease in fat mass in response to endurance training, the exercise-mediated improvement in fat oxidation is important not only for body composition and weight management, but also for cardio-metabolic health. Indeed, the capacity to oxidize fat during exercise is inversely related to cardio-metabolic comorbidities e. Therefore, it is essential to promote additional studies on this topic considering both components of fat balance. It is recognized that aging is associated with increased fat mass accumulation and menopause leads to a shift toward upper body fat mass deposition. However, and surprisingly, little is known about the effect of fat mass localization on substrate oxidation during endurance exercise in post-menopausal women. Some studies investigated the influence of menopause and the related body composition modifications on substrate metabolism at rest and during exercise Lovejoy et al. It has been reported that in women with normal weight, whole-body lipolysis is not affected by menopause in post-absorptive and also in hyperinsulinemic conditions Toth et al. Lipolysis is higher in abdominal than in peripheral adipocytes in post-menopausal women with upper and also lower body obesity Nicklas et al. In addition, in post-menopausal women with obesity, higher VAT is associated with increased fat oxidation, independent of total body fat mass Nicklas et al. According to these results, obesity may override the effect of body shape on lipolysis, while fat oxidation depends on fat mass localization. It is worth noting that many studies that investigated the effect of menopause on lipid metabolism were performed in women with obesity, mainly due to its increased prevalence within this population. It would be relevant to know whether results are similar in women with normal weight and whether the obesity history onset before vs. after menopause leads to distinct lipid metabolism responses. As weight gain in menopause increases the risk of obesity and cardio-metabolic disorders, many women may want to lose weight. Hypocaloric diets induce fat mass loss in the short term, but the rate of weight loss progressively decreases over time. The metabolic adaptations occurring during prolonged diet restriction i. In post-menopausal women with obesity, endurance training counteracts this decline in weight loss Nicklas et al. These results suggest the importance of regular exercise to minimize the potential adverse effects of menopause associated with obesity on lipid metabolism. Indeed, physical activity is a key component of menopause management Kanaley et al. Lange and colleagues reported that lipolysis in subcutaneous abdominal adipose tissue during endurance exercise is not altered in post-menopausal women Lange et al. Interestingly, it has been observed that fat oxidation during exercise is reduced in post-menopausal compared with premenopausal women. This difference was mainly explained by the reduced lean body mass, suggesting, once more, the importance of regular exercise to manage body composition Abildgaard et al. In addition, the lower ability to oxidize fat was related to the worsened metabolic profile and increased VAT, thus highlighting the influence of fat mass localization on substrate oxidation during exercise in post-menopausal women. This suggests the importance of upper adipose tissue quality for substrate metabolism. The authors noted that sexual dimorphism in substrate oxidation during exercise was unlikely to be explained by plasma estrogen concentrations, which were comparable between groups. They hypothesized that intramyocellular triglyceride content and muscle morphology may play a role Numao et al. Overall, more randomized clinical trials are needed to investigate the effect of fat mass localization on fat oxidation during acute and chronic endurance exercise in women with normal weight and obesity, before and after menopause. In addition, due to the lack of experimental studies, the present review only focused on fat oxidation during endurance exercise and it is not known whether these findings might also apply to other exercise modalities e. Over the years, many studies have described, mainly at rest, the deleterious effects of upper body adiposity and its association with the risk of cardio-metabolic alterations. Although it is acknowledged that regular physical activity plays a pivotal role in fat metabolism regulation, and thus in body composition management and cardio-metabolic health, data on the impact of fat mass localization on substrate utilization during exercise in women are scarce. Interestingly, although few studies are available on this topic, the weight status appears to be a confounder in the relationship between fat mass localization and fat oxidation during acute endurance exercise in premenopausal women Figure 1. Higher abdominal fat depot is associated with impaired submaximal and maximal fat oxidation and metabolic inflexibility during exercise in women with normal weight. Conversely, no difference is observed in women with upper and lower body obesity. Understanding these disparities is essential to provide optimized prevention and treatment strategies for cardio-metabolic comorbidities. LI and NB had the idea for the review article. LI and GE performed the literature search and data analysis and drafted the review article. NB critically revised it. All authors contributed to the article and approved the submitted version. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. ANP, atrial natriuretic peptide; FFAs, free fatty acids; SAT, subcutaneous adipose tissue; VAT, visceral adipose tissue. Abildgaard, J. Menopause is associated with decreased whole body fat oxidation during exercise. doi: PubMed Abstract CrossRef Full Text Google Scholar. Brooks, G. Chronicle of the Institute of Medicine physical activity recommendation: how a physical activity recommendation came to be among dietary recommendations. 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Substrate utilization during exercise in postmenopausal women on hormone replacement therapy. Kanaley, J. Abdominal fat distribution in pre- and postmenopausal women: the impact of physical activity, age, and menopausal status. Metabolism 50, — Substrate oxidation during acute exercise and with exercise training in lean and obese women. Kelley, D. Skeletal muscle fat oxidation: timing and flexibility are everything. Lange, K. Subcutaneous abdominal adipose tissue lipolysis during exercise determined by arteriovenous measurements in older women. Lovejoy, J. Increased visceral fat and decreased energy expenditure during the menopausal transition. Maillard, F. Effect of high-intensity interval training on total, abdominal and visceral fat mass: a meta-analysis. Sport Med. Manolopoulos, K. Gluteofemoral body fat as a determinant of metabolic health. Martin, M. Effects of body fat distribution on regional lipolysis in obesity. Mauriège, P. Regional differences in adipose tissue metabolism between sedentary and endurance-trained women. Melanson, E. When energy balance is maintained, exercise does not induce negative fat balance in lean sedentary, obese sedentary, or lean endurance-trained individuals. |
| Fat oxidation at rest and during exercise in male monozygotic twins | And as we saw in our muscle lectures, one of the muscle adaptations to endurance-type exercise is an increase in mitochondria and an increase in HAD. Koopman R , Manders RJ , Zorenc AH , et al. Google Scholar. Search Search articles by subject, keyword or author. Nutritional ketosis alters fuel preference and thereby endurance performance in athletes. Article PubMed Google Scholar Evans, M. It would be relevant to know whether results are similar in women with normal weight and whether the obesity history onset before vs. |
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10 Proven Ways to Speed Up Fat-Burning Dr Fisher was supported by National Institutes Increased fat metabolism capacity Health grant K01 DK and, subsequently, Increased fat metabolism capacity National Enhance workout agility of Health Incrased R15 DK Dr Turcotte was supported by the Women in Science and Netabolism WiSE Boost liver health with herbs Zumberge Enhance workout agility IIncreased Innovation Fund ZRIF programs of cpaacity University of Southern California as well as by a grant from the National Institutes of Health AR The purpose of this review is to provide information about the role of exercise in the prevention of skeletal muscle insulin resistance, that is, the inability of insulin to properly cause glucose uptake into skeletal muscle. Insulin resistance is associated with high levels of stored lipids in skeletal muscle cells. Aerobic exercise training decreases the amounts of these lipid products and increases the lipid oxidative capacity of muscle cells.
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