On the other hand, determination of plasma-derived fatty acid oxidation using stable isotope tracers has long been questioned, and only since the introduction of the acetate recovery factor in 19 could the oxidation of labeled fatty acids be reliably determined 20 , The molecular adaptation of skeletal muscle to low-intensity endurance training is largely unknown.

GLUT4, the major glucose transporter in skeletal muscle, and hexokinase II, which catalyzes the phosphorylation of glucose to glucosephosphate, are two key genes involved in glucose utilization. LPL is responsible for hydrolysis of plasma triglycerides and directs the released free fatty acids FFAs into the tissue Inside the muscle cell, ACC2 has recently been suggested to control the rate of fatty acid oxidation and triglyceride storage Finally, the skeletal muscle-specific uncoupling protein-3 UCP3 has also been suggested to be involved in fatty acid metabolism, but the exact function is still under debate Therefore, the third aim of the present study was to examine the effect of low-intensity endurance training on the expression of the above-mentioned genes.

The characteristics of the six healthy nonobese male volunteers are presented in Table 1. The nature and risks of the experimental procedure were explained to the subjects, and all subjects gave written informed consent. The study was approved by the Medical-Ethical Committee of Maastricht University.

Subjects participated in two stable isotope experiments, separated by 1 week, to measure total and plasma-derived fatty acid oxidation in random order. In these tests, an infusion of either [U- 13 C]palmitate or [1,2- 13 C]acetate was given for 2 h at rest and 1 h during exercise.

Acetate is directly converted to acetyl-CoA, and the recovery of acetate can be used to correct [ 13 C]palmitate oxidation for loss of label in the tricarboxylic acid TCA cycle, as previously described 19 , On a separate day, a muscle biopsy was taken after an overnight fast.

Immediately after the last stable isotope experiment, the training period was started. After the week training program, a second muscle biopsy was taken 6—7 days after the last training session.

The two stable isotopes experiments were repeated 7—8 and 14—15 days after the end of the week training program in random order. In this way, it was prevented that the last training session could influence the measurements. Three days before the first stable isotope experiment, subjects were asked to write down their food intake and to consume the same food items before every other stable isotope experiment.

Subjects were asked not to consume any products with a high abundance of 13 C carbohydrates derived from C4 plants such as maize and sugar cane 1 week before and during the entire experimental period.

Subjects were asked to refrain from physical activity 2 days before the sampling of the muscle biopsy and before the stable isotope experiments. Subjects trained three times per week for 12 weeks. Training duration for subjects per session was Heart rate was monitored continuously during the training sessions Polar Electro, Oy, Finland.

After 4 and 8 weeks of exercise training, a maximal aerobic exercise test was performed, and the training workload and duration were adjusted if necessary.

All training sessions took place at the university under the supervision of a professional trainer. One week before and after the training program, body density was determined by underwater weighing in the fasted state.

Body weight was measured with a digital balance, accurate to 0. Lung volume was measured simultaneously with the helium dilution technique using a spirometer Volugraph ; Mijnhardt. Body fat percentage was calculated using the equations of Siri Fat-free mass, in kilograms, was calculated by subtracting fat mass from total body mass.

One week before and after the training program, each subject performed an incremental exercise test on an electronically braked cycle ergometer Lode Excalibur to determine maximal oxygen consumption V o 2max and maximal power output W max.

Subjects started cycling at 75 W for 5 min. Thereafter, workload was increased by 50 W every 2. When subjects were approaching exhaustion, as indicated by heart rate and subjective scoring, the increment was reduced to 25 W.

Heart rate was registered continuously using a Polar Sport tester Kempele, Finland. Oxygen consumption and carbon dioxide production were measured using open circuit spirometry Oxycon-β; Mijnhardt.

At a. after an overnight fast, subjects underwent an isotope infusion test. Teflon catheters were inserted in an antecubital vein for isotope infusion and retrogradely into a contralateral dorsal hand vein for sampling of arterialized venous blood. After placement of the catheters, subjects rested on a bed, and the cannulated hand was placed in a hotbox, in which air was circulated at 60°C to obtain arterialized venous blood.

After 30 min, baseline oxygen consumption and carbon dioxide production was measured, and breath and blood samples were collected. Immediately thereafter, subjects were given an intravenous dose of 0. Then, at time zero, a constant intravenous infusion of either [U- 13 C]palmitate 0.

With these infusion rates, the amount of 13 C infused during palmitate and acetate infusion are similar. Blood samples and breath samples were taken at 0, , , and min at rest and , , and min during exercise. At rest, V o 2 and V CO 2 were measured continuously during the first 90 min using open circuit spirometry Oxycon-β.

During exercise, V o 2 and V CO 2 were measured immediately before the measurement of breath 13 CO 2 enrichment. To determine the exact infusion rate, the concentration of palmitate in the infusate was measured for each experiment using analytical gas chromatography GC using heptadecanoic acid as internal standard see sample analysis.

The acetate concentration was measured in each infusate with an enzymatic method Boehringer Mannheim, Mannheim, Germany. Muscle biopsies were taken from the mid-thigh region from M.

vastus lateralis according to the technique of Bergstrom et al. The subjects were required to abstain from training or vigorous exercise 48 h before the biopsy. The biopsy was used for isolation of total RNA using the acid phenol method of Chomozynski and Sacchi 28 , with an additional DNAse digestion step with concomitant acid phenol extraction and ethanol precipitation.

The mRNA levels of LPL, hexokinase II, GLUT4, ACC2, and UCP3 were quantified by RT-competitive PCR For the assays, the RT reaction was performed from 0. The competitive PCR assays were performed as previously described 30 — To improve the quantification of the amplified products, fluorescent dye-labeled sense oligonucleotides were used.

The PCR products were separated and analyzed on an ALFexpress DNA sequencer Pharmacia with the Fragment Manager Software. Total RNA preparations and RT-competitive PCR assays of the two skeletal muscle samples from the same individual before and after weight loss were performed simultaneously.

Oxygen saturation Hemoximeter OSM2; Radiometer, Copenhagen, Denmark was determined immediately after sampling in heparinized blood and used to check arterialization. Fifteen milliliters of arterialized venous blood was sampled in tubes containing EDTA to prevent clotting and immediately centrifuged at 3, rpm 1, g for 10 min at 4°C.

Plasma substrates were determined using the hexokinase method Roche, Basel for glucose, the Wako NEFA nonesterified fatty acid C test kit Wako Chemicals, Neuss, Germany for FFAs, and the glycerolkinase-lipase method Boehringer Mannheim for glycerol and triglycerides.

For determination of plasma palmitate, FFAs were extracted from plasma, isolated by thin-layer chromatography, and derivated to their methyl esters. From palmitate oxidation, plasma-derived fatty acid oxidation was then calculated by dividing palmitate oxidation rate by the fractional contribution of palmitate to the total FFA concentration.

Differences in measured variables before and after training were tested using paired t tests. Repeated measures one-way ANOVA were used to detect differences in variables in time. For testing differences in blood parameters between treatments, areas under the concentration versus time curve where calculated for 0— min at rest and — during exercise.

On average, subjects completed a total of 31 ± 1. Therefore, the average exercise duration per week was 2. The week training program had no influence on percentage body fat or V o 2max Table 1.

At rest, total fat oxidation was not significantly influenced by the week training program ± 18 vs. Similarly, plasma-derived fatty acid oxidation was not significantly influenced by the week training program ± 24 vs. Plasma-derived fatty acid oxidation during exercise was not significantly influenced by the training program ± 88 vs.

Rate of appearance of FFA was not influenced by the training program, neither at rest ± 41 vs. The percentage of R a that was oxidized was also not influenced by the training program, neither at rest 40 ± 4 vs.

At rest, carbohydrate oxidation was not significantly affected by the training program ± 9 vs. Carbohydrate oxidation during exercise tended to be lower after training 1, ± vs.

Energy expenditure, both at rest 4. Acetate recovery, both at rest Plasma triglyceride concentrations Fig.

Both at rest and during exercise, the average concentrations for plasma glucose at rest: 4. The week training program had no effect on two genes involved in the transport and oxidation of blood glucose: hexokinase II 2. However, the expression of two genes encoding for key enzymes in fatty acid metabolism were affected by the training program: skeletal muscle ACC2 was significantly lower after training ± 24 vs.

The expression of UCP3 The effect of endurance training on the contribution of different fat sources to total fat oxidation after endurance training is under debate.

Part of this controversy could be explained by the methodological difficulties in using [ 13 C]- and [ 14 C]-fatty acid tracers to estimate the oxidation of plasma fatty acids, especially in the resting state However, Sidossis et al.

We showed that this acetate recovery is reproducible 25 but has a high interindividual variation and is influenced by infusion period, metabolic rate, respiratory quotient, and body composition 21 and therefore needs to be determined in every individual under similar conditions and at similar time points as the measurement of plasma-derived fatty acid oxidation.

In the present study, we therefore measured the acetate recovery factor at all time points in each individual both before and after the training program at least 7 days separated from the last training session to exclude the influence of the last exercise bout on the measurements and were therefore able to correct plasma-derived fatty acid oxidation rate for loss of label in the TCA cycle.

With the available stable isotope tracer methodology, we cannot distinguish between IMTG- or VLDL-derived fatty acid oxidation.

Using electron microscopy, it has previously been shown that endurance-trained athletes have increased IMTG concentrations 36 , and because endurance athletes have an increased fat oxidation capacity, it seems logical that this increased IMTG storage after endurance training is an adaptation mechanism to allow IMTG oxidation during exercise.

The localization of the IMTG near the mitochondria would make these triglyceride pools an efficient source of substrate, especially during exercise.

However, biochemical analysis of IMTGs is problematic, and therefore the use of IMTG remains controversial.

On the other hand, the contribution of VLDL-derived fatty acids to fat oxidation during exercise is also still under debate 18 , The increased expression of LPL mRNA after training, as observed in our study, which is in accordance with previous studies showing increased LPL activity after endurance training in rodents 38 , 39 , and the reduced plasma triglyceride levels after the training program suggest that VLDL-derived fatty acids contribute significantly to total fat oxidation.

Alternatively, an increase in LPL after training might serve to provide fatty acids for the replenishment of IMTGs that have been oxidized during exercise Certainly, further studies are needed to clarify the contribution of IMTG- and VLDL-derived fatty acid oxidation to total fat oxidation.

Another important aspect of the present study is that we have examined the effect of a low-intensity training program for only 2 h per week. Because endurance training has been shown to increase the capacity to oxidize fatty acids, it has been proposed to be beneficial in overcoming the disturbances in fat oxidation often observed in obesity and diabetes 9.

To investigate the mechanisms behind the changes in substrate oxidation after the endurance-training program, we measured mRNA levels of several genes involved in glucose and fatty acid metabolism. A muscle biopsy was taken 6—7 days before the training program and 6—7 days after the last training session to exclude the influence of acute exercise on mRNA expression.

The expression of two genes involved in regulatory steps of glucose metabolism, i. As mentioned above, mRNA expression of LPL, which hydrolyzes plasma triglycerides and directs the released FFAs into the tissue 22 , tended to increase after training, suggesting that the capacity of skeletal muscle to hydrolyze VLDL triglycerides may be improved by the training program.

Inside the muscle cell, ACC2 activity has recently been suggested to control the rate of fatty acid oxidation and triglyceride storage ACC2 catalyzes the carboxylation of acetyl-CoA to form malonyl-CoA, an intermediate that inhibits the activity of CPT1.

CPT1 catalyzes the rate-limiting step in the transfer of fatty acyl-CoA into mitochondria, where they undergo oxidation. Although we were not able to measure ACC2 enzyme activity, it is tempting to speculate that a decrease in ACC2 activity after training was responsible for the observed training-induced increase in fat oxidation.

Because high levels of malonyl-CoA have been associated with insulin resistance 42 , the reduction of ACC2 with endurance training could possibly be beneficial in the treatment of type 2 diabetes. Finally, we determined the expression of the human UCP3, which has recently also been implicated in the transport of fatty acids across the inner mitochondrial membrane In a cross-sectional study, we have previously found that UCP3 mRNA was lower in trained than in untrained subjects In the present study, we did not find a significant effect of the training program on UCP3 mRNA expression, suggesting that the training program was not severe enough to result in changes in UCP3 mRNA.

Remarkably, we recently found that, in the same study, UCP3 protein content was significantly decreased after training in all subjects The reason for the discrepancy between the effect of training on UCP3 mRNA expression and protein cannot be deduced from the present study but might involve posttranslational regulation, although the number of subjects is too limited to make such a conclusion.

The mechanism behind this adaptation seems to involve a chronic upregulation of LPL mRNA expression and a chronic downregulation of ACC2, potentially leading to lower malonyl-CoA concentration and less inhibition of CPT1.

In contrast to moderate- to high-intensity endurance training, the mild training protocol did not increase hexokinase II and GLUT4 expression, indicating that specifically fat oxidation was improved.

This study was supported by a grant from the Netherlands Organization for Scientific Research NWO to P. and a grant from the Netherlands Heart Foundation to D. The laboratories are members of the Concerted Action FATLINK FAIR-CT , supported by the European Commission. The authors thank Paulette Vallier for help in mRNA analysis and Dr.

Diraison for making and validating the ACC2 competitor. Address correspondence and reprint requests to Dr. Schrauwen, Department of Human Biology, Maastricht University, P.

Box , MD Maastricht, the Netherlands. E-mail: p. schrauwen hb. Sign In or Create an Account. Search Dropdown Menu. header search search input Search input auto suggest.

filter your search All Content All Journals Diabetes. Advanced Search. User Tools Dropdown. Sign In. Skip Nav Destination Close navigation menu Article navigation. Volume 51, Issue 7. Previous Article Next Article. Fat oxidation rates increase from low to moderate intensities and then decrease when the intensity becomes high.

The mode of exercise can also affect fat oxidation, with fat oxidation being higher during running than cycling. Endurance training induces a multitude of adaptations that result in increased fat oxidation.

The duration and intensity of exercise training required to induce changes in fat oxidation is currently unknown. Ingestion of carbohydrate in the hours before or on commencement of exercise reduces the rate of fat oxidation significantly compared with fasted conditions, whereas fasting longer than 6 h optimizes fat oxidation.

Fat oxidation rates have been shown to decrease after ingestion of high-fat diets, partly as a result of decreased glycogen stores and partly because of adaptations at the muscle level.

However, comparisons of MFO and Fat max between-modalities have not been as conclusive. The original study reported significantly greater MFO 0. A further study in a similar subject population failed to observe a significant difference in MFO, but did observe a greater Fat max during running Chenevière et al.

The reason for this disparate result in terms of MFO is not easily discernible, but could be related to between-study differences indirect calorimetry analysis of 1 vs. It is therefore recommended that the exercise modality in which Fat max tests are performed be considered when between-study and intra-individual comparisons are made, and by those preparing for multi-modal endurance competitions such as triathlons.

It has been demonstrated that the training status, sex, and acute and chronic nutritional status of the subject population or individual under study are clear determinants of MFO and Fat max , with a possible effect of exercise modality.

These determining factors must be considered when interpreting results between-studies and in serial intra-individual measurement. Given the interest in measurement of MFO and Fat max in research and non-research settings, it would be prudent to generate normative values from existing data in order to contextualize individually measured values and define the fat oxidation capacity of given research cohorts.

However, in order to do this, the aforementioned determinants of MFO and Fat max need to be considered. Accordingly, published MFO and Fat max values were synthesized from studies with homogeneous cohorts performing assessments after an overnight fast on a cycle ergometer.

These criteria were applied in order to generate sufficient data to produce meaningful normative values. Studies were subsequently partitioned into five populations: endurance-trained, lean males Achten et al. Baseline values were used for intervention studies. For synthesis, a sample size-weighted mean and SD for MFO was calculated for each population as described above for sex-mediated comparisons see section Sex.

Subsequently, normative percentile values were generated for each population assuming a within-population normal distribution Tables 1 , 2. Table 1. Normative percentile values for MFO g. Table 2. A trend toward greater MFO with increasing training status was observed Table 1 , and in males compared to females, which supports the evidence from individual studies presented above.

These normative percentile values might therefore be used by exercise physiologists to contextualize individual measurements and define the fat oxidation capacity of given research cohorts, whilst acknowledging the aforementioned determinants of MFO when making inferences.

It is worth noting that no data was available for endurance-trained female populations, which is a pertinent area for future research. It should also be noted that none of this data was derived from studies in which participants ingested a high-fat or ketogenic diet, which is known to increase fat oxidation during exercise Phinney et al.

Indeed, in many of the studies in endurance-trained males participants were specifically instructed to ingest a high-carbohydrate meal the evening before testing Achten et al.

Therefore, these values are likely only of relevance to those ingesting a traditional mixed diet. Many determinants of MFO and Fat max have been identified in the ~16 years since the original protocol was developed Achten et al. However, given the practical utility of this protocol as a training monitoring tool in elite sport and as an indication of health status, further research is warranted to better understand what factors must be considered when measuring MFO and Fat max , as is research concerned with training effects on these variables and their relevance to endurance performance Figure 2.

Figure 2. Schematic illustration of the identified determinants of maximal fat oxidation during graded protocols black and key identified unknown factors gray. An unexplored parameter likely to alter MFO and Fat max is environmental temperature. Environmental heat stress increases muscle glycogenolysis, hepatic glucose output, and whole-body carbohydrate oxidation rates, whilst reducing fat oxidation rates at given intensities Febbraio et al.

This is attributed to independent effects of rising core temperature, enhanced muscle temperature, greater plasma catecholamine concentrations, and progressive dehydration Febbraio et al. Given these effects, it might be hypothesized that MFO decreases in the heat compared to temperate conditions, although it is also possible that MFO is shifted to a lower Fat max.

Elucidating this effect is a relevant consideration for endurance sport and military contexts given the likely negative effects of environmental heat on self-selected work intensity. The effect of cold environments on substrate metabolism during prolonged exercise is less certain.

Some investigations have reported augmented carbohydrate utilization in cold vs. temperate conditions Galloway and Maughan, ; Layden et al. Interestingly, Galloway and Maughan Galloway and Maughan, reported greater fat oxidation rates during moderate intensity cycling at 11 vs.

These disparities are not easily reconciled, and may be a result of interactions between the specific environmental conditions and exercise modality cycling vs.

running Gagnon et al. Direct investigation of the impact of environmental temperature on laboratory measures of MFO and Fat max , and the environmental thresholds at which they occur, is therefore warranted.

This data would have strong applied relevance given the diverse environmental conditions in which endurance competitions take place Racinais et al. MFO is generally upregulated in response to exercise training Mogensen et al. Training-induced increases in MFO have been consistently observed in sedentary populations Mogensen et al.

Therefore, the existing literature suggests MFO is a malleable parameter that can be increased by both aerobic or interval training, particularly in sedentary populations. Indeed, alongside long-standing observations of adaptations to fat metabolism in response to moderate-intensity training Howald et al.

The most favorable training regimen for increasing MFO cannot presently be discerned. Training studies have generally utilized either prolonged moderate-intensity aerobic exercise Mogensen et al. Interestingly, differences in the magnitude of training-induced increases in MFO were not observed for moderate and high-intensity interval training in these studies Venables and Jeukendrup, ; Alkahtani et al.

Furthermore, whilst promising effects of training with low-glycogen availability on whole-body fat oxidation rates during prolonged exercise have been observed Yeo et al. There is also a notable absence of data concerning the responsiveness of MFO and Fat max to training in endurance-trained cohorts.

As endurance-trained individuals already have elevated MFO compared to lesser-trained populations, it remains to be determined if these individuals can accrue further advances in MFO through optimized training practices.

It would also be useful to discern if training-induced changes in MFO reflect alterations in substrate metabolism during prolonged exercise, as the relatively short-duration of this protocol makes it a viable monitoring tool in elite sport. Therefore, whilst it has been demonstrated that exercise training per se improves MFO in untrained populations, this effect remains to be elucidated in trained populations, and the most appropriate training regimen for increasing MFO is unknown.

These are worthy directions for future research given the likely importance of fat oxidation capacity in endurance sport and military settings, and the apparent relationship between MFO and insulin sensitivity Robinson et al.

If an individual makes extensive use of fat oxidation to support metabolism during prolonged exercise at their competitive or operational intensity, this should reduce the requirement for endogenous carbohydrate oxidation, and therefore muscle glycogen depletion, which is linked to fatigue Bergström et al.

Indeed, at a given absolute workload, significantly higher whole-body fat oxidation and lower muscle glycogenolysis have been observed in trained compared to untrained males van Loon et al.

A link between MFO, Fat max , and endurance exercise performance is further supported by cross-sectional evidence demonstrating enhanced MFO in trained compared to untrained cohorts Nordby et al.

However, the importance of MFO and Fat max for exercise performance has not yet been comprehensively studied, and such research is warranted.

Metabolically, a cross-sectional study of elite ultra-distance runners demonstrated greater MFO and Fat max in those adapted to ketogenic diets, but the rate of glycogenolysis in working skeletal muscle during prolonged exercise was not significantly different compared to those ingesting a high-carbohydrate diet, despite higher whole-body fat oxidation rates Volek et al.

Therefore, MFO, Fat max , and whole-body fat oxidation rates were dissociated from skeletal muscle glycogenolysis during prolonged endurance exercise between these groups, which might question the hypothesis linking MFO and Fat max to endurance exercise performance via muscle glycogen sparing.

However, it is possible this dissociation was an artifact of the measurement site, and that a carbohydrate sparing effect in the ketogenic group was observed in the liver, as observed previously Webster et al.

An interesting avenue for future research might therefore be to determine if MFO and Fat max are indicators of the degree of endogenous carbohydrate utilization and skeletal muscle glycogenolysis during prolonged exercise within a homogenous group of endurance-trained athletes, and consequently if such an effect has implications for endurance exercise performance.

Such data would provide indication of the functional relevance of monitoring MFO and Fat max in endurance-trained athletes, and could serve to build on existing models of endurance exercise performance McLaughlin et al.

This review has systematically identified several key determinants of MFO and Fat max. These include training status, sex, acute nutritional status, and chronic nutritional status, with the possibility of an effect of exercise modality. Accordingly, normative percentile values for MFO and Fat max in different subject populations are provided to contextualize individually measured values and define the fat oxidation capacity of given research cohorts.

However, the effect of environmental conditions on MFO and Fat max remain to be established, as does the most appropriate means of training MFO and Fat max , particularly in endurance-trained cohorts.

Furthermore, direct links between MFO, Fat max , and rates of muscle glycogenolysis during prolonged exercise remain to be established, as do relationships between MFO, Fat max , and exercise performance. This information might add to existing models of endurance exercise performance, and indicate how useful MFO and Fat max monitoring might be in endurance sport.

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. EM is funded by an Education New Zealand scholarship no role in preparation of the manuscript.

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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. Open Access This article is distributed under the terms of the Creative Commons Attribution 4.

Reprints and permissions. Karppinen, J. et al. Fat oxidation at rest and during exercise in male monozygotic twins. Eur J Appl Physiol , — Download citation. Received : 29 January Accepted : 24 October Published : 31 October Issue Date : December Anyone you share the following link with will be able to read this content:.

Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative. Download PDF. Abstract Purpose We aimed to investigate if hereditary factors, leisure-time physical activity LTPA and metabolic health interact with resting fat oxidation RFO and peak fat oxidation PFO during ergometer cycling.

Methods We recruited 23 male monozygotic twin pairs aged 32—37 years and determined their RFO and PFO with indirect calorimetry for 21 and 19 twin pairs and for 43 and 41 twin individuals, respectively.

Conclusions Hereditary factors were more important than LTPA for determining fat oxidation at rest and during exercise. Exercise Snacks and Other Forms of Intermittent Physical Activity for Improving Health in Adults and Older Adults: A Scoping Review of Epidemiological, Experimental and Qualitative Studies Article 08 January Physical activity in older age: perspectives for healthy ageing and frailty Article Open access 02 March A Review of Obesity, Physical Activity, and Cardiovascular Disease Article 01 September Use our pre-submission checklist Avoid common mistakes on your manuscript.

Introduction Fat oxidation rates at rest Goedecke et al. Leisure-time physical activity LTPA The LTPA level was determined with two separate interviews and the Baecke questionnaire. Peak oxygen uptake VO 2peak and peak fat oxidation PFO A graded incremental exercise test with a gas-exchange analysis was performed on the first day of the laboratory visit.

Metabolic health A standard 2-h OGTT followed the resting metabolism measurement. Ethical approval Good clinical and scientific practices and guidelines, as well as the Declaration of Helsinki, were followed while conducting the study.

Statistical analysis Statistical analysis was carried out with IBM SPSS Statistics Results Participant characteristics Table 1 presents the participant characteristics.

Table 2 The intraclass correlation coefficients ICCs between MZ co-twins Full size table. Full size image. Table 3 Characteristics of the long-term-discordant MZ twin pairs Full size table. Table 4 Results of the twin individual-based analysis Full size table.

Discussion For the first time, our study data showed that fat oxidation rates at rest and during exercise were similar between MZ co-twins, even though the study group was enriched with pairs who had discordant LTPA habits. Abbreviations AUC: Area under the curve DXA: Dual-energy x-ray absorptiometry ICC: Intraclass correlation coefficient LBM: Lean body mass LTPA: Leisure-time physical activity MET: Metabolic equivalent of task MZ: Monozygotic OGTT: Oral glucose tolerance test PFO: Peak fat oxidation REE: Resting energy expenditure RER: Respiratory exchange ratio RFO: Resting fat oxidation VCO 2 : Volume of carbon dioxide VO 2 : Volume of oxygen VO 2peak : Peak oxygen uptake.

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