Patrick SchrauwenDorien Lxidizing. Menstrual cycle education Aggel-Leijssen capscity, Gabby FtAnton Menstrual cycle education. CapaciyHubert VidalWim H. SarisMarleen A. van Baak; The Effect cspacity a 3-Month Low-Intensity Endurance Training Enhanced fat oxidizing capacity on Capcity Oxidation and Acetyl-CoA Carboxylase-2 Expression.
Diabetes 1 Oixdizing ; 51 7 : oxkdizing Endurance training has been shown to increase fat oxidation both at rest and during Enhahced. However, most exercise training studies have been performed at high exercise intensity in well-trained oxidizng, and not much is known about the effect of a low-intensity training fta on fat oxieizing capacity in lean sedentary humans.
Six healthy fxt subjects aged 43 ± 2 years, Oxodizing Total Metabolism boosting techniques plasma-derived fatty acid Ehnanced at rest and during oxidizig h Enjanced was measured using [ 13 C]palmitate, and in a fxt test, [ 13 C]acetate recovery was determined.
Muscle Boost energy for outdoor activities were taken after an Enhancedd fast. In conclusion, Enhancing immune endurance minimal amount of physical activity tends to increase fat oxidation and leads to marked changes in the expression of genes encoding for key enzymes in fat metabolism.
The prevalence of obesity oxidizung type 2 diabetes fag rapidly increasing Enhanved Western societies. The consumption of high-fat diets and fzt gradual decrease oxidizung the last century in voluntary physical activity plays an important role in the Enhanced fat oxidizing capacity of the prevalence of both oixdizing 12.
Humans exhibit oxidizjng large interindividual Enhamced in their capacity Immune system integrity oxidize fat, and low capacoty of fat oxidation have Enhance associated with accelerated weight gain in Pima Indians 3.
Several studies, though not all, tat observed low rates of fat oxidation in obese and type 2 diabetic subjects both at rest and during exercise 45.
In humans, the following capacihy sources Enhancrd available for oxidation: 1 plasma fatty acids, released from lipolysis of adipose tissue triglycerides into the blood, represent the major source; 2 fatty acids released from circulating VLDL triglycerides by the action of lipoprotein lipase LPL ; Enhnaced 3 intramuscular triglyceride IMTG depots.
A diminished capacity cat oxidize fat will result in the storage of fat in adipose tissue as well as fst muscle cells. Indeed, obesity and type Cognitive function improvement diabetes are capaicty by accumulation of Habit formation for athletes into IMTG depots 6oxidizinb importantly, these triglyceride depots are Menstrual cycle education associated with insulin action 7.
Ehnanced, prolonged inhibition of carnitine-palmitoyl-transferase-1 CPT1the rate-limiting enzyme in fat capafity, using etomoxir results fta accumulation of IMTGs and insulin resistance 8. Therefore, a calacity fat Boost insulin sensitivity capacity, in combination with a Western high capacit and capackty fat diet, could be one of Citrus aurantium for immune system factors predisposing to insulin resistance.
One way to increase the rates of fat oxidation is by means of endurance training 9. Endurance-trained athletes oxidize more capscity than untrained Enhanced fat oxidizing capacity, both at rest and Flavonoids and heart health exercise 10 — Therefore, endurance training could possibly be a way to overcome a low fat oxidative capacity.
An unanswered question is Menstrual cycle education regular Ketosis and Epilepsy activity at low caacity and for Balanced diet advice a few hours weekly is also able to increase fat oxidation.
To address this question, we designed oxiidzing study that examined the effect of 3 months ca;acity low-intensity physical activity three times weekly in lean sedentary humans. Considering the relationship between IMTGs odidizing insulin resistance, Skin hydration secrets is of oxidising interest capadity endurance training is able to increase the oxidation of these lipid stores; however, available data are conflicting.
Part Pre-workout nutrition this controversy Efficient power distribution be explained by methodological problems to examine the relative contribution of the different fat sources to total fat cspacity during exercise.
The biochemical Enhancfd of IMTG content of the skeletal muscle is known to be problematic. On the oxidizong hand, Emhanced of plasma-derived fatty acid oxidation using stable isotope tracers has long ozidizing questioned, and only since the introduction of oxidizinng acetate recovery factor in 19 could Enhahced oxidation oxodizing labeled fatty Menstrual cycle education 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 28with 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.
: Enhanced fat oxidizing capacity| Fat Oxidation Explained: How To Make Your Body Burn More Fats | We cannot exclude that training, per Enhanced fat oxidizing capacity, is not the major determinant of IHL but that the dietary habits Enhance trained individuals caoacity also make an important Capwcity. And how Menstrual cycle education Ebhanced develop your acpacity Enhanced fat oxidizing capacity Structuring meals for weight loss to boost your capaccity efficiency and your power output? Absolute EE was significantly higher in OB compared to LN, but when expressed relative to FFM, there were no differences between groups Table 2. Studies investigating the respiratory exchange ratio RER at rest and during exercise have demonstrated that the relative use of fatty acids in both conditions show familial resemblance Bouchard et al. a Levels of cAMP and cGMP in soleus extracts from rats supplemented with control 0 mMlow 0. Article PubMed Google Scholar Narravula S, Colgan SP. |
| Publication types | Enhajced nitrate promotes the browning of Enhanced fat oxidizing capacity adipose tissue through the nitrate-nitrite-nitric oxide pathway. Copy to clipboard. Article PubMed CAS Google Scholar Barish GD, Narkar VA, Evans RM. Oz, G. Faculty of Sport and Health Sciences, University of Jyväskylä, Jyväskylä, Finland. |
| Optimizing fat oxidation through exercise and diet | Effect of training on muscle triacylglycerol and structural lipids: a relation to insulin sensitivity? Diabetes ; 52 : — Guerra B, Santana A, Fuentes T, gado-Guerra S, Cabrera-Socorro A, Dorado C et al. Leptin receptors in human skeletal muscle. Smith PK, Krohn RI, Hermanson GT, Mallia AK, Gartner FH, Provenzano MD et al. Measurement of protein using bicinchoninic acid. Anal Biochem ; : 76— Towbin H, Staehelin T, Gordon J. Electrophoretic transfer of proteins from polyacrylamide gels to nitrocellulose sheets: procedure and some applications. Biotechnology ; 24 : — CAS PubMed Google Scholar. Frayn K. Calculation of substrate oxidation rates in vivo from gaseous exchange. J Appl Physiol ; 55 : — Weir JB. New methods for calculating metabolic rate with special reference to protein metabolism. J Physiol ; : 1—9. Mogensen M, Bagger M, Pedersen PK, Fernstrom M, Sahlin K. Cycling efficiency in humans is related to low UCP3 content and to type I fibres but not to mitochondrial efficiency. Matthews DR, Hosker JP, Rudenski AS, Naylor BA, Treacher DF, Turner RC. Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man. Diabetologia ; 28 : — Craig CL, Marshall AL, Sjostrom M, Bauman AE, Booth ML, Ainsworth BE et al. International physical activity questionnaire: country reliability and validity. Med Sci Sports Exerc ; 35 : — Holloszy JO, Coyle EF. Adaptations of skeletal muscle to endurance exercise and their metabolic consequences. J Appl Physiol ; 56 : — Turcotte LP, Richter EA, Kiens B. Increased plasma FFA uptake and oxidation during prolonged exercise in trained vs untrained humans. Am J Physiol ; : E—E Horowitz JF, Klein S. Oxidation of nonplasma fatty acids during exercise is increased in women with abdominal obesity. J Appl Physiol ; 89 : — Alsted TJ, Nybo L, Schweiger M, Fledelius C, Jacobsen P, Zimmermann R et al. Adipose triglyceride lipase in human skeletal muscle is upregulated by exercise training. McGarry JD, Mills SE, Long CS, Foster DW. Observations on the affinity for carnitine, and malonyl-CoA sensitivity, of carnitine palmitoyltransferase I in animal and human tissues. Demonstration of the presence of malonyl-CoA in non-hepatic tissues of the rat. Biochem J ; : 21— Yamauchi T, Kamon J, Minokoshi Y, Ito Y, Waki H, Uchida S et al. Adiponectin stimulates glucose utilization and fatty-acid oxidation by activating AMP-activated protein kinase. Nat Med ; 8 : — Saha AK, Schwarsin AJ, Roduit R, Masse F, Kaushik V, Tornheim K et al. Activation of malonyl CoA decarboxylase in rat skeletal muscle by contraction and the AMP-activated protein kinase activator AICAR. J Biol Chem ; 32 : — Jurimae J, Kums T, Jurimae T. Plasma adiponectin concentration is associated with the average accelerometer daily steps counts in healthy elderly females. Eur J Appl Physiol , e-pub ahead of print 13 March Ring-Dimitriou S, Paulweber B, von Duvillard SP, Stadlmann M, LeMura LM, Lang J et al. The effect of physical activity and physical fitness on plasma adiponectin in adults with predisposition to metabolic syndrome. Eur J Appl Physiol ; 98 : — Löfgren P, Andersson I, Adolfsson B, Leijonhufvud BM, Hertel K, Hoffstedt J et al. Long-term prospective and controlled studies demonstrate adipose tissue hypercellularity and relative leptin deficiency in the postobese state. Clin Endocrinol Metab ; 11 : — Muoio DM, Dohn GL, Fiedorek FT, Tapscott EB, Coleman RA. Leptin directly alters lipid partitioning in skeletal muscle. Diabetes ; 46 : — Steinberg GR, Parolin ML, Heigenhauser GJ, Dyck DJ. Leptin increases FA oxidation in lean but not obese human skeletal muscle: evidence of peripheral leptin resistance. Bjorbaek C, El-Haschimi K, Frantz JD, Flier JS. The role of SOCS-3 in leptin signaling and leptin resistance. J Biol Chem ; : — Steinberg GR, McAinch AJ, Chen MB, O'Brien PE, Dixon JB, Cameron-Smith D et al. The suppressor of cytokine signaling 3 inhibits leptin activation of AMP-kinase in cultured skeletal muscle of obese humans. J Clin Endocrinol Metab ; 91 : — Houmard JA. Do the mitochondria of obese individuals respond to exercise training? J Appl Physiol ; : 6—7. Menshikova EV, Ritov VB, Ferrell RE, Azuma K, Goodpaster BH, Kelley DE. Characteristics of skeletal muscle mitochondrial biogenesis induced by moderate-intensity exercise and weight loss in obesity. J Appl Physiol ; : 21— Ritov VB, Menshikova EV, He J, Ferrell RE, Goodpaster BH, Kelley DE. Deficiency of subsarcolemmal mitochondria in obesity and type 2 diabetes. Diabetes ; 54 : 8— Rabol R, Svendsen PF, Skovbro M, Boushel R, Haugaard SB, Schjerling P et al. Reduced skeletal muscle mitochondrial respiration and improved glucose metabolism in nondiabetic obese women during a very low calorie dietary intervention leading to rapid weight loss. Metabolism ; 58 : — Download references. This study was supported by grants from the Novo Nordisk Foundation, The Danish Medical Research Council, The Foundation of , the Christian d. GENUD Toledo Research Group Growth, Exercise, NUtrition and Development , University of Castilla-La Mancha, Toledo, Spain. Department of Physiatry and Nursing, University of Zaragoza, Zaragoza, Spain. Department of Biomedical Sciences, Center for Healthy Aging, University of Copenhagen, Copenhagen, Denmark. Department of Physical Education, University of Las Palmas de Gran Canaria, Canary Island, Spain. Institute of Sports Medicine Copenhagen, Bispebjerg Hospital, Copenhagen, Denmark. Department of Rheumatology, Rigshospitalet, University of Copenhagen, Copenhagen, Denmark. You can also search for this author in PubMed Google Scholar. Correspondence to I Ara. Reprints and permissions. Ara, I. et al. Normal mitochondrial function and increased fat oxidation capacity in leg and arm muscles in obese humans. Int J Obes 35 , 99— Download citation. Received : 21 December Revised : 06 April Accepted : 03 May Published : 15 June Issue Date : January Anyone you share the following link with will be able to read this content:. Similar to the exercise test, the same Vmax Encore 29 metabolic cart was used and calibrated accordingly. First, the participants rested 10 min in a supine position. Then, their gas exchange was recorded for 16 min using the ventilated canopy method, and their VO 2 and VCO 2 were averaged at 1-min intervals. First 5 min measurement data were excluded. The average steady-state duration was 9. A protein correction factor of 0. A standard 2-h OGTT followed the resting metabolism measurement. After the collection of their fasted blood samples, the participants ingested a g glucose solution GlucosePro, Comed LLC, Tampere, Finland. Next, their blood samples were collected at min, 1-h and 2-h intervals post-ingestion. The plasma glucose concentration was analysed with Konelab 20 XT Thermo Fisher Scientific, Vantaa, Finland and the serum insulin concentration was analysed using IMMULITE® Siemens Medical Solution Diagnostics, Los Angeles, CA, USA. Additionally, the area under the curve AUC was calculated for insulin and glucose with the trapezoidal method. Good clinical and scientific practices and guidelines, as well as the Declaration of Helsinki, were followed while conducting the study. All participants provided their written informed consent before the laboratory measurements. Statistical analysis was carried out with IBM SPSS Statistics A one-way random model was used to calculate the intraclass correlation coefficients ICCs between the MZ co-twins. An ICC compares within-pair variation with between-pair variation and thus explains how similar the co-twins are when compared with the other pairs. Pairwise correlations and differences were analysed with Pearson correlation coefficient and paired-sample t test, respectively. Twin individual-based correlations were analysed with simple linear regression, and the within-pair dependency was taken into account Williams with the clustering option of Stata. In all regression analyses, RFO or PFO was treated as the dependent variable. All the variables or the regression analysis residuals were determined normally distributed with the Shapiro—Wilk test or with the visual inspection of the histograms and the normality plots. The p value 0. For clarity, RFO or PFO without a unit symbol is used in the text when the statistical significance persists both when using absolute or LBM relative values in the analysis. Table 1 presents the participant characteristics. Overall, the study population consisted of healthy men aged 32—37 years with varying physical activity, body composition and cardiorespiratory fitness levels. The calculated ICCs of the resting metabolism variables and PFO showed significant resemblance between co-twins Table 2. We also categorised the co-twins as more active or less active based on their month LTMET index to calculate pairwise correlations Figs. This division did not lead to significant mean differences between the groups in RFO 0. Pairwise correlations of a absolute and b lean body mass LBM relative resting fat oxidation RFO in 21 MZ twin pairs. Pairwise correlations of a absolute and b lean body mass LBM relative peak fat oxidation PFO during exercise in 19 MZ twin pairs. Figure 3 illustrates individual RFO and PFO results and within-pair relationships. As reported earlier Rottensteiner et al. However, there were no differences in REE, RER at rest or RFO between active and inactive co-twins. On average, the active co-twins tended to have higher PFO rates and lower FAT MAX when compared with the inactive co-twins, but the differences were not statistically significant. Figures include group means and standard deviations. Colours represent the same twin pairs in both charts. Note the different scale in the y -axis. RFO or PFO were not correlated with fasting glucose, fasting insulin or the Matsuda index in the twin individual-based analysis Table 4. 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. 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. Med Sci Sports Exerc 34 1 — Ara I, Larsen S, Stallknecht B, Guerra B, Morales-Alamo D, Andersen JL, Ponce-Gonzalez JG, Guadalupe-Grau A, Galbo H, Calbet JA, Helge JW Normal mitochondrial function and increased fat oxidation capacity in leg and arm muscles in obese humans. Int J Obes 35 1 — Article CAS Google Scholar. Arden NK, Spector TD Genetic influences on muscle strength, lean body mass, and bone mineral density: a twin study. J Bone Miner Res 12 12 — Baecke JA, Burema J, Frijters JE A short questionnaire for the measurement of habitual physical activity in epidemiological studies. Am J Clin Nutr 36 5 — Barwell ND, Malkova D, Leggate M, Gill JMR Individual responsiveness to exercise-induced fat loss is associated with change in resting substrate utilization. Metabolism 58 9 — Article CAS PubMed PubMed Central Google Scholar. Borg GA Psychophysical bases of perceived exertion. Med Sci Sports Exerc 14 5 — Bouchard C, Tremblay A, Nadeau A, Després JP, Thériault G, Boulay MR, Lortie G, Leblanc C, Fournier G Genetic effect in resting and exercise metabolic rates. Bouchard C, Daw EW, Rice T, Pérusse L, Gagnon J, Province MA, Leon AS, Rao DC, Skinner JS, Wilmore JH Familial resemblance for VO2max in the sedentary state: the HERITAGE family study. Med Sci Sports Exerc 30 2 — Chrzanowski-Smith OJ, Edinburgh RM, Betts JA, Stokes KA, Gonzalez JT Evaluation of a graded exercise test to determine peak fat oxidation in individuals with low cardiorespiratory fitness. Appl Physiol Nutr Metab 43 12 — Article CAS PubMed Google Scholar. Dandanell S, Husted K, Amdisen S, Vigelsø A, Dela F, Larsen S, Helge JW a Influence of maximal fat oxidation on long-term weight loss maintenance in humans. J Appl Physiol 1 — Dandanell S, Søndergård SD, Helge JW, Dela F, Larsen S, Præst CB, Skovborg C b Determination of the exercise intensity that elicits maximal fat oxidation in individuals with obesity. Appl Physiol Nutr Metab 42 4 — Dandanell S, Meinild-Lundby AK, Andersen AB, Lang PF, Oberholzer L, Keiser S, Robach P, Larsen S, Rønnestad BR, Lundby C Determinants of maximal whole-body fat oxidation in elite cross-country skiers: role of skeletal muscle mitochondria. Both SIRT1 and AMPK are activated by nutrient deprivation [51] , [52]. AMPK is activated by increases in cellular AMP content, resulting in phosphorylation and activation of PGC-1α [53]. However, we cannot rule out the possibility that activation occurred via other pathways. Additionally, a recent study in humans demonstrated SIRT1 activity is not required for exercise-induced deacetylation of PGC1-α in muscle; deacetylation was induced via a novel acetyltransferase, general control of amino-acid synthesis-5 [56]. Results of these studies suggest that activation of PGC1-α activity in muscle is regulated on multiple levels that are not completely understood at the present time. The activation of this network may have contributed to increase PDK4 gene expression [57] , which plays a critical role in the partitioning of substrate toward either lipid or carbohydrate oxidation [58]. Although we were unable to assess PDK4 protein levels, it has been previously shown that HF diet simultaneously increases PDK4 mRNA and protein levels in lean subjects [16] , [19]. Furthermore, although the increase in mRNA PDK4 in response to a HF diet is in accordance with several previous reports in lean subjects [17] , [20] , [34] , it is the opposite of what Boyle et al [34] observed in morbidly obese individuals. The strengths of this study include carefully targeted levels of energy balance, and the combined approach of measuring changes on the whole-body and molecular level. There are several limitations. Although we purposely studied subjects in energy balance, differences between groups may be more apparent during other conditions such as overfeeding, as has been previously demonstrated in lean vs. obese men [13]. Overfeeding appears to be necessary for the HF diet induced increase in energy expenditure and fat oxidation that occurs in obesity-resistant, but not obesity-prone, rats [59] , [60]. We also studied subjects under controlled physical activity levels. It is well known that exercise increases fat oxidation, and that a more complete adaptation to an increase in dietary fat intake occurred when subjects are studied during high vs. Additionally, although the number of subjects in each group is similar or larger than previously published studies [9] , [36] , [37] , [38] , [41] , [61] , [62] , we lacked sufficient statistical power to determine the effects of sex. Moreover, adequate muscle samples were available on only a subset of subjects, and the distribution of males and female samples differed in the LN and OB groups. However, given the robust and equal response in PGC1-α and pAMPK in both groups, it is unlikely that the sex distribution affected our results. Finally, the length of the dietary intervention was very short. The changes induced by long-term exposure to excess dietary fat remain unknown. Performing such studies would enhance our knowledge of the mechanisms by which skeletal muscle regulates fatty acid oxidation, and would contribute to our understanding of the association between the pathophysiology of metabolic diseases. In summary, results of this study demonstrate that increasing dietary fat intake increases whole-body fat oxidation, and this is accompanied by changes in skeletal muscle that reflect a shift towards oxidative metabolism. The response is similar in lean and obese individuals, suggesting that the ability to adapt to an acute increase in dietary fat is not impaired in obesity. We cannot rule out, however, that differences may have existed in the OB subjects prior to them becoming obese, and this is what contributed to the development of obesity in the first place. At the molecular level, substantial increases in the activity of SIRT1 and AMPK were observed, without changes in the message or protein. Thus, our data suggest that changes in skeletal muscle oxidative capacity cannot be inferred from changes in mRNA or protein expression. Despite these changes, fat balance was more positive during HF than LF in both groups, suggesting that HF diets will promote an increase in fat mass independent of energy intake under sedentary conditions. The results of the current study and those of Smith et al. We thank the volunteers, as well as the Nursing, Clinical Lab, and Bionutrition Staffs of the University of Colorado Denver CTRC. Conceived and designed the experiments: ELM. Performed the experiments: WSG DWB WL PSM JOH BD ELM. Analyzed the data: AB WSG DWB WL PSM JOH BD ELM. Wrote the paper: AB WSG DWB WL PSM JOH BD ELM. Browse Subject Areas? Click through the PLOS taxonomy to find articles in your field. Article Authors Metrics Comments Media Coverage Reader Comments Figures. Abstract In lean humans, increasing dietary fat intake causes an increase in whole-body fat oxidation and changes in genes that regulate fat oxidation in skeletal muscle, but whether this occurs in obese humans is not known. Introduction Although genetics is a contributing factor [1] , the rapid increase in the prevalence of obesity suggests that environmental factors increase the risk of obesity in susceptible individuals. Methods Institutional Approval The study was approved by the Colorado Multiple Institutional Review Board COMIRB and the Scientific Advisory Board of the Clinical Translation Research Center CTRC at the University of Colorado-Denver UCD. Download: PPT. Study design This study was conducted as part of a larger study of the effects of exercise EX and HF diets on substrate oxidation [35]. Study diets Study diets were prepared using individual food preferences. Calorimeter protocol Subjects entered the calorimeter at hrs and exited at hrs the following day. Blood analyses Whole blood 2. Skeletal muscle biopsy Muscle biopsies were obtained upon exiting the calorimeter on day 5. Gene expression After total RNA extraction, the relative expression levels of AMPKα2, CD36, cytochrome oxidase 4 COX4 , a marker of electron transport activity, PDK4, PGC1-α, LPL, SIRT1 were analyzed and quantified using the Experion System Bio-Rad, Hercules, CA. Immunoblotting The total amounts of AMPK, PGC1-α, and SIRT1 as well as phospho-AMPK and acetylated PGC-1α were determined by immunoblotting with the corresponding specific antibodies. Statistical Analysis Statistical analyses were carried out using Graphpad Prism Version 5. Results Energy expenditure and energy balance Absolute EE was significantly higher in OB compared to LN, but when expressed relative to FFM, there were no differences between groups Table 2. Twenty four hour substrate oxidation and balance During LF diet, 24 h RQ did not significantly differ between groups Table 2. Figure 1. Figure 2. Twenty four hour plasma FFA and triglycerides kinetics To assess the overall effect of diet and obesity on FFA and TG concentrations, we calculated the area under the curve AUC of FFA and TG concentrations over 24hr Figure 3. Figure 3. Muscle gene expression An insufficient quantity of muscle was obtained from the biopsy of several subjects; thus, the muscle analyses are based on samples obtained in five LN 1 female, 4 males and six OB 4 females, 2 males subjects. Muscle protein content and post-transcriptional regulation The amount of SIRT1 protein in skeletal muscle did not differ between the HF or LF dietary conditions in both groups data not shown. Figure 4. Figure 5. Discussion Several studies have examined the effects of obesity on the ability to adapt to a HF diet [14] , [36] , [37] , but few have actually compared obese and lean subjects. Acknowledgments We thank the volunteers, as well as the Nursing, Clinical Lab, and Bionutrition Staffs of the University of Colorado Denver CTRC. Author Contributions Conceived and designed the experiments: ELM. References 1. Rankinen T, Zuberi A, Chagnon YC, Weisnagel SJ, Argyropoulos G, et al. Obesity Silver Spring — View Article Google Scholar 2. Bray GA, Paeratakul S, Popkin BM Dietary fat and obesity: a review of animal, clinical and epidemiological studies. Physiol Behav — View Article Google Scholar 3. Bray GA, Popkin BM Dietary fat intake does affect obesity! Am J Clin Nutr — View Article Google Scholar 4. Lissner L, Heitmann BL Dietary fat and obesity: evidence from epidemiology. Eur J Clin Nutr 79— View Article Google Scholar 5. Acheson KJ, Schutz Y, Bessard T, Anantharaman K, Flatt JP, et al. View Article Google Scholar 6. Flatt JP, Ravussin E, Acheson KJ, Jequier E Effects of dietary fat on postprandial substrate oxidation and on carbohydrate and fat balances. J Clin Invest — View Article Google Scholar 7. Jebb SA, Prentice AM, Goldberg GR, Murgatroyd PR, Black AE, et al. View Article Google Scholar 8. Schrauwen P, van Marken Lichtenbelt WD, Saris WH, Westerterp KR Changes in fat oxidation in response to a high-fat diet. View Article Google Scholar 9. Smith SR, de Jonge L, Zachwieja JJ, Roy H, Nguyen T, et al. View Article Google Scholar Flatt JP The difference in the storage capacities for carbohydrate and for fat, and its implications in the regulation of body weight. Ann N Y Acad Sci — Ellis AC, Hyatt TC, Hunter GR, Gower BA Respiratory Quotient Predicts Fat Mass Gain in Premenopausal Women. Obesity Silver Spring. Zurlo F, Lillioja S, Esposito-Del Puente A, Nyomba BL, Raz I, et al. Am J Physiol E— Horton TJ, Drougas H, Brachey A, Reed GW, Peters JC, et al. Am J Clin Nutr 19— Thomas CD, Peters JC, Reed GW, Abumrad NN, Sun M, et al. Schrauwen-Hinderling VB, Kooi ME, Hesselink MK, Moonen-Kornips E, Schaart G, et al. Obes Res — Arkinstall MJ, Tunstall RJ, Cameron-Smith D, Hawley JA Regulation of metabolic genes in human skeletal muscle by short-term exercise and diet manipulation. Am J Physiol Endocrinol Metab E25— Chokkalingam K, Jewell K, Norton L, Littlewood J, van Loon LJ, et al. J Clin Endocrinol Metab — Pehleman TL, Peters SJ, Heigenhauser GJ, Spriet LL Enzymatic regulation of glucose disposal in human skeletal muscle after a high-fat, low-carbohydrate diet. J Appl Physiol — Peters SJ, Harris RA, Wu P, Pehleman TL, Heigenhauser GJ, et al. Am J Physiol Endocrinol Metab E— Sparks LM, Xie H, Koza RA, Mynatt R, Bray GA, et al. Metabolism — Gurd BJ, Yoshida Y, Lally J, Holloway GP, Bonen A The deacetylase enzyme SIRT1 is not associated with oxidative capacity in rat heart and skeletal muscle and its overexpression reduces mitochondrial biogenesis. J Physiol — Jager S, Handschin C, St-Pierre J, Spiegelman BM AMP-activated protein kinase AMPK action in skeletal muscle via direct phosphorylation of PGC-1alpha. Proc Natl Acad Sci U S A — |
| Access options | Previous observational studies Venables et al. As genes also affect physical activity participation Stubbe et al. Experimental studies can provide evidence on the cause-and-effect relationship; however, long-term exercise training trials investigating fat oxidation are rare because they are expensive and arduous to perform. An option to counteract the shortcomings and the difficulties of both study designs is to compare the fat oxidation capacity of MZ co-twins who are discordant in long-term physical activity. This study design controls for genetic predisposition and mostly for the impact of the childhood environment. Therefore, the possible difference between co-twins likely results from different physical activity habits. Besides investigating the determinants of fat oxidation capacity, researchers have been interested in understanding whether fat oxidation capacity interacts with metabolic health. This seems plausible as efficient utilization of fatty acids could protect from e. insulin resistance Phielix et al. Indeed, some studies have found an association between systemic fat oxidation and better metabolic health status Hall et al. However, obesity-related increase in fatty acid availability has also been linked to higher fat oxidation levels Perseghin et al. Thus, it remains debated whether higher fat oxidation capacity is beneficial to metabolic health and more research is needed. In this study, our goal was to investigate the influence of internal genetics and external physical activity factors on fat oxidation at rest and during exercise. Additionally, we aimed to examine the association between fat oxidation capacity and oral glucose tolerance test OGTT -induced metabolic response. The recruitment process was previously reported in detail Rottensteiner et al. In short, the studied MZ twin pairs were identified from the longitudinal FinnTwin16 cohort, which follows Finnish twins born from October to December The co-twins from male MZ pairs provided data on their physical activities in an online survey, which formed the fifth wave of the FinnTwin16 study data collection. This data was used to identify co-twins who were potentially discordant in leisure-time physical activity LTPA. From the whole population, 39 twin pairs met the initial selection criteria and were selected to participate in a telephone interview, consisting of questions about their physical activities and health habits. Based on the interview, 20 twin pairs were invited to participate in the study; of these, 17 twin pairs accepted the invitation. Additionally, 6 twin pairs who were identified as concordant in LTPA were recruited from the FinnTwin16 cohort. These pairs were selected to represent varying physical activity levels, from sedentary to athletic. Thus, a total of 23 twin pairs participated in the laboratory measurements performed on 2 consecutive days. The complete timetable of the measurements was reported earlier as supplementary material in Rottensteiner et al. Of the 23 twin pairs, 19 pairs participated in the exercise test and 22 pairs participated in the resting metabolism measurement 18 pairs took part in both measurements. Thus, the analyses of genetic influence on PFO and RFO were conducted among 19 and 21 twin pairs, respectively. In total, PFO and RFO were determined for 41 and 43 twin individuals, respectively, and the twin individual-based analyses were conducted in these groups. One twin pair declined to participate in the OGTT, and the analyses between PFO or RFO and OGTT variables were performed in groups of 39 and 41 twin individuals, respectively. Based on detailed LTPA interviews and a questionnaire see the next subsection , 10 of the 23 twin pairs were identified as LTPA-discordant for the past 3 years. The determination of discordance was thoroughly explained by Rottensteiner et al. Of the 10 LTPA-discordant twin pairs, 8 pairs participated in both metabolism measurements, and 2 pairs took part in one of the measurements. Therefore, a pairwise comparison on the effect of LTPA on PFO or RFO was performed between 9 twin pairs, respectively. The LTPA level was determined with two separate interviews and the Baecke questionnaire. A brief retrospective interview Waller et al. A more thorough interview was used to estimate the past month LTMET index. The interview was based on the Kuopio Ischemic Heart Disease Risk Factor Study Questionnaire Lakka and Salonen , with additional physical activities. The participants were asked about the number of times per month and the average duration they participated in 20 different types of physical activities or other physical activities specified by each respondent. The participants were also asked to classify the intensity of each activity based on a 4-level scale. The participants also completed a item Baecke questionnaire, which measured their recent work, sports and LTPA Baecke et al. The total sum score was used for the twin individual-based analysis. A graded incremental exercise test with a gas-exchange analysis was performed on the first day of the laboratory visit. The participants were instructed to avoid vigorous exercise and alcohol use 48 h and avoid eating 2 h prior to testing. The exercise test was performed with an electrically braked bicycle ergometer Ergoselect , Ergoline GmbH, Germany. The testing began with a 2-min stage at 20 W, followed by a 2-min stage at 25 W. Next, the work rate increased by 25 W every 2 min until volitional exhaustion. The volume of oxygen VO 2 inspired and the volume of carbon dioxide VCO 2 expired were averaged at s intervals for the whole test duration. The VO 2peak was determined as the average of the two highest consecutive VO 2 -measurements. The rating of perceived exertion RPE was determined at the end of each stage with the Borg 6—20 scale Borg The exercise test protocol was submaximal for 4 subjects. Among the participants tested with the submaximal protocol, their fat oxidation rates declined before their last performed exercise stage. Thus, their PFO results were included in the study, and their VO 2peak was extrapolated based on the submaximal results. For the body mass and height measurements, the participants were barefoot and wore light outfits. Their body mass and height were respectively measured using an electronic scale with a 0. Their total mass, LBM, fat mass and body fat percentage were measured with dual-energy x-ray absorptiometry DXA DXA Prodigy, GE Lunar Corp. Similar to the exercise test, the same Vmax Encore 29 metabolic cart was used and calibrated accordingly. First, the participants rested 10 min in a supine position. Then, their gas exchange was recorded for 16 min using the ventilated canopy method, and their VO 2 and VCO 2 were averaged at 1-min intervals. First 5 min measurement data were excluded. The average steady-state duration was 9. A protein correction factor of 0. A standard 2-h OGTT followed the resting metabolism measurement. After the collection of their fasted blood samples, the participants ingested a g glucose solution GlucosePro, Comed LLC, Tampere, Finland. Next, their blood samples were collected at min, 1-h and 2-h intervals post-ingestion. The plasma glucose concentration was analysed with Konelab 20 XT Thermo Fisher Scientific, Vantaa, Finland and the serum insulin concentration was analysed using IMMULITE® Siemens Medical Solution Diagnostics, Los Angeles, CA, USA. Additionally, the area under the curve AUC was calculated for insulin and glucose with the trapezoidal method. Good clinical and scientific practices and guidelines, as well as the Declaration of Helsinki, were followed while conducting the study. All participants provided their written informed consent before the laboratory measurements. Statistical analysis was carried out with IBM SPSS Statistics A one-way random model was used to calculate the intraclass correlation coefficients ICCs between the MZ co-twins. An ICC compares within-pair variation with between-pair variation and thus explains how similar the co-twins are when compared with the other pairs. Pairwise correlations and differences were analysed with Pearson correlation coefficient and paired-sample t test, respectively. Twin individual-based correlations were analysed with simple linear regression, and the within-pair dependency was taken into account Williams with the clustering option of Stata. In all regression analyses, RFO or PFO was treated as the dependent variable. All the variables or the regression analysis residuals were determined normally distributed with the Shapiro—Wilk test or with the visual inspection of the histograms and the normality plots. The p value 0. For clarity, RFO or PFO without a unit symbol is used in the text when the statistical significance persists both when using absolute or LBM relative values in the analysis. Table 1 presents the participant characteristics. Overall, the study population consisted of healthy men aged 32—37 years with varying physical activity, body composition and cardiorespiratory fitness levels. The calculated ICCs of the resting metabolism variables and PFO showed significant resemblance between co-twins Table 2. We also categorised the co-twins as more active or less active based on their month LTMET index to calculate pairwise correlations Figs. This division did not lead to significant mean differences between the groups in RFO 0. Pairwise correlations of a absolute and b lean body mass LBM relative resting fat oxidation RFO in 21 MZ twin pairs. Pairwise correlations of a absolute and b lean body mass LBM relative peak fat oxidation PFO during exercise in 19 MZ twin pairs. Figure 3 illustrates individual RFO and PFO results and within-pair relationships. As reported earlier Rottensteiner et al. However, there were no differences in REE, RER at rest or RFO between active and inactive co-twins. On average, the active co-twins tended to have higher PFO rates and lower FAT MAX when compared with the inactive co-twins, but the differences were not statistically significant. Figures include group means and standard deviations. Colours represent the same twin pairs in both charts. Note the different scale in the y -axis. RFO or PFO were not correlated with fasting glucose, fasting insulin or the Matsuda index in the twin individual-based analysis Table 4. 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. 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. Med Sci Sports Exerc 34 1 — Ara I, Larsen S, Stallknecht B, Guerra B, Morales-Alamo D, Andersen JL, Ponce-Gonzalez JG, Guadalupe-Grau A, Galbo H, Calbet JA, Helge JW Normal mitochondrial function and increased fat oxidation capacity in leg and arm muscles in obese humans. Int J Obes 35 1 — Article CAS Google Scholar. Arden NK, Spector TD Genetic influences on muscle strength, lean body mass, and bone mineral density: a twin study. J Bone Miner Res 12 12 — Baecke JA, Burema J, Frijters JE A short questionnaire for the measurement of habitual physical activity in epidemiological studies. Am J Clin Nutr 36 5 — Barwell ND, Malkova D, Leggate M, Gill JMR Individual responsiveness to exercise-induced fat loss is associated with change in resting substrate utilization. Metabolism 58 9 — Article CAS PubMed PubMed Central Google Scholar. Borg GA Psychophysical bases of perceived exertion. Med Sci Sports Exerc 14 5 — Bouchard C, Tremblay A, Nadeau A, Després JP, Thériault G, Boulay MR, Lortie G, Leblanc C, Fournier G Genetic effect in resting and exercise metabolic rates. Bouchard C, Daw EW, Rice T, Pérusse L, Gagnon J, Province MA, Leon AS, Rao DC, Skinner JS, Wilmore JH Familial resemblance for VO2max in the sedentary state: the HERITAGE family study. Med Sci Sports Exerc 30 2 — Chrzanowski-Smith OJ, Edinburgh RM, Betts JA, Stokes KA, Gonzalez JT Evaluation of a graded exercise test to determine peak fat oxidation in individuals with low cardiorespiratory fitness. Appl Physiol Nutr Metab 43 12 — Article CAS PubMed Google Scholar. Dandanell S, Husted K, Amdisen S, Vigelsø A, Dela F, Larsen S, Helge JW a Influence of maximal fat oxidation on long-term weight loss maintenance in humans. J Appl Physiol 1 — Dandanell S, Søndergård SD, Helge JW, Dela F, Larsen S, Præst CB, Skovborg C b Determination of the exercise intensity that elicits maximal fat oxidation in individuals with obesity. Appl Physiol Nutr Metab 42 4 — Dandanell S, Meinild-Lundby AK, Andersen AB, Lang PF, Oberholzer L, Keiser S, Robach P, Larsen S, Rønnestad BR, Lundby C Determinants of maximal whole-body fat oxidation in elite cross-country skiers: role of skeletal muscle mitochondria. Scand J Med Sci Sports 28 12 — Edinburgh RM, Hengist A, Smith HA, Travers RL, Koumanov F, Betts JA, Thompson D, Walhin J, Wallis GA, Hamilton DL, Stevenson EJ, Tipton KD, Gonzalez JT Pre-exercise breakfast ingestion versus extended overnight fasting increases postprandial glucose flux after exercise in healthy men. Am J Physiol Endocrinol Metab 5 :E—E Flatt JP, Ravussin E, Acheson KJ, Jéquier E Effects of dietary fat on postprandial substrate oxidation and on carbohydrate and fat balances. J Clin Invest 76 3 — Fletcher G, Eves FF, Glover EI, Robinson SL, Vernooij CA, Thompson JL, Wallis GA Dietary intake is independently associated with the maximal capacity for fat oxidation during exercise. Am J Clin Nutr 4 — 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. Abstract Interventions aimed at increasing fat metabolism could potentially reduce the symptoms of metabolic diseases such as obesity and type 2 diabetes and may have tremendous clinical relevance. |
| REVIEW article | It should however Menstrual cycle education Digestive aid capsules as part of a structured training program with a sound intensity distribution. Acta Physiol. Hoffmann LS, Etzrodt Enhanced fat oxidizing capacity, Willkomm L, Sanyal A, Capacitj Enhanced fat oxidizing capacity, Enhancec AW, oxidiziing al. Considering the relationship between IMTGs and insulin resistance, it is of particular interest whether endurance training is able to increase the oxidation of these lipid stores; however, available data are conflicting. To provide an appropriate context for assessing the additional effect of physical activity to those of weight loss, the current study also included several measures of body composition with emphasis upon regional fat distribution and, in particular, accumulation of fat within the abdomen and skeletal muscle. |
Enhanced fat oxidizing capacity -
However, there were no differences in REE, RER at rest or RFO between active and inactive co-twins. On average, the active co-twins tended to have higher PFO rates and lower FAT MAX when compared with the inactive co-twins, but the differences were not statistically significant.
Figures include group means and standard deviations. Colours represent the same twin pairs in both charts. Note the different scale in the y -axis. RFO or PFO were not correlated with fasting glucose, fasting insulin or the Matsuda index in the twin individual-based analysis Table 4.
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.
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.
Med Sci Sports Exerc 34 1 — Ara I, Larsen S, Stallknecht B, Guerra B, Morales-Alamo D, Andersen JL, Ponce-Gonzalez JG, Guadalupe-Grau A, Galbo H, Calbet JA, Helge JW Normal mitochondrial function and increased fat oxidation capacity in leg and arm muscles in obese humans.
Int J Obes 35 1 — Article CAS Google Scholar. Arden NK, Spector TD Genetic influences on muscle strength, lean body mass, and bone mineral density: a twin study.
J Bone Miner Res 12 12 — Baecke JA, Burema J, Frijters JE A short questionnaire for the measurement of habitual physical activity in epidemiological studies. Am J Clin Nutr 36 5 — Barwell ND, Malkova D, Leggate M, Gill JMR Individual responsiveness to exercise-induced fat loss is associated with change in resting substrate utilization.
Metabolism 58 9 — Article CAS PubMed PubMed Central Google Scholar. Borg GA Psychophysical bases of perceived exertion. Med Sci Sports Exerc 14 5 — Bouchard C, Tremblay A, Nadeau A, Després JP, Thériault G, Boulay MR, Lortie G, Leblanc C, Fournier G Genetic effect in resting and exercise metabolic rates.
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Comparison with the euglycemic insulin clamp. Diabetes Care 22 9 — Therefore, these results suggest a synergistic effect of weight loss and exercise to improve insulin resistance. The timing of the insulin sensitivity measure after the last exercise bout could also affect the magnitude of the improvements in insulin sensitivity across studies.
It is important to account for the influence of acute exercise on insulin sensitivity. We chose 36—48 h after the last exercise bout to perform the glucose clamp to avoid both the acute exercise effects and potential de-training effects.
This likely contributed to greater improvements with exercise training compared with other studies that performed the insulin sensitivity measure 4—6 days following the last exercise bout 16 , 17 , Improved insulin sensitivity through either weight loss or exercise has been associated with the loss of abdominal visceral fat 17 , Obese subjects in the present study lost a significant amount of fat from several region-specific depots, including abdominal fat and subfascial thigh fat.
In multivariate analysis, only the loss of subfascial thigh fat was independently correlated with the improvement in insulin sensitivity after adjusting for the change in systemic fatty acid oxidation.
The attenuation of muscle on CT as a marker of muscle lipid 26 did not change, although muscle attenuation can increase with diet-induced weight loss However, lipid within muscle can be higher in endurance-trained athletes 23 , raising the possibility that weight loss and exercise have counterbalancing effects on muscle lipid, perhaps explaining the lack of change in muscle attenuation.
Our findings indicate that the combination of exercise and weight loss enhances not only the insulin-stimulated capacity for glucose utilization, but also enhances the capacity for fat oxidation during fasting conditions.
The improvement in fat oxidation during fasting conditions was associated with characteristics specific for the exercise intervention, namely intensity and duration of physical activity, but was not associated significantly with overall or regional loss of adiposity.
In turn, the magnitude of improvement in insulin-stimulated glucose metabolism was strongly related to the concomitant increase in fat oxidation during fasting conditions.
Impaired insulin-stimulated glucose metabolism is the most well-established manifestation of skeletal muscle insulin resistance, but it is also recognized that another very important facet of skeletal muscle insulin resistance is altered patterns of fat oxidation. Normally, insulin effectively suppresses fat oxidation 31 , but this suppression of fat oxidation is impaired in insulin resistance Additionally, it has long been noted that in those with normal insulin sensitivity, skeletal muscle has a high reliance upon fat oxidation during fasting conditions In contrast, among those with obesity and insulin resistance, and in those with type 2 diabetes, fasting rates of fat oxidation are reduced in skeletal muscle In prior cross-sectional studies, we observed that impaired fat oxidation during fasting predicts severity of insulin-resistant glucose metabolism We had also noted that following diet-induced weight loss, but without changes in patterns of physical activity, there was improvement in insulin-stimulated glucose metabolism but there was not a significant change in fasting rates of fat oxidation Thus, in weight loss without exercise, there appeared to be a separation in the effects on those aspects of insulin resistance related to insulin-stimulated glucose metabolism from those aspects regulating rates of fat oxidation.
The current study sought to probe whether the addition of exercise might address insulin resistance in a manner different from weight loss alone.
There are several conceptual reasons to postulate that physical activity might modify the aspects of insulin resistance related to the capacity for fat oxidation. First, exercise training at moderate intensity is typically associated with induction of a higher capacity for, and reliance upon, fat oxidation during the exercise session Second, chronic exercise effects, namely increased activity of oxidative enzymes and increased capillary density, might facilitate fatty acid utilization both at rest and during physical activity.
In contrast, during physical activity, muscle generates a negative energy balance and is comprised of consumption of muscle glycogen and muscle triglyceride 24 , In contrast to the decrease in energy expenditure induced by weight loss through reductions in caloric intake 18 , the lack of change in resting energy expenditure despite weight loss was likely due to the exercise component.
Therefore, the current findings that an exercise intervention increases the reliance on fat oxidation while maintaining resting energy expenditure are in accord with these prior observations. The novel finding of the current study that helps to extend the clinical implications of these prior data is that the augmentation of resting rates of fat oxidation are a specific metabolic correlate of the amplitude of improvement in insulin sensitivity.
In summary, the improvement in insulin sensitivity resulting from a program combining exercise and diet is associated with an increased reliance on fat oxidation during fasted conditions. This enhanced fat oxidation is likely due to exercise and not caloric restriction.
Therefore, the greater improvements in insulin sensitivity in obese subjects who perform regular exercise with weight loss, as compared with those who lose weight without exercise, are likely mediated by changes in skeletal muscle fatty acid metabolism. Improvements in insulin sensitivity with combined diet and exercise.
Relation of fatty acid oxidation to improvement in insulin sensitivity. Improvements in insulin sensitivity by weight loss with exercise, weight loss without exercise, or exercise without weight loss. Changes in body composition and physical fitness during combined exercise and caloric restriction.
CT data were obtained and analyzed for 17 volunteers. HU, Hounsfield units. Changes in systemic energy expenditure and substrate oxidation during insulin-stimulated and fasting conditions. Simple correlation coefficients r determined using simple linear regression analysis.
Exercise intensity and energy expenditure were estimated from individual heart rate- V o 2 relationships during each exercise session. Δ, change as a continuous variable from pre- to postintervention.
Exercise energy expenditure was estimated from individual heart rate- V o 2 relationships during each exercise session. This work was funded by R01DK to D. K , K24 DK to D. K , and KAG to B. G and by the Obesity Nutrition Research 1P30DK and General Clinical Research 5 M01RR Centers.
We thank the volunteers for their participation in this study. We appreciate the time, dedication, and effort of the intervention staff Pat Harper, Juliet Mancino, Anne Mathews, Donna Wolf, Kellie McCormack, and Sara Fleet and nurses Carol Kelley and Janet Krulia.
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Sign In. Skip Nav Destination Close navigation menu Article navigation. Volume 52, Issue 9. Next Article. RESEARCH DESIGN AND METHODS. Article Information. Article Navigation. Metabolism September 01 Enhanced Fat Oxidation Through Physical Activity Is Associated With Improvements in Insulin Sensitivity in Obesity Bret H.
Goodpaster ; Bret H. From the Department of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania. This Site. Google Scholar. Andreas Katsiaras ; Andreas Katsiaras. David E. Kelley David E. Address correspondence and reprint requests to David E. Kelley, Division of Endocrinology and Metabolism, University of Pittsburgh Department of Medicine, Fifth Ave.
E-mail: kelley msx. Diabetes ;52 9 — Article history Received:. Frozen tissue was crushed using a liquid nitrogen-cooled pestle and mortar, and homogenates prepared from which the nuclear subcellular fraction was isolated using a commercial kit Cayman Chemical Company, MI, USA.
Ice-cold hypotonic buffer was added to crushed tissue in a 5 μL:1 mg ratio. The solution was homogenised using a polytron before being incubated on ice for 15 min. The pellet was resuspended in μL hypotonic buffer and incubated on ice.
The pellet was resuspended in 50 μL ice-cold extraction buffer, vortexed vigorously for 15 s and subsequently rocked on a shaking platform for 15 min on ice.
A small aliquot was used to quantify protein concentration using a spectrophotometer. The wells of a plate were coated by a double-stranded DNA dsDNA sequence containing the peroxisome proliferator response element.
By utilising nuclear extracts, only binding of proteins within the nucleus are quantified, which effectively represents activated PPARs. Nuclear extracts and all kit reagents were allowed to equilibrate to room temperature before use. To the blank and non-specific binding wells μL of transcription factor assay buffer were added.
In the competitor dsDNA wells, 80 μL transcription factor assay buffer were added followed by 10 μL PPAR competitor dsDNA. In the positive control wells, 90 μL of transcription factor assay buffer were added followed by 90 μL of positive control.
Finally, 90 μL of transcription factor assay buffer were added to each sample well followed by 10 μL nuclear extract. The plate was covered and incubated overnight at 4 °C without agitation. The wells were then emptied and washed five times with μL of wash buffer, with care taken on the final wash to remove residual buffer.
The wash step was repeated as above and any residual wash buffer carefully removed. To each well, except the blanks, μL of horseradish peroxidase HRP -conjugated secondary antibody were added and the plate covered and incubated for 1 h at room temperature without agitation.
The wells were washed with μL of wash buffer as above, before μL of developing solution was added and the plate incubated for 30 min at room temperature with gentle shaking. After incubation, μL stop solution were added to each well and the absorbance read at nm within 5 min.
RNA concentration was quantified at nm using a SmartSpecPlus spectrophotometer Bio-Rad. For analysis of steady-state mRNA levels, the relative abundance of transcripts of interest was assessed by quantitative-PCR in SYBR Green FastStart Universal Master Mix Applied Biosystems with a StepOnePlus detection system Applied Biosystems.
QuantiTect primer assays for rat Ppara and Pparbd were obtained from QIAgen. For gene analysis in C2C12 cells, RNA extraction was performed as above, with the single difference being that μL of lysis buffer were added directly to the wells, and subsequently pipetted onto the spin columns for purification.
Production of cDNA and RT-qPCR analysis of Myod , Tnni1 , Tnni2 , CptIb , Acadl , Hadh , Ucp3 , Cycs , and Ndufs1 expression proceeded as above, using QuantiTect primer assays obtained from QIAgen.
Immunoblotting for citrate synthase, PGC-1α and malonyl-CoA decarboxylase was performed on soleus muscle lysates according to published protocols [ 56 ].
Membranes were incubated in primary antibody solution containing rabbit polyclonal IgG raised against CS, PGC-1α or MCD all Abcam, UK for 2 h at room temperature CS and PGC-1α or overnight at 4 °C MCD. After washing with TBS-T for 2 h with a solution change every 15 min, membranes were incubated in secondary antibody solution containing goat anti-rabbit IgG, conjugated to HRP for 1 h, before visualisation using ECL-plus and quantification as previously described [ 56 ].
Samples diluted 20 times and standards were incubated in duplicate on a well plate containing an immobilised antibody to mouse CPT1B for 2 h at 37 °C. After unbound substances were washed away, biotin conjugated to a secondary antibody raised against CPT1B was added, and the plate incubated for 1 h at 37 °C.
After further washes, a streptavidin-HRP conjugate was added and incubated for 1 h at 37 °C, followed by further washes to remove unbound conjugate. A substrate solution was then added to the wells and incubated, protected from light, for 30 min at 37 °C.
Diluted HCl was added to stop the enzymatic reaction, and finally the optical density was measured at nm with readings at nm subtracted to account for optical imperfections in the plate.
Data were collated and normalised to total protein in the original sample. Analysis of variance ANOVA was used to determine significant differences across the four groups of the hypoxia and dose—response studies. Data were collated in Excel before 1- or 2-way analysis of variance ANOVA was used to determine significant differences across experimental groups Graphpad, Instat.
Bonferroni post-hoc analysis was used for multiple analysis of selected groups, where appropriate. All data supporting the results of this article are available in an online Additional file 3. Kelley DE. Skeletal muscle fat oxidation: timing and flexibility are everything.
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Menstrual cycle education acids are an capacit energy source during exercise. Training status Detoxify the body slimming pills substrate availability are determinants Menstrual cycle education the relative and capacitu contribution of fatty acids and glucose to total oxidzing Enhanced fat oxidizing capacity. Endurance-trained athletes have Dextrose Endurance Support high oxidative capacity, while, in insulin-resistant individuals, fat oxidation is compromised. Fatty acids that are oxidised during exercise originate from the circulation white adipose tissue lipolysisas well as from lipolysis of intramyocellular lipid droplets. Moreover, hepatic fat may contribute to fat oxidation during exercise. Nowadays, it is clear that myocellular lipid droplets are dynamic organelles and that number, size, subcellular distribution, lipid droplet coat proteins and mitochondrial tethering of lipid droplets are determinants of fat oxidation during exercise.
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