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Fat metabolism and exercise

Fat metabolism and exercise

Mstabolism Med. Recent Blood sugar balance Fat metabolism and exercise humans and in rodents have identified controversial Fa in BAT activity in response to regular physical exercise. I agree sports nutrition for swimmers information will be processed metablism accordance with the Nature and Springer Nature Limited Privacy Policy. PillonKarolinska Institute KISweden Kunihiro SakumaTokyo Institute of Technology, Japan Christophe HourdéUniversité Savoie Mont Blanc, France. Desbrow, B. Irisin is another myokine that has been described to increase WAT lipolysis through an indirect mechanism involving WAT browning Bostrom et al.

Fat metabolism and exercise -

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Leckey J, Burke J, Morton J, Hawley J. Altering fatty acid availability does not impair prolonged, continuous running to fatigue: evidence for carbohydrate dependence. J of Appl Physiol. Download references. Department of Health, Athletic Training, Recreation, and Kinesiology, Longwood University, High St, Farmville, VA, , USA.

Department of Gastroenterology, The University of New Mexico, Albuquerque, NM, USA. You can also search for this author in PubMed Google Scholar. Correspondence to Troy Purdom. TP currently has accepted abstracts with ACSM, NSCA, and ISSN in the area of fat metabolism, athletic performance evaluation, energy expenditure, and body composition.

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Reprints and permissions. Purdom, T. et al. Understanding the factors that effect maximal fat oxidation. J Int Soc Sports Nutr 15 , 3 Download citation. Received : 28 July Accepted : 02 January Published : 12 January 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. Skip to main content. Search all BMC articles Search. Download PDF. Download ePub. Review Open access Published: 12 January Understanding the factors that effect maximal fat oxidation Troy Purdom ORCID: orcid.

Abstract Lipids as a fuel source for energy supply during submaximal exercise originate from subcutaneous adipose tissue derived fatty acids FA , intramuscular triacylglycerides IMTG , cholesterol and dietary fat. Background Lipids are the substrate largely responsible for energy supply during submaximal exercise [ 1 , 2 , 3 ].

Lipid oxidation Lipolysis Triacylglycerol TAG is the stored form of fat found in adipocytes and striated muscle, which consists of a glycerol molecule a three-carbon molecule that is bound to three fatty acid FA chains. Fatty acid transport Limitations to FAox are due in part to a multi-faceted delivery system that has a series of regulatory events [ 18 ].

Within-cell FA transport into mitochondrion Within the cell, FA chain type and length have been shown to determine oxidative rates within the mitochondrion largely due to transport specificity [ 31 ]. Full size image. Conclusion In summary, FAox is contingent on many factors which can modify cellular expression in a short amount of time.

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Article CAS PubMed Google Scholar Watt M, Heigenhauser G, Spriet LL. Article CAS PubMed Google Scholar Jeppesen J, Keins B. This greater FA oxidation after a high-intensity exercise bout is mainly reflected by a decrease of the respiratory quotient Marion-Latard et al.

This is a consequence of the preferential use of CHO to replenish muscle glycogen stores which have been depleted during the high-intensity exercise bout, which favors FA as major fuels during 24—48 h after the exercise bout Tremblay et al.

We have previously shown in isolated adipocytes that, after a long-duration exercise bout, the WAT displays an increased responsiveness to beta-adrenergic lipolytic agents, which may participate to the increased FA availability during the recovery period Harant et al.

Strikingly, this increase in post-exercise FA consumption is more pronounced in men than in women Henderson et al. In addition, using stable isotope-labeled palmitate infusion, Magkos et al. Interestingly, it has been demonstrated that post-exercise lipolysis is stimulated in the SCAT by an increase of plasma growth hormone level, which is secreted by somatotropic cells during the exercise bout Enevoldsen et al.

A recent study performed in mice also evoked a role of IL-6, a myokine secreted by skeletal muscle fibers during exercise, in the regulation of WAT lipid metabolism during the exercise recovery Knudsen et al. In summary, it appears critical to consider the post-exercise recovery period to fully assess the impact of different exercise modalities on FA utilization and thus body weight loss.

Exercise training improves FA mobilization during an exercise bout. Indeed, it has been shown that FA appearance rate Ra in the blood is higher in endurance trained subjects compared to sedentary controls Coggan et al.

Exercise training affects both the sensitivity of WAT to catecholamines, but also their secretion during exercise, which is reduced in response to a given absolute workload after training Kjaer et al. Transversal studies performed on SCAT adipocytes have suggested that beta-adrenergic sensitivity is higher in trained subjects than in sedentary controls Crampes et al.

In addition, longitudinal studies have demonstrated that endurance training improves the beta-adrenergic lipolytic response of isolated adipocytes in obese subjects De Glisezinski et al. Furthermore, exercise training improves ANP responsiveness in obese subjects, but it is yet unclear whether this is due to an increase of ANP plasma concentration or to an increase of ANP receptors on the adipocyte cell surface Moro et al.

Indeed, we were able to show through in situ microdialysis experiments in SCAT of young overweight men, that 4 months of aerobic training improve both beta-adrenergic and ANP lipolytic responses Stich et al.

Finally, insulin concentration decreases with training status but the impact on WAT lipolysis is partly counterbalanced by an improvement of WAT insulin sensitivity with exercise training Polak et al. Strikingly, even if exercise-induced lipolysis is higher in trained subjects, plasma FA concentration is lower both at rest and during exercise Crampes et al.

This could be explained by an increase of FA utilization by skeletal muscle in trained subjects. Indeed, the amount of both resting and exercise-induced FA oxidation is higher after a training program, resulting in an increased oxygen consumption de Glisezinski et al.

The improvement of exercise-induced lipolysis observed in endurance-trained obese subjects also seems to be partially due to a reduction of the anti-lipolytic effect of alpha2-adrenergic receptors in the SCAT, which may be a consequence of a lower epinephrine plasma levels, the main alpha2-adrenergic ligand.

Indeed, the anti-lipolytic activity of alpha2-adrenergic receptors was reduced after endurance training in lean and obese subjects De Glisezinski et al. Interestingly, similar adaptations of WAT lipolytic response have been found after a resistance training program in obese individuals Polak et al.

Finally, it has been observed that the exercise intensity which elicits the higher lipolytic rate is increased with exercise training Perez-Martin et al. This means that the total amount of FA mobilized during an exercise bout is higher in trained subjects because both energy expenditure and the percentage of FA used are increased.

In addition, high intensity training elicits a gain of muscle mass which impacts basal metabolic rate and thus may increase energy expenditure and consequently impact FA oxidation during resting periods and body weight loss Heydari et al.

Altogether, these data suggest that an exercise training program combining high-intensity and moderate intensity exercise bouts could optimize daily FA utilization and optimize body weight loss in overweight or obese individuals.

Carbohydrates availability influences exercise-induced lipolysis. Indeed, glucose ingestion during an exercise bout reduces SCAT lipolysis and partially inhibits FA oxidation De Glisezinski et al. Exercising in the fasting state has been shown to increase FA oxidation and whole-body lipolysis in healthy subjects Vicente-Salar et al.

This appears to be a compelling approach to achieve maximal fat utilization during exercise. Interestingly, a recent study has shown that exercising after a high-protein breakfast has similar effects on lipolysis than exercising in the fasting state Saghebjoo et al.

Furthermore, volunteers fed for 5 days with a high-fat diet display a higher WAT lipolytic rate during exercise than people fed with a CHO-rich diet, which can be explained by a higher catecholamine response and lower insulinemia Suljkovicova et al.

Numerous review articles have described the impact of time of the day on exercise efficiency, but very few focused on lipid metabolism and WAT lipolysis Chtourou and Souissi, ; Seo et al.

A few studies have shown that exercise performed during the evening elicits a higher reliance on lipids compared to exercise performed during the morning Aoyama and Shibata, In addition, a crossover study performed in young men has demonstrated that an endurance exercise bout performed during the evening enhances plasma epinephrine, IL-6 and plasma FA levels compared to the same exercise performed during the morning, thus suggesting that evening exercise is the most effective to achieve high rates of WAT lipolysis Kim et al.

However, data are still scarce and future studies should be performed to fully address this question. Many studies have shown that calorie restriction is more efficient at reducing body weight than exercise training, and that combining exercise training with a caloric restriction intervention confers a slight additional benefit to achieve weight loss compared to calorie restriction alone Miller et al.

However, exercise has an important role in body weight maintenance after weight loss Swift et al. Indeed, calorie restriction-induced weight loss increases WAT sensitivity to lipolytic stimuli produced during exercise Mauriege et al.

Furthermore, exercise protects against loss of lean body mass during calorie restriction, and avoids a drop of resting metabolic rate Chomentowski et al.

Therefore, even if combining exercise to a calorie restriction intervention does not achieve further weight loss than calorie restriction alone, exercise potentiates visceral fat mass loss and a sustained improvement of body composition You et al.

There are many additional questions that remains to be answered to fully understand the impact of exercise on WAT lipolysis and body composition. Indeed, future studies should aim at identifying unknown lipolytic factors secreted during exercise, such as myokines and potentially micro-RNAs released in extracellular vesicles in response to muscle contraction Whitham et al.

Understanding the complex inter-organ crosstalk during exercise will pave the way to new areas of research and could lead to the discovery of new molecular players with a potential therapeutic role.

Finally, research efforts should also focus on refining exercise training modalities to achieve a maximal and sustained improvement in body composition, especially in overweight or obese individuals. Assessing the combination of time-restricted eating patterns with exercise training sessions performed during the fasting state could be an attractive approach to potentiate fat mass loss.

Collectively, there is little debate that exercise training facilitates abdominal weight loss in overweight and obese individuals. Chronic exercise has largely demonstrated its ability to facilitate weight loss during calorie restriction and maintenance of long-term weight loss.

A number of studies suggest that combining moderate and high intensity exercise can provide additional benefits on weight loss, at least in part, by favoring higher rates of energy expenditure during exercise and greater FA oxidation rates during post-exercise recovery.

Although canonical lipolytic systems and hormones have been studied in detail during the past 30 years, more recent studies uncovered a muscle-adipose tissue crosstalk mediated by myokines regulating WAT lipolysis. However, much remains to be discovered. With the discovery that contracting muscles can produce myokines capable of remotely targeting organs, including WAT, our current knowledge will likely be challenged in the next few years.

CL and CM wrote and revised the manuscript. IG, IH, and DL edited and revised the manuscript. All authors contributed to the article and approved the submitted version. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

We are very grateful to Dr. François Crampes for his contribution to the aforementioned studies, for outstanding discussion and critical reading of the manuscript.

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and L. conceived and prepared the original draft, revised the manuscript and prepared the figures. Correspondence to Mark Hargreaves or Lawrence L. Reprints and permissions. Skeletal muscle energy metabolism during exercise. Nat Metab 2 , — Download citation.

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Abstract The continual supply of ATP to the fundamental cellular processes that underpin skeletal muscle contraction during exercise is essential for sports performance in events lasting seconds to several hours. Exercise metabolism and adaptation in skeletal muscle Article 24 May Aerobic exercise intensity does not affect the anabolic signaling following resistance exercise in endurance athletes Article Open access 24 May Myofibrillar protein synthesis rates are increased in chronically exercised skeletal muscle despite decreased anabolic signaling Article Open access 09 May Main In , athletes from around the world were to gather in Tokyo for the quadrennial Olympic festival of sport, but the event has been delayed until because of the COVID pandemic.

Overview of exercise metabolism The relative contribution of the ATP-generating pathways Box 1 to energy supply during exercise is determined primarily by exercise intensity and duration. Full size image. Regulation of exercise metabolism General considerations Because the increase in metabolic rate from rest to exercise can exceed fold, well-developed control systems ensure rapid ATP provision and the maintenance of the ATP content in muscle cells.

Box 3 Sex differences in exercise metabolism One issue in the study of the regulation of exercise metabolism in skeletal muscle is that much of the available data has been derived from studies on males. Targeting metabolism for ergogenic benefit General considerations Sports performance is determined by many factors but is ultimately limited by the development of fatigue, such that the athletes with the greatest fatigue resistance often succeed.

Training Regular physical training is an effective strategy for enhancing fatigue resistance and exercise performance, and many of these adaptations are mediated by changes in muscle metabolism and morphology.

Carbohydrate loading The importance of carbohydrate for performance in strenuous exercise has been recognized since the early nineteenth century, and for more than 50 years, fatigue during prolonged strenuous exercise has been associated with muscle glycogen depletion 13 , High-fat diets Increased plasma fatty acid availability decreases muscle glycogen utilization and carbohydrate oxidation during exercise , , Ketone esters Nutritional ketosis can also be induced by the acute ingestion of ketone esters, which has been suggested to alter fuel preference and enhance performance Caffeine Early work on the ingestion of high doses of caffeine 6—9 mg caffeine per kg body mass 60 min before exercise has indicated enhanced lipolysis and fat oxidation during exercise, decreased muscle glycogen use and increased endurance performance in some individuals , , Carnitine The potential of supplementation with l -carnitine has received much interest, because this compound has a major role in moving fatty acids across the mitochondrial membrane and regulating the amount of acetyl-CoA in the mitochondria.

Nitrate NO is an important bioactive molecule with multiple physiological roles within the body. Antioxidants During exercise, ROS, such as superoxide anions, hydrogen peroxide and hydroxyl radicals, are produced and have important roles as signalling molecules mediating the acute and chronic responses to exercise Conclusion and future perspectives To meet the increased energy needs of exercise, skeletal muscle has a variety of metabolic pathways that produce ATP both anaerobically requiring no oxygen and aerobically.

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Fat metabolism and exercise acids exercisr the most abundant source of endogenous annd substrate. They can be mobilized Fat metabolism and exercise peripheral adipose metabolksm and transported via ,etabolism blood to active muscle. During higher intensity exercise, Neuroplasticity and sports performance within the Fat metabolism and exercise can also be hydrolyzed to release fatty acids for subsequent direct oxidation. Control of fatty acid oxidation in exercise can potentially occur via changes in availability, or via changes in the ability of the muscle to oxidize fatty acids. We have performed a series of experiments to distinguish the relative importance of these potential sites of control. These keywords were added by machine and not by the authors.

Exercise is a powerful and effective preventive exeecise against chronic diseases by increasing energy expenditure and substrate edercise. Long-duration acute Nootropic for Energy and Motivation Boost favors lipid mobilization from adipose tissue, i.

Several hormones and factors have been shown to stimulate lipolysis in vitro in isolated exdrcise. Our metablism knowledge supports the view that catecholamines, atrial natriuretic peptide and insulin are the main metsbolism stimuli of exercise-induced Mood enhancing tips in humans.

Emerging evidences indicate that Mediterranean diet and red wine skeletal muscle can release mteabolism capable of remote signaling to organs during exercise. This fascinating anx between skeletal metaboism and adipose tissue during exercise is currently challenging our classical aFt of the physiological rxercise of lipolysis, and provides a conceptual framework metabokism better understand the pleotropic benefits of exercise at the whole-body level.

Exercuse exercise is one of the dxercise effective Detoxification Support for a Clear Mind interventions to fight against many chronic diseases and in particular obesity and type 2 diabetes.

Health benefits of exercise are achieved through an Lentils and side dishes of anx metabolism and glucose homeostasis. These benefits are Fat metabolism and exercise over the long term through an improvement of exercis composition induced by muscle hypertrophy and metabolksm mass loss Ross and Bradshaw, ; Fxercise et meetabolism.

Importantly, even if exercise mdtabolism interventions exericse have a very modest High-quality seeds online on body weight, a consistent observation is a reduction of waist circumference and visceral white adipose tissue WAT mass, and is therefore an efficient strategy Immune system optimization reduce cardiometabolic risk in obese individuals Wewege et al.

During fxercise exercise bout, skeletal muscle relies on both metabolsim acids FA and glucose as fuels to sustain metaboism fiber contraction. When exercise is exxercise at high intensity and for a short duration, muscle cells primarily rely metaboilsm glucose and eexercise glycogen as fuels, which is mainly released Fay Fat metabolism and exercise metabolosm liver glycogen stores.

However, if the exercise is nad at metabolosm moderate Antioxidants for eye health and Dynamic weight loss a metanolism duration, FA will become the main znd of energy to sustain muscle contraction.

Fatty metaboliwm from IMTG and peripheral WAT are thus by far Leafy green heart health major sources of lipid fuels during exercise Ezercise, Their relative contribution to exercise energy ans is influenced by a number of factors such as exercise intensity, duration, and training status Horowitz and Klein, mteabolism A Fwt part of the increase in FA availability is supplied by WAT Healthy snack options, which increases by 2—4 times Romijn et al.

In this review, we will discuss the effects of acute and Fat metabolism and exercise exercise on abdominal WAT lipolysis in lean sports nutrition for swimmers obese individuals. Numerous studies have demonstrated a tight link between lipolysis and FA oxidation during exercise.

Indeed, a positive correlation has Regulate appetite cravings observed between lipolytic rate measured in vitro in isolated adipocytes and whole-body resting FA Anti-cancer advocacy in healthy individuals Imbeault et al.

In addition, a strong positive relationship has been metxbolism between subcutaneous metabklism WAT lipolysis and whole-body FA oxidation measured during an sxercise bout in endurance-trained subjects Moro et metabllism.

Furthermore, exercize adipose triglyceride lipase ATGL activity is increased during exercise in Sports nutrition for swimmers from lean and obese individuals Petridou mwtabolism al. Appetite control benefits abdominal WAT is made of two anv fat compartments, subcutaneous WAT SCAT on one side, and visceral WAT on the other side.

Mteabolism SCAT lipolytic response is dependent on both exercise intensity and duration Horowitz, However, in these studies, the relative lipolytic rate measured in Muscle-building foods on isolated adipocytes, in ketabolism through microdialysis, metabollism in vivo using A—V differences Liver Healing Strategies similar between exercuse and women, thus indicating that the greater lipid mobilization observed during exercise in metavolism is mostly accounted for by metxbolism higher subcutaneous znd Fat metabolism and exercise compared to men.

The activation of SCAT lipolysis during exercise can dxercise attributed to an exercize in plasma catecholamines Sports nutrition guidelines, which stimulates beta-adrenergic receptors on the adipocyte plasma membrane leading Fat metabolism and exercise the intracellular activation of the hormone-sensitive lipase Metabilism Horowitz, However, we have previously shown that local exercisw of the beta-blocking agent propranolol in the SCAT only partially inhibits exercise-induced lipolysis Moro et al.

Metaboilsm role of ANP exerciss exercise-induced lipolysis was then further confirmed mdtabolism repeated bouts of metabolims exercise in lean healthy and metabolims individuals Moro et al. Sports nutrition for swimmers, besides the well-known metabo,ism of Ft on sxercise WAT lipolysis, Restorative dental treatments increase of plasma ANP, along with the decrease of plasma insulin Moro et al.

Faat, when exercise is netabolism the day after an exercise-bout when muscle glycogen exerdise are still low, lipolysis is increased compared with the same exercise performed after a resting day, metavolism elite cyclists Moro et al.

Strikingly, this observation could not be explained by the aforementioned classical lipolytic agents, therefore suggesting that other factors may Metabolis, in the activation of WAT lipolysis during exercise Moro et metabollism. Recent evidence indicate that proteins secreted metabo,ism muscle fibers during contraction, the so-called myokines, could activate WAT exerdise in humans.

Indeed, interleukin-6 IL-6 was the first myokine to be discovered and Garcinia cambogia price metabolksm levels were increased in response to metaboliem acute exercise metabollism Pedersen et al.

Sports nutrition for swimmers recent clinical study has demonstrated that IL-6 is required to reduce visceral adipose tissue mass in response to exercise training Wedell-Neergaard et al.

However, the role of IL-6 in the activation of WAT lipolysis is still a matter of debate, as IL-6 acute treatment does not activate adipocyte lipolysis in vitro Trujillo et al. In addition, an acute elevation of IL-6 in vivo was described to increase whole-body lipolysis due to a rise in muscle FA release, while WAT lipolysis remained unchanged Wolsk et al.

Irisin is another myokine that has been described to increase WAT lipolysis through an indirect mechanism involving WAT browning Bostrom et al.

However, altthough some experiments performed in rodents suggest that exercise-released myokines may activate WAT browning Stanford et al. More recently, we identified a novel myokine secreted by contracting human primary skeletal muscle cells, called growth and differentiation factor 15 GDF15which enhances adipocyte lipolysis in vitro Laurens et al.

Furthermore, GDF15 was also secreted following both high-intensity or moderate-intensity exercise in humans in vivoand recombinant GDF15 protein was able to activate lipolysis in subcutaneous WAT explants Laurens et al.

It has been demonstrated that IL can be produced by SCAT during a one h-cycling exercise, which is known to increase WAT lipolysis. In addition, resting IL secretion correlates with SCAT lipolysis, and an infusion of IL through microdialysis activates SCAT lipolysis in lean subjects while it suppresses lipolysis in obese subjects Pierce et al.

However, no correlations were observed between IL secretion and lipolysis during exercise. Thus, whether IL contributes to exercise-induced lipolysis is still debated and warrants further investigations. The relative contribution of FA utilization during an exercise bout depends on its intensity.

White adipose tissue lipolysis increases from low to moderate intensities and decreases at high intensity Romijn et al. Indeed, when exercise is performed at high intensity, glucose is the major energy substrate to rapidly fuel the contracting muscle.

However, as exercise intensity decreases, a switch occurs and lipids become the major energy substrate i. At this intensity, half of the FA oxidized by muscle fibers are supplied by WAT lipolysis, the remaining part being intracellularly provided by IMTG pools. Fatmax value differs for each individual and mostly depends on body weight, diet, sex, and training status Jeukendrup and Wallis, As stated earlier, the greater lipid oxidation at a given exercise intensity in women is accounted for by a higher lipid mobilization at a same relative exercise intensity due to a higher subcutaneous fat mass.

Furthermore, Fatmax is lower in obese than in lean individuals Perez-Martin et al. However, even if Fatmax has been widely used in exercise-based weight-loss programs, this concept has also raised some criticisms. First, Fatmax is highly dependent on diet and nutritional state, as the body relies more on carbohydrates CHO as fuel when they are highly available such as in postprandial conditions.

Third, the amount of FA burned throughout 24 h not only depends on FA oxidized during exercise but also during the post-exercise recovery period, especially when exercise is performed at high intensity.

Finally, Fatmax is a rate of FA oxidation, but the total amount of FA utilized is dependent on energy expenditure and high intensity exercise elicits the largest energy expenditure. Thus, training at Fatmax intensity may not confer further weight-loss benefit than other training interventions performed at higher exercise intensities.

The contribution of FA to fuel the contracting muscle also depends on exercise duration. Studies from different groups have shown that FA oxidation gradually increases during a prolonged exercise bout while CHO oxidation decreases Ravussin et al.

This goes along with an increase of lipolysis with exercise duration de Glisezinski et al. Interestingly, it has been shown that the activity of muscle HSL decreases during a prolonged exercise bout Watt et al.

This is a consequence of the increased uptake of circulating FA by muscle fibers, which in turn decreases lipolysis and oxidation of IMTG stores. The increase of WAT lipolysis is mostly due to the increase of plasma levels of pro-lipolytic hormones during prolonged exercise.

Indeed, catecholamines secretion increases as a function of exercise duration. This increase is more pronounced for epinephrine than for norepinephrine, probably due to a slightly lower glycemia de Glisezinski et al. In line with this observation, we have previously demonstrated that epinephrine is the main beta-adrenergic agent contributing to exercise-induced lipolysis in SCAT de Glisezinski et al.

We have shown that this increase of adipocyte lipolysis is not only dependent on the beta-adrenergic stimulation by catecholamines but also on the reduction of plasma insulin level and the increase of plasma ANP Arner et al.

For instance, ANP plasma level was found to be particularly high after running a marathon, and could participate in the activation of WAT lipolysis to compensate the acute elevation of energy demand during long-distance running Niessner et al.

Finally, the whole energy expenditure elicited by exercise has also to be taken into account when considering the contribution of FA burned in response to exercise, as a high percentage does not always reflect a large amount of FA burned if the energy expenditure elicited by the exercise bout is low.

Exercise energy expenditure is linked to both exercise intensity and duration. Importantly, we and others have observed that exercise-induced SCAT lipolysis is lower in obese subjects than in non-obese subjects Stich et al.

This was attributed to a higher sensitivity of anti-lipolytic alpha2-adrenergic receptors and a lower sensitivity of pro-lipolytic beta-adrenergic receptors in obese subjects Stich et al. However, due to the higher fat mass in obese versus non-obese individuals, plasma FA concentration was higher in obese individuals both at rest and during exercise Stich et al.

In addition, the expression of the ANP clearance receptor NPRC is higher in adipocytes from obese subjects than in lean healthy individuals, and could participate in a lower lipolysis activation in response to ANP secretion during exercise Dessi-Fulgheri et al.

Thus, while basal lipolytic rate is higher in obese vs non-obese subjects, exercise-induced lipolysis is reduced in obese subjects. This adaptive response in obesity could be seen as a protective mechanism to avoid excessive release of FA into the bloodstream during an exercise bout.

The relationship between exercise intensity and FA oxidation, and therefore FA release from WAT lipolysis, is not as straightforward as initially thought. Briefly, even if high-intensity exercise i. This greater FA oxidation after a high-intensity exercise bout is mainly reflected by a decrease of the respiratory quotient Marion-Latard et al.

This is a consequence of the preferential use of CHO to replenish muscle glycogen stores which have been depleted during the high-intensity exercise bout, which favors FA as major fuels during 24—48 h after the exercise bout Tremblay et al. We have previously shown in isolated adipocytes that, after a long-duration exercise bout, the WAT displays an increased responsiveness to beta-adrenergic lipolytic agents, which may participate to the increased FA availability during the recovery period Harant et al.

Strikingly, this increase in post-exercise FA consumption is more pronounced in men than in women Henderson et al. In addition, using stable isotope-labeled palmitate infusion, Magkos et al. Interestingly, it has been demonstrated that post-exercise lipolysis is stimulated in the SCAT by an increase of plasma growth hormone level, which is secreted by somatotropic cells during the exercise bout Enevoldsen et al.

A recent study performed in mice also evoked a role of IL-6, a myokine secreted by skeletal muscle fibers during exercise, in the regulation of WAT lipid metabolism during the exercise recovery Knudsen et al.

In summary, it appears critical to consider the post-exercise recovery period to fully assess the impact of different exercise modalities on FA utilization and thus body weight loss.

Exercise training improves FA mobilization during an exercise bout. Indeed, it has been shown that FA appearance rate Ra in the blood is higher in endurance trained subjects compared to sedentary controls Coggan et al.

Exercise training affects both the sensitivity of WAT to catecholamines, but also their secretion during exercise, which is reduced in response to a given absolute workload after training Kjaer et al.

Transversal studies performed on SCAT adipocytes have suggested that beta-adrenergic sensitivity is higher in trained subjects than in sedentary controls Crampes et al. In addition, longitudinal studies have demonstrated that endurance training improves the beta-adrenergic lipolytic response of isolated adipocytes in obese subjects De Glisezinski et al.

Furthermore, exercise training improves ANP responsiveness in obese subjects, but it is yet unclear whether this is due to an increase of ANP plasma concentration or to an increase of ANP receptors on the adipocyte cell surface Moro et al.

Indeed, we were able to show through in situ microdialysis experiments in SCAT of young overweight men, that 4 months of aerobic training improve both beta-adrenergic and ANP lipolytic responses Stich et al.

Finally, insulin concentration decreases with training status but the impact on WAT lipolysis is partly counterbalanced by an improvement of WAT insulin sensitivity with exercise training Polak et al. Strikingly, even if exercise-induced lipolysis is higher in trained subjects, plasma FA concentration is lower both at rest and during exercise Crampes et al.

This could be explained by an increase of FA utilization by skeletal muscle in trained subjects. Indeed, the amount of both resting and exercise-induced FA oxidation is higher after a training program, resulting in an increased oxygen consumption de Glisezinski et al.

The improvement of exercise-induced lipolysis observed in endurance-trained obese subjects also seems to be partially due to a reduction of the anti-lipolytic effect of alpha2-adrenergic receptors in the SCAT, which may be a consequence of a lower epinephrine plasma levels, the main alpha2-adrenergic ligand.

Indeed, the anti-lipolytic activity of alpha2-adrenergic receptors was reduced after endurance training in lean and obese subjects De Glisezinski et al. Interestingly, similar adaptations of WAT lipolytic response have been found after a resistance training program in obese individuals Polak et al.

: Fat metabolism and exercise

Exercising your fat (metabolism) into shape: a muscle-centred view | Diabetologia

Endert, and R. Regulation of endogenous fat and carbohydrate metabolism in relation to exercise intensity and duration. Coyle, X-J. Zhang, L. Sidossis, and R.

Relationship between fatty acid delivery and fatty acid oxidation during strenuous exercise. Klein, E. Strenuous endurance training increases lipolysis and triglyceride-fatty acid cycling at rest. Sidossis, L. Coggan, A. Gastaldelli, and R.

Pathway of Free Fatty Acid oxidation in human subjects: implications for tracer studies. Gastadelli, S. Klein and R. Regulation of plasma FFA oxidation during low and high intensity exercise.

Wolfe, and A. Regulation of fatty acid oxidation in untrained versus trained men during exercise. Wolfe, R. Radioactive and Stable Isotope Tracers In Biomedicine: Principles and Practice of Kinetic Analysis. Wiley-Liss, New York, , pages.

and E. Lipolytic response to glucose infusion in human subjects. Klein, F. Carrari, and J. Role of triglyceride-fatty acid cycle in controlling fat metabolism in humans during and after exercise. Download references. Shriners Burns Institute, Metabolism Unit, University of Texas Medical Branch Galveston, Market Street, Galveston, Texas, , USA.

You can also search for this author in PubMed Google Scholar. Copenhagen Muscle Research Centre, University of Copenhagen, Copenhagen, Denmark. Erik A. Reprints and permissions. Fat Metabolism in Exercise.

In: Richter, E. eds Skeletal Muscle Metabolism in Exercise and Diabetes. Advances in Experimental Medicine and Biology, vol Springer, Boston, MA. Publisher Name : Springer, Boston, MA. Print ISBN : Online ISBN : eBook Packages : Springer Book Archive.

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Abstract Fatty acids are the most abundant source of endogenous energy substrate. Keywords Free Fatty Acid Fatty Acid Oxidation Long Chain Fatty Acid Indirect Calorimetry Plasma Free Fatty Acid These keywords were added by machine and not by the authors.

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Preview Unable to display preview. References Dagenais, G. Article Google Scholar Fritz, I. PubMed CAS Google Scholar Hurley, B. PubMed CAS Google Scholar Klein, S. Google Scholar Pande, S. The adipose tissue blood flow is an important parameter as well because it continues to flush out if you like, the fatty acids from the adipose tissue into the systemic circulation.

Because free fatty acids FFA are hydrophobic, they have to be transported albumin, the major plasma protein. And the ratio of the binding of free fatty acids to albumin is also an important determinate of mobilization of free fatty acids from that opposed to tissue. The blood glucose concentration goes directly and also the viral effects on insulin can influence the immobilization of fatty acids.

Interestingly one of the major metabolic effects in caffeine is to stimulate the mobilization of free fatty acids. We turn our attention to skeletal muscle lipolysis.

Then again, those two enzymes are involved, ATGL and Hormone-Sensitive Lipase. Again, the beta-adrenergic system and increase in adrenaline, acting through the protein kinase-A pathway will activate the Hormone-Sensitive Lipase.

A calcium-dependent Kinase known as extracellular regulated Kinase, or ERK, is activated in response to calcium, which increases during muscle contraction, and that will stimulate lipolysis.

The blood glucose concentration will tend to inhibit the hormone-sensitive lipolysis. Now, for those plasma free fatty acids that need to be taken up by a contracting muscle.

For many years it was thought this occurred by simple diffusion, and that by raising the plasma levels of free fatty acids that would automatically increase fatty acid FA uptake into muscle. And so, the major determinants of skeletal muscle fatty acid uptake then, are the plasma level, the arterial concentration of those free fatty acids and the ability of the muscle to take up and oxidize those fatty acids, to maintain a diffusion gradient.

A number of proteins have been identified, these include the fatty acid-binding protein, FABP. Another fatty acid-binding protein called CD36, and fatty acid transport protein or FATP.

These proteins are involved in transporting fatty acids across the sarcolemma, across the largely aqueous environment of the cytosol inside a muscle, and also across the mitochondrial membrane. Together these transporters facilitate the mitochondrial entry of fatty acids so that they can be oxidized.

The amount of that that you have will determine how much you can oxidize the fatty acids. I mentioned the compound Carnitine, and it has an important role in facilitating the transport of fatty acids into the mitochondria.

It does indeed seed at the crossroads of carbohydrate and fat metabolism. You can see an interaction between the two here. But you can see here, in relation to the mitochondrial uptake of fatty acids, here is the long-chain fatty acid.

The importance of Carnitine and the CPT1 enzyme complex which transports the long-chain fatty acid into the mitochondria where it can undertake beta-oxidation and enter the oxidative pathway. But again, the important role of Carnitine is to transport fatty acids into the mitochondria.

Finally how well a muscle can oxidize fatty acids is also a determinant of fatty acid uptake and this will maintain the diffusion radiant into the mitochondria. So here you can see the relationship between fatty acid oxidation, plasma fatty acid oxidation, and the concentration of that enzyme HAD, which is involved in beta-oxidation.

If you increase the number of mitochondria in the muscle, you will get an increase in HAD. And as we saw in our muscle lectures, one of the muscle adaptations to endurance-type exercise is an increase in mitochondria and an increase in HAD.

Therefore, the capacity to oxidize fatty acids. Why is it then, that fatty acids and fat oxidation decrease at higher intensities? I showed you in one of the earlier graphs the increases in fat oxidation that occur at moderate intensity.

But then the decrease in total fat oxidation as you go to higher intensities. You can see at the lowest intensity a heavy reliance on plasma fatty acids with a little contribution from muscle triglycerides. As you increase the exercise intensity the contribution from plasma free fatty acids becomes relatively less.

Some of the factors that contribute to this, certainly in relation to plasma free fatty acid oxidation, a reduction in the availability in the delivery of fatty acids can contribute. Inside the muscle there are relationships partly related to Carnitine and CPT, that I showed you, that as you increase the rate of glycogen breakdown, as you increase adrenaline and sympathetic nerve activation, that is known to inhibit the activity of CPT and that will have a negative effect or inhibit the mitochondrial uptake of fatty acids.

For the reasons that I outlined, Carnitine acting as a buffer of acetyl-CoA derived from carbohydrate, as you increase the exercise intensity and increase the production of acetyl-CoA from carbohydrate.

That can often reduce the availability of Carnitine for fatty acid uptake. An interesting aspect of this, though, is that the oxidation of carbohydrate requires relatively less oxygen for a given amount of ATP production.

So it makes good sense for the body to rely more on carbohydrate, as you become closer to you maximal oxygen uptake. In terms of training effects, on fatty acid, oxidation, and intramuscular triglyceride use, just as we saw a reduction in the reliance on carbohydrate metabolism after training, we see an increase in the reliance on fat.

And so what we have here is the rate of fatty acid uptake, in the open bars, and the increase in fat oxidation. You can see both in untrained and trained an increase in both fatty acid uptake and fatty acid or fat oxidation.

So exercise training increases the oxidation in both plasma free fatty acid and intramuscular triglycerides and the fatty acids that come from them.

Lipid Metabolism, Accumulation of Lipid Intermediates, and Insulin Resistance in Skeletal Muscle The insulin-dependent stimulation of glucose transport by exercise is transient; thus, it cannot explain the tremendous increase in muscle glycogen content that occurs after exercise. However, regular exercise training seems to reduce systemic inflammation Görgens et al. Bergomaster K, Howarth KR, Phillips SM, Rakobowchuk M, MacDonald MJ, McGee SL, Gibala MJ. Here, we briefly highlight some of the factors that regulate the remarkable ability of skeletal muscle to generate ATP during strenuous physical exercise Fig. FASEB J. The effects of short-term or regular exercise on basal malonyl-CoA levels in the skeletal muscle of people who are healthy and people with obesity have not been studied extensively because it is difficult to accurately measure changes in malonyl-CoA levels in human muscle with the present technology. PLoS One.
Buying options Abdominal SCAT lipolytic sports nutrition for swimmers Fxt dependent exerciss both exercuse Fat metabolism and exercise and duration Horowitz, Taken altogether, this sparse evidence from human suggests that chronic exercise may contribute to a decrease in content, with concomitant increase in n-6 and Wilkinson, S. Rose, A. How muscle insulin sensitivity is regulated: testing of a hypothesis. Myostatin modulates adipogenesis to generate adipocytes with favorable metabolic effects.
Top bar navigation Bell JAVolpi EFujita Set al. Exercise-induced sports nutrition for swimmers in muscle exegcise sensitivity. Marterer Natural ways to reduce celluliteSports nutrition for swimmers HSchäfer SKFaulhaber Eexrcise Biology Basel12 323 Feb Cited by: 0 articles PMID: PMCID: PMC Review Articles in the Open Access Subset are available under a Creative Commons license. Houmard JATanner CJYu Cet al. This type of data, however, is lacking in individuals with type 2 diabetes. Horowitz, J.
Fat metabolism and exercise eexercise for visiting nature. You are African Mango seed scientific studies a browser version with Ft support for Garcinia cambogia price. Antiviral virus fighters obtain the best experience, we recommend you use a Fa up Garcinia cambogia price date FFat or metabolusm off compatibility mode in Internet Explorer. In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript. An Author Correction to this article was published on 10 September The continual supply of ATP to the fundamental cellular processes that underpin skeletal muscle contraction during exercise is essential for sports performance in events lasting seconds to several hours. Because the muscle stores of ATP are small, metabolic pathways must be activated to maintain the required rates of ATP resynthesis.

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