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Fat metabolism and exercise

Fat metabolism and exercise

Impact of physical exercise on Pancreatic trauma adipose Fat metabolism and exercise ajd acid profile and inflammation in response to a high-fat diet regimen. Article CAS PubMed PubMed Central Google Scholar Nybo, L. Acid-base balance during repeated bouts of exercise: influence of HCO 3.

Fat metabolism and exercise -

The increased expression of FAox transport and oxidative cell proteins CD36, CPT-1, HAD, etc. that results in an increase FAox are a result of exercise intensity [ 24 , 49 ]. The Lima-Silva et al. Thus, FAox adaptation potential is related to training at higher exercise intensities rather than non-descript chronic exercise adaptation.

Additionally, it has also been shown that carnitine concentrations are a direct limitation of FAox Fig. Interestingly, efforts to mitigate the limitations of free carnitine on MFO at high exercise intensities have been unsuccessful [ 24 ].

Exercise intensity may further influence MFO by influencing catecholamine concentrations which have regulatory effects on lipolysis [ 16 ], glycogenolysis, as well as gluconeogenesis [ 12 ].

Increased epinephrine concentrations that parallel increases in exercise intensity stimulate both glycogenolysis and gluconeogenesis [ 12 ]. As exercise intensity increases, so does catecholamine concentrations facilitating a concurrent increase of serum CHO and FAs into the blood [ 12 ].

The crossover concept. The relative decrease in energy derived from lipid fat as exercise intensity increases with a corresponding increase in carbohydrate CHO. The crossover point describes when the CHO contribution to substrate oxidation supersedes that of fat. MFO: maximal fat oxidation.

Adapted from Brooks and Mercier, The concept of the crossover point represents a theoretical means to understand the effect of exercise intensity on the balance of CHO and FA oxidation [ 4 ] Fig.

More specifically, the crossover concept describes the point that exercise intensity influences when the CHO contribution relevant to energy demand exceeds FAox. The limitations of FAox at higher intensities is due to the vast amount of acetyl-CoA produced by fast glycolysis [ 24 , 38 ].

The abrupt increase in total acetyl-CoA production at high intensity is due to fast glycolysis flooding the cell with potential energy, which suppresses FA mitochondrial transport potential resulting in decreased FAox Fig. Notably, the large inter-individual fluctuation of when the crossover point occurs at a given exercise intensity can be attributed in part to training status [ 39 , 40 ].

Training status has been shown to effect catecholamine release and receptor sensitivity [ 12 ], endogenous substrate concentrations, and cellular transport protein expression; all of which contribute to the variability of when MFO occurs relevant to exercise intensity [ 1 ].

Nonetheless, MFO occurs in all populations regardless of training status, nutritional influence, etc. Another factor that significantly influences FAox is the duration of exercise [ 13 , 45 , 48 ]. Throughout a prolonged exercise bout, changes in hormonal and endogenous substrate concentrations trigger systematic changes in substrate oxidation [ 20 , 51 ].

Studies show that endurance training promotes reliance on endogenous fuel sources for up to min of submaximal exercise [ 47 , 51 , 52 ]. Exercise duration has a large effect on the origin of FAs for oxidative purposes.

While the initiation of exercise relies heavily on endogenous fuel sources IMTG and glycogen , reductions in IMTG concentrations have been shown to occur when exercise duration exceeds 90 min [ 45 ]. Increases in both epinephrine and plasma LCFA concentrations were observed when exercise exceeded 90 min with a simultaneous reduction in HSL activity.

Therefore the increase in serum LCFAs [ 20 , 45 ] and the saturation of HSL to epinephrine [ 16 , 46 ] are postulated to inhibit HSL reducing IMTG oxidation when exercise exceeds 90 min [ 20 ].

The shift from intramuscular fuel sources to serum derived FAs after 2 h of submaximal exercise parallel changes in blood glucose concentrations.

Trained subjects however experienced a reduction in muscular CHO uptake during the same time frame compared with the untrained. This suggests that the trained subjects were able to maintain FAox despite substrate origin during prolonged exercise to stave off CHO usage for high intensity exercise [ 51 ].

While the exercise intervention used in this study is not typically classified as endurance exercise, the exercise protocol does clarify the variation in the origin of substrate oxidation over time, and expands on the diverse effects exercise duration has on substrate oxidation.

Training duration has a large influence on FA and CHO oxidation during prolonged submaximal exercise. However, training status has little influence on the origin of FAs during the first min of submaximal exercise. Nonetheless, trained subjects are able to maintain higher workloads with decreased metabolic work HR for longer periods compared to untrained individuals based on the ability to maintain FAox for longer durations [ 45 ].

Despite the training status effect on FAox, exercise duration will dictate substrate origin during submaximal exercise [ 20 , 45 , 51 ].

Variability in FAox owing to sex exist due to the inherent hormonal differences specific to men and women [ 53 , 54 , 55 , 56 ]. In a comprehensive study with over men and premenopausal women, the energy contribution of fat was significantly higher in women vs.

Studies have consistently shown that premenopausal women have a significantly greater ability to oxidize fat during exercise [ 2 , 57 , 58 ].

The sex differences in fat oxidation [ 58 , 59 ] during exercise is attributed to the increased circulation of estrogens [ 53 , 54 , 60 ]. Evidence suggests that estrogen directly stimulates AMPK [ 29 ] and PGC-1α activity [ 60 ], which is thought to increase the downstream FAox transport protein CD36 and beta-oxidative protein HAD [ 30 ].

Additionally, beta-oxidative proteins that oxidize LCFA oxidation have been shown to be regulated in part by estrogen [ 54 , 60 ]. The result of increased beta-oxidative proteins is directly related to increased FAox potential [ 29 , 54 ]. Interestingly, when men were supplemented with estrogen, increases in FAox were observed along with increased cellular expression of beta-ox proteins within eight days of supplementation [ 60 ].

Circulating estrogen is naturally higher for premenopausal women compared to men. Additionally, fluctuation in estrogen levels is inherent throughout the menstrual cycle [ 53 , 59 ]. Estrogens are generally higher during the follicular phase of the menstrual cycle compared to the luteal phase [ 29 ].

Paradoxically, elevated estrogens during the follicular phase do not affect FAox when compared to the luteal phase [ 29 , 53 ]. Nevertheless, elevations in endogenous circulating estrogens inherent to premenopausal women increase the expression of cellular proteins responsible for increased FA transport and oxidation compared to men.

Cellular protein expression and the corresponding endogenous vs. systematic substrate oxidation vary according to dietary macronutrient intake [ 19 , 35 , 61 ]. It has been recently shown that high fat diets promote FAox and have performance enhancement capabilities [ 3 , 60 ].

However, definitive conclusions regarding pre-exercise macronutrient dominant diets and exercise performance improvements are contingent on specific exercise applications [ 62 ] that are directed by exercise duration and intensity [ 63 , 64 , 65 ].

Diets that have higher proportions of a specific macronutrient e. High fat diets increase IMTG concentrations while decreasing glycogen levels within muscle [ 17 , 35 ]. Alternatively, high CHO diet conditions increase glycogen concentrations while IMTGs decrease [ 17 ].

However, post-exercise predominant macronutrient CHO consumption has been shown to influence cellular protein expression in as little as 2 hrs [ 69 ]. The plasticity of cellular changes relevant to chronic adaptation are compromised when macronutrient content is altered [ 65 , 67 ].

Macronutrient proportion and timing has been shown to have effects on cellular adaptation [ 32 ] as well as the physiological response to exercise [ 70 , 71 , 72 ].

High fat diets increase beta-ox potential at rest [ 66 ] and during exercise [ 34 ], however, the limitations of high fat diets including short term adaptation 5dys reside with high intensity exercise [ 70 , 72 , 73 ]. Pyruvate dehydrogenase is the enzyme responsible for oxidizing pyruvate as the final substrate of the glycolytic pathway.

The deleterious cellular adaptation of reduced PDH activity due to high fat diets has been found to compromise high intensity exercise performance potential [ 35 , 63 , 67 ]. Adapting the body to high fat diets allows the body to increase IMTG storage as well as increase FAox [ 21 , 35 ].

However, crossover diet applications where the body was adapted to a high fat diet prior to short term high CHO loading h was shown to maintain IMTG stores [ 65 ] while increasing glycogen stores [ 72 ], partially restore glycolytic enzymes [ 35 ], as well as partially restore CHOox [ 67 ].

Alternating pre-exercise macronutrient specificity has the potential to be effective in accommodating the stress of sustained high intensity exercise due to both ideal cellular protein expression, and adequate storage of IMTG and muscle glycogen. The reduction in PDH activity due to high fat diets is a limiting factor to the necessary CHO oxidation at high intensity exercise despite adequate endogenous energy stores.

Maintaining the ability to store and oxidize fat after acclimating to a high fat diet while restoring the ability to oxidize CHO with short-term CHO loading is an ideal physiological state for endurance exercise performance.

Current research asserts that high fat diets favorably enhance FAox at both rest and during exercise [ 3 , 74 ]. However, exercise intensity dictates substrate utilization regardless of dietary influence, training status, and exercise duration.

Because of this, high fat diets are sometimes encouraged during preparatory off-season training when training volumes are high and exercise intensities are low to moderate [ 74 ]. More research into the short-term macronutrient manipulation effect on endogenous substrate concentrations, plasticity of cellular expression, and preferential substrate oxidation are necessary to ascertain if there is benefit on exercise performance outcomes.

In summary, FAox is contingent on many factors which can modify cellular expression in a short amount of time. Macronutrient availability, training status, sex, exercise intensity, and duration all influence cellular adaptation, systematic FA transport, and FAox.

Additionally, more investigation into the ideal nutritional timing and content that will favorably influence the physiological adaptations of FAox during endurance exercise is warranted. Nonetheless, exercise prescriptions and dietary recommendations need to take into account specific exercise goals duration, intensity, sport specific to facilitate a training plan that will elicit the ideal substrate oxidation adaptations relevant to improve sport performance.

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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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Metabolosm your Fat metabolism and exercise browser doesn't qnd Javascript or Oxidative stress-induced diseases is currently turned off. In the latter case, please turn metabolismm Javascript support in your web browser and reload this page. Moitzi AMKönig D. Nutrients15 1304 Jul Cited by: 0 articles PMID: Charoensap TKilding AEMaunder E. Eur J Appl Physiol918 May Exerclse Physiology Forskolin and joint health Contraction Muscle Fibers Fat metabolism and exercise Adaptations Exercise Fuels CHO Fat metabolism and exercise Mwtabolism Metabolism Oxygen Uptake Cardiovascular Fat metabolism and exercise Respiratory Responses VO2 Max Temperature Regulation Heat Abd Balance Fatigue Sprinting Exerfise Genes Practical Case Example. Learn about exercie metabolism exeecise a fuel source. Fatty acids are stored in the muscle and in the adipose tissue. Learn about the interactions between fatty acids from the bloodstream plasma and muscle. Study lipase, hormone-sensitive lipase, and the breakdown of triglycerides. The lecture will cover important aspects of interactions between fatty acids and other fuel sources as utilized and influenced by increasing or decreasing exercise intensity. These fatty acids can come either from the bloodstream, which has been derived from the adipose tissue triglyceride stores or from the triglycerides that are stored within the muscle. Fat metabolism and exercise

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