Fat Metabolism During Exercise: A Review - Part II: Regulation of Metabolism and the Effects of Training

Jeukendrup, A. E.; Saris, W.H.M.; Wagenmakers, Anton J. M.

doi:10.1055/s-2007-971921

Cited by 105 publications

(79 citation statements)

References 65 publications

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“…Third, dietary capsaicin increased the mitochondrial mass and respiratory function, and promoted a fiber transformation from glycolytic type II fibers to more oxidative type I fibers. It is known that type I fibers contain more mitochondria and produce more ATP from lipid oxidation but less from glycolysis compared to type II fibers, thus providing stable energy for a longer time with less lactic acid accumulation [3,31,37].…”

Section: Discussionmentioning

confidence: 99%

TRPV1 activation improves exercise endurance and energy metabolism through PGC-1α upregulation in mice

et al. 2011

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Impaired aerobic exercise capacity and skeletal muscle dysfunction are associated with cardiometabolic diseases. Acute administration of capsaicin enhances exercise endurance in rodents, but the long-term effect of dietary capsaicin is unknown. The capsaicin receptor, the transient receptor potential vanilloid 1 (TRPV1) cation channel has been detected in skeletal muscle, the role of which remains unclear. Here we report the function of TRPV1 in cultured C2C12 myocytes and the effect of TRPV1 activation by dietary capsaicin on energy metabolism and exercise endurance of skeletal muscles in mice. In vitro, capsaicin increased cytosolic free calcium and peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) expression in C2C12 myotubes through activating TRPV1. In vivo, PGC-1α in skeletal muscle was upregulated by capsaicin-induced TRPV1 activation or genetic overexpression of TRPV1 in mice. TRPV1 activation increased the expression of genes involved in fatty acid oxidation and mitochondrial respiration, promoted mitochondrial biogenesis, increased oxidative fibers, enhanced exercise endurance and prevented high-fat diet-induced metabolic disorders. Importantly, these effects of capsaicin were absent in TRPV1-deficient mice. We conclude that TRPV1 activation by dietary capsaicin improves energy metabolism and exercise endurance by upregulating PGC-1α in skeletal muscles. The present results indicate a novel therapeutic strategy for managing metabolic diseases and improving exercise endurance.

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Section: Discussionmentioning

confidence: 99%

TRPV1 activation improves exercise endurance and energy metabolism through PGC-1α upregulation in mice

et al. 2011

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“…2,9 One mechanism underlying the positive effect of Ex on obesity might be its ability to increase energy expenditure, prompting an increase in fat oxidation from dietary intake or bodily reserves. 28,29 Furthermore, Ex might be most effective in weight control when it is combined with improved eating habits. However, Obesity suppression and tea catechins T Murase et al little is known about the combined effects of Ex and food components, including tea Cat, on the development of obesity.…”

Section: Discussionmentioning

confidence: 99%

Reduction of diet-induced obesity by a combination of tea-catechin intake and regular swimming

et al. 2005

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Objective: Obesity is a metabolic disorder resulting from imbalance between metabolizable energy intake and energy expenditure. It is known to be a strong risk factor for lifestyle-related diseases. Here, we investigated the effects of long-term intake of tea catechins (Cat) in combination with regular exercise (Ex) on the development of obesity in C57BL/6 mice. Design: We compared body weight, adipose tissue mass, plasma parameters and b-oxidation activity in mice fed a low-fat diet (5% triglyceride (TG); LF), a high-fat diet (30% TG; HF), a HF diet supplemented with 0.5% (w/w) tea Cat, a HF diet in addition to swimming Ex or a HF diet plus 0.5% tea Cat in addition to swimming Ex (Cat þ Ex) for 15 weeks. Oxygen consumption and respiratory quotients were measured using indirect calorimetry. Results: Tea-Cat intake in combination with swimming Ex suppressed HF diet-induced body-weight gain by 18 and 22%, respectively, compared to Ex and tea-Cat intake on their own. Visceral fat accumulation and the development of hyperinsulinemia and hyperleptinemia were also reduced in the HF þ Cat þ Ex group. Muscular b-oxidation activity in this group was 69 and 52% higher, respectively, than that in the HF and HF þ Cat groups. Lipid oxidation, determined using indirect calorimetry, was higher in the HF þ Cat þ Ex group, suggesting increased lipid utilization at the individual level. Conclusion: These results indicate that intake of tea Cat, together with regular Ex helps to reduce diet-induced obesity. This effect might be attributed, at least in part, to the activation of whole-body energy metabolism.

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“…In resting muscle there is some indication that the glucose ± fatty acid cycle (Randle cycle) is operative, however under conditions of exercise the mechanism of regulation is currently debated. 15 A possible regulation could also occur through malonyl-CoA. The increase in the use of lipids as a substrate with long-term exercise of low intensity is probably related to the increase in plasma free fatty acids, 5,15 .…”

Section: Muscle Mitochondria Set the Demand For Oxygen And Substratesmentioning

confidence: 99%

“…15 A possible regulation could also occur through malonyl-CoA. The increase in the use of lipids as a substrate with long-term exercise of low intensity is probably related to the increase in plasma free fatty acids, 5,15 . However, again we do not know how the muscle cell selects between the two substrates and what governs use of intracellular versus extracellular substrates.…”

Section: Muscle Mitochondria Set the Demand For Oxygen And Substratesmentioning

confidence: 99%

Skeletal muscle substrate metabolism

Hoppeler

1999

Int J Obes

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Endurance power of muscles is determined largely by the capacities to oxidize substrates in mitochondria in the process of making ATP by oxidative phosphorylation. This review explores physiological and morphological factors that may cause limitation of carbohydrate and fat utilization by muscle cells. The pathways for oxygen and substrates converge in muscle mitochondria. In mammals, a structural limitation of carbohydrate and lipid transfer from the microvascular system to muscle cells is reached at a moderate work intensity (that is, at 40 ± 50% of V Á O 2 max). At higher work rates intracellular substrate stores must be used for oxidation. Because of the importance of these intracellular stores for aerobic work we ®nd larger intramyocellular substrate stores in endurance trained athletes. The transfer limitations for carbohydrates and lipids on the level of the sarcolemma implies that the design of the respiratory cascade from lungs to muscle mitochondria re¯ects primarily oxygen demand.

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Fat Metabolism During Exercise: A Review - Part II: Regulation of Metabolism and the Effects of Training

Cited by 105 publications

References 65 publications

TRPV1 activation improves exercise endurance and energy metabolism through PGC-1α upregulation in mice

TRPV1 activation improves exercise endurance and energy metabolism through PGC-1α upregulation in mice

Reduction of diet-induced obesity by a combination of tea-catechin intake and regular swimming

Skeletal muscle substrate metabolism

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