Depletion of glycogen is thought to be a potential aspect of the

Depletion of glycogen is thought to be a potential aspect of the stimulation of mitochondrial biogenesis [35]. Exercise in the current study was sufficient to lower muscle glycogen levels ~40%,

which is believed to be capable of stimulating AMPK, an upstream covalent modifier of PGC-1α [5, 36, 37]. In the current study glycogen depletion and carbohydrate oxidation did not differ between trials during the 1 h of exercise, indirectly suggesting that AMPK activity was similar between trials. This is supported by others, as carbohydrate ingestion during cycling is not thought to EPZ015938 alter glycogen utilization [14, 38]. As well, carbohydrate ingestion during cycling does not appear to alter AMPK signaling in humans [39]. This may explain why GLUT4 was not different between trials, since AMPK is thought to be a potent simulator of GLUT4 transcription [40]. Despite this lack of effect of carbohydrate ingestion on GLUT4, UCP3 mRNA expression was LY2603618 in vitro attenuated by carbohydrate ingestion. This suggests that the UCP3 gene may be more sensitive to fat oxidation. We showed a significant effect of carbohydrate ingestion on RER, with the P trial demonstrating greater fat reliance by the end of the exercise bout. We unfortunately do not have substrate oxidation data for the 3 h of recovery prior to the last biopsy, when mRNA expression

was sampled. However since the P trial received no carbohydrate into the recovery period, it is quite possible that the greater fat oxidation during the later stages of exercise continued into recovery in the P trial and subsequently attenuated the UCP3 mRNA expression. This is supported by evidence that elevated circulating fatty acids are associated with the upselleck compound regulation of skeletal muscle expression of UCP3 [14, 41–43]. We do not have evidence of circulating free fatty acids (FFA) in the current study, but it is well established that fasted exercise in

the absence of carbohydrate delivery elevates FFA compared to carbohydrate trials [44]. Although fat oxidation appears to coincide with UCP3 expression, the metabolic role of this protein in skeletal muscle remains unclear as it suggests a loss of exercise efficiency Meloxicam by uncoupling the proton gradient created in the electron transport chain from ATP synthesis. However, besides fat oxidation, UCP3 has been implicated as being important in the control of thermogenesis and the regulation of oxidative stress [45]. The long term implications of the attenuation of UCP3 expression following exercise with carbohydrate supplementation in this study and others has yet to be determined [14, 43]. It is intriguing to think that lower UCP3 mRNA may play a role in previous evidence of the carbohydrate attenuating effect on fat oxidation with exercise training [44, 46]. These studies demonstrated that low carbohydrate availability (fat adapted) resulted in greater rates of fat oxidation even when glycogen levels were restored with a day on a high carbohydrate diet.

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