Abstract
PurposeCarbohydrate (CHO) restriction could be a potent metabolic regulator of endurance exercise-induced muscle adaptations. Here, we determined whether post-exercise CHO restriction following strenuous exercise combining continuous cycling exercise (CCE) and sprint interval exercise could affect the gene expression related to mitochondrial biogenesis and oxidative metabolism in human skeletal muscle.MethodsIn a randomized cross-over design, 8 recreationally active males performed two cycling exercise sessions separated by 4 weeks. Each session consisted of 60-min CCE and six 30-s all-out sprints, which was followed by ingestion of either a CHO or placebo beverage in the post-exercise recovery period. Muscle glycogen concentration and the mRNA levels of several genes related to mitochondrial biogenesis and oxidative metabolism were determined before, immediately after, and at 3 h after exercise.ResultsCompared to pre-exercise, strenuous cycling led to a severe muscle glycogen depletion (> 90%) and induced a large increase in PGC1A and PDK4 mRNA levels (~ 20-fold and ~ 10-fold, respectively) during the acute recovery period in both trials. The abundance of the other transcripts was not changed or was only moderately increased during this period. CHO restriction during the 3-h post-exercise period blunted muscle glycogen resynthesis but did not increase the mRNA levels of genes associated with muscle adaptation to endurance exercise, as compared with abundant post-exercise CHO consumption.ConclusionCHO restriction after a glycogen-depleting and metabolically-demanding cycling session is not effective for increasing the acute mRNA levels of genes involved in mitochondrial biogenesis and oxidative metabolism in human skeletal muscle.
Highlights
Carbohydrate (CHO) is a crucial macronutrient used to fuel skeletal muscle during exercise and restore glycogen after exercise (Bergstrom et al 1967)
It is conceivable that performing a strenuous exercise session consisting of cycling exercise (CCE) followed by sprint interval exercise (SIE), and which results in a drastic muscle glycogen depletion (Cheng et al 2020), could answer the question as to whether post-exercise CHO restriction enhances the acute expression of PGC1A and other mitochondrial biogenesisrelated genes
Our results indicated that post-exercise CHO restriction following a strenuous cycling session that combined CCE and SIE did not amplify the mRNA levels of genes associated with muscle adaptation to endurance exercise
Summary
Carbohydrate (CHO) is a crucial macronutrient used to fuel skeletal muscle during exercise and restore glycogen after exercise (Bergstrom et al 1967). It is conceivable that performing a strenuous exercise session consisting of CCE followed by SIE, and which results in a drastic muscle glycogen depletion (Cheng et al 2020), could answer the question as to whether post-exercise CHO restriction enhances the acute expression of PGC1A and other mitochondrial biogenesisrelated genes In this context where both severe muscle glycogen depletion and high metabolic stress are induced, we hypothesized that post-exercise CHO restriction may be beneficial to potentiate the acute molecular response associated with stimulation of mitochondrial biogenesis and oxidative metabolism. To test this hypothesis, we determined the effect of post-exercise CHO restriction following an exercise session combining CCE and SIE on the acute gene expression related to exercise-induced muscle adaptations in humans
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