IntroductionThe importance of endogenous muscle glycogen as a primary fuel source during exertion (particularly for intense endurance bouts) has been a fundamental concept in exercise physiology for half a century (Bergstrom et al. ; Pernow & Saltin, ). Accordingly, carbohydrate‐rich diets have been traditionally recommended for athletes to ensure the replenishment of muscle glycogen stores to meet the metabolic demands of intense training exercise sessions and competitions (Bartlett et al. ). However, training with low muscle glycogen availability might induce some beneficial metabolic adaptations in the muscle tissue, including activation of key cell signalling kinases (e.g. protein kinase, AMP‐activated, catalytic subunit α 1 and p38 mitogen‐activated protein kinase (p38MAPK)), transcription factors (e.g. protein 53 (p53), peroxisome proliferator‐activated receptor delta (PPARδ)) and transcriptional co‐activators (e.g. peroxisome proliferator‐activated receptor‐1α (PGC‐1α)) (Bartlett et al. ), increased fat oxidation (Lane et al. ), or delayed liver glycogenolysis (Webster et al. ). Elucidating the muscle metabolic adaptations to endurance exercise training as a function of glycogen availability is of interest as it may help to gain insight into the mechanisms that mediate the muscle adaptations to this type of training. This issue can be solved effectively by studying McArdle's disease because it allows the investigation of the effects of
The Journal of Physiology – Wiley
Published: Jan 15, 2018
Keywords: ; ; ; ; ;
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