Carbohydrate feeding during recovery alters the skeletal muscle metabolic response to repeated sessions of high-intensity interval exercise in humans.
Exercise training under conditions of reduced carbohydrate (CHO) availability has been reported to augment gains in skeletal muscle oxidative capacity; however, the underlying mechanisms are unclear. We examined the effect of manipulating CHO intake on the acute metabolic response to high-intensity interval exercise, including signaling cascades linked to mitochondrial biogenesis. Ten men performed two trials in random order separated by >or=1 wk. Each trial consisted of a morning (AM) and afternoon (PM) training session (5 x 4 min cycling at approximately 90-95% of heart rate reserve) separated by 3 h of recovery during which subjects ingested a high-CHO drink (HI-HI) or nonenergetic placebo (HI-LO) before PM exercise. Biopsies (vastus lateralis) revealed that muscle phosphocreatine and ATP content were similar after AM exercise but decreased to a greater extent during PM exercise in HI-LO vs. HI-HI. Phosphorylation of p38 mitogen-activated protein kinase (MAPK) and AMP-activated protein kinase (AMPK) increased approximately 4-fold and 2-fold, respectively, during AM exercise with no difference between conditions. After PM exercise, p38 MAPK phosphorylation was higher in HI-LO vs. HI-HI, whereas AMPK was not different between conditions. Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1 alpha) gene expression increased approximately 8-fold during recovery from AM exercise and remained elevated during PM exercise with no differences between conditions. Cytochrome oxidase subunit 4 (COXIV) mRNA was also elevated 3 h after AM exercise, with no difference between conditions. These data provide evidence that p38 MAPK is a nutrient-sensitive signaling molecule that could be involved in the altered skeletal muscle adaptive response reported after exercise training under conditions of restricted CHO intake, but further research is required to confirm this hypothesis.
Cochran
Andrew J R
AJ
Exercise Metabolism Research Group, Department of Kinesiology, McMaster University, Hamilton, ON L8S 4K1, Canada.
Little
Jonathan P
JP
Tarnopolsky
Mark A
MA
Gibala
Martin J
MJ
D055372:AMP-Activated Protein Kinases / Q000378:metabolism; D000222:Adaptation, Physiological; D000255:Adenosine Triphosphate / Q000378:metabolism; D000284:Administration, Oral; D001628:Beverages; D001706:Biopsy; D001786:Blood Glucose / Q000378:metabolism; D004040:Dietary Carbohydrates / Q000008:administration & dosage / Q000378:metabolism*; D003576:Electron Transport Complex IV / Q000235:genetics; D004734:Energy Metabolism; D015444:Exercise; D006339:Heart Rate; D006360:Heat-Shock Proteins / Q000378:metabolism; D006801:Humans; D007328:Insulin / Q000097:blood; D019344:Lactic Acid / Q000097:blood; D008297:Male; D008931:Mitochondria, Muscle / Q000378:metabolism; D009119:Muscle Contraction; D053580:Muscle Strength; D009752:Nutritional Status; D000071248:Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha; D010725:Phosphocreatine / Q000378:metabolism; D010766:Phosphorylation; D052097:Quadriceps Muscle / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D020127:Recovery of Function; D015398:Signal Transduction; D013997:Time Factors; D014157:Transcription Factors / Q000378:metabolism; D055815:Young Adult; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism
D001786:Blood Glucose; D004040:Dietary Carbohydrates; D006360:Heat-Shock Proteins; D007328:Insulin; C486497:PPARGC1A protein, human; D000071248:Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha; D012333:RNA, Messenger; D014157:Transcription Factors; D010725:Phosphocreatine; D019344:Lactic Acid; D000255:Adenosine Triphosphate; D003576:Electron Transport Complex IV; D048051:p38 Mitogen-Activated Protein Kinases; D055372:AMP-Activated Protein Kinases