title: Mitochondrial nutrients stimulate performance and mitochondrial biogenesis in exhaustively exercised rats.
abstract: The aim of this study was to investigate the effects of a combination of nutrients on physical performance, oxidative stress and mitochondrial biogenesis in rats subjected to exhaustive exercise. Rats were divided into sedentary control (SC), exhaustive exercise (EC) and exhaustive exercise with nutrient supplementation (EN). The nutrients include (mg/kg/day): R-α-lipoic acid 50, acetyl-L-carnitine 100, biotin 0.1, nicotinamide 15, riboflavin 6, pyridoxine 6, creatine 50, CoQ10 5, resveratrol 5 and taurine 100. Examination of running distances over the 4-week period revealed that EN rats ran significantly longer throughout the entire duration of the exhaustive exercise period compared with the EC rats. Nutrient supplementation significantly inhibited the increase in activities of alanine transaminase, lactate dehydrogenase and creatine kinase, reversed increases in malondialdehyde, inhibited decreases in glutathione S-transferase and total antioxidant capacity in plasma, and suppressed the elevation of reactive oxygen species and apoptosis in splenic lymphocytes. Nutrient supplementation increased the protein expression of mitochondrial complexes I, II and III, mtDNA number and transcription factors involved in mitochondrial biogenesis and fusion in skeletal muscle. These findings suggest that mitochondrial nutrient supplementation can reduce exhaustive exercise-induced oxidative damage and mitochondrial dysfunction, thus leading to enhancement of physical performance and of fatigue recovery.
authors.affiliation: Key Laboratory of General Administration of Sport, Shanghai Research Institute of Sports Science, Shanghai, China.
authors.forename: M
authors.initials: M
authors.lastname: Sun
authors.forename: F
authors.initials: F
authors.lastname: Qian
authors.forename: W
authors.initials: W
authors.lastname: Shen
authors.forename: C
authors.initials: C
authors.lastname: Tian
authors.forename: J
authors.initials: J
authors.lastname: Hao
authors.forename: L
authors.initials: L
authors.lastname: Sun
authors.forename: J
authors.initials: J
authors.lastname: Liu
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D004272:DNA, Mitochondrial / Q000378:metabolism; D019587:Dietary Supplements; D004798:Enzymes / Q000097:blood; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D008928:Mitochondria / Q000187:drug effects* / Q000378:metabolism / Q000648:ultrastructure; D063269:Mitochondrial Turnover / Q000187:drug effects*; D018763:Muscle Fatigue / Q000187:drug effects; D018482:Muscle, Skeletal / Q000187:drug effects* / Q000378:metabolism / Q000648:ultrastructure; D018384:Oxidative Stress / Q000187:drug effects*; D010807:Physical Endurance / Q000187:drug effects; D050050:Protein Carbonylation / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000097:blood; D014157:Transcription Factors / Q000378:metabolism
chemical_list: D004272:DNA, Mitochondrial; D004798:Enzymes; D017382:Reactive Oxygen Species; D014157:Transcription Factors; D008315:Malondialdehyde