Increased peak oxygen consumption of trained muscle requires increased electron flux capacity.
The importance of the training-induced increase in mitochondrial capacity in realizing the increase in maximal O2 consumption (VO2max) of trained muscle was evaluated using an isolated perfused rat hindlimb preparation at a high blood flow (approximately 80 ml.min-1.100 g-1) during tetanic contractions. Rats trained for 8-12 wk by treadmill running exhibited an approximately 25% increase in muscle VO2max (5.62 +/- 0.31 to 7.06 +/- 0.64 mumol.min-1.g-1), an increase in mitochondrial enzyme activity (approximately 70% for cytochrome oxidase and approximately 55% for NADH cytochrome-c reductase), and an increase in tissue capillarity (14%) that is expected to increase the O2 exchange capacity of the tissue. Muscle VO2max of sedentary (n = 34) and trained (n = 30) animals was determined, and electron transport capacity was acutely managed with myxothiazol, a tight-binding inhibitor of complex III. Inhibition of complex III was similar among 1) the low- and high-oxidative fibers and 2) the superficial and deep mitochondrial populations within muscle. Inhibition of NADH cytochrome-c reductase activity resulted in reductions in muscle VO2max with similar dose responses (mean effective dose of approximately 0.2 microM) of myxothiazol added to the perfusion medium. The extraction of O2 by the contracting muscle decreased as VO2max declined. The increase in muscle VO2max observed in the muscle of trained animals was eliminated when its electron transport capacity was reduced to that observed in normal sedentary rat muscle. Thus, the exercise-induced adaptation of an increased muscle mitochondrial content appears to be essential for trained muscle to exhibit its increased O2 flux capacity. The results of the present experiment illustrate the importance of mitochondrial adaptations in muscle remodeled by exercise training.
Robinson
D M
DM
Department of Physiology, State University of New York Health Science Center, Syracuse 13210.
Ogilvie
R W
RW
Tullson
P C
PC
Terjung
R L
RL
D000818:Animals; D001783:Blood Flow Velocity; D004579:Electron Transport; D006614:Hindlimb / Q000098:blood supply; D008689:Methacrylates; D008931:Mitochondria, Muscle / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism*; D009119:Muscle Contraction / Q000187:drug effects / Q000502:physiology; D018482:Muscle, Skeletal / Q000098:blood supply / Q000187:drug effects / Q000378:metabolism*; D009210:Myofibrils / Q000187:drug effects / Q000201:enzymology; D009245:NADH Dehydrogenase / Q000037:antagonists & inhibitors / Q000378:metabolism; D010101:Oxygen Consumption / Q000187:drug effects; D010477:Perfusion; D010805:Physical Conditioning, Animal / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013844:Thiazoles / Q000097:blood / Q000494:pharmacology
D008689:Methacrylates; D013844:Thiazoles; C030517:myxothiazol; D009245:NADH Dehydrogenase