Control of muscle VO2 kinetics: a role for metabolic rate?

Abstract

Control of skeletal muscle oxygen uptake (VO2) kinetics is mediated by ADP feedback, oxygen and substrate delivery and mitochondrial content. Controversy remains whether mitochondrial enzyme activation at exercise onset contributes to this control. We tested the hypothesis that VO2 kinetics would be speeded by increased metabolic rate, in pump‐perfused, tetanically‐stimulated muscle (i.e. independent of O2 delivery and muscle recruitment dynamics). The gastrocnemius of 6 anaesthetized, ventilated dogs was isolated and the tendon attached to a force transducer. Blood flow was pump‐controlled at a constant flow (1.09 ± 0.25 L.kg−1.min−1; mean ± SD). Isometric tetanic contractions (50 Hz; 200 ms duration) were elicited via supramaximal sciatic nerve stimulation. Metabolic rate was manipulated using 3 min of stimulation at 0.33 Hz (S1) immediately followed by 3 min at 0.67 Hz (S2); also following prior contractions at 0.67 Hz and 2 min recovery (PS1, PS2). Muscle VO2 was determined contraction‐by‐contraction. τVO2 was lower in S1 (11.4±2.4 s; p<0.05) than S2 (17.6±2.9 s), PS1 (16.6±4.6 s) and PS2 (16.1±2.5 s). Unexpectedly VO2 kinetics were fastest at the lowest stimulation frequency without prior contractions. This implies that any putative role of mitochondrial activation in VO2 kinetic control may be countered by a reduction in cellular energy state (e.g. less negative ΔGATP). Supported by BBSRC: BB/F019521/1