Slowed muscle oxygen uptake kinetics with raised metabolism are not dependent on blood flow or recruitment dynamics

Oxygen uptake kinetics (τV̇O2) are slowed when exercise is initiated from a raised metabolic rate. Whether this reflects the recruitment of muscle fibres differing in oxidative capacity, or slowed blood flow (Q̇) kinetics is unclear. This study determined τV̇O2 in canine muscle in situ, with experimental control over muscle activation and Q̇ during contractions initiated from rest and a raised metabolic rate. The gastrocnemius complex of nine anaesthetised, ventilated dogs was isolated and attached to a force transducer. Isometric tetanic contractions (50 Hz; 200 ms duration) via supramaximal sciatic nerve stimulation were used to manipulate metabolic rate: 3 min stimulation at 0.33 Hz (S1), followed by 3 min at 0.67 Hz (S2). Circulation was initially intact (SPON), and subsequently isolated for pump-perfusion (PUMP) above the greatest value in SPON. Muscle V̇O2 was determined contraction-by-contraction using an ultrasonic flowmeter and venous oximeter, and normalised to tension-time integral (TTI). τV̇O2/TTI and τQ̇ were less in S1_SPON (mean ± s.d.: 13 ± 3 s and 12 ± 4 s, respectively) than in S2_SPON (29 ± 19 s and 31 ± 13 s, respectively; P < 0.05). τV̇O2/TTI was unchanged by pump-perfusion (S1_PUMP, 12 ± 4 s; S2_PUMP, 24 ± 6 s; P < 0.001) despite increased O₂ delivery; at S2 onset, venous O₂ saturation was 21 ± 4% and 65 ± 5% in SPON and PUMP, respectively. V̇O2 kinetics remained slowed when contractions were initiated from a raised metabolic rate despite uniform muscle stimulation and increased O₂ delivery. The intracellular mechanism may relate to a falling energy state, approaching saturating ADP concentration, and/or slowed mitochondrial activation; but further study is required. These data add to the evidence that muscle V̇O2 control is more complex than previously suggested.