Effects of prior contractions on muscle microvascular oxygen pressure at onset of subsequent contractions

In humans, pulmonary oxygen uptake (V̇ O2 ) kinetics may be speeded by prior exercise in the heavy domain. This ‘speeding’ arises potentially as the result of an increased muscle O 2 delivery ( Q̇ O2 ) and/or a more rapid elevation of oxidative phosphorylation. We adapted phosphorescence quenching techniques to determine the Q O2 ‐to‐O 2 utilization ( Q̇ O2 /V̇ O2 ) characteristics via microvascular O 2 pressure ( P O2,m ) measurements across sequential bouts of contractions in rat spinotrapezius muscle. Spinotrapezius muscles from female Sprague‐Dawley rats ( n = 6 ) were electrically stimulated (1 Hz twitch, 3–5 V) for two 3 min bouts (ST 1 and ST 2 ) separated by 10 min rest. P O2,m responses were analysed using an exponential + time delay (TD) model. There was no significant difference in baseline and Δ P O2,m between ST 1 and ST 2 (28.5 ± 2.6 vs. 27.9 ± 2.4 mmHg, and 13.9 ± 1.8 vs. 14.1 ± 1.3 mmHg, respectively). The TD was reduced significantly in the second contraction bout (ST 1 , 12.2 ± 1.9; ST 2 , 5.7 ± 2.2 s, P < 0.05), whereas the time constant of the exponential P O2,m decrease was unchanged (ST 1 , 16.3 ± 2.6; ST 2 , 17.6 ± 2.7 s, P > 0.1). The shortened TD found in ST 2 led to a reduced time to reach 63 % of the final response of ST 2 compared to ST 1 (ST 1 , 28.3 ± 3.0; ST 2 , 20.2 ± 1.8 s, P < 0.05). The speeding of the overall response in the absence of an elevated P O2,m baseline (which had it occurred would indicate an elevated Q O2 /V̇ O2 ) or muscle blood flow suggests that some intracellular process(es) (e.g. more rapid increase in oxidative phosphorylation) may be responsible for the increased speed of P O2,m kinetics after prior contractions under these conditions.