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

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Abstract
In humans, pulmonary oxygen uptake (V̇O2) kinetics may be speeded by prior exercise in the heavy domain. This ‘speeding’ arises potentially as the result of an increased muscle O2 delivery (Q̇O2) and/or a more rapid elevation of oxidative phosphorylation. We adapted phosphorescence quenching techniques to determine the QO2-to-O2 utilization (Q̇O2/V̇O2) characteristics via microvascular O2 pressure (PO2,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 (ST1 and ST2) separated by 10 min rest. PO2,m responses were analysed using an exponential + time delay (TD) model. There was no significant difference in baseline and ΔPO2,m between ST1 and ST2 (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 (ST1, 12.2 ± 1.9; ST2, 5.7 ± 2.2 s, P < 0.05), whereas the time constant of the exponential PO2,m decrease was unchanged (ST1, 16.3 ± 2.6; ST2, 17.6 ± 2.7 s, P > 0.1). The shortened TD found in ST2 led to a reduced time to reach 63 % of the final response of ST2 compared to ST1 (ST1, 28.3 ± 3.0; ST2, 20.2 ± 1.8 s, P < 0.05). The speeding of the overall response in the absence of an elevated PO2,m baseline (which had it occurred would indicate an elevated QO2/V̇O2) 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 PO2,m kinetics after prior contractions under these conditions.