Combination of hyperoxia and a right-shifted HbO₂ dissociation curve delays VO₂ kinetics during maximal contractions in isolated muscle

Acute enhancement of peripheral O-2 diffusion may accelerate skeletal muscle O-2 uptake (VO2) kinetics and lessen fatigue during transitions from rest to maximal contractions. Surgically isolated canine gastrocnemius muscles in situ (n=6) were studied during transitions from rest to 4-min of electrically stimulated isometric tetanic contractions at VO(2)peak, in two conditions: normoxia (CTRL) and hyperoxia (FIO2=1.00) + administration of a drug (RSR-13) which right-shifts the Hb-O-2 dissociation curve (Hyperoxia+RSR13). Prior to and during contractions muscles were pump-perfused with blood at constant elevated flow ( ) and infused with the vasodilator adenosine. Arterial (CaO2) and muscle venous (CvO(2)) O-2 concentrations were determined at rest and at 5-7 s intervals during contractions; VO2 was calculated as (.)(CaO2-CvO(2)). PO2 at 50% of Hb saturation (standard P-50) and mean microvascular PO2 (PmvO(2)) were calculated by the Hill equation and a numerical integration technique. P-50 (42 +/- 7 (x +/- SD) mmHg vs. 33 +/- 2, P=0.02) and PmvO(2) (218 +/- 73 mmHg vs. 49 +/- 4, P=0.003) were higher Hyperoxia+RSR13. Muscle force and fatigue were not different in the two conditions. VO2 kinetics (monoexponential fitting) were unexpectedly slower in Hyperoxia+RSR13, due to a longer time delay (TD) (9.9 +/- 1.7 s vs. 4.4 +/- 2.2 [P=0.001]), whereas the time constant (t) was not different (13.7 +/- 4.3 s vs. 12.3 +/- 1.9 [P=0.37]); the mean response time (TD+t) was longer in Hyperoxia+RSR13 (23.6 +/- 3.5 s vs. 16.7 +/- 3.2 [P=0.003]). Increased O-2 availability deriving, in Hyperoxia+RSR13, from higher PmvO(2) and from presumably greater intramuscular O-2 stores, did not accelerate the primary component of the VO2 kinetics, and delayed the metabolic activation of oxidative phosphorylation.