The role of oxygen in determining phosphocreatine onset kinetics in exercisina humans

P-31-magnetic resonance spectroscopy was used to study phosphocreatine (PCr) onset kinetics in exercising human gastrocnemius muscle under varied fractions of inspired O-2 (F-IO2). Five male subjects performed three identical work bouts (5 min duration; order randomised) at a submaximal workload while breathing 0.1, 0.21 or 1.0 F-IO2. Either a single or double exponential model was fitted to the PCr kinetics. The phase Itau (0.1, 38.6 +/- 7.5; 0.21, 34.5 +/- 7.9; 1.0, 38.6 +/- 9.2 s) and amplitude, A(1) (0.1, 0.34 +/- 0.03; 0.21, 0.28 +/- 0.05; 1.0, 0.28 +/- 0.03,% fall in PCr) were invariant (both P > 0.05) across F 102 trials. The initial rate of change in PCr hydrolysis at exercise onset, calculated as A(1)/tau(1) (%PCr reduction s(-1)),was the same across F-IO2 trials. A PCr slow component (phase II) was present at an F-IO2, of 0.1 and 0.21; however, breathing 1.0 F-IO2, ablated the slow component. The onset of the slow component resulted in a greater (P < 0.05) overall percentage fall in PCr (both phase I and 11) as F-IO2, decreased (0.43 0.05, 0.34 0.05, 0.28 0.03) for 0.1, 0.21 and 1.0 F-IO2, respectively. These data demonstrate that altering F-IO2, does not affect the initial phase I PCr onset kinetics, which supports the notion that O-2 driving pressure does not limit PCr kinetics at the onset of submaximal exercise. Thus, these data imply that the manner in which microvascular and intracellular P-O2, regulates PCr hydrolysis in exercising muscle is not due to the initial kinetic fall in PCr at exercise onset.