The role of oxygen in determining phosphocreatine onset kinetics in exercising humans.

31P-magnetic resonance spectroscopy was used to study phosphocreatine (PCr) onset kinetics in exercising human gastrocnemius muscle under varied fractions of inspired O(2) (F(IO(2))). 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(IO(2)). Either a single or double exponential model was fitted to the PCr kinetics. The phase I tau (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(IO(2)) 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(IO(2)) trials. A PCr slow component (phase II) was present at an F(IO(2)) of 0.1 and 0.21; however, breathing 1.0 F(IO(2)) ablated the slow component. The onset of the slow component resulted in a greater (P< or = 0.05) overall percentage fall in PCr (both phase I and II) as F(IO(2)) decreased (0.43 +/- 0.05, 0.34 +/- 0.05, 0.28 +/- 0.03) for 0.1, 0.21 and 1.0 F(IO(2)), respectively. These data demonstrate that altering F(IO(2)) 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(O(2)) regulates PCr hydrolysis in exercising muscle is not due to the initial kinetic fall in PCr at exercise onset.