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Received February 4, 2004
Revised February 27, 2004
Accepted after revision May 23, 2004
1 Gold Coast Campus Griffith University
2 University of California-San Diego
* To whom correspondence should be addressed. E-mail: l.haseler{at}griffith.edu.au.
31P-magnetic resonance spectroscopy was used to study phosphocreatine (PCr) onset kinetics in exercising human gastrocnemius muscle under varied fractions of inspired O2 (FIO2). 5 male subjects performed 3 identical work bouts (5-min duration; order randomized) at a submaximal workload while breathing 0.1, 0.21 or 1.0 FIO2. Either a single or double exponential model was fit 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, A1, (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 FIO2 trials. The initial rate of change in PCr hydrolysis at exercise onset, calculated as A1/tau1 (%PCr reduction/s), was the same across FIO2 trials. A PCr slow component (phase II) was present at an FIO2 of 0.1 and 0.21, however breathing 1.0 FIO2 ablated the slow component. The onset of the slow component resulted in a greater (p < 0.05) overall % fall in PCr (both phase I and II) as FIO2 decreased (0.43 ±± 0.05, 0.34 ± 0.05, 0.28 ± 0.03) for 0.1, 0.21 and 1.0 FIO2 respectively. These data demonstrate that altering FIO2 does not affect the initial phase I PCr onset kinetics, which supports the notion that O2 driving pressure does not limit PCr kinetics at the onset of submaximal exercise. Thus, these data infer that the manner in which microvascular and intracellular PO2 regulates PCr hydrolysis in exercising muscle is not due to the initial kinetic fall in PCr at exercise onset.
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