Phosphocreatine hydrolysis during submaximal exercise: the effect of FIO2.
There is evidence that the concentration of the high-energy phosphate metabolites may be altered during steady-state submaximal exercise by the breathing of different fractions of inspired O2 (FIO2). Whereas it has been suggested that these changes may be the result of differences in time taken to achieve steady-state O2 uptake (V(O2)) at different FIO2 values, we postulated that they are due to a direct effect of O2 tension. We used 31P-magnetic resonance spectroscopy during constant-load, steady-state submaximal exercise to determine 1) whether changes in high-energy phosphates do occur at the same V(O2) with varied FIO2 and 2) that these changes are not due to differences in V(O2) onset kinetics. Six male subjects performed steady-state submaximal plantar flexion exercise [7.2 +/- 0.6 (SE) W] for 10 min while lying supine in a 1.5-T clinical scanner. Magnetic resonance spectroscopy data were collected continuously for 2 min before exercise, 10 min during exercise, and 6 min during recovery. Subjects performed three different exercise bouts at constant load with the FIO2 switched after 5 min of the 10-min exercise bout. The three exercise treatments were 1) FIO2 of 0.1 switched to 0.21, 2) FIO2 of 0.1 switched to 1.00, and 3) FIO2 of 1.00 switched to 0.1. For all three treatments, the FIO2 switch significantly (P </= 0.05) altered phosphocreatine: 1) 55.5 +/- 4.8 to 67.8 +/- 4.9% (%rest); 2) 59.0 +/- 4.3 to 72.3 +/- 5.1%; and 3) 72.6 +/- 3.1 to 64.2 +/- 3.4%, respectively. There were no significant differences in intracellular pH for the three treatments. The results demonstrate that the differences in phosphocreatine concentration with varied FIO2 are not the result of different V(O2) onset kinetics, as this was eliminated by the experimental design. These data also demonstrate that changes in intracellular oxygenation, at the same work intensity, result in significant changes in cell homeostasis and thereby suggest a role for metabolic control by O2 even during submaximal exercise.
Haseler
L J
LJ
Division of Physiology, Department of Medicine, University of California, San Diego, La Jolla, California 92093, USA. lhaseler@ucsd.edu
Richardson
R S
RS
Videen
J S
JS
Hogan
M C
MC
D000328:Adult; D015444:Exercise / Q000502:physiology*; D006801:Humans; D006868:Hydrolysis; D000860:Hypoxia; D001239:Inhalation / Q000502:physiology*; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D018482:Muscle, Skeletal / Q000502:physiology*; D010101:Oxygen Consumption / Q000502:physiology*; D010725:Phosphocreatine / Q000378:metabolism*; D012146:Rest / Q000502:physiology
D010725:Phosphocreatine