Molé 1999 Am J Physiol
| Molé PA, Chung Y, Tran TK, Sailasuta N, Hurd R, Jue T (1999) Myoglobin desaturation with exercise intensity in human gastrocnemius muscle. https://doi.org/10.1152/ajpregu.1999.277.1.R173 |
» Am J Physiol 277:R173-80. PMID: 10409271 Open Access
Mole PA, Chung Y, Tran TK, Sailasuta N, Hurd R, Jue T (1999) Am J Physiol
Abstract: The present study evaluated whether intracellular partial pressure of O2 (PO2) modulates the muscle O2 uptake (VO2) as exercise intensity increased. Indirect calorimetry followed VO2, whereas nuclear magnetic resonance (NMR) monitored the high-energy phosphate levels, intracellular pH, and intracellular PO2 in the gastrocnemius muscle of four untrained subjects at rest, during plantar flexion exercise with a constant load at a repetition rate of 0.75, 0.92, and 1.17 Hz, and during postexercise recovery. VO2 increased linearly with exercise intensity and peaked at 1.17 Hz (15. 1 ± 0.37 watts), when the subjects could maintain the exercise for only 3 min. VO2 reached a peak value of 13.0 ± 1.59 mL O2.min-1.100 mL leg volume-1. The 31P spectra indicated that phosphocreatine decreased to 32 % of its resting value, whereas intracellular pH decreased linearly with power output, reaching 6.86. Muscle ATP concentration, however, remained constant throughout the exercise protocol. The 1H NMR deoxymyoglobin signal, reflecting the cellular PO2, decreased in proportion to increments in power output and VO2. At the highest exercise intensity and peak VO2, myoglobin was approximately 50 % desaturated. These findings, taken together, suggest that the O2 gradient from hemoglobin to the mitochondria can modulate the O2 flux to meet the increased VO2 in exercising muscle, but declining cellular PO2 during enhanced mitochondrial respiration suggests that O2 availability is not limiting VO2 during exercise.
• Bioblast editor: Gnaiger E
Labels: MiParea: Respiration, Exercise physiology;nutrition;life style
Stress:Hypoxia Organism: Human Tissue;cell: Skeletal muscle
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