Myoglobin desaturation with exercise intensity in human gastrocnemius muscle

The present study evaluated whether intracellular partial pressure of O₂ ($P{O}_2$ ) modulates the muscle O₂ uptake (V˙o₂) as exercise intensity increased. Indirect calorimetry followedV˙o₂, whereas nuclear magnetic resonance (NMR) monitored the high-energy phosphate levels, intracellular pH, and intracellular$P{O}_2$ 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.V˙o₂ 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.V˙o₂ reached a peak value of 13.0 ± 1.59 ml O₂ ⋅ min⁻¹ ⋅ 100 ml leg volume⁻¹. The³¹P 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$P{O}_2$ , decreased in proportion to increments in power output andV˙o₂. At the highest exercise intensity and peakV˙o₂, myoglobin was ∼50% desaturated. These findings, taken together, suggest that the O₂ gradient from hemoglobin to the mitochondria can modulate the O₂flux to meet the increasedV˙o₂ in exercising muscle, but declining cellular $P{O}_2$ during enhanced mitochondrial respiration suggests that O₂ availability is not limitingV˙o₂ during exercise.