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Energy metabolism in relation to oxygen partial pressure in human skeletal muscle during exercise.

ABSTRACT: 1. The intramuscular oxygen partial pressure (pO2) in human gastrocnemius muscle was monitored during exercise and compared with metabolite concentrations reflecting the energy and the redox state in the tissue. Ten normal subjects and ten patients with peripheral vascular occlusive disease were investigated. 2. In normal subjects the pO2 at the end of exercise was related to the intensity of the exercise, expressed as effect (J/s) per contraction. 3. In both patients and normal subject the pO2 was related to the [ATP]/[ADP] ratio, the [lactate/[pyruvate] ratio and the phosphocreatine concentration in the muscle tissue at rest and during exercise. 4. At each pO2 value, a lower [lactate/[pyruvate] ratio was found in the muscle tissue of the patients compared with that of normal subjects. This was interpreted as a beneficial effect of the higher oxidative-enzyme capacity in the muscle of the patients. 5. The results show the importance of pO2 for the regulation of the energy and the redox state of the tissue. During exercise the changes induced in pO2 and thus the energy state will stimulate the respiratory rate. This might be an important link in triggering the oxidative-enzyme capacity in response to physical training as well as in peripheral vascular occlusive disease.

SUBMITTER: Bylund-Fellenius AC

PROVIDER: S-EPMC1163530 | biostudies-other | 1981 Nov

REPOSITORIES: biostudies-other

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Project description:Skeletal muscle can maintain ATP concentration constant during the transition from rest to exercise, whereas metabolic reaction rates may increase substantially. Among the key regulatory factors of skeletal muscle energy metabolism during exercise, the dynamics of cytosolic and mitochondrial NADH and NAD+ have not been characterized. To quantify these regulatory factors, we have developed a physiologically based computational model of skeletal muscle energy metabolism. This model integrates transport and reaction fluxes in distinct capillary, cytosolic, and mitochondrial domains and investigates the roles of mitochondrial NADH/NAD+ transport (shuttling) activity and muscle glycogen concentration (stores) during moderate intensity exercise (60% maximal O2 consumption). The underlying hypothesis is that the cytosolic redox state (NADH/NAD+) is much more sensitive to a metabolic disturbance in contracting skeletal muscle than the mitochondrial redox state. This hypothesis was tested by simulating the dynamic metabolic responses of skeletal muscle to exercise while altering the transport rate of reducing equivalents (NADH and NAD+) between cytosol and mitochondria and muscle glycogen stores. Simulations with optimal parameter estimates showed good agreement with the available experimental data from muscle biopsies in human subjects. Compared with these simulations, a 20% increase (or approximately 20% decrease) in mitochondrial NADH/NAD+ shuttling activity led to an approximately 70% decrease (or approximately 3-fold increase) in cytosolic redox state and an approximately 35% decrease (or approximately 25% increase) in muscle lactate level. Doubling (or halving) muscle glycogen concentration resulted in an approximately 50% increase (or approximately 35% decrease) in cytosolic redox state and an approximately 30% increase (or approximately 25% decrease) in muscle lactate concentration. In both cases, changes in mitochondrial redox state were minimal. In conclusion, the model simulations of exercise response are consistent with the hypothesis that mitochondrial NADH/NAD+ shuttling activity and muscle glycogen stores affect primarily the cytosolic redox state. Furthermore, muscle lactate production is regulated primarily by the cytosolic redox state.

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Energy metabolism in relation to oxygen partial pressure in human skeletal muscle during exercise.

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