Effect of low pO₂ on Qo₂, Na²² efflux, and contractility of muscles

¹ Department of Physiology, College of Medicine, State University of Iowa, Iowa City, Iowa

Previous experiments suggested that the in vivo consumption of O₂ by the cell is normally limited by the pO₂ in the cellular environment. We suggested that if the pO₂ exceeds a certain minimal level, some or all of the energy from the "extra" respiration may be directly converted to heat. To further test the hypothesis, 39 isolated frog sartorii were placed in respirometers containing Ringer-bicarbonate solution (at 22 or 27 C) equilibrated with gas mixtures of various oxygen tensions. (All gases contained 2% CO₂.) The Qo₂ of muscles exposed to 98% O₂ for 6–7 hr reached a stable value which was about 200% of the stable value for muscles exposed to 25% O₂ for the same period of time. In other experiments the depression of the Qo₂ in 25% O₂ was shown to be reversible. The ability to develop tension, as judged by occasional test contractions, was not impaired in 25% O₂. The amount of lactic acid liberated from the muscles was small and was independent of the pO₂. In additional experiments with similar muscles exposed to either 25% O₂ or 98% N₂ for 5–7 hr, neither the Na²² efflux nor resting membrane potential differed significantly from the values obtained in 98% O₂. The data are consistent with the hypothesis.

Key Words: skeletal muscle metabolism • pO₂-Qo₂ relationship • in vitro O₂ consumption • membrane potentials

Submitted on July 17, 1964