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

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Abstract
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.