The effect of prolonged hypoxia on striated muscle pH regulation.

Abstract

The extracellular acid-base status of mammals exposed to low inspired PO2 for prolonged periods of time has been studied extensively (Bouverot, 1985). However, less is known regarding the intracellular acid-base status during prolonged hypoxia. In a previous study we observed that the intracellular pH of striated muscles of rats subjected to 3 weeks of hypobaric hypoxia was not significantly different from that of normoxic rats (Gonzalez and Clancy, 1986b). However, when the cells were acid-loaded by rendering the animals hypercapnic, the decreases in intracellular pH of tibialis anterior, quadriceps and diaphragm were significantly less than in hypercapnic normoxic rats. The magnitude of cell pH regulation, as measured by the apparent non-bicarbonate buffer value, ranged from 3 (tibialis anterior) to 12 (diaphragm) times greater in the hypobaric hypoxic than the normoxic animals. This augmentation of striated muscle pH regulation during hypercapnia in hypobaric hypoxic rats could result from increased physicochemical buffering and/or increased efflux of proton equivalents. The question arises as to whether augmentation of these cellular pH- regulating mechanisms resulted from intrinsic changes in the cell interior and/or the sarcolemma engendered by the prolonged hypoxia or whether extracellular factors which enhance these cellular pH-regulating mechanisms were increased to a greater extent in the hypercapnic hypoxic rats than in the hypercapnic normoxic rats. To resolve this question cell pH regulation of diaphragms from prolonged hypoxic and normoxic rats was studied under in vitro conditions. Under these conditions the contribution of extracellular factors to cell pH regulation was the same in diaphragms from hypoxic and normoxic rats. Therefore, any difference in cell pH regulation should be attributable to intrinsic changes in one or more of the cell pH-regulating mechanisms.