Key result
Lowering extracellular pH depresses lactate accumulation in isolated frog muscle.
Why the study?
Environmental stressors such as low temperature, extracellular acidosis, and anoxia play a key role in metabolic regulation, but their combined effects on metabolic rate in anoxia-tolerant muscle are not fully understood.
In isolated frog muscle, extracellular pH and temperature regulate anaerobic glycolysis and lactate accumulation during anoxia.
No direct implications for cardiac ischemia management; leaves open pH-temperature effects on glycolysis in mammalian models.
Environmental stress, such as low temperature, extracellular acidosis and anoxia, is known to play a key role in metabolic regulation. The aim of the present study was to gain insight into the combined temperature-pH regulation of metabolic rate in frog muscle, i.e. an anoxia-tolerant tissue. The rate of exergonic metabolic processes occurring in resting isolated muscles was determined at 15 degrees C and 25 degrees C as well as at extracellular pH values higher (7.9), similar (7.3) and lower (7.0) than the physiological intracellular pH. (31)P and (1)H nuclear magnetic resonance spectroscopy high-resolution measurements were carried out at 4.7 T in isolated frog (Rana esculenta) gastrocnemius muscle during anoxia to assess, by means of reference compounds, the concentration of all phosphate metabolites and lactate. Intra- and extracellular pH was also determined. In the range of examined temperatures (15-25 degrees C), the temperature dependence of anaerobic glycolysis was found to be higher than that of PCr depletion (Q(10)=2.3). High-energy phosphate metabolism was confirmed to be the initial and preferential energy source. The rate of phosphocreatine hydrolysis did not appear to be affected by extracellular pH changes. By contrast, independent of the intracellular pH value, at the higher temperature (25 degrees C) a lowering of the extracellular pH from 7.9 to 7.0 caused a depression in lactate accumulation. This mechanism was ascribed to the transmembrane proton concentration gradient. This parameter was demonstrated to regulate glycolysis, probably through a reduced lactate efflux, depending on the activity of the lactate-H(+) co-transporter. The calculated intracellular buffer capacity was related to intra- and extracellular pH and temperature. At the experimental extracellular pH of 7.9 and at a temperature of 15 degrees C and 25 degrees C, calculated intracellular buffering capacity was 29.50 micromol g(-1) pH unit(-1) and 69.98 micromol g(-1) pH unit(-1), respectively.
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Vezzoli et al. (2003) studied this question. Temperature and extracellular pH changes was evaluated on Rate of exergonic metabolic processes (anaerobic glycolysis, PCr depletion, lactate accumulation). In isolated frog muscle, lowering extracellular pH from 7.9 to 7.0 at 25 degrees C depressed lactate accumulation, while the temperature dependence of anaerobic glycolysis was higher than PCr depletion.
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