pH recovery from a proton load in rat cardiomyocytes: effects of chronic exercise

The ability of cardiomyocytes to recover from a proton load was examined in the hearts of exercise-trained and sedentary control rats in CO 2 /[Formula: see text]-free media. Acidosis was created by the NH 4 Cl prepulse technique, and intracellular pH (pH i ) was determined using fluorescence microscopy on carboxy-SNARF-1 AM-loaded isolated cardiomyocytes. CO 2 -independent pH i buffering capacity (β i ) was measured by incrementally reducing the extracellular NH 4 Cl concentration in steps of 50% from 20 to 1.25 mM. β i increased as pH i decreased in both exercise-trained and sedentary control groups. However, the magnitude of increase in β i as a function of pH i was found to be significantly ( P < 0.001) greater in the exercise-trained group compared with the sedentary control group. The rate of pH i recovery from an imposed proton load was found to not be different between the exercise-trained and control groups. The Na + /H + exchanger-dependent H + extrusion rate during the recovery from an imposed proton load, however, was found to be significantly greater in the exercise-trained group compared with the control group. By increasing β i and subsequently the Na + /H + exchanger-dependent H + extrusion rate, exercise training may provide cardiomyocytes with the ability to better handle an intracellular excess of H + generated during hypoxia/ischemic insults and may serve in a cardioprotective role. These data may be predictive of two positive outcomes: 1) increased exercise tolerance by the heart and 2) a protective mechanism that limits the degree of myocardial acidosis and subsequent damage that accompanies ischemia-reperfusion stress. NEW & NOTEWORTHY The enhanced ability to deal with acidosis conferred by exercise training is likely to improve exercise tolerance and outcomes in response to myocardial ischemia-reperfusion injury.