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 CO₂/[Formula: see text]-free media. Acidosis was created by the NH₄Cl prepulse technique, and intracellular pH (pH_i) was determined using fluorescence microscopy on carboxy-SNARF-1 AM-loaded isolated cardiomyocytes. CO₂-independent pH_i buffering capacity (β_i) was measured by incrementally reducing the extracellular NH₄Cl 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.