Abstract
Cardiac cellular responses to acute exercise remain undescribed. We present a model for mimicking acute aerobic endurance exercise to freshly isolated cardiomyocytes by evoking exercise-like contractions over prolonged periods of time with trains of electrical twitch stimulations. We then investigated immediate contractile, Ca(2+) , and metabolic responses to acute exercise in perfused freshly isolated left ventricular rat cardiomyocytes, after a matrix-design optimized protocol and induced a mimic for acute aerobic endurance exercise by trains of prolonged field twitch stimulations. Acute exercise decreased cardiomyocyte fractional shortening 50%-80% (p < .01). This was not explained by changes to intracellular Ca(2+) handling (p > .05); rather, we observed a weak insignificant Ca(2+) transient increase (p = .11), while myofilament Ca(2+) sensitivity increased 20%-70% (p < .05). Acidic pH 6.8 decreased fractional shortening 20%-70% (p < .05) because of 20%-30% decreased Ca(2+) transients (p < .05), but no difference occurred between control and acute exercise (p > .05). Addition of 1 or 10 mM La(-) increased fractional shortening in control (1 mM La(-) : no difference, p > .05; 10 mM La(-) : 20%-30%, p < .05) and acute exercise (1 mM La(-) : 40%-90%, p < .01; 10 mM La(-) : 50%-100%, p < .01) and rendered acute exercise indifferent from control (p > .05). Intrinsic autofluorescence showed a resting NAD(state) of 0.59 ± 0.04 and FAD(state) of 0.17 ± 0.03, while acute exercise decreased NADH/FAD ratio 8% (p < .01), indicating intracellular oxidation. In conclusion, we show a novel approach for studying immediate acute cardiomyocyte responses to aerobic endurance exercise. We find that acute exercise in cardiomyocytes decreases contraction, but Ca(2+) handling and myofilament Ca(2+) sensitivity compensate for this, while acidosis and reduced energy substrate and mitochondrial ATP generation explain this.