Mechanism of contraction rhythm homeostasis for hyperthermal sarcomeric oscillations of neonatal cardiomyocytes.

The heart rhythm is maintained by oscillatory changes in [Ca2+ ]. However, it has been suggested that the rapid drop in blood pressure that occurs with a slow decrease in [Ca2+ ] preceding early diastolic filling is related to the mechanism of rapid sarcomere lengthening associated with spontaneous tension oscillation at constant intermediate [Ca2+ ]. Here, we analyzed a new type of oscillation called hyperthermal sarcomeric oscillation. Sarcomeres in rat neonatal cardiomyocytes that were warmed at 38-42 °C oscillated at both slow (~ 1.4 Hz), Ca2+ -dependent frequencies and fast (~ 7 Hz), Ca2+ -independent frequencies. Our high-precision experimental observations revealed that the fast sarcomeric oscillation had high and low peak-to-peak amplitude at low and high [Ca2+ ], respectively; nevertheless, the oscillation period remained constant. Our numerical simulations suggest that the regular and fast rthythm is maintained by the unchanged cooperative binding behavior of myosin molecules during slow oscillatory changes in [Ca2+ ].