Increased heart rate reduced crossbridge formation in beating rat whole heart

Heart rate is one of the determinant factors of cardiac performance. However, there is no direct evidence for the effect of heart rate on the actin-myosin interaction. Purpose: To test the effect of heart rates on actin-myosin interaction in hearts with X-ray diffraction analysis using SPring-8. Methods: Seven isolated isovolumically contracting rat hearts were mounted so that the X-ray beam (15.0 keV) passed the subepicardial region. We recorded X-ray diffraction images and LV pressure at heart rates of 120 and 300bpm under 0 mmHg end-diastolic pressure. Between two different heart rates, we compared 1) the amount and the duration of actin-myosin interaction from the intensity ratio reduction of inner (1,0) and outer (1,1) X-ray diffraction, and 2) myofilament lattice spacing from the position of inner X-ray diffraction. Results: In all hearts, we did not detect incomplete relaxation at both heart rates. Increasing heart rate from 120 to 300bpm significantly decreased the intensity ratio reduction at the end-systole (0.92 ± 0.15 vs. 1.58 ± 0.17unitless, p<;0.01) suggesting a smaller amount of actin-myosin interaction, but did not change myofilament lattice spacing (36.2 ± 0.5 vs. 36.7 ± 0.5 nm, NS). Conclusion: Increasing HR reduces the actin-myosin interaction without causing incomplete relaxation, indicating intact intracellular Ca²⁺ handling. These results may derive from shortening of Ca²⁺-myofilament interaction.