While cardiac beats are traditionally thought to be driven by intracellular Ca²⁺ transients, the beat frequency in vivo is so high that Ca²⁺ cannot fall sufficiently during diastole—a long‑standing paradox. This Opinion article offers a fresh perspective: Hyperthermal Sarcomeric Oscillations (HSOs)—high‑speed contraction–relaxation oscillations that cardiomyocyte sarcomeres exhibit autonomously at ≥ 37 °C—may provide the mechanical basis for the rapid ventricular expansion that occurs with every heartbeat (early diastolic filling).
Experimental evidence from cultured cardiomyocytes shows that HSOs periodically lengthen sarcomeres even when Ca²⁺ remains elevated, with a period close to the heartbeat itself. Because Contraction Rhythm Homeostasis (CRH) keeps the period constant while allowing amplitude and waveform to follow Ca²⁺ fluctuations, Ca²⁺ oscillations and mechanical vibrations remain synchronized, enabling swift tension release despite residual Ca²⁺.
The paper reviews HSO research since 2015—its discovery, 500 fps nanometric measurements, and mathematical models including reverse strokes—and proposes an integrative hypothesis: “At the top of the cardiac hierarchy, the heart exploits HSOs to transform stochastic molecular motions into a robust beating rhythm.” The hypothesis is consistent with in situ molecular data obtained by synchrotron X‑ray diffraction, suggesting that HSOs likely occur in vivo.
Future challenges include direct demonstration of HSOs during intact heartbeats and functional analyses under Ca²⁺ period modulation. Success in these areas could illuminate heart‑failure mechanisms and improve the fidelity of heartbeat simulations.