By focusing a 1,455 nm laser to generate a microscopic heat pulse, adult rat cardiomyocytes were made to shorten in a beat‑like manner—even though no excitation–contraction coupling (ECC) calcium signal was involved. This study quantitatively characterizes the phenomenon and clearly demonstrates “heat‑driven contraction,” a mode of contraction that bypasses the core Ca²⁺ dynamics of ECC.
At an ambient temperature of 36 °C, a rapid rise of only ≈ 4 °C triggered contraction, whereas at 25 °C a ≥ 11 °C pulse was required, revealing high temperature sensitivity near physiological temperature.
No intracellular Ca²⁺ transients were detected with Fluo‑4, and the same contraction occurred in skinned cells placed in Ca²⁺‑free solution.
The data suggest that the heat pulse weakens tropomyosin–actin interactions, shifting the thin‑filament on/off equilibrium toward the “on” state and directly promoting actin–myosin binding.
Significance
The heat‑pulse method provides a novel platform for non‑invasive, localized activation of cardiac or skeletal muscle without genetic manipulation—distinct from electrical or optogenetic stimulation. Because it controls contraction while bypassing Ca²⁺‑dependent regulation, it is a powerful tool for disease models with impaired Ca²⁺ release and for drug testing. From the standpoint of thin‑filament thermosensitivity, the findings laid groundwork for later concepts such as Hyperthermal Sarcomeric Oscillations (HSOs) and Contraction Rhythm Homeostasis (CRH). Potential applications include safety evaluation under febrile or hyperthermic conditions, and the development of local hyperthermia therapies or photothermal devices.
Article information & citation
Kotaro Oyama, Akari Mizuno, Seine A. Shintani, Hideki Itoh, Takahiro Serizawa, Norio Fukuda, Madoka Suzuki, Shin’ichi Ishiwata.
Microscopic heat pulses induce contraction of cardiomyocytes without calcium transients. Biochemical and Biophysical Research Communications 417, 607–612 (2012).