Can temperature-dependent changes in myocardial contractility explain why fish only increase heart rate when exposed to acute warming?

Fish increase heart rate (f_H), not stroke volume (V_S), when acutely warmed as a way to increase cardiac output (Q). To assess whether aspects of myocardial function may have some basis in determining temperature-dependent cardiac performance, we measured work and power (shortening, lengthening and net) in isolated segments of steelhead trout (Oncorhynchus mykiss) ventricular muscle at the fish's acclimation temperature (14^oC), and at 22^oC, when subjected to increased rates of contraction (30–105 min⁻¹, emulating increased f_H) and strain amplitude (8-14%, mimicking increased V_S). At 22^oC, shortening power (indicative of Q) increased in proportion to f_H, and the work required to re-lengthen (stretch) the myocardium (fill the heart) was largely independent of f_H. In contrast, the increase in shortening power was less than proportional when strain was augmented, and lengthening work approximately doubled when strain was increased. Thus, the derived relationships between f_H, strain, and myocardial shortening power and lengthening work, suggest that: increasing f_H would be preferable as a mechanism to increase Q at high temperatures; or in fact, may be an unavoidable response given constraints on muscle mechanics as temperatures rise. Interestingly, at 14^oC, lengthening work increased substantially at higher f_Hs, and the duration of lengthening (i.e., diastole) became severely constrained when f_H was increased. These data suggest that myocardial contraction / twitch kinetics greatly constrain maximal f_H at cool temperatures, and may underlie observations that fish elevate V_S to an equal or greater extent than f_H to meet demands for increased Q at lower temperatures.