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°C), and at 22°C, 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°C, 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°C, lengthening work increased substantially at higher f(H), 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.