The air-breathing Alaska blackfish (Dallia pectoralis) remodels ventricular Ca2+ cycling with chronic hypoxic submergence to maintain ventricular contractility

Abstract

The Alaska blackfish ( Dallia pectoralis ) is a facultative air-breather endemic to northern latitudes where it remains active in winter under ice cover in cold hypoxic waters. To understand the changes in cellular Ca 2+ cycling that allow the heart to function in cold hypoxic water, we acclimated Alaska blackfish to cold (5 °C) normoxia or cold hypoxia (2.1–4.2 kPa; no air access) for 5–8 weeks. We then assessed the impact of the acclimation conditions on intracellular Ca 2+ transients (Δ[Ca 2+ ] i ) of isolated ventricular myocytes and contractile performance of isometrically-contracting ventricular strips. Measurements were obtained at various contractile frequencies (0.2–0.6 Hz) in normoxia, during acute exposure to hypoxia, and reoxygenation at 5 °C. The results show that hypoxia-acclimated Alaska blackfish compensate against the depressive effects of hypoxia on excitation-contraction coupling by remodelling cellular Δ[Ca 2+ ] i to maintain ventricular contractility. When measured at 0.2 Hz in normoxia, hypoxia-acclimated ventricular myocytes had a 3.8-fold larger Δ[Ca 2+ ] i peak amplitude with a 4.1-fold faster rate of rise, compared to normoxia-acclimated ventricular myocytes. At the tissue level, maximal developed force was 2.1-fold greater in preparations from hypoxia-acclimated animals. However, maximal attainable contraction frequencies in hypoxia were lower in hypoxia-acclimated myocytes and strips than preparations from normoxic animals. Moreover, the inability of hypoxia-acclimated ventricular myocytes and strips to contract at high frequency persisted upon reoxygenation. Overall, the findings indicate that hypoxia alters aspects of Alaska blackfish cardiac myocyte Ca 2+ cycling, and that there may be consequences for heart rate elevation during hypoxia, which may impact cardiac output in vivo .

Does the ventricle limit cardiac contraction rate in the anoxic turtle (Trachemys scripta)? I. Comparison of the intrinsic contractile responses of cardiac chambers to the extracellular changes that accompany prolonged anoxia exposure

“…The following parameters were quantified: F max , time-to-peak force ( T PF ) and time-to-half relaxation ( T 0.5R ). Duration of contraction ( T DC ) was calculated by adding T PF + T 0.5R and average rates of contraction ( Rate rise ) and 50% relaxation ( Rate 50% relax ) were calculated by dividing F max by T PF and 0.5 x F max by T 0.5R , respectively ( Kubly and Stecyk, 2019 ; Shiels et al, 2022 ; Stecyk et al, 2021 ). F max is expressed as mN mm −2 , where mean cross-sectional area was calculated using the strip wet mass, length, and an assumed muscle density of 1.06 g cm −3 ( Layland et al, 1995 ).…”