Abstract

Tolerance to acute environmental warming in fish is partly governed by the functional capacity of the heart to increase systemic oxygen delivery at high temperatures. However, cardiac function typically deteriorates at high temperatures, due to declining heart rate and an impaired capacity to maintain or increase cardiac stroke volume, which in turn has been attributed to a deterioration of the electrical conductivity of cardiac tissues and/or an impaired cardiac oxygen supply. While autonomic regulation of the heart may benefit cardiac function during warming by improving myocardial oxygenation, contractility and conductivity, the role of these processes for determining whole animal thermal tolerance is not clear. This is in part because interpretations of previous pharmacological in vivo experiments in salmonids are ambiguous and were confounded by potential compensatory increases in coronary oxygen delivery to the myocardium. Here, we tested the previously advanced hypothesis that cardiac autonomic control benefits heart function and acute warming tolerance in perch (Perca fluviatilis) and roach (Rutilus rutilus); two species that lack coronary arteries and rely entirely on luminal venous oxygen supplies for cardiac oxygenation. Pharmacological blockade of β-adrenergic tone lowered the upper temperature where heart rate started to decline in both species, marking the onset of cardiac failure, and reduced the critical thermal maximum (CTmax) in perch. Cholinergic (muscarinic) blockade had no effect on these thermal tolerance indices. Our findings are consistent with the hypothesis that adrenergic stimulation improves cardiac performance during acute warming, which, at least in perch, increases acute thermal tolerance.

Highlights

  • Upper thermal tolerance in fish is partly governed by the cardiovascular systems capacity to maintain tissue oxygen delivery during warming

  • Exacerbated venous hypoxemia is detrimental in fish species that lack a coronary arterial circulation where the luminal venous oxygen supply represents the sole route

  • While Gilbert et al (2019) found that both cholinergic and β-adrenergic blockade with atropine and sotalol, respectively, reduced ­CTmax and the temperature at which heart rate started to decline in juvenile rainbow trout, we found no such effects when using a similar pharmacological protocol in adult trout (Ekström et al 2014)

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Summary

Introduction

Upper thermal tolerance in fish (i.e., the temperature beyond which the fish cannot survive) is partly governed by the cardiovascular systems capacity to maintain tissue oxygen delivery during warming (see Eliason and Anttila 2017; Ekström et al 2016a, 2019; Gollock et al 2006; Badr et al 2016). Adrenergic or cholinergic autonomic regulation of the heart was hypothesized to be important determinants of ­CTmax and overall cardiac performance during acute warming (Gilbert et al 2019; Ekström et al 2014, 2019). This stems from the idea that a controlled cholinergic slowing of heart rate at elevated temperatures could be beneficial by circumventing AV block by reducing the pacemaker rate to within the functional rate limits of the ventricle (Gilbert et al 2019), lowering overall cardiac workload and oxygen demand, and/or improving myocardial oxygenation by extending the duration for luminal oxygen diffusion (Farrell 2007). We tested the prediction that pharmacological blockade of cholinergic or adrenergic cardiac control systems would reduce the temperature at which heart rate starts to decline during warming, and result in lowered ­CTmax

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