Autonomic cardiac regulation facilitates acute heat tolerance in rainbow trout:<i>in situ</i>and<i>in vivo</i>support

Abstract

Acute warming in fish increases heart rate (<i>f</i>_H) and cardiac output to peak values, after which performance plateaus or declines and arrhythmia may occur. This cardiac response can place a convective limitation on systemic oxygen delivery at high temperatures. To test the hypothesis that autonomic cardiac regulation protects cardiac performance in rainbow trout during acute warming, we investigated adrenergic and cholinergic regulation during the onset and progression of cardiac limitations. We explored the direct effects of adrenergic stimulation by acutely warming an <i>in situ</i> working perfused heart until arrhythmia occurred, cooling the heart to restore rhythmicity and rewarming with increasing adrenergic stimulation. Adrenergic stimulation produced a clear, dose-dependent increase in the temperature and peak <i>f</i>_H achieved prior to the onset of arrhythmia. To examine how this adrenergic protection functions in conjunction with cholinergic vagal inhibition <i>in vivo</i>, rainbow trout fitted with ECG electrodes were acutely warmed in a respirometer until they lost equilibrium (CT_max) with and without muscarinic (atropine) and β-adrenergic (sotalol) antagonists. Trout exhibited roughly equal and opposing cholinergic and adrenergic tone on <i>f</i>_H that persisted up to critical temperatures. β-Adrenergic blockade significantly lowered peak <i>f</i>_H by 14-17%, while muscarinic blockade significantly lowered the temperature for peak <i>f</i>_H by 2.0<b>°</b>C. Moreover, muscarinic and β-adrenergic blockers injected individually or together significantly reduced CT_max by up to 3<b>°</b>C, indicating for the first time that cardiac adrenergic stimulation and cholinergic inhibition can enhance acute heat tolerance in rainbow trout at the level of the heart and the whole animal.