Atlantic cod were subjected to 12–15 min swimming exercise at 2/3 body lengths s-1 in a Blazka-type swim tunnel. Pre- and postbranchial blood pressures, cardiac output (ventral aortic blood flow) and heart rate were continuously recorded, and blood samples for measurement of arterial and mixed venous oxygen tension were taken before and at the end of the exercise period. In a second group of fish, subjected to similar exercise regimes, blood samples were taken for analysis of the plasma concentrations of catecholamines. Pre- and postbranchial blood pressures and cardiac output increase during exercise, while the mixed venous oxygen tension decreases. The effect on cardiac output is due to an increase of both heart rate and stroke volume. There are no significant changes in either systemic or branchial vascular resistances, or in the plasma concentrations of catecholamines. Injection of the adrenergic neurone-blocking drug bretylium produces a decrease in postbranchial blood pressure in resting cod, due to a decrease in the systemic vascular resistance. Exercising cod treated with bretylium have a significantly lower pre- and postbranchial blood pressure than exercising control cod. This is due mainly to a dramatic reduction in the systemic vascular resistance. The alpha-adrenoceptor antagonist phentolamine does not further affect the blood pressure in cod treated with bretylium. It is concluded that the exercise hypertension observed in cod depends on the effect of adrenergic vasomotor fibres maintaining the systemic vascular resistance, and also on the increase in cardiac output. An adrenergic innervation of the heart may play some role in the control of cardiac performance both at rest and during exercise, but the main cardioregulatory mechanism is likely to be non-adrenergic, most probably including cardiac control via variation of the cholinergic vagal cardioinhibitory tonus.

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