No evidence for pericardial restraint in the snapping turtle () following pharmacologically induced bradycardia at rest or during exercise.

Most animals elevate cardiac output during exercise through a rise in heart rate (), whereas stroke volume (V) remains relatively unchanged. Cardiac pacing reveals that elevating alone does not alter cardiac output, which is instead largely regulated by the peripheral vasculature. In terms of myocardial oxygen demand, an increase in is more costly than that which would incur if V instead were to increase. We hypothesized that must increase because any substantial rise in V would be constrained by the pericardium. To investigate this hypothesis, we explored the effects of pharmacologically induced bradycardia, with ivabradine treatment, on V at rest and during exercise in the common snapping turtle () with intact or opened pericardium. We first showed that, in isolated myocardial preparations, ivabradine exerted a pronounced positive inotropic effect on atrial tissue but only minor effects on ventricle. Ivabradine reduced in vivo, such that exercise tachycardia was attenuated. Pulmonary and systemic V rose in response to ivabradine. The rise in pulmonary V largely compensated for the bradycardia at rest, leaving total pulmonary flow unchanged by ivabradine, although ivabradine reduced pulmonary blood flow during swimming (exercise × ivabradine interaction, < 0.05). Although systemic V increased, systemic blood flow was reduced by ivabradine both at rest and during exercise, despite ivabradine's potential to increase cardiac contractility. Opening the pericardium had no effect on , V, or blood flows before or after ivabradine, indicating that the pericardium does not constrain VS in turtles, even during pharmacologically induced bradycardia.