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Most animals elevate cardiac output during exercise through a rise in heart rate ( f H ), whereas stroke volume (V S ) remains relatively unchanged. Cardiac pacing reveals that elevating f H alone does not alter cardiac output, which is instead largely regulated by the peripheral vasculature. In terms of myocardial oxygen demand, an increase in f H is more costly than that which would incur if V S instead were to increase. We hypothesized that f H must increase because any substantial rise in V S would be constrained by the pericardium. To investigate this hypothesis, we explored the effects of pharmacologically induced bradycardia, with ivabradine treatment, on V S at rest and during exercise in the common snapping turtle ( Chelydra serpentina) 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 f H in vivo, such that exercise tachycardia was attenuated. Pulmonary and systemic V S rose in response to ivabradine. The rise in pulmonary V S 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, P < 0.05). Although systemic V S 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 f H , V S , or blood flows before or after ivabradine, indicating that the pericardium does not constrain VS in turtles, even during pharmacologically induced bradycardia.