When oxygen delivery to active skeletal muscle is insufficient for the metabolic demands, afferent nerves within muscles are activated, which elicit reflex increases in heart rate (HR), cardiac output (CO), and arterial pressure (AP), termed the muscle metaboreflex (MMR). To what extent the increases in CO are the result of increased ventricular contractility is unclear. A widely accepted index of contractility is maximal left ventricular elastance (Emax), the slope of the end-systolic pressure-volume relationship, such as during rapidly imposed reductions in preload. The objective of the present study was to determine whether MMR activation elicits increases in Emax. Experiments were performed using conscious dogs chronically instrumented to measure left ventricular pressure and volume at rest and during mild or moderate treadmill exercise with and without partial hindlimb ischemia to elicit MMR responses. At both workloads, MMR activation significantly increased CO, HR, AP, and maximum rate of change of left ventricular pressure. During both mild and moderate exercise, MMR activation increased Emax to 159.6 Ϯ 8.83 and 155.8 Ϯ 6.32% of the exercise value under free-flow conditions, respectively. We conclude that the increase of ventricular elastance associated with MMR activation indicates that a substantial increase in ventricular contractility contributes to the rise in CO during dynamic exercise. elastance; pressor response; cardiac function DURING DYNAMIC EXERCISE, when oxygen delivery to active skeletal muscle is insufficient to meet the metabolic demands, metabolites (e.g., lactic acid, adenosine, potassium, diprotonated phosphate, H ϩ , arachidonic acid products, and others) accumulate within the active muscle and stimulate group III and IV afferent neurons. These sensory neurons project to the central nervous system, eliciting a reflex pressor response consisting of increases in efferent sympathetic nerve activity (SNA), mean arterial pressure (MAP), heart rate (HR), cardiac output (CO), plasma levels of vasoactive hormones, and peripheral vasoconstriction termed the muscle metaboreflex (MMR) (1, 2, 8, 12, 14, 19, 21, 25-28, 30, 32, 33, 35-38, 42, 44). These mechanisms act in concert to partially restore blood flow and arterial oxygen delivery to the hypoperfused muscles (27,31). Previous studies have shown that in normal dogs exercising at mild and moderate workloads, the increases in MAP elicited by this MMR activation are mainly due to increases in CO. The rise in CO likely results from increases in ventricular performance, HR, and central blood volume mobilization (26, 35). In this way the MMR-induced increases in ventricular performance act to sustain or slightly increase stroke volume (SV) despite decreases in ventricular filling time due to the reflex tachycardia (2, 26, 44). Furthermore, O'Leary an Augustyniak (26) showed that in normal dogs in which HR was fixed at 225 beats/min during mild exercise, MMR activation caused such a rise in SV that the increases in CO were approximately equal to t...