Elevations in skin blood flow and sweating during heat stress are driven through an integration of elevated internal and skin temperatures, with internal temperature being the primary controller. Passive heat stress increases cardiac output through elevated heart rate coupled with maintained stroke volume, the latter of which is achieved by improved systolic function and maintained diastolic function in healthy individuals. The contribution of thermal inputs from the skin in mediating these cardiac responses is unknown. This study tested the hypothesis that cardiac responses during heat stress are primarily mediated by internal temperature. To test this hypothesis, eight healthy (AB) and seven spinal cord injured (SCI) volunteers underwent a lower body heat stress; heating applied only to insensate skin in the SCI subjects. Echocardiographic indices of diastolic and systolic function were performed at normothermia and after an increase in internal temperature of approximately ~1.0 °C. Cardiac output (CO2 rebreathing) increased during heat stress in both groups, but the increase was smaller in SCI (1.7±0.4(SD) l/min) relative to AB (2.3±1.0 l/min; P=0.06). The table shows the effects of heat stress on indices of diastolic and systolic function. These data suggest that improved ventricular systolic function during heat stress primarily occurs by increases in internal temperature, with little to no influence from skin thermoceptors. Notably, smaller increases in atrial and ventricular systolic function in SCI subjects may contribute to their impaired increase in cardiac output during heat stress.