Introduction: Counter rotation in the left ventricular (LV) base and apex during systole and diastole plays an important role in the filling and emptying of the LV. Heat stress leads to increased cardiac work, evidenced by a rise in heart rate (HR) and cardiac output at rest. Whilst the influence of heat stress on LV dimensions has been assessed (Crandall et al. 2008) the effects on cardiac twisting (systolic rotation) and untwisting (diastolic rotation) remain unknown. In order to further elaborate the influence of passive heating on LV function, the present study sought to evaluate the hypothesis that passive heat stress increases LV rotation and rotation rate. Methods: Six active male subjects (21±2yr) completed the study, remaining fully hydrated throughout. Measurements were made at 4 different thermal conditions: 1) Control (Tcore ~37°C, Tskin ~32°C), 2) skin hyperthermia (Tc ~37°C, Tsk ~36°C), 3) skin and mild core hyperthermia (Tc ~38°C, Tsk ~37°C), and 4) high skin and core hyperthermia (Tc ~39°C, Tsk ~38°C). Echocardiographic images were acquired at each stage of heat stress. Two-dimensional images were analysed for LV basal and apical peak rotation (ROT_bas, ROT_api) and rotation rates (ROTR_bas, ROTR_api) and ejection fraction (EF). Mean arterial pressure (MAP) was measured online via a canula inserted in the radial artery. HR was assessed throughout the trial using a three lead ECG. A repeated measures ANOVA was used to detect effects over time and paired student t-test was applied post-hoc to ascertain differences between conditions. Alpha was set at 0.05, Bonferroni adjustment was made for repeated comparisons. Results: ROT_bas increased significantly between skin hyperthermia and high skin and core hyperthermia (-6.5±3.1 vs. -11.3±3.5°, p<0.05). ROT_api (p>0.05) was unaltered. Systolic and late diastolic ROTR_bas increased significantly between control and high skin and core hyperthermia (-88±13 vs. -161±48 s^-1 & 25±10 vs. 76±19 s^-1, p<0.05). Late diastolic ROTR_api increased significantly between control and high skin and core hyperthermia (-6±12 vs. -47±31 s^-1, p<0.05). EF also increased between control and high core hyperthermia (61±4 vs. 76±7%, p<0.05). MAP remained constant throughout the experiment (p>0.05) and HR significantly increased between control and high core hyperthermia (62±14 vs. 119±14 beats*min^-1, p<0.05). Conclusion: Similar to previous studies we demonstrated an increase in systolic function with passive heating, as evidenced by an increase in EF. Our findings suggest that heat stress also increases LV systolic ROT_bas, systolic and late diastolic ROTR_bas and late diastolic ROTR_api. The enhanced twisting and untwisting rate of the LV may facilitate the pronounced increase in EF observed with increased core temperature.