The Acute Effect of Hot Water Immersion on Cardiac Function in Individuals with Cervical Spinal Cord Injury

<b>Background/Objectives:</b> Thermotherapy is expected to assist in the prevention of arteriosclerosis and cardiovascular disease in individuals with spinal cord injuries. This study aimed to investigate the impact and underlying mechanisms of whole-body heat stress on cardiac function in patients with cervical spinal cord injury (CSCI) and healthy controls using head-out hot water immersion (HHWI). <b>Methods:</b> Eight male patients with complete motor CSCI and nine healthy controls were recruited. Participants were immersed for 60 min in water set at 2 °C above the resting esophageal temperature. Esophageal temperature, heart rate, and arterial pressure were monitored throughout the experiment. Before and after HHWI, echocardiography was used to measure indices of left ventricular diastolic capacity (E, E', and A), left atrial contractility (A and A'), and left ventricular contractility [S' and isovolumic acceleration (IVA)]. <b>Results:</b> Both groups exhibited an increase in body temperature and heart rate, while blood pressure remained stable. In the control group, there was a significant increase in E (67.0 ± 22.6 to 89.1 ± 13.6), E' (9.5 ± 3.8 to 15.1 ± 4.1), A (50.0 ± 15.2 to 75.8 ± 18.2), A' (8.1 ± 1.6 to 14.8 ± 5.9), S' (8.7 ± 1.4 to 15.1 ± 4.5) and isovolumic acceleration (IVA) (104.2 ± 14.7 to 151.1 ± 20.6). In the CSCI group, only A (49.5 ± 9.9 to 56.9 ± 10.9) and IVA (94.4 ± 27.2 to 134.7 ± 27.7) showed a significant change. <b>Conclusions:</b> In the control group, heat stress increased left atrial contractility, left ventricular dilatation, and left ventricular contractility, while in patients with CSCI, left atrial contractility and left ventricular contractility improved, but there was no improvement in left ventricular diastolic function. This discrepancy in the impact of HHWI on cardiac function suggests that the sympathetic nervous system predominantly influences left ventricular dilatation during whole-body heat stress. However, other factors may also contribute to left atrial and ventricular contractility.