Exploring changes in electrocardiography during passive heat strain in healthy adults

Introduction: Heat stress places significant strain on the cardiovascular system. Hyperthermia elevates heart rate through direct temperature effects on pacemaker cells, sympathetic activation, and vagal withdrawal. To support heat loss, skin blood flow increases, requiring higher cardiac output driven by rising heart rate. The heart’s electrical conduction system maintains rhythmic pumping and can be assessed non-invasively via electrocardiography (ECG), an over century old clinical tool for detecting cardiovascular disease and arrhythmias. Since cardiovascular problems are a major reason for medical visits during extreme heat events, ECG monitoring may offer a simple biomarker of heat-related cardiovascular strain, particularly as ECG abnormalities are present in heat stroke patients. However, limited work has explored how the typical ECG waveform is modified during heat stress in healthy adults. This preliminary study sought to examine changes in ECG components during common laboratory heat-stress protocols in healthy adults which increase heart rate but with different core temperature responses. Methods: Two passive heat stress protocols were conducted: i) a water perfusion suit (WPS) model, and ii) ambient heat exposure (AH). In the WPS model, 10 participants (5 females; 23±2yrs, 1.7±0.1m, 73.6±10.8kg) were passively heated by circulating 49°C water through the suit until core temperature increased ~1.0°C above baseline. ECG traces were captured pre-heating, and following a 0.5°C and 1.0°C rise in core temperature. In the AH model, 29 participants (14 females, 38±19yrs; 1.7±0.1m; 80.0±17.2kg) remained seated in a climate-controlled room (40°C & 25%RH) for 120 minutes. ECG traces were captured prior to heat stress, and every 30 minutes of heat exposure. In both heat stress models, lead II of a 4-lead ECG was captured at 1000 Hz for one minute, and the following components were extracted from each heart beat and averaged within each trace: P-, R-, and T-wave amplitude, ST segment, QRS duration, and PR and QT interval. Within each protocol, components were compared between baseline and end exposure. Additionally, linear regression analyses were performed to examine associations between each component and heart rate within protocol. Results: The mean rise in heart rate during the WPS model was higher (28±7 BPM) compared to AH (10±10 BPM, p< 0.001), with a greater change in core temperature at end exposure with WPS compared to AH (+0.9°C, p< 0.001). From baseline to end heat stress, a shortening of the uncorrected QT interval (-53±17ms, P< 0.001) and PR interval (-17±6ms) was detected with WPS. During WPS, rises in heart rate are strongly associated with uncorrected QT shortening (R 2 =0.88, p< 0.001), and moderately associated with shortening of the corrected QT (R 2 =0.35, P< 0.001), PR interval (R 2 =0.22, p=0.001), and ST duration (R 2 =0.35, p< 0.001); and with T-wave amplitude reduction (R 2 =0.28, p=0.003). With respect to AH, no differences in ECG components or relationships with heart rate were observed. Across all trials, ECG components remained within normal clinically defined thresholds. Conclusion: Preliminary results suggest that changes in ECG components can be observed during passive heat exposure, and are more pronounced with greater hyperthermia and rises in heart rate. Funding: This research was supported by Dr. Ravanelli’s Lakehead University Research Funding and the Natural Sciences and Engineering Research Council of Canada Discovery Grant (PIN#2022-05096). This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.