INTRODUCTION:
Exercise and hot water immersion (HWI) stress the cardiovascular system through multiple mechanisms. Exercise elevates cardiac output (CO) via increased venous return from the skeletal muscle pump and concomitant chronotropic and inotropic responses. During HWI, CO is maintained or elevated through similar cardiac adjustments amid hydrostatic and thermoregulatory shifts in central blood volume. We hypothesised that prior high intensity interval exercise (HIIE) would augment cardiac loading during HWI, compared to HIIE with thermoneutral water immersion (TWI) and time-matched passive heating.
METHODS:
Twelve adults (24±5 years; 6 females; V̇O2max 39±8 mL·kg^-1·min^-1) completed three randomised crossover conditions in a repeated-measures design: (i) 30-min HIIE followed by 30-min HWI (41°C; ExHWI), (ii) 30-min HIIE followed by TWI (35°C; ExTWI), and (iii) 60-min HWI without prior exercise (HWI60). Transthoracic echocardiography assessed left ventricular structure and function pre and during (20 and 50 min) each condition. Heart rate (HR) and rectal temperature (Trec) were measured throughout. Linear mixed-effects models assessed Condition, Time, and interaction effects.
RESULTS:
HIIE increased HR (from ~62 to ~180 bpm) and CO (from ~3.3 to ~10.0 L·min^-1; Time p<0.001). During HWI60, CO increased from ~3.1 to ~5.7 L·min^-1 at 20 min (without exercise-induced tachycardia). During immersion, HR was higher in ExHWI (104±14 bpm) than ExTWI (86±12 bpm) and HWI60 (78±11 bpm; Condition × Time p<0.001), while stroke volume (SV) was maintained across conditions at 20 min (p=0.565). At 50 min, CO was 6.0±1.4 L·min^-1 in ExHWI, 4.7±1.4 L·min^-1 in ExTWI and 5.6±1.4 L·min^-1 in HWI60 (p=0.150). Left ventricular end-diastolic volume (an index of ventricular filling) decreased during HIIE (~17%; p<0.001) and recovered more slowly following ExHWI (98±23 mL), compared with ExTWI (111±33 mL) and HWI60 (108±30 mL) at 50 min (Condition × Time p<0.001). Peak Trec was higher in ExHWI (38.5±0.2°C) than ExTWI (37.3±0.5°C; p<0.001) and similar to HWI60 (38.3±0.2°C; p=0.251).
CONCLUSION:
Prior HIIE prolonged cardiac and thermal strain during HWI and reduced ventricular filling compared with HWI60 and ExTWI conditions, indicating a preload-limited haemodynamic profile despite maintained SV. These findings show that prior exercise modifies haemodynamic responses during subsequent heat exposure, whereas passive heating alone elevates CO to levels approaching HIIE. Together, these results demonstrate that hydrostatic and thermal stimuli can mimic or augment exercise-associated cardiac loading, supporting passive heating as a potential conditioning stimulus and advancing understanding of acute heat-exercise interactions.