Repeated exposure to passive heat stress ('heat therapy') has widespread physiological benefits, including cellular protection against novel stressors. Increased heat shock protein (HSP) expression and upregulation of circulating factors may impart this protection. We tested the isolated abilities of mild heat pretreatment and serum from human subjects (n = 10) who had undergone 8 weeks of heat therapy to protect against cellular stress following hypoxia-reoxygenation (H/R), a model of ischaemic cardiovascular events. Cultured human umbilical vein endothelial cells were incubated for 24 h at 37°C (control), 39°C (heat pretreatment) or 37°C with 10% serum collected before and after 8 weeks of passive heat therapy (four to five times per week to increase rectal temperature to ≥ 38.5°C for 60 min). Cells were then collected before and after incubation at 1% O for 16 h (hypoxia; 37°C), followed by 20% O for 4 h (reoxygenation; 37°C) and assessed for markers of cell stress. In control cells, H/R increased nuclear NF-κB p65 protein (i.e. activation) by 106 ± 38%, increased IL-6 release by 37 ± 8% and increased superoxide production by 272 ± 45%. Both heat pretreatment and exposure to heat therapy serum prevented H/R-induced NF-κB activation and attenuated superoxide production; by contrast, only exposure to serum attenuated IL-6 release. H/R also decreased cytoplasmic haemeoxygenase-1 (HO-1) protein (known to suppress NF-κB), in control cells (-25 ± 8%), whereas HO-1 protein increased following H/R in cells pretreated with heat or serum-exposed, providing a possible mechanism of protection against H/R. These data indicate heat therapy is capable of imparting resistance against inflammatory and oxidative stress via direct heat and humoral factors.

METHODS: Data was collected on 41 active adults who completed a 11km road race. Age (mean±standard deviation [SD]): 44.7±15.7 years; VO 2 max: 42.7±9.2 ml/kg/min; percent body fat: 22.4±9.6%. CRI was assessed at baseline for 10 minutes in a supine position in a thermoneutral environment. At the road race, CRI was assessed for 2 minutes pre-race and post-race in the supine position. Heart rate and oxygen saturation were assessed alongside CRI. Environmental conditions were captured surrounding the race. Core temperature was assessed post-race. Descriptive statistics (mean±SD) were calculated and paired-samples t-tests were utilized to compare baseline to pre-race, baseline to post-race, and pre-race to post-race. RESULTS: Post-race CRI (mean ± SD: 0.70±0.32) significantly diminished compared to baseline values (0.91±0.07; p<0.001). Post-race CRI was significantly diminished (p<0.001) compared to pre-race CRI measures (mean±SD: 0.88±0.09). Resting heart rate increased from baseline (mean±SD: 59.6±10.4 bpm) to pre-race (65.4±11.2 bpm) and to post-race (85.1±16.9 bpm). Runners were characterized as hyperthermic following the race (core temperature: 38.90±1.20 ºC). Environmental conditions upon finishing the race were 22.78 ºC, 53% RH, and 21.67 ºC WBGT. CONCLUSIONS: Following physically demanding exercise in the heat, CRI monitoring may be able to detect changes resulting from increased physiological stress and may be utilized to prevent collapse. Future studies should assess the extent to which thermal stress is correlated to changes in CRI.

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