Proceedings of The Physiological Society

Future Physiology (Leeds, UK) (2017) Proc Physiol Soc 39, PC24

Poster Communications

Elevated core temperature: not only useful in the context of exercise to combat chronic low-grade inflammation?

S. Hoekstra1, N. C. Bishop1, S. H. Faulkner1, C. A. Leicht1

1. The Peter Harrison Centre for Disability Sport, Loughborough University, Loughborough, United Kingdom.

Regular exercise is suggested to be effective in reducing chronic low-grade inflammation, which in turn could enhance insulin sensitivity (1). Since the increase in body temperature during exercise is one of the proposed inducers of the beneficial acute inflammatory response, passive heating could be an alternative strategy to combat chronic low-grade inflammation in individuals without the physical capacity to engage in sufficient exercise (2). This study investigates both the acute inflammatory response to hot water immersion (HWI) as well as the chronic effects of a HWI intervention period. Ten sedentary, overweight (BMI: 31.0±4.2 kg/m2), healthy males were immersed in water set at 39°C for 1 hour, whilst 1 hour of seated rest at ambient temperature was used as control condition. Blood was drawn from an antecubital vein pre, post and 2 hours post-session. A resting blood sample was taken 3 days after completion of a 2-week intervention period consisting of 10 HWI sessions (5 sessions of 45 min followed by 5 sessions of 60 min). Main outcome measures were monocyte intracellular heat shock protein 72 (iHsp72), the distribution of CD14++/CD16-, CD14++/CD16+ and CD14+/CD16++ monocyte subsets, plasma interleukin (IL)-6, plasma heat shock protein 72 (eHsp72) and fasting blood glucose concentrations. The acute and chronic effects of HWI were assessed using repeated measures ANOVA. Acutely, HWI increased rectal temperature from 37.1±0.6°C to 38.7±0.4°C. The plasma concentration of IL-6 (p<0.001) and the percentage of CD14++/CD16+ (p=0.004) and CD14+/CD16++ (p=0.008) monocytes were significantly higher compared to control immediately post-HWI, whilst iHsp72 and eHsp72 were not changed after the HWI session at any time point (p=0.57). Resting levels of IL-6, iHsp72 and the distribution of monocyte subsets were not changed following the 2-week intervention period (p>0.29), whilst there was a trend for a decrease in resting eHsp72 concentration (p=0.10). However, fasting blood glucose levels were significantly lowered following the intervention period (4.42±1.01 mmol/L to 3.98±1.11 mmol/L; p=0.03). A single HWI session did induce an acute inflammatory response. This was, however, not accompanied by an acute elevation of iHsp72 or eHsp72, possibly because the exposure to heat and the associated high rectal temperatures were not maintained for long enough. Although the 10 HWI sessions did not significantly alter the inflammatory markers at rest, the lowering in fasting blood glucose concentration may indicate a positive change in glucose metabolism and/or insulin sensitivity, suggesting that HWI may induce some of the positive metabolic effects found after exercise training.

Where applicable, experiments conform with Society ethical requirements