Passive heat therapy: a ready route to vascular health?

Humans are exquisitely adaptable to their environment. Heat, for instance, stimulates cutaneous smooth muscle relaxation in an attempt to maintain a homeostatic core body temperature. Though simple in concept, it is more complex in mechanism; local factors such as cytokines, heat shock proteins and prostaglandins work in conjunction with centrally mediated reflexes to regulate flow appropriate to the external environment. Moreover, repeated exposure to heat stress leads to decreased threshold for cutaneous vasodilatation (Yamazaki & Hamasaki, 2003) and sweat gland hypertrophy (Pritchett et al. 2015). However, repeated core body temperature elevation can elicit more generalized effects on the vasculature than previously thought. Recently, a 30 year prospective study found significantly reduced frequency of cardiovascular related deaths in those with greater frequency and duration of sauna bathing (Laukkanen et al. 2015). In this issue of The Journal of Physiology, Brunt et al. have explored possible underlying mechanisms linking heat therapy to improved physiological health (Brunt et al. 2016). Specifically, they examined the effects of 8 weeks of heat therapy on endothelial dependent dilatation, arterial stiffness, intima media thickness and blood pressure in a cohort of young, healthy, sedentary individuals. Heat sufficient to raise core body temperature to ∼39°C for up to 90 min increased flow mediated dilatation (FMD) and reduced femoral arterial stiffness and compliance, carotid intima media thickness and arterial pressures. Overall, these vascular changes reflect those that are typically associated with improved cardiovascular health. These findings are important in that significant vascular improvements in a group of young healthy individuals could pertain to greater adaptations in populations with vascular pathophysiology. Though the results as a whole are interesting, there are some inconsistencies. Neither carotid stiffness nor compliance were changed but thickness was less after heat therapy. This suggests that the impact of heat therapy on carotid structure was insufficient to result in functional alterations, but it is possible that longer exposure could further decrease thickness to the point that functional improvement might be observed. Additionally, femoral artery stiffness decreased and compliance increased though thickness was unchanged. This would suggest that the more muscular femoral artery may be impacted by alterations in either locally produced vasodilators or sympathetic outflow. In support of the former, heat shock proteins released in response to heat stress improve NO signalling thereby elevating FMD (McClung et al. 2008). And, in fact, Brunt et al. (2016) found that FMD was increased with heat exposure. In support of the latter mechanism, decreased noradrenaline (norepinephrine) levels can manifest as decreased arterial stiffness and increased compliance (Palatini et al. 2011). Interestingly, sympathetic nerve activity changes seasonally and is lowest in the summer (Cui et al. 2015), suggesting that heat exposure can directly influence sympathetic outflow to the vasculature. These data are particularly interesting because of their potential clinical application. Few treatment modalities are as widely accessible, safe in both the general (Kukkonen-Harjula et al. 2006) and disease (Basford et al. 2009) populations, and cost effective as heat therapy. Moreover, other markers of disease such as glycated haemoglobin (Krause et al. 2015), total cholesterol and LDL cholesterol (Gryka et al. 2014) have been shown to decrease with heat therapy. Populations that have a limited ability to perform aerobic exercise could potentially benefit from this treatment. It has been hypothesized that some part of the adaptations to aerobic exercise training is mediated by the increase in core temperature (Welc et al. 2016). Therefore, heat therapy could potentially serve as a supplementary treatment for these restricted patients. For example, heat therapy reduces resting heart rate in those with spinal cord injury (Gass et al. 2002) and reduces noradrenaline release in those with heart failure (Basford et al. 2009). Ultimately, these findings show immense promise and should prompt further research into the potential for heat therapy as a treatment modality. None declared.