Key Points
- Until recently, a majority of prior investigations have focused on the cardiovascular adjustments that occur during acute heat exposure. Therefore, little was known regarding the recovery period that follows acute exposure or how these responses may vary across the life span or in pathophysiological conditions.
- In this review, we discuss how the recovery period is not simply a passive return to thermal and cardiovascular homeostasis, but represents a dynamic phenomenon with distinct physiological adjustments that differ from those that occur during heat exposure.
- We highlight recent studies from our group and others that have characterized the cardiovascular adjustments that occur after acute passive heat exposure. Special emphasis will be placed on underlying mechanisms and clinical implications. Finally, we postulate that these acute cardiovascular adjustments may predict the long-term adaptive response to chronic heat exposure (i.e., heat therapy).
INTRODUCTION
Until recently, a majority of prior investigations have focused on the cardiovascular adjustments that occur during acute heat exposure. Therefore, little was known regarding the recovery period that follows acute exposure or how these responses may vary across the life span or in pathophysiological conditions. Work from our group and others has demonstrated that the recovery period is not simply a passive return to thermal and cardiovascular homeostasis, but represents a dynamic phenomenon with distinct physiological adjustments that differ from those that occur during heat exposure. Often these adjustments represent key changes in traditional (e.g., blood pressure) and nontraditional risk factors (e.g., vascular function) that may be of benefit to various populations. In addition, these acute adjustments may set the foundation for long-term adaptations associated with chronic heat exposure (i.e., heat therapy) (1–5). Thus, a holistic understanding of the acute cardiovascular adjustments that occur after heat exposure is critical to our understanding of the therapeutic potential of this nonpharmacological therapy within the acute setting and beyond. To that end, the purpose of this brief review is to highlight recent studies that have characterized the cardiovascular adjustments that occur after acute heat exposure. Special emphasis will be placed on underlying mechanisms and clinical implications. Finally, we postulate that these acute cardiovascular adjustments may predict the long-term adaptive response to heat therapy.
THE RECOVERY PERIOD
What is the importance of studying the recovery period after heat exposure? As highlighted elegantly by Luttrell and Halliwill (6), recovery from a stressor is not simply a passive return to “baseline,” but rather it represents a period in which one may be at risk or vulnerable to negative health outcomes, whereas in others, it may represent a period in which the cardiovascular system is primed for adaptation. Interest in the physiology of recovery, particularly within the context of heat exposure, has grown over the last decade owing largely to studies highlighting the efficacy of heat therapy to induce beneficial cardiovascular adaptations (1–5). For the purpose of this review, we will define the recovery period as the 24 h after the termination of acute passive heat exposure that is sufficient in magnitude to increase body core temperature and local skin/tissue temperature. This period represents the time frame in which studies have demonstrated that the function, regulation, and control of the cardiovascular system differs from a preheat baseline. In addition, these adjustments may occur beyond the time frame in which thermoregulatory homeostasis has been reestablished.
During passive heat exposure, body core and tissue temperatures are augmented primarily by increasing skin temperature, an effect that can be modulated by conditions that influence convective and evaporative heat transfer. In contrast, during aerobic exercise, body core temperature increases secondary to augmented metabolic heat production. Upon the cessation of exercise, heat loss thermoeffectors (cutaneous vasodilation and sweating) are suppressed, thereby mediating a sustained elevation in body core and muscle temperatures despite the attenuation of metabolic heat production (7). As such, recovery of thermoregulatory function after exercise is likely to differ relative to that after passive heat exposure. In addition, recovery of thermoregulatory function may vary between passive heating paradigms that utilize various mediums to transfer heat (e.g., Finnish sauna vs hot water immersion). We are unaware of any investigations that have directly compared recovery of thermoregulatory function after exercise and passive heat exposure or across various heating paradigms. Nevertheless, thermal homeostasis seems to be restored within 0.5–2 h after most forms of passive heat exposure, but the rate in which this occurs may vary depending on the duration and magnitude of exposure. In addition, active cooling strategies may speed thermal recovery relative to passive cooling, which relies primarily on ambient air temperature. The cardiovascular system seems to recover more slowly, although studies in this area have largely been confined to the initial phase (i.e., ≤3 h). Thus, the extent to which these changes persist beyond the initial recovery period remains understudied.
Several factors should be considered when studying recovery of the cardiovascular system after acute heat exposure. First, the timing in which measurements are made after the termination of heat exposure should always be considered, particularly as it relates to body core and skin temperatures. That is, the assessment of cardiovascular function may vary substantially if measured immediately after heat exposure, when body core and skin temperatures are significantly elevated relative to 2 h into recovery when temperature homeostasis likely has been restored. Second, and somewhat related to the first point, the heating paradigm should be considered relative to the outcome measures and the extent to which body core temperature is increased. Finally, posture should be considered as it has significant influence on the cardiovascular system and associated control mechanisms. Investigators should consider a recovery posture that mimics what one might experience outside of the laboratory (e.g., seated, semirecumbent, or ambulatory), or the supine position whereby the influence of hydrostatic pressure is limited.
EXPERIMENTAL APPROACHES TO EXPLORE RECOVERY FROM ACUTE HEAT EXPOSURE
A number of paradigms have been utilized to examine recovery of the cardiovascular system after acute heat exposure. Three of the most common approaches are hot water immersion, use of a water-perfused suit, and dry and far infrared sauna bathing. Hot water immersion typically utilizes a temperature range of 38°C–42°C and can easily and rapidly increase body core temperature (8). With water immersion, participants can be immersed to varying depths, with some using knee-down immersion (9–12) and others utilizing waist-down (13–15) or chest-down immersion (16,17). Water-perfused suits were first utilized in human thermal physiology investigations over a half-century ago by the late Dr. Loring Rowell (18). These nylon suits are lined with vinyl tubes that are spaced ~1 to 2 cm apart and connected to a water heater and pump system. Investigators can heat participants by perfusing hot water through the vinyl tubes to clamp skin temperature at ~38°C to 40°C. Some studies have utilized only the trousers (19–21), whereas others have used the entire suit (22,23). Dry saunas, also known as traditional Finnish saunas, typically operate at 80°C–100°C with a low relative humidity. Most studies utilizing dry saunas expose participants to heating cycles lasting 8–15 min separated by short periods of thermoneutral recovery or cold-water showering (24–26), whereas others have utilized a 30-min continuous exposure (27). Far infrared saunas generate an infrared wavelength of 6–12 μm that can easily penetrate human skin up to 2 inches, essentially inducing a deep heating effect. Infrared saunas, such as those typically used in Waon therapy, operate at ~60°C, and exposure lasts ~15 min and is followed immediately by a 30-min period in which participants are covered with blankets (28). Finally, pulsed short-wave diathermy generates high-frequency currents that increase tissue kinetic energy to induce deep tissue heating (29–31). Unlike other heating modalities, the effects of pulsed short-wave diathermy are localized and not accompanied by an increase in body core temperature. Thus, pulsed short-wave diathermy allows investigators to isolate the effects of localized heat exposure. A number of factors should be considered when determining which heating paradigm best fits the experimental design. Specifically, heating duration, target body core temperature (i.e., intensity), population, and primary outcome measures are key factors that should be weighed when deciding which heating paradigm is most appropriate to achieve the overall goals of an investigation.
CARDIOVASCULAR ADJUSTMENTS IN RECOVERY FROM ACUTE HEAT EXPOSURE
Hemodynamics
The human cardiovascular system undergoes significant hemodynamic adjustments during passive heat exposure. These adjustments go beyond the scope of this review, but readers are referred to seminal reviews by Rowell (32,33) and a more recent in-depth review by Crandall and Wilson (34). The cardiovascular adjustments described hereinafter will first be presented for healthy adults and will set the stage for a later section that discusses clinical implications.
Central hemodynamics
We recently characterized the central hemodynamic adjustments that occur after 45-min lower-leg hot water immersion that was sufficient to increase intestinal temperature by ~0.7°C in a cohort of young and aged adults (11). Mean arterial blood pressure was reduced 30 min into recovery for the aged adults, whereas it was well maintained in young adults. However, Francisco and colleagues (17) later demonstrated that 60 min of chest-down hot water immersion, which increased rectal temperature by ~1.5°C, reduced mean arterial blood pressure in young adults through 60 min of recovery. Importantly, the blood pressure-lowering effect observed by our group and by that of Francisco and colleagues seems to be mediated by an increase in systemic vascular conductance that is not fully offset by a modest increase in cardiac output. More recently, Campbell et al. (35) reported a numerical reduction in systolic, diastolic, and mean arterial pressure in young adults after whole-body hot water immersion (Δ rectal temperature of ~1.5°C) that tended to be smaller in magnitude relative to that which occurs after cycle exercise performed in the heat. Interestingly, they also reported an absence of a hypotensive response after sauna exposure, despite an increase in rectal temperature of ~1.2°C. Finally, Didier and colleagues (36) reported that systolic, diastolic, and mean arterial pressure did not differ from baseline in young adults when measured 24 h after whole-body hot water immersion (Δ rectal temperature of 1.2°C). Combined, these studies provide evidence suggesting that the adjustment in arterial blood pressure that occurs after acute heat exposure is not universal and may vary depending on the intensity, duration, and the population being studied.
Our understanding of splanchnic and renal hemodynamics in recovery from acute heat exposure is limited. To our knowledge, splanchnic hemodynamics have not been assessed in the recovery period, whereas only one study has examined renal hemodynamics. Chapman et al. (37) used Doppler ultrasound to measure renal and segmental artery blood velocity after whole-body heat exposure (water-perfused suit) sufficient to increase intestinal temperature by ~1.2°C. They demonstrated that the reduction in renal blood velocity and an increase in vascular resistance that occurs during heat stress are restored to baseline immediately upon active skin cooling. In addition, vasoconstrictor responsiveness to a cold pressor test also returned to baseline after an attenuation during heat stress. These data highlight that the renal circulation undergoes substantial adjustments during heat stress but returns to baseline in the recovery period.
Peripheral hemodynamics
Arm (10,17) and leg (10,11,17) blood flow remain elevated upward of ~30 min after acute heat exposure (Δ body core temperature of ≥0.6°C) and contribute to the increase in systemic vascular conductance. This hyperemic response seems to resolve thereafter in young healthy adults (17) but persists for upward of ~40 min in middle-aged and older adults (25). Vasodilation within the cutaneous circulation is thought to be the primary mediator of the sustained hyperemic response after heat exposure. However, it is possible that the skeletal muscle circulation also contributes, given the increase in muscle blood flow that occurs during heat exposure (38,39) and the sustained elevation in muscle temperature that persists well into the recovery period (11).
Shear stress (i.e., the frictional drag of red blood cells along the endothelium) is considered one of the primary mechanisms mediating vascular adaptation in response to heat exposure. During acute heat exposure, conduit artery shear stress shifts from an oscillatory pattern (i.e., having antegrade and retrograde shear) with a low mean shear to a purely antegrade profile with a high mean shear that approximates values measured during low-intensity aerobic exercise (40). Biological sex and underlying pathophysiology (12,14) seem to influence shear patterns that occur during acute heat stress. For example, Larson and colleagues (41) demonstrated that the increase in antegrade shear rate (an index of shear stress) during hot water immersion (Δ rectal temperature of ~1.0°C) is greater in women because of a combination of increased blood velocity and a smaller cross-sectional area of the brachial artery. Coombs et al. (12) demonstrated that, relative to age-matched control participants, the increase in brachial and femoral artery antegrade shear rate is attenuated in individuals with spinal cord injury when exposed to lower-leg hot water immersion that was sufficient to increase intestinal temperature by ~0.7°C. Interestingly, Thomas and colleagues (14), demonstrated that popliteal artery, but not brachial artery, antegrade shear rate is augmented during hot water immersion (Δ tympanic temperature of ~1.8°C) in patients with peripheral arterial disease compared with age-matched control participants, an effect that is likely due to smaller cross-sectional area of the vessel.
The conduit artery shear patterns induced by acute heat exposure are sustained into the recovery period (Fig. 1). To that end, we recently demonstrated that superficial femoral artery antegrade shear rate was elevated and retrograde shear rate reduced in young and aged adults up to 30 min after lower-leg hot water immersion (11). Using an identical heating intervention, Cheng et al. (10) demonstrated that brachial artery shear rate returns to baseline 30 min after exposure, whereas the shift was still present in the superficial femoral artery. Francisco et al. (17) demonstrated that the shift in the shear profile is sustained in the brachial (~40 min) and femoral (~20 min) arteries after chest-down hot water immersion. Together, these studies suggest that the intensity of exposure may influence the recovery of shear patterns and that there may be some limb dependency. It should be noted that other physical hemodynamic stimuli such as circumferential stretch and shear frequency that occurs secondary to the increase in heart rate induced by heat exposure could contribute to the beneficial adjustments in the recovery period (42,43).
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Figure 1: Representative superficial femoral artery blood velocity tracings obtained via Doppler ultrasound. Data are shown for a 67-year-old woman before (top panel), through 45 min of knee-down hot water immersion (middle panel), and 30 min into recovery (bottom panel). Significant retrograde blood flow is present at baseline, but is abrogated during heat exposure and persists in the recovery period. TAMV, time-average mean blood velocity. Created with
BioRender.com.
Cerebral hemodynamics
Similar to other circulations, the cerebrovasculature undergoes significant adjustments during heat exposure. However, to our knowledge, only one study has characterized cerebral hemodynamics in recovery from acute heat exposure. This is particularly surprising given the clinical implications of heat therapy on the pathophysiology of Alzheimer’s disease and related dementias (44). Amin and colleagues (45) demonstrated that relative to baseline, internal carotid artery and vertebral artery blood flow and shear rate were unchanged through 80 min of recovery after 30 min of chest-down hot water immersion that increased rectal temperature by ~1.5°C. Interestingly, this hemodynamic response was similar to that observed after moderate-intensity treadmill running and 5 × 4-min high-intensity interval exercise that were time and core temperature matched to the heating condition.
Neurovascular Adjustments
Neural control
The mechanism/s mediating the sustained increase in systemic vascular conductance and reduction in arterial blood pressure after acute heat exposure are yet to be fully elucidated. We recently utilized the microneurography technique to directly measure sympathetic nerve traffic in young and aged adults before and in recovery from acute leg heating (19). We found that the reduction in arterial blood pressure that occurs in aged adults 30 min after acute leg heating is mediated, in part, by a sympathoinhibitory effect that alters the compensatory neural response to hypotension. That is, the characteristic increase in muscle sympathetic nerve activity that occurs in response to hypotension is absent in aged adults after heat exposure despite a marked reduction in arterial blood pressure and is suggestive of altered central neural cardiovascular control. In young adults, arterial blood pressure is well maintained because of increased sympathetic nerve activity that restrains the increase in systematic vascular conductance. Despite the adjustments in basal sympathetic outflow after heat exposure, there is no change in the transduction of this signal into vascular resistance (i.e., neurovascular transduction). These findings are summarized in Figure 2. The extent to which these results vary after other heating paradigms or in other populations is unclear but remains an exciting area of future investigation.
Figure 2: Neural control of the circulation. In Engelland
et al. (
19), we found that arterial blood pressure was well maintained in young adults after acute leg heating due to increased sympathetic nerve activity, which restrains the increase in systemic vascular conductance. However, in aged adults, sympathetic nerve activity did not differ from preheat despite a marked reduction in arterial blood pressure, suggesting that acute heat exposure induces a sympathoinhibitory effect that alters the compensatory neural response to hypotension. That is, the characteristic increase in muscle sympathetic nerve activity that occurs in response to hypotension is absent in aged adults after heat exposure despite the marked reduction in arterial blood pressure. Neurovascular transduction did not differ from preheat to recovery for either age group. Arrows denote the directional change, relative to baseline, that occurs 30 min into the recovery period. †
P < 0.05 versus young; *
P < 0.05 versus preheat. MSNA, muscle sympathetic nerve activity. Created with
BioRender.com.
Vasodilator function
The assessment of vasodilator function after acute heat exposure can span the entire arterial tree from large conduit arteries to the microcirculation. To date, flow-mediated dilation and postocclusive reactive hyperemia are the most widely utilized techniques to simultaneously assess macrovascular and microvascular function in humans, respectively. Along these lines, Tinken et al. (46) were the first to demonstrate that acute heat exposure via forearm hot water immersion improved brachial artery flow-mediated dilation in young men. We later demonstrated that knee-down hot water immersion improved flow-mediated dilation in the superficial femoral artery and leg postocclusive reactive hyperemia in aged adults (11). These improvements are not ubiquitous between limbs or across the human life span. For example, knee-down hot water immersion has no effect on vasodilator function measured in the leg of young healthy adults, but does seem to augment brachial artery flow-mediated dilation and forearm postocclusive reactive hyperemia (10,11). In addition, Coombs et al. (42) demonstrated that increasing esophageal temperature by ~1.3°C via a water-perfused suit and isolated forearm heating, which clamped skin temperature at ~38°C improved brachial artery flow-mediated dilation in young men. These adjustments seem to persist well beyond the initial recovery phase as Didier and colleagues (36) demonstrated recently that brachial artery flow-mediated dilation was augmented in young adults for 24 h after whole-body hot water immersion. However, these findings are not universal as Brunt et al. (16) demonstrated that chest-down hot water immersion that was sufficient to increase rectal temperature by ~1.5°C had no effect on brachial artery flow-mediated dilation and forearm postocclusive reactive hyperemia in young adults. It is unclear why vasodilator function measured in the arm differs between these studies but may be related to the timing of measurements as Brunt et al. performed their assessment 60 min into recovery relative to the studies of Coombs et al. and Cheng et al., who made their assessments at 10 and 30 min after exposure, respectively. In addition, the results of Didier et al. should be interpreted judiciously as they did not include a thermoneutral time control.
The acute improvement in microvascular function assessed via postocclusive reactive hyperemia was thought to be mediated by adjustments in the cutaneous and skeletal muscle circulations. However, this had yet to be confirmed because of methodological challenges associated with differentiating blood flow between these vascular beds using whole-limb measurement techniques such as Doppler ultrasound or venous occlusion plethysmography. We recently utilized skeletal muscle microdialysis to bypass the cutaneous circulation and directly assess endothelial-dependent and endothelial-independent vasodilation by measuring the local hyperemic response to graded infusions of acetylcholine and sodium nitroprusside in aged adults (13). We demonstrated that endothelial-dependent and endothelial-independent vasodilations are improved in the microcirculation of skeletal muscle in aged humans at ~90 min after waist-down hot water immersion (Δ intestinal temperature of ~1.0°C). These findings suggest that the improvement in microvascular function induced by acute heat exposure extends to the cutaneous and skeletal muscle circulations in aged adults.
Endothelial ischemia–reperfusion injury
Interventions that rapidly restore vessel patency to reestablish blood flow during an ischemic event can simultaneously augment tissue and organ damage — a condition known as ischemia–reperfusion injury (47). Although a number of mechanisms are thought to contribute to ischemia–reperfusion injury, endothelial dysfunction has emerged as a strong contributor to the overall condition. In humans, endothelial ischemia–reperfusion injury is induced in the brachial artery by 20-min arm circulatory arrest via rapid cuff inflation followed by 20-min reperfusion (48,49). The magnitude of endothelial ischemia–reperfusion injury can then be assessed immediately thereafter via brachial artery flow-mediated dilation. Using this experimental model, Brunt and colleagues (16) were the first to demonstrate that acute heat exposure via chest-down hot water immersion (Δ rectal temperature of ~1.8°C) protects against endothelial ischemia–reperfusion injury in young adults. This finding was later replicated by our group using knee-down hot water immersion (9), which suggests that this heating paradigm may be an alternative approach that is equally efficacious at protecting against endothelial ischemia-reperfusion injury relative to the more intense heating interventions.
The mechanism/s mediating protection against endothelial ischemia–reperfusion injury after acute heat exposure are yet to be fully elucidated. Using an ex vivo preparation, Brunt et al. (50) provided evidence that the direct effect of heat exposure on endothelial cells and humoral factors released in response to elevated body core temperature contribute to the protection against ischemia–reperfusion injury. However, the ex vivo preparation utilized in their study did not incorporate a physiological shear stress stimulus. Therefore, we performed an experiment where we utilized arterial compression to manipulate brachial artery blood velocity during acute heat exposure, which allowed us to isolate the contribution of shear stress versus the direct effect of heat and the release of humoral factors (23). Surprisingly, despite inhibiting the increase in shear stress induced by whole-body heat exposure (Δ intestinal temperature of ~1.2°C), we found that endothelial function remained protected after ischemia–reperfusion injury in young adults (Fig. 3). This finding supports the ex vivo data from Brunt et al. that the direct effect of heat on endothelial cells and humoral factors are the primary mechanisms mediating the protective response after heat exposure.
Figure 3: Heat exposure, shear stress, and endothelial ischemia–reperfusion (I/R) Injury. In Hemingway
et al. (
23), we utilized arterial compression to manipulate brachial artery blood velocity during acute heat exposure to isolate the contribution of shear stress to the protection of endothelial function after ischemia–reperfusion injury. Raw Doppler tracings show the characteristic increase in brachial artery blood velocity induced by whole-body heat exposure and the effectiveness of arterial compression to inhibit this response. Despite inhibiting the increase in shear stress during heat exposure, endothelial function remained protected after ischemia–reperfusion injury. Created with
BioRender.com.
Until recently, our understanding of the efficacy of acute heat exposure to protect against endothelial ischemia–reperfusion in populations other than young healthy adults was limited. However, we recently exposed older adults (69 ± 8 yr) to whole-body heat exposure sufficient to increase body core temperature by 1.2°C (22). We found that endothelial function was protected after ischemia–reperfusion injury (assessed ~60 min into recovery) and was similar in magnitude to that measured in young adults. These findings suggest that acute heat exposure protects endothelial function after ischemia–reperfusion injury across the human life span.
CLINICAL IMPLICATIONS
Exercise training remains a strong nonpharmacological therapeutic approach to reduce cardiovascular morbidity and mortality, per American Heart Association/American College of Sports Medicine position statements (51,52). However, only 12% of at-risk individuals report participating in any form of exercise, and 50% of these individuals have no intention of incorporating exercise into their daily routine (53,54). In addition, if exercise training is undertaken, long-term adherence is extremely low and there is no consensus regarding appropriate measures to improve adherence (55,56). Thus, those individuals who are unwilling or unable to exercise stand to benefit most from acute and chronic heat exposure, provided that these interventions overcome the issues associated with exercise training.
Tei and colleagues (28) were the first to report that acute heat exposure induces beneficial cardiovascular adjustments in a clinical population. In this seminal study, they demonstrated that diastolic blood pressure was reduced secondary to increased systemic vascular conductance 30 min after Waon therapy that increased pulmonary artery blood temperature by ~1.2°C in patients with congestive heart failure (i.e., heart failure with reduced ejection fraction). Pulmonary artery, pulmonary capillary wedge, and right atrial pressures measured via a Swan-ganz catheter were attenuated after heat exposure. In addition, ejection fraction increased from 24% ± 8% to 28% ± 8%. Interestingly, these clinical outcomes were nearly identical when compared with those after chest-down hot water immersion that increased arterial blood temperature by ~1.2°C.
Several groups have examined the cardiovascular adjustments after acute heat exposure in patients with peripheral arterial disease. Neff et al. (21) and Thomas et al. (14) demonstrated that systolic, diastolic, and mean arterial blood pressures were reduced for 30–60 min after lower body heat exposure, a response that seems to be mediated, in part, by sustained peripheral blood flow (and shear stress) and reduced circulating concentrations of the potent vasoconstrictor, endothelin-1. Kuhlenhoelter et al. (20) later demonstrated that gene expression for several angiogenic factors (e.g., vascular endothelial growth factor) is upregulated in skeletal muscle after lower body heat exposure that was accompanied by a modest increase in intestinal temperature of ~0.5°C. Importantly, these cardiovascular adjustments translate to improved performance on a graded treadmill test (57) and the 6-min walk test (58), although there seems to be no effect on the time to claudication onset.
There is some evidence suggesting that acute Finnish sauna bathing induces beneficial adjustments in patients with coronary artery disease. Gravel and colleagues (24) replicated traditional Finnish sauna bathing by having participants perform 2 × 10-min sauna exposures separated by a 10-min thermoneutral recovery, an approach that increased intestinal temperature by ~0.6°C. Endothelium-dependent vasodilation assessed via flow-mediated dilation of the brachial artery was augmented ~50 min after heat exposure, whereas there was no effect on microvascular function assessed using forearm postocclusive reactive hyperemia. The former finding is particularly important given evidence suggesting that endothelium-dependent dilation of the brachial artery is a surrogate for coronary artery vasodilator function (59).
Finally, individuals without overt cardiovascular disease but who are at risk also stand to benefit from acute heat exposure. For example, Laukkanen and colleagues (27) reported an immediate reduction in systolic and diastolic blood pressure in a large cohort of middle-aged adults with at least one cardiovascular risk factor during a 30-min Finnish sauna bathing session that increased tympanic temperature by ~2.0°C. Importantly, the reduction in systolic blood pressure was sustained 30 min into recovery and was accompanied by a reduction in arterial stiffness measured via pulse wave velocity. However, the latter observation likely does not reflect a true change in stiffness that results from modulation of the structural components of the vessel wall, but more likely is mediated by the change in blood pressure.
PREDICTION OF LONG-TERM ADAPTATION
Acute aerobic exercise induces a blood pressure–lowering effect that persists well into the recovery period, a phenomenon known as postexercise hypotension. Despite this phenomenon first being identified at the turn of the 20th century (60) and despite the significant advancement in our understanding of the mechanisms mediating this response since then, the predictability or relation to the long-term adaptive response associated with chronic exercise training was unknown until recently. Elegant work from Liu et al. (61) and Hecksteden et al. (62) provided strong evidence demonstrating that the acute blood pressure–lowering effect induced by aerobic exercise could serve as a proxy for the adaptive response associated with chronic exercise training. Indeed, we postulate that a similar phenomenon occurs with acute and chronic heat exposure (Fig. 4). Evidence in support of this postulation is provided by Tei and colleagues (28), who demonstrated that the reduction in blood pressure and systemic vascular resistance induced by acute Waon therapy is similar in magnitude to that measured in a separate cohort of patients with congestive heart failure after 2 weeks of therapy (63). Despite this evidence, future work is needed to systematically assess the relation between the cardiovascular adjustments that occur in recovery from acute heat exposure and the long-term adaptive response to heat therapy and to what extent these responses may vary between populations and across heating paradigms.
Figure 4: Conceptual framework highlighting the postulation that the cardiovascular adjustments that occur in recovery from acute heat exposure may serve as a proxy for the long-term adaptations associated with heat therapy. Acute heat exposure increases body core and tissue temperature, thereby augmenting blood flow and shear stress and triggering the release of endocrine, autocrine, and paracrine factors. These responses that occur during heat exposure are likely driving the cardiovascular adjustments that occur in the recovery period. The extent to which these acute cardiovascular adjustments may serve as a proxy for the long-term adaptive response to chronic heat therapy remains unknown. Created with
BioRender.com.
MOVING THE FIELD FORWARD
Despite the recent advancements in our understanding of the cardiovascular adjustments that occur after acute heat exposure, many questions still remain. Hereinafter, we outline several key physiological questions, the answers to which will significantly advance the field. First, it is clear from some of the studies presented in this review that “one size does not fit all.” That is, a given heat exposure may induce certain cardiovascular adjustments in one population, but responses may differ substantially in other populations when exposed to the same heat stress. Moving forward, investigations should focus on identifying which populations stand to benefit the most and the least from a given heat exposure. In doing so, scientists and clinicians alike can design acute and chronic heating interventions tailored for a specific population. Second, the underlying mechanisms mediating the various cardiovascular adjustments that occur after acute heat exposure remain largely unexplored. To that end, future studies should focus on identifying the temperature-dependent signaling mechanisms that mediate these adjustments and how they may vary in pathophysiological conditions. Third, emphasis should be placed on developing studies that examine the extent to which the cardiovascular adjustments that occur after acute heat exposure subserves responses in other tissues and organ systems. For example, could the increase in peripheral blood flow and microvascular function that occurs after acute heat exposure facilitate the augmentation of insulin-stimulated glucose uptake that occurs in skeletal muscle (64)? Unraveling the Gordian knot that connects the physiology across multiple organ systems after acute heat exposure will undoubtably advance the field. Finally, examining the extent to which acute heat exposure may alter the physiological response to a novel stressor (i.e., a cross-tolerance effect), such as hypoxia, cold stress, and mental stress, is ripe for investigation (65).
SUMMARY
Recovery of the cardiovascular system after acute heat exposure is not simply a return to homeostasis, but is a dynamic phenomenon that is accompanied by distinct physiological adjustments. These adjustments represent key changes in traditional and nontraditional risk factors that may be of benefit to various populations. In addition, these adjustments may even be used to predict the long-term adaptive response associated with heat therapy.
Acknowledgments
The authors would like to thank Amy M. Moore, RN, and Dr. Albert H. Olivencia-Yurvati for their continued clinical support of their work. The authors would also like to thank Dr. Justin Lawley for comments on this manuscript. All figures were made using BioRender.com.
Funding was provided by the National Institutes of Health (R01 AG059314, T32 AG020494), the Texas Chapter of the American College of Sports Medicine Student Research Development Award, and laboratory startup funds from the University of North Texas Health Science Center.
The authors have no competing interests to declare.
Author contributions: S.A.R. drafted the manuscript. S.A.R., R.E.R., and H.W.H. revised it critically for intellectual content.
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