Background
Acute exposure to high ambient temperatures (e.g., hot-humid conditions) can overwhelm heat dissipating and regulatory mechanisms in the body, thereby inducing thermal load known as
‘heat stress’. The ensuing physiological strain, notably, impaired cardiovascular (CV) [
1] and metabolic function [
2], is associated with acute reductions in functional performance in both hot [
3] and temperate [
4] conditions. At its extreme, heat strain can significantly increase heat-related illness morbidity and mortality risk [
5]. However, controlled, and repeated exposure (> 5 days) to whole-body hyperthermia has been shown to induce physiological adaptations, e.g., increased sweat rate, that mitigate the deleterious effects of exercise in the heat [
6]. Heat acclimation (HA) may even promote cross-adaptation in temperate conditions [
7] and a greater resistance to various exercise stressors (e.g., hypoxia) [
8,
9].
Over the past decade, the additive effect of combined exercise and heat has emerged as a novel and attractive strategy to improve endurance performance not only in hot conditions, but also in temperate conditions [
10‐
14]. Indeed, reductions in basal core temperature (T
core) [
10,
15,
16], a greater sweat rate [
7,
10] and cutaneous blood flow [
7], which collectively augment cutaneous heat loss, are hallmark thermoregulatory responses to exercise HA. These adaptations translate to improvements in cardiac filling pressures and blood velocities [
17], plasmatic volume [
11,
16,
17], heart rate (HR), and blood pressure (BP) [
18]. Reductions in arterial stiffness and improved endothelial function also follow passive chronic heat exposure [
19,
20], suggesting improvement in CV risk profile [
21] in sedentary adults. Taken together, these findings suggest that combined exercise and HA may influence several factors determining O
2 supply to the active muscles (e.g., cardiac output, vascular resistance) and blood flow redistribution, which could theoretically amplify the adaptations induced by exercise training alone.
To this regard, a seminal study by Lorenzo et al. demonstrated that 10 sessions of low- to moderate-intensity cycling (elite endurance cyclists; maximal oxygen consumption [VO
2max]: ~ 67 ml/kg/min) in the heat (38˚C) induced plasma volume (PV) expansion, augmenting stroke volume (SV) and ventricular compliance, which in turn improved cardiac output (CO) and VO
2max in temperate conditions [
11]. However, this effect was subsequently attributed to the greater relative intensity of the training modality in the heat rather than an additive ergogenic benefits from heat stress. In fact, using a counter-balanced crossover study design with exercise intensity matched between conditions, VO
2max and time-trial performance were unchanged after 10 consecutive sessions of moderate-intensity continuous cycling in the heat (38˚C) in trained individuals (VO
2max: ~ 61 ml/kg/min) [
22]. Importantly, the thermophysiological adaptations to exercise coupled with thermal load have primarily been investigated using low-intensity, long term (> 10 days) HA (LTHA) protocols, which are time intensive and difficult to implement [
23].
In this regard, high-intensity interval exercise, i.e., HIIT, is an effective, time-efficient training paradigm [
24]. HIIT incorporates intervals of quick, high intensity exercise bouts, i.e., exercise above the lactate threshold, and long, lower intensity
“active recovery” exercise bouts repeated in succession. Conventional HIIT sessions last no more than 30 min and has been known to elicit robust metabolic (e.g., improved fat oxidation) [
25,
26] and cardiovascular (e.g., improved blood pressure regulation and vascular function) [
24,
27] adaptations. Interestingly, whether the physiological adaptations induced by short-term HA and high-intensity exercise training can translate into improved performance in temperate conditions or elicit antagonistic effects is currently still debated [
28,
29].
For example, using a parallel study design, Karlsen et al. reported no significant effects of 2 weeks of HA (34˚C) on VO
2max and a 43 km cycling performance test in temperate conditions outdoor in competitive cyclist (VO
2max: ~ 4.8 l/min) training ~ 15 h. a week, including 2.5 h. of high-intensity interval exercise [
30]. Although this field-based study provided important insight into HA in well-trained athletes, the interaction between high-intensity exercise training and HA was not directly tested as the participants maintained their training routine during the study period. Using a design to test the interaction between HA and 3 weeks of high-intensity training (3 sessions per week, ~ 33˚C), McCleave et al. documented a 3.3% improvement in the performance during a 3 km running test conducted in temperate condition outdoor in well-trained runners (peak oxygen consumption [VO
2peak]: ~ 62–65 ml/kg/min) [
31]. Surprisingly, running performance was not improved immediately after the intervention, but 3 weeks later, i.e., when plasma and blood volume values had returned to baseline, such that the physiological adaptations responsible for this delayed performance improvement were unclear.
To date, the effects of combined high-intensity interval exercise (HIIE) and short-term HA on performance, and the underlying physiological adaptation, in a temperate environment are still poorly understood. Furthermore, studies have primarily focused on elite/semi-elite athletes, although recreational athletes routinely exercise in hot environments. Accordingly, the goal of the present pilot study was to determine the potential interaction of low-volume HIIE and short-term heat exposure on CV function (i.e., heart rate [HR], HR variability [HRV], blood pressure [BP], peripheral mean arterial pressure [pMAP]), arterial stiffness (pulse wave velocity [PWV]), whole-body VO
2peak, and performance during a 5 km treadmill time-trial in active young adults. Based upon prior findings [
7,
11,
31], we hypothesized that HIIE combined with heat exposure would improve, to a greater extent, CV function and aerobic performance compared to a temperate group undergoing a HIIE program at the same relative intensity.
Discussion
The present pilot study examined, in active young, healthy adults, the potential interaction of low-volume HIIE and short-term heat stress on the autonomic nervous system, markers of CV function, and aerobic endurance performance. The main findings of this study are that six sessions of HIIE with added heat exposure: 1) elicited significant reductions in arterial stiffness, as measured by pulse wave velocity, that were of large effect size, 2) markedly decreased central and peripheral systolic BP (~ 7–8 mmHg decrease in MAP), which, in the absence of a change in resting HR and HRV, suggests a decrease in total peripheral resistance, but 3) did not significantly improve aerobic function, assessed as VO2peak and 5-km treadmill time trial performance, as compared to an intensity-matched temperate HIIE group. Together, these data demonstrate a potential added benefit of heat exposure to high-intensity exercise training on CV health. This exercise paradigm is therefore an enticing training strategy that warrants further investigation.
HIIT & short-term heat stress: aerobic performance
In non-acclimated athletes, the thermoregulatory imposed by heat stress, in both hot and temperate conditions, is pronounced and a known deterrent to exercise performance [
50]. This has roused interest in different training modalities to sustain HA and exercise performance, and in particular, the application of combined high-intensity exercise and heat to amplify training adaptations. As little as five, 27-min sessions of cycle ergometry HIIT at temperatures of 22 °C, 36% RH was sufficient to improve RPE and TC during a submaximal exercise test in the heat in elite Australian football athletes (VO
peak: ~ 48 ml/kg/min) [
23]. However, resting HR, T
core, and VO
2peak were unaffected, suggesting only partial HA. Likewise, 3 weeks of high-intensity training 3 sessions per week (~ 33˚C) improved 3 km running performance in temperate condition outdoor by 3.3% [
31]. However, this beneficial effect on performance was delayed, reaching significance 3 weeks after the intervention, i.e., when hematological adaptations had weaned off, such that no clear underlying physiological mechanisms could be identified. Thermoperceptual adaptations in the short-term (≤ 5 days) have been documented in elite cyclists [
28] (VO
2peak: > 55 ml/kg/min) and active young adults (VO
2peak: ~ 3.75 l/min) [
16], with reductions in resting HR and rectal temperature suggesting rapid and full HA in both studies. While these adaptations undoubtedly result in improved performance in hot conditions [
7,
10,
12‐
14], it is unclear if they provide additional benefits in temperate conditions. Interestingly, failure to observe improvements in indices of aerobic performance (e.g., Cooper Test) [
15], and even an impaired cycling capacity due to overreaching in the study by Reeve et al. calls into question the performance efficacy of this HA paradigm. In addition, using a parallel study design, Karlsen et al. reported no effects of 2 weeks of HA (34˚C) on VO
2max and 43 km cycling performance test in temperate conditions outdoor in competitive cyclist training ~ 15 h. a week, including 2.5 h. of high-intensity exercise [
30].
The disparity between thermophysiological and performance adaptions is in agreement with the present results. Resting HR, as well as RPE and TS, were unaffected by the current HIIE-H protocol. Although thermophysiological alterations respond positively to as little as 5 days of thermal exposure [
51], the present data suggests our thermal stimuli (6 days of low-volume HIIE-H) was inadequate to induce full HA. Nevertheless, improvements in BP, MAP, and PWV underscore that, irrespective of the degree of HA, HIIE-H induced favorable modifications in CV function. This translated to a nonsignificant 6% increase in VO
2peak, which matches the 5–8% increase in VO
2max documented by Lorenzo et al. using a longer HA in trained cyclists, and opposes Kelly et al., the latter using a similar HIIT protocol to the present study in profession football athletes. Importantly, however, is that the change in VO
2peak was nonsignificant and likewise did not reflect in an improvement in 5 km time-trial performance. Wardenaar et al. also reported an insignificant, yet meaningful, 4% improvement in Cooper Test performance with a 5-day HA program in collegiate athletes, and it has been argued that longer duration exercise stimuli (10 vs. 5 days) is needed for aerobic performance adaptations to ensue [
40]. Such differences in exercise-heat intensity and duration likely explain the incongruent results, which warrants further research.
HIIT & heat stress: blood pressure
Although HR was unaffected by HIIE with heat stress, the improved BP profile suggests a cardioprotective benefit to this exercise-heat paradigm, albeit only in a small group of individuals. However, this reduction in BP parallels that observed with long-term PHT protocols, which have demonstrated improvements in vascular function and BP regulation in various populations [
52]. For example, Brunt et al. demonstrated a -10-mmHg improvement in MAP, owing to decreased arterial stiffness and improved endothelial function, with eight weeks of passive heat therapy in young sedentary adults [
20]. Likewise, MAP tended to improve at a similar magnitude (-8 mmHg) after the HIIT-H intervention and was accompanied by a reduction in PWV (-0.3 m/s), a well-established marker of vascular stiffness. Although nonsignificant, the ~ 6% improvement in MAP does hold clinical value, and more importantly, follows the -7 and -10 mmHg reductions in resting central and peripheral SBP, respectively. Thus, it appears that six sessions of HIIE under short-term thermal load may improve BP profile, similar to the effects of several weeks (40 session, 90 min/session) of acute whole-body heat therapy [
19] in healthy, middle-aged adults, but warrants further investigation which a larger cohort of participants.
To the best of our knowledge, this is the first study to investigate BP and, indirectly, vascular alterations to HIIE under heat stress. Previous exercise HA studies have reported improvements in CO, and consequently, aerobic exercise performance (VO
2max), likely attributed to PV expansion [
11,
14]. PV expansion, in theory, could increase BP and thus CV event risk. Nevertheless, the reduction in BP and MAP in the present study, with no change in HRV (e.g., no change in cardiac autonomic function), suggests a capacity of the systemic circulation to enhance cardiac contractile function in the face of PV expansion. Therefore, a potential for a decrease in peripheral resistance induced by combined HIIE and heat stress appear outweigh the potential deleterious effects of increased PV on BP regulation. Future research assessing both PV and BP are needed as we are limited by a lack of PV data in the current study. However, such improvements in BP may be of clinical importance, especially when considering factors such as adherence, thermal tolerance, and the ability to safely induce CV adaptions in a time-efficient manner, which warrants further attention.
HIIT & heat stress: cardiac autonomic function
HRV is a non-invasive assessment of cardiac autonomic balance (i.e., sympathetic and parasympathetic tone) [
43], providing a unique window into autonomic nervous system factors regulating adaptations to physiological insults (e.g., heat). The marginal and nonsignificant increase in HRV, coupled with no change in HR, in the HIIE-H group therefore suggests little or no role of neural adaptions, specifically estimated cardiac autonomic function. This contrasts with the 10% increase in HRV, and 5% reduction in HR, that has been observed with 11 days of on-field soccer training in hot humid conditions in well-trained male soccer athletes [
53]. In conjunction with PV expansion and an enhanced CO [
11], previous studies suggest that mitigation of sympathetic neural drive to cardiac muscle is one physiological means by which myocardial efficiency is enhanced with exercise in the heat (Frank-Starling Mechanism: CO = SV X HR). This disparity may allude to different mechanisms of adaptions for the different heat, duration (long- vs. short-term) and exercise (high- vs. moderate-intensity) modalities. Indeed, follow-up studies that directly measure PV, CO, and HRV following low-volume HIIT with heat are required to test this hypothesis.
HIIT & heat stress: arterial stiffness
In line with the reduced peripheral resistance hypothesis, there was a significant 6% decrement in PWV in our heat group. PWV is a validated assessment of arterial stiffness, the latter an independent risk factor for CV diseases (e.g., atherosclerosis) [
54], and the former itself a strong predictor of CV morbidity and mortality. In accordance with our findings, eight weeks of Hot Yoga (40.5 °C, 40–60% RH) reduced brachial-ankle PWV to a similar magnitude (~ 0.5 m/s), albeit in older [
55] and overweight/obese adults [
56]. Thus, although our practical (but nonsignificant) ~ 0.3 m/s improvement in PWV was short of the 1 m/s observed with 12 weeks of whole-body hot water immersion and deemed clinically significant [
19], this response was elicited in a markedly shorter timeframe and in healthy individuals. Collectively, in the present HIIE-H paradigm, factors downstream from central neural drive appear to be the dominant mechanism at play, and specifically, suggests enhanced endothelial function, perhaps mediated through heat shock proteins (HSP) [
57] and transient receptor potential cation channel subfamily V (TRPV) channel [
58] augmenting endothelial nitric oxide synthase activity and NO production. This hypothesis will benefit from future studies that interrogate peripheral vascular resistance with robust assessments of vascular endothelial function, such as flow-mediated dilation (FMD) and passive leg movement (PLM) and assessment of circulating factors (e.g., HSPs) that might be explanatory in the enhanced vascular endothelial function, that may be superior with HIIE-H.
Experimental considerations
Several methodological considerations might explain the disparity in the present results. The small sample size (
n = 10) may not be statistically powered to detect performance adaptations, although several physiological variables were significantly altered (VO
2peak, PWV, pSBP, cSBP) and establish effect sizes for sample size estimations in subsequent studies. Importantly, the application of continuous (90 min), low-moderate intensity (50% VO
2max) exercise, at a higher frequency (≥ 10 days), might allow for a stronger training and heat stimulus. It is therefore conceivable that our lower volume HIIE protocol was appropriate to improve aerobic capacity and CV function at almost half the frequency (6 vs. 10 days) of traditional LTHA protocols, but not sufficient to induce performance adaptations. Future studies should explore longer interventions of HIIT with heat stress to test this hypothesis. Furthermore, it has been shown that females exhibit slower HA kinetics (e.g., increased active sweat gland concentration) and performance adaptations (e.g., improved power output) than males [
59]. We were underpowered to investigate sex differences and to account for sex as a covariate, but it is possible that there may be sex specificity (e.g., time-trial performance) and certain trends (e.g., MAP) driven by female participants (
n = 6). This is a topic that has recently garnered traction in the heat literature, warranting further attention. Lastly, a better understanding of the role of dietary and physical activity habits, as well as familiarization and reproducibility of the tests performed, is needed to contextualize the effects of heat and HIIE.
Conclusions
Despite no appreciable differences in HR and indices of HRV (i.e., SDNN and RMSSD), six sessions of HIIE in hot-humid conditions significantly improved central and peripheral BP, and accordingly, MAP, compared to HIIE performed at the same relative intensity in temperate conditions. These effects appeared to be mediated by decreased arterial stiffness, as indicated by reductions in PWV, and, perhaps, an enhanced vascular endothelial function. Importantly, contrary to traditional exercise-heat paradigms of long duration (> 60 min) and frequency (> 36 sessions), the utilization of low-volume HIIT elicited favorable CV and performance adaptations of similar magnitude in a time-efficient manner. Furthermore, given that adaptations were documented in young, healthy, and recreationally active participants, there is a potential for this exercise-heat paradigm with clinical populations in need of a rapid and potent intervention to improve their CV risks profile, proposing an enticing avenue for future research with careful safety monitoring.
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