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. Author manuscript; available in PMC: 2024 Jul 1.
Published in final edited form as: Microvasc Res. 2023 Apr 5;148:104536. doi: 10.1016/j.mvr.2023.104536

The acute effect of whole-body heat therapy on peripheral and cerebral vascular reactivity in Black and White females

Zachary T Martin 1, John D Akins 1, Emily R Merlau 1, John O Kolade 1, Iman O Al-daas 1, Natalia Cardenas 1, Joshua K Vu 1, Kyrah K Brown 1, R Matthew Brothers 1,*
PMCID: PMC10908357  NIHMSID: NIHMS1967271  PMID: 37024072

Abstract

Among females in the U.S., Black females suffer the most from cardiovascular disease and stroke. While the reasons for this disparity are multifactorial, vascular dysfunction likely contributes. Chronic whole-body heat therapy (WBHT) improves vascular function, but few studies have examined its acute effect on peripheral or cerebral vascular function, which may help elucidate chronic adaptative mechanisms. Furthermore, no studies have investigated this effect in Black females. We hypothesized that Black females would have lower peripheral and cerebral vascular function relative to White females and that one session of WBHT would mitigate these differences. Eighteen young, healthy Black (n = 9; 21 ± 3 yr; BMI: 24.7 ± 4.5 kg/m2) and White (n = 9; 27 ± 3 yr; BMI: 24.8 ± 4.1 kg/m2) females underwent one 60 min session of WBHT (49 °C water via a tube-lined suit). Pre- and 45 min post-testing measures included post-occlusive forearm reactive hyperemia (peripheral microvascular function, RH), brachial artery flow-mediated dilation (peripheral macrovascular function, FMD), and cerebrovascular reactivity (CVR) to hypercapnia. Prior to WBHT, there were no differences in RH, FMD, or CVR (p > 0.05 for all). WBHT improved peak RH in both groups (main effect of WBHT: 79.6 ± 20.1 cm/s to 95.9 ± 30.0 cm/s; p = 0.004, g = 0.787) but not Δ blood velocity (p > 0.05 for both groups). WBHT improved FMD in both groups (6.2 ± 3.4 % to 8.8 ± 3.7 %; p = 0.016, g = 0.618) but had no effect on CVR in either group (p = 0.077). These data indicate that one session of WBHT acutely improves peripheral micro- and macrovascular but not cerebral vascular function in Black and White females.

Keywords: Health disparity, Endothelial function, Hypertension, African American women, Cardiovascular disease prevention

1. Introduction

In the United States, race- and ethnicity-related disparities in cardiovascular health and function persist (Brothers et al., 2019). Indeed, Black females are disproportionately affected by cardiovascular and cerebrovascular diseases, having ~40 % higher total cardiovascular disease and twofold greater stroke prevalence relative to White females (Tsao et al., 2022). Furthermore, an emerging body of research suggests that young, otherwise healthy Black females exhibit blunted vascular function (Brothers et al., 2019; D’Agata et al., 2021; Patik et al., 2018a; Akins et al., 2022; D’Agata et al., 2021), indicating that alterations in vascular health likely begin long before the presence of overt disease. These findings highlight an important opportunity in early life for implementation of interventional approaches specifically targeting vascular function and overall cardiometabolic health.

One such emerging strategy is whole-body heat therapy (Brunt and Minson, 2021) (e.g., sauna bathing, hot water immersion). Heat therapy is a novel preventive and therapeutic modality that has been used for the treatment and prevention of diseases and other ailments for centuries (Miyata and Tei, 2010; Serbulea and Payyappallimana, 2012; Peräsalo, 1988; Laukkanen et al., 2015); however, scientific research regarding its efficacy has only recently gained widespread attention, particularly as it relates to cardiovascular disease (Brunt and Minson, 2021; Cheng and MacDonald, 2019). Numerous studies have demonstrated improvements in various indices of cardiovascular health and function following chronic whole-body heat therapy (Pizzey et al., 2021), including peripheral vascular function (Bailey et al., 2016) and arterial stiffness (Brunt et al., 2016a), among other factors (Brunt et al., 2016b; Masuda et al., 2004). However, to our knowledge, no studies have examined the impact of either acute or chronic whole-body heat therapy on cerebral vascular function and limited studies have examined the acute (one-session) effect of heat therapy on peripheral vascular function (Cheng and MacDonald, 2019), but have generally demonstrated beneficial peripheral vascular effects (Richey et al., 2022; Romero et al., 2017; Brunt et al., 2016c; Ganio et al., 2011). This is important as a better understanding of whether heat therapy acutely alters peripheral and cerebral vascular function, particularly in populations with elevated risk for and prevalence of various conditions associated with altered vascular function will be critical for understanding long-term adaptive responses and which factors might dictate improvements in cardiovascular health (Romero et al., 2022). Lastly, no studies have been designed to examine the impact of acute or chronic heat therapy specifically in young Black females, an understudied population (Feldman et al., 2019; Brown Speights et al., 2017), despite having among the highest risk for and prevalence of cardiovascular disease and stroke (Tsao et al., 2022). Together, this knowledge may help improve our understanding of the mechanisms by which chronic heat therapy impacts vascular health (Cheng and MacDonald, 2019; Romero et al., 2022) and serve as a catalyst for more research into the preventive and therapeutic effects of heat therapy. Therefore, we tested the hypothesis that Black females would have lower peripheral and cerebral vascular reactivity relative to White females and that one 60 min session of whole-body heat therapy would improve these responses and this improvement would be augmented in the Black females.

2. Materials and methods

2.1. Ethical approval

Ethical approval was obtained from the University of Texas at Arlington Institutional Review Board (#2020–0054). All participants were informed of the experimental procedures and risks before participating. Verbal and written informed consent were obtained from each participant. The experimental protocols aligned with the guidelines set forth by the Declaration of Helsinki except for registration in a database.

2.2. Participants

Twenty Black (n = 10) and White (n = 10) females were recruited from the Dallas-Fort Worth Metroplex (Texas, USA) via flyers, social media, and word-of-mouth from November 2021 to May 2022. Participants were included if they self-reported being of Black or White race/ethnicity, female, a BMI between 18.5 and 29.9 kg/m2, and age between 18 and 40 yr. Participants were excluded if they reported a history of smoking within 2 years or being a current smoker; taking vasoactive medications; or having overt cardiovascular (including hypertension), metabolic, or neurological disease. One White participant was screened out due to a diagnosis of anxiety and depression. Data from one Black participant could not be included due to equipment complications, leaving a total of 18 participants (n = 9 Black females and n = 9 White females).

2.3. Study design and protocol

Testing occurred following a minimum 6 h fast, at least an 8 h abstention from caffeine and medications/supplements, and at least a 24 h abstention from alcohol and vigorous exercise. To improve the generalizability of our findings (Stanhewicz and Wong, 2020), we did not control for the menstrual cycle. During a single visit to the laboratory, participants underwent testing for peripheral and cerebral vascular reactivity before and 45 min after one 60 min session of heat therapy (protocol schematic provided in Fig. 1). Participants remained in the supine position throughout all phases of the research protocol, which was developed from reviewing the relevant acute heat therapy literature (e.g., (Brunt et al., 2016c; Romero et al., 2022)). Internal body temperature (Tint) was controlled throughout pre-testing, whole-body heating, recovery, and post-testing via a tube-lined, water-perfused suit (Med-Eng; Ottawa, ON, Canada) that covered the entire body except for the head, forearms, hands, and feet. During baseline, recovery, and post-testing, 34 °C (thermoneutral) water was circulated through the suit. For the heating stimulus, 49 °C water was circulated, and 3 blankets were placed on top of the participant as pilot testing revealed that this was necessary to ensure a swift Tint response. The target ΔTint was +1.0 °C greater than baseline Tint. In an effort to prevent further increases in Tint, if the participant reached the target ΔTint, the blankets were removed, and the water temperature was reduced to 44 °C until the 60 min mark was reached (n = 12). If the participant did not reach the target ΔTint within 60 min, heating was terminated at the 60 min mark, which was immediately followed by 45 min of thermoneutral recovery (n = 6). The average ΔTint for those who did not reach the target ΔTint within 60 min was 0.74 ± 0.12 °C. Since this is still a robust heating stimulus (Crandall and Wilson, 2015), all participants were included in the final analyses.

Fig. 1.

Fig. 1.

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Experimental protocol schematic. Tint, Internal body temperature; MCA, Middle cerebral artery blood velocity; PETCO2, Partial pressure of end-tidal carbon dioxide.

2.4. Measurements

2.4.1. Initial measurements & instrumentation

Height and weight were measured using a stadiometer and digital scale (Seca 769; Seca North America; Chino, CA, USA) and waist-to-hip ratio was measured/calculated according to the American College of Sports Medicine guidelines (ACSM, 2017). Tint was continuously monitored via an ingested telemetric temperature pill (HQ, Inc.; Palmetto, FL, USA; n = 17) or a sublingual thermocouple (Sable Systems International; North Las Vegas, NV, USA; n = 1 due to pill swallowing intolerance). Brachial artery blood flow, middle cerebral artery blood velocity (MCAv), heart rate (HR), intermittent blood pressure (BP), and partial pressure of end-tidal CO2 (PETCO2) were measured throughout heating and recovery as described below in the pre-/post-testing sections. Data were collected via PowerLab (ADInstruments – North America; Colorado Springs, CO, USA) and saved for offline analysis.

2.4.2. Brachial artery flow-mediated dilation & forearm reactive hyperemia

Following 15 min of supine rest, measures of microvascular and macrovascular function were performed during baseline and post-testing as previously described (Thijssen et al., 2019). Briefly, the right arm was abducted and supported at heart level while a pneumatic cuff was wrapped around the forearm ~1 cm distal to the antecubital fossa. The brachial artery was insonated ~5–10 cm proximal to the antecubital fossa via an adjustable frequency (10–13 MHz) linear array Doppler ultrasound probe (LOGIQ P5; GE Healthcare; Chicago, IL, USA), held in place by a stereotactic probe holder at an angle of 60°. B-mode images of the brachial artery were optimized to ensure delineation between the vessel wall and lumen during offline analysis. The probe was then set to duplex mode (pulsed frequency of 5 MHz) for simultaneous imaging of the artery and blood velocity, with the sample volume set to include the entire artery without extending beyond its wall. Brachial artery diameter (D; cm) and blood velocity (Vblood; cm/s) were continuously recorded throughout a 2 min baseline period, after which the cuff was inflated to 220 mm Hg to occlude circulation to the forearm for 5 min (Rapid Cuff Inflation System; D. E. Hokanson, Inc.; Bellevue, WA, USA). Upon cuff release, D and Vblood were recorded for a 3 min recovery period. Digital video of the entire protocol was recorded and saved (Elgato/CORSAIR; Fremont, CA, USA) for later analysis using a commercially available edge-detection and velocity tracking software (FMD Studio; Quipu; Pisa, Italy). Brachial artery flow-mediated dilation (%FMD) was defined as ((Dpeak − Dbaseline)/Dbaseline)× 100. Angle-corrected Vblood was calculated as the full area of the Doppler envelope each second and averaged between anterograde and retrograde velocity (Vmean). Reactive hyperemia (RH) was calculated as the peak (1 s) as well as the relative (absolute Δ and percentage) increase in blood velocity following cuff release. Blood flow, in ml/min, was calculated as π(D/2)2 × Vmean × 60 and shear rate, as s−1, was calculated as 4× Vmean/D. Shear rate AUC for RH/FMD testing was calculated as the sum of the second-by-second shear rate above baseline up to Dpeak.

2.4.3. Cerebral vascular function

Cerebral vascular function was assessed as the cerebral vasodilatory reactivity to steady-state hypercapnia as previously described in detail by our lab and others (Miller et al., 2019; Junejo et al., 2020; Portegies et al., 2014; Tucker et al., 2020). While supine, heart rate was monitored via ECG (CardioCard; Nasiff Associates; Central Square, NY, USA) and brachial artery BP was measured via an oscillometric electrosphygmomanometer (Tango M2; SunTech Medical; Morrisville, NC, USA). PETCO2 and peripheral oxygen saturation (SpO2) (Capnocheck® Plus; BCI/Smiths Medical; Minneapolis, MN, USA) along with respiratory rate (Pneumotrace II; UFI; Morro Bay, CA, USA) were also continuously measured. Continuous beat-to-beat BP was monitored via finger photoplethysmography (Finometer PRO; Finapres Medical Systems; Enschede, Netherlands). Left MCAv was measured using a 2 MHz probe (TOC Neurovision; Multigon Industries; Yonkers, NY, USA) fixed at the temporal window with a headband. The participants were then fitted with a mouthpiece and 3-way stopcock valve (Hans Rudolph, Inc.; Shawnee, KS, USA) that led to either ambient air or a 5 L rubber bag (GPC Medical Ltd.; New Delhi, Delhi, India) pre-filled with a 6 % CO2 gas mixture (21 % O2, nitrogen balance). Baseline data were collected for 3 min while the participant breathed ambient air, after which the valve was switched so that the participant began breathing air from the bag, which was continuously supplied with 6 % CO2. Following 3 min of steady-state hypercapnia, the valve was switched back to ambient air and data collection continued for a 3 min recovery period. Data from the last minute of baseline and the last minute of hypercapnia were selected and used in the analysis. Cerebrovascular conductance index (CVCi) was calculated as CVCi = MCAv/MAP, and cerebrovascular reactivity was assessed as ΔMCAv/Δ PETCO2, ΔCVCi/Δ PETCO2, and %CVCi/Δ PETCO2.

2.5. Physiological response to heating data analysis

Tint data were captured as follows. Baseline: 5 min of data prior to cerebral vascular pre-testing. Peak: 1 min of clean data during the last 5 min of heating. Post RH-FMD testing: 5 min of data immediately prior to arterial occlusion. Post cerebral vascular testing: 5 min of data immediately prior to administering 6 % CO2. Heart rate data were captured as follows. Baseline: 2 min of data during the RH-FMD baseline. Peak: data from the last 30 s of heating. Post RH-FMD testing: 2 min of data during the RH-FMD baseline. Post cerebral vascular testing: 3 min of data during the cerebral vascular testing baseline. Blood pressure data were captured as follows. Baseline: the average of 3 consecutive brachial artery blood pressures obtained immediately prior to beginning the RH-FMD pre-testing. Peak: brachial artery blood pressure obtained during the last 5 min of heating. Cerebral vascular post-testing: the average of 5 brachial artery blood pressures taken immediately after cerebral vascular testing.

Pre- and post-testing baseline brachial artery blood flow, shear rate, and diameter as well as forearm vascular conductance, PETCO2, MCAv, and CVCi data were taken as the average values during the respective baseline for the RH-FMD and cerebral vascular tests. Peak values for these variables were taken from 1 min of clean data during the last 5 min of heating.

2.6. Statistical analysis

All data were processed using GraphPad Prism 9 (v. 9.4.0; GraphPad Software, LLC, San Diego, CA, USA) and SPSS 28 (IBM; Armonk, New York, USA). The data were assessed for normality via the D’Agostino-Pearson normality test, and non-normally distributed data were transformed. However, results from tests run on the transformed data did not differ from those of the non-transformed data. Therefore, to retain the physiological relevance of the data, only results from the non-transformed data are reported. Participant characteristics were compared via two-tailed Welch’s t-tests or the Mann-Whitney U test (waist-to-hip ratio only). For the remaining outcomes, a mixed-effects model was used to examine the influence of time/heating and group on the dependent variables. For a significant interaction or main effect with 3 or more time points, post-hoc multiple comparisons were performed via Dunnett’s or Šídák’s tests, where appropriate. For statistically significant results of key variables, effect sizes were calculated as Hedge’s g. Peak blood velocity data from one Black female were excluded due to being a statistical outlier as determined by the ROUT method. All data are presented as mean ± SD, and the level for statistical significance was set a priori at α = 0.05.

3. Results

3.1. Participant characteristics

Participant characteristics are provided in Table 1. Although the White participants were older than the Black participants (p = 0.045), there were no differences between groups in BMI and waist-to-hip ratio nor resting HR, BP, and Tint (p > 0.05 for all).

Table 1.

Participant characteristics.

Black females Mean ± SD (n = 9) White females Mean ± SD (n = 9) p value
Age (years) 21 ± 3 27 ± 7 0.045
Body mass index (kg/m2) 24.7 ± 4.5 24.8 ± 4.1 0.940
Waist-to-hip ratio (au) 0.85 ± 0.20 0.77 ± 0.07 0.546
Heart rate (bpm) 67 ± 6 62 ± 10 0.209
Systolic blood pressure (mm Hg) 116 ± 4 113 ± 12 0.506
Diastolic blood pressure (mm Hg) 71 ± 5 71 ± 5 0.947
Baseline internal body temperature (°C) 37.1 ± 0.2 37.2 ± 0.2 0.364
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Note: Comparisons were made via two-tailed Welch’s t-tests or the Mann-Whitney U test (waist-to-hip ratio only).

3.2. General physiological responses

General thermoregulatory and cardiovascular responses to 60 min of passive heating and the subsequent recovery period are provided in Fig. 2. In response to heating, Tint and HR increased in both groups (p <0.001 for both; Fig. 2A and B, respectively). Six participants (50 % Black females) did not reach the target ΔTint of +1.0 °C, but still received a robust heating stimulus (ΔTint: 0.74 ± 0.12 °C). The average time to reach the target ΔTint was 53 ± 7 min (n = 12). Tint recovered to baseline values prior to cerebral vascular testing (p = 0.119) but not RH-FMD (p = 0.008) post-testing (Fig. 2A). Further, HR did not return to baseline during either post-test (p = 0.003 for both; Fig. 2B). In both groups, heating caused systolic BP to increase (p = 0.015; Fig. 2C) and diastolic BP to decrease (p = 0.012; Fig. 2D), thereby resulting in no change in mean arterial BP (p = 0.903; Fig. 2E). Although mean arterial BP (Fig. 2E) remained at baseline values for RH-FMD post-testing (p = 0.988), it was elevated for cerebral vascular post-testing (p = 0.001), due to elevated SBP (p = 0.038; Fig. 2C) and DBP (p < 0.001; Fig. 2D).

Fig. 2.

Fig. 2.

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General physiological responses to whole-body heating in Black (n = 9) and White (n = 8–9) females. Data from one White female were not available for CVMR because they did not perform the test. A) Internal body temperature. B) Heart rate. C) Systolic blood pressure. D) Diastolic blood pressure. E) Mean arterial blood pressure. Data were analyzed via a mixed-effects model. BL, Baseline; Peak, Measurement taken at the end of heating; RH-FMD, Reactive hyperemia and flow-mediated dilation post-heating tests; CVMR, Cerebral vasomotor reactivity post-heating test. *p < 0.05 vs. BL; **p < 0.01 vs. BL; ***p < 0.001 vs BL. Data are presented as mean ± SD.

As shown in Fig. 3, heating increased forearm blood flow, forearm vascular conductance, and shear rate (p < 0.001 for all; Fig. 3A, B, and C, respectively) in both groups, which did not entirely return to baseline for RH-FMD post-testing (p < 0.05 for all). Brachial artery diameter increased during heating (p < 0.001) and returned to baseline for post-testing in both groups (p = 0.362; Fig. 3D).

Fig. 3.

Fig. 3.

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Upper limb vascular responses to whole-body heating in Black (n = 9) and White (n = 9) females. A) Forearm blood flow. B) Forearm vascular conductance. C) Brachial artery shear rate. D) Brachial artery diameter. Data were analyzed via a mixed-effects model. BL1, Baseline during pre-testing; Peak, measurement taken at end of heating session; BL2, Baseline during post-heating tests. *p < 0.05 vs. BL1; **p < 0.01 vs. BL1; ***p < 0.001 vs BL1. Data are presented as mean ± SD.

Across groups, heating caused a reduction in PETCO2 (p < 0.001; Fig. 4A), thereby reducing MCAv similarly in both groups (p < 0.001, g = 1.513; Fig. 4B), while CVCi was reduced to a greater extent in Black (p < 0.001, g = 2.039; Fig. 4C) relative to White (p = 0.038, g = 1.166; Fig. 4C) females. Despite PETCO2 returning to baseline values (p = 0.095; Fig. 4A), baseline MCAv remained lower for both groups for cerebral vascular post-testing (p = 0.022, g = 0.672; Fig. 4B), while CVCi remained lower only for White females (p = 0.006, g = 1.476; Fig. 4C).

Fig. 4.

Fig. 4.

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Respiratory and cerebral vascular responses to whole-body heating in Black (n = 9) and White (n = 8) females. Data were not available for any time point in one White female because they did not undergo cerebral vascular reactivity testing. Data were not available for two additional White females at Peak due to intolerance associated with the measurement. A) Partial pressure of end-tidal carbon dioxide. B) Middle cerebral artery blood velocity. C) Cerebral vascular conductance index. Data were analyzed via a mixed-effects model. BL1, Baseline during pre-testing; Peak, measurement taken at end of heating session; BL2, Baseline during post-testing; PETCO2, Partial pressure of end-tidal carbon dioxide; MCAv, Middle cerebral artery blood velocity; CVCi, Cerebral vascular conductance index. *p < 0.05 vs. BL1; ***p < 0.001 vs BL1; §, p < 0.05 vs. BL1 in White females only; §§, p < 0.01 vs. BL1 in White females only; §§§, p < 0.001 vs BL1 in Black females only. Data are presented as mean ± SD.

3.3. Forearm reactive hyperemia & brachial artery flow-mediated dilation

When expressed as peak blood velocity, there was a main effect of heating for forearm RH (79.6 ± 20.1 cm/s to 95.9 ± 30.0 cm/s; p = 0.004, g = 0.787; Fig. 5A). Despite a significant interaction (p = 0.041), there were no within-group differences in Δ blood velocity (p > 0.05 for both groups; Fig. 5B). Although the percentage change in blood velocity was lower for both groups during post-testing (p = 0.010; Fig. 5C), this was attributable to elevated resting blood flow following recovery from heating (Fig. 3A).

Fig. 5.

Fig. 5.

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Post-occlusive forearm reactive hyperemia (A, B, and C) and brachial artery flow-mediated dilation (D, E, and F) measures before and 45 min after one 60 min session of whole-body heat therapy in Black (n = 8–9) and White (n = 9) females. A) Peak brachial artery blood velocity. B) Absolute change in brachial artery blood velocity (peak minus baseline). C) Percentage change in brachial artery blood velocity (baseline to peak). D) Absolute change in brachial artery diameter (peak minus baseline). E) Percentage change in brachial artery diameter (baseline to peak). F) Brachial artery shear rate area under the curve (above baseline, to peak diameter). Data were analyzed via a mixed-effects model and are presented individually and as group means for each time point. Note: despite a significant interaction, multiple comparisons testing revealed no within group differences in absolute change in brachial artery blood velocity (B).

Whether expressed as absolute change (0.19 ± 0.11 mm to 0.28 ± 0.11 mm; p = 0.009, d = 0.687; Fig. 5D) or percentage change (6.2 ± 3.4 % to 8.8 ± 3.7 %; p = 0.016, d = 0.618; Fig. 5E) in blood vessel diameter, brachial artery endothelial function was improved in both groups following one session of whole-body heat therapy. Importantly, resting brachial artery diameter was not different between or within groups for pre- or post-testing (Fig. 3D). Furthermore, the shear rate area under the curve, which is the stimulus for vasodilation, was not different between or within groups across testing conditions (Fig. 5F).

3.4. Hypercapnic cerebrovascular reactivity

Cerebrovascular reactivity to hypercapnia was not altered in either group following one session of whole-body heat therapy. Whether expressed as ΔMCAv/ΔPETCO2 (Fig. 6A), ΔCVCi/ΔPETCO2 (Fig. 6B), or %CVCi/ΔPETCO2 (Fig. 6C), no significant interactions or main effects were detected (p > 0.05 for all).

Fig. 6.

Fig. 6.

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Hypercapnic cerebral vascular reactivity measures expressed as ΔMCAv/ΔPETCO2 (A), ΔCVCi/ΔPETCO2 (B), and %CVCi/ΔPETCO2 (C) before and 45 min after one 60 min session of whole-body heat therapy in Black (n = 9) and White (n = 8) females. Data were not available for one White female because they did not undergo cerebral vascular reactivity testing. MCAv, Middle cerebral artery blood velocity; PETCO2, Partial pressure of end-tidal carbon dioxide. Data were analyzed via a mixed-effects model and are presented individually and as group means for each time point.

4. Discussion

The primary finding of this study is that one session of whole-body heat therapy acutely improves peripheral micro- and macrovascular but not cerebral vascular function in young, healthy Black and White females. Contrary to our hypothesis, Black females did not have blunted peripheral and cerebral vascular function relative to White females during pre-testing, and potential reasons for this are provided below. Nevertheless, the improvement in peripheral micro- and macrovascular function among both groups, and in particular Black females, is notable given the existing literature demonstrating blunted vascular function among Black females (Brothers et al., 2019; D’Agata et al., 2021; Patik et al., 2018a; Akins et al., 2022; D’Agata et al., 2021).

4.1. Brachial artery flow-mediated dilation

Brachial artery FMD testing is a common approach for assessing endothelial function (Deanfield et al., 2007) and is predictive of CVD morbidity and mortality (Huang et al., 2007; Ras et al., 2013; Shechter et al., 2009a; Shechter et al., 2009b). Numerous studies have shown that behavioral and lifestyle interventions are capable of inducing improvements in FMD (Woo et al., 2004; Heiss et al., 2007; Gainey et al., 2016). Here, we demonstrated that one session of whole-body heat therapy improves FMD in Black and White females. Previous research examining the acute effect of heat therapy on conduit artery endothelial function in a similar fashion to the present study is equivocal, with some studies demonstrating an improvement (Gravel et al., 2021) and others showing no effect (Brunt et al., 2016c; Behzadi et al., 2022; Gravel et al., 2019; Engelland et al., 2020). In the present study, the improvement in FMD across groups, including a near doubling (~5 to 10 %) in Black females, is notable, especially considering that the shear rate AUC was not acutely impacted by heating. These findings indicate that heat therapy acutely improves vascular endothelial function in Black and White females, which may contribute to lowering atherosclerotic cardiovascular disease risk in these populations. Although it is likely that the observed improvements in FMD are attributable to upregulated endothelial nitric oxide pathways from elevated brachial artery shear stress during heating, further work will be required to tease out precise mechanisms.

Although we hypothesized that Black females would have lower FMD relative to White females, which would thus be improved to a greater extent in Black females, baseline FMD was not different between groups. Our group (Martin et al., 2022) and others (D’Agata et al., 2021) have previously reported lower FMD in Black relative to White females. The lack of this baseline difference here may be attributable to resting measures being conducted while participants were in a 34 °C water-perfused suit, which is slightly warmer than skin temperature. Although this possibility remains to be tested, the acute effect of slightly warmer skin temperature may have improved resting FMD in Black females.

4.2. Forearm reactive hyperemia

Post-occlusive RH testing is commonly utilized to assess microvascular function (Rosenberry and Nelson, 2020), and blunted responses are predictive of future CVD risk (Huang et al., 2007; Anderson et al., 2011). In the present study, one session of whole-body heat therapy improved forearm microvascular reactivity as indexed by peak blood velocity, but not Δ blood velocity. However, given that baseline blood velocity remained elevated for post-testing, it is likely that, in this circumstance, it is more appropriate to focus on the peak blood velocity response. Interestingly, our finding of improved microvascular function is in contrast with other studies (Brunt et al., 2016c; Gravel et al., 2021; Behzadi et al., 2022; Gravel et al., 2019) where there was no acute effect of heat therapy on reactive hyperemia. This may be due to the differential influence of the mode of heating (e.g., hot water immersion, sauna) or the population studied (e.g., older adults with cardiometabolic disease) on acute microvascular changes. Nevertheless, the observed improvements in RH in the present study have implications for lowering CVD risk in Black and White females, especially since microvascular dysfunction may be a unique contributor to CVD in females (Taqueti et al., 2017; Taqueti and Di Carli, 2018).

4.3. Hypercapnic cerebrovascular reactivity

Cerebral vascular reactivity serves as an index of cerebral vascular function and is predictive of all-cause, cardiovascular, and non-cardiovascular mortality (Portegies et al., 2014; Ainslie and Duffin, 2009). To our knowledge, there are very limited studies that have examined the impact of whole-body heat therapy on cerebral hemodynamics and vascular function (Amin et al., 2022). To this end, this is the first study to examine the acute effect of whole-body heat therapy on cerebral vascular reactivity to hypercapnia. In the present study, whole-body heating alone induced the expected reductions in PETCO2, which is attributable to hyperthermia-induced hyperventilation (Tsuji et al., 2016; Brothers et al., 2009; Nelson et al., 2011). This reduction in PETCO2 was not surprisingly accompanied by reductions in cerebral vascular conductance during the passive heating phase (Crandall and Wilson, 2015). Accordingly, although we did not expect improvements in cerebral vascular reactivity due to increases in shear stress in cerebral arteries, per se, we did anticipate cerebral vascular reactivity to be improved secondary to other heating-induced mechanisms (e.g., upregulation/alteration of heat shock proteins and other circulating factors) (Brunt and Minson, 2021). The lack of an acute effect of heat therapy does not preclude the possibility that chronic heat therapy may be beneficial for cerebral vascular health; however, our data indicate that any benefits to the cerebral circulation likely do not stem from acute improvements in cerebral vascular reactivity.

4.4. Experimental considerations

Although these findings are critical to both the health disparities and heat therapy literatures, there are some experimental considerations worth discussing. First, it needs to be acknowledged that the root causes of cardiovascular health and function disparities among Black females are undoubtedly multifactorial and likely stem from structural racism1 (Carnethon et al., 2017; Churchwell et al., 2020; Ferdinand and Nasser, 2017), which contributes to adverse cardiovascular health in this population (Vaccarino et al., 2021; Bushnell et al., 2014; Lee et al., 2021). Accordingly, this and other work that examines the efficacy of lifestyle/behavioral interventions related to CVD in populations who experience health inequities must be put into the greater context of addressing disparities via multi-pronged approaches, including policy-level efforts to address social determinants of health stemming from structural racism (Javed et al., 2022; Paskett et al., 2016). In this regard, the current research does not directly address the underlying causes of the health disparity between Black and White females. Rather, it provides new information regarding a novel preventive/therapeutic modality for CVD. Nevertheless, the investigation of personal/behavioral strategies designed to improve health in populations experiencing disparities is also critical (Paskett et al., 2016), particularly in the short term. Secondly, we chose not to control for the menstrual cycle in order to improve the generalizability/external validity of the findings (Stanhewicz and Wong, 2020). However, in doing so, we acknowledge that internal validity may be partially hindered given the mixed literature available on the effect of menstrual cycle phase on vascular responses to laboratory perturbations (Stanhewicz and Wong, 2020; Stanhewicz and Wong, 2020; Wenner and Stachenfeld, 2020). TCD ultrasound does not measure the diameter of the MCA. Therefore, MCAv, as reported in this study, only provides an index of cerebral blood flow. Accordingly, it is possible that the hypercapnic challenges caused larger increases in cerebral blood flow than were detected in this study via MCAv (Verbree et al., 2014). That being said, TCD remains an often utilized methodological approach for assessing cerebral vascular responsiveness during various perturbations (Ainslie and Duffin, 2009; Brothers and Zhang, 2016); however, future studies should consider the use of MRI-based MCA imaging or utilize duplex Doppler ultrasound to image the internal carotid artery. In addition, for forearm RH, resting blood flow did not return to pre-testing values, which may have resulted in missing an effect of heat therapy on Δ blood velocity. We made every reasonable effort to allow these values to return to baseline by circulating thermoneutral water to promote cooling and providing a 45 min recovery period. Future studies should consider a longer recovery period, if possible. A time control was not performed for this study because a previous study in our lab demonstrated that RH-FMD and cerebral vascular reactivity to hypercapnia are unchanged after ~4 h (Patik et al., 2018b), which is the approximate duration of the present study. Finally, although the tube-lined suit is very effective for administering heat stress in a controlled laboratory setting, it may not be representative of typical heat therapy modalities. Indeed, hot water immersion or dry saunas would likely produce slightly different results due to their inherent differences. Nevertheless, our study may serve as a starting point for more “field-based” studies in this regard.

4.5. Conclusion

Whole-body heat therapy is an emerging novel preventive and therapeutic modality for addressing cardiovascular disease. Here, we acutely applied the technique in the setting of a known health disparity whereby Black females are disproportionately affected by stroke and CVD. Importantly, several studies have demonstrated reduced vascular function in young, otherwise healthy Black and White adults (D’Agata et al., 2021; Hurr et al., 2018; Hurr et al., 2015), which opens the door for strategies to reduce the risk of overt CVD by improving vascular function in younger individuals (Beck et al., 2013). Our findings demonstrate that one session of heat therapy acutely improves micro- and macrovascular function in young, healthy Black and White females. However, there was no acute effect of whole-body heat therapy on cerebral vascular function. Taken together, whole-body heat therapy may be a promising approach for improving endothelial function in Black and White females; however, more chronic whole-body heat therapy studies in these specific populations are warranted.

Acknowledgments

The authors would like to thank the participants for their time and effort in this study.

Funding

This research was supported by start-up funds from The University of Texas at Arlington (RMB) and a Student Research Development Award from the Texas Chapter of the American College of Sports Medicine (JDA). Aspects of the project were supported by NIH R15 HL156128 (RMB). ZTM was supported by an American Heart Association Predoctoral Fellowship (#915133).

Footnotes

Declaration of competing interest

The authors declare there are no competing interests, financial or otherwise.

CRediT authorship contribution statement

ZTM contributed to the study design, data collection, data analysis, data interpretation, and drafted and contributed to the editorial process of the manuscript. JDA contributed to the study design, data interpretation, and editorial process of the manuscript. ERM, JOK, IOA, NC, and JKV contributed to the data collection, data analysis, data interpretation, and editorial process of the manuscript. KKB contributed to the data interpretation, and editorial process of the manuscript. RMB contributed to the study design, data analysis, data interpretation, and contributed to the editorial process of the manuscript. All authors approved the final version of this manuscript.

1

Structural racism refers to “the normalization and legitimization of an array of dynamics—historical, cultural, institutional, and interpersonal—that routinely advantage White people while producing cumulative and chronic adverse outcomes for people of color” (Lawrence and Keleher, 2004).

Data availability

Data will be made available on request.

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Data Availability Statement

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