Home-based heat therapy lowers blood pressure and improves endothelial function in older adults

Abstract

Advancing age is associated with vascular dysfunction and hypertension, both of which increase cardiovascular event risk. Heat therapy has emerged as a novel intervention to improve cardiovascular health in various populations. Therefore, we tested the hypothesis that home-based lower body heat therapy would reduce blood pressure and improve endothelium-dependent vasodilation in older adults. Ambulatory blood pressure monitoring was performed in 19 older adults (67 ± 7 yrs) before and after 8 weeks of a sham intervention or heat therapy. Endothelium-dependent vasodilation of the superficial femoral artery was assessed via flow-mediated dilation. Participants were provided with a pair of tube-lined pants connected to a portable water circulator to perform the home-based sessions. Water temperature was set to 31 °C for sham and 51 °C for heat therapy, resulting in target skin temperatures of ~33 °C and ~40 °C, respectively. Participants were instructed to wear the pants 4 days per week for 60 min each session. Adherence was 100% for both groups. Heat therapy reduced ambulatory daytime systolic blood pressure by Δ −5 ± 8 mmHg, but was unchanged for the sham group (Δ 1 ± 6 mmHg; P = 0.04). Likewise, heat therapy increased flow-mediated dilation (P = 0.02), whereas there was no change across time for the sham group (P = 0.5). These results combined with a strong adherence rate suggest that home-based lower body heat therapy could be an alternative nonpharmacological intervention to reduce blood pressure and improve vascular function, ultimately reducing long-term cardiovascular event risk in older adults.

Graphical Abstract

Introduction

The human arterial vasculature undergoes profound changes across the lifespan. This “vascular aging” manifests as structural (e.g., rarefaction) and functional (e.g., endothelial dysfunction) maladaptations that increase cardiovascular event risk (1–3). Exercise training remains a strong nonpharmacological intervention to promote healthy aging (4, 5). However, only 14% of older adults report participating in any form of exercise and 50% of older adults have no intention of incorporating exercise into their daily routine (6, 7). Therefore, alternative approaches are needed to preserve vascular health and reduce cardiovascular event risk in older adults.

Chronic heat exposure (i.e., heat therapy) via sauna bathing or whole-body hot tub immersion has emerged as a novel strategy to improve clinical and physiological outcomes (e.g., blood pressure, endothelial function, and arterial stiffness) in a number of populations (8–11). However, whole-body heat exposure can require expensive equipment, and may require trained personnel to ensure participant safety, especially for those more at risk for heat-related illness (e.g., older adults) (12). Thus, heat exposure targeting only the lower body offers an opportunity to leverage the benefits of whole-body heat therapy while managing safety and convenience. To that end, our group and others have demonstrated that acute leg heating reduces arterial blood pressure and improves vascular function in older adults (13–15). While these acute cardiovascular adjustments may offer insight into possible long-term adaptations, the effect of heat therapy on cardiovascular function in this population has not been tested experimentally (16).

Therefore, the purpose of this study was to examine the extent to which 8 weeks of home-based lower body heat therapy alters cardiovascular function in older adults. We tested the hypothesis that home-based lower body heat therapy would reduce ambulatory blood pressure and improve endothelium-dependent vasodilation in older adults. In addition, we hypothesized that adherence rate for home-based heat therapy would exceed 75%.

Methods

Ethical Approval and Participants.

Written informed consent was obtained from participants following a verbal and written explanation of all experimental procedures. This study was approved by the North Texas Regional Institutional Review Board (Project No. 2022-090) and was performed in accordance with the principles outlined in the Declaration of Helsinki. This study was registered at clinicaltrials.gov (NCT05706181). Men and post-menopausal women, aged 55–80 yrs, were included in the study if they were deemed free from cardiovascular and metabolic disease following the completion of an in-depth medical health history questionnaire and a resting 12-lead electrocardiogram. Individuals with controlled hypothyroidism or hypercholesterolemia were permitted to enroll. Participants were required to abstain from caffeine, alcohol, vitamins/supplements, and strenuous physical activity for at least 24h before experimentation. Women were 17 ± 11 yr from cessation of menstruation and were not currently using hormone replacement therapy. Current physical activity was quantified via The Rapid Assessment of Physical Activity (17). This questionnaire uses a 10-point scale where a score of 1 represents a sedentary lifestyle and a score of 10 represents an active lifestyle that incorporates aerobic, strength, and flexibility activities. Participant physical characteristics, fasting blood characteristics, and physical activity status are shown in Table 1. Participant medication usage is shown in Table 2.

Table 1.

Participant Characteristics

	Sham	Heat Therapy
Women/Men, N	7/1	9/2
Age (yrs)	68 ± 6	65 ± 6
Time post menopause (yr)	20 ± 7	14 ± 10
Height (cm)	166 ± 5	165 ± 8
Weight (kg)	67 ± 10	73 ± 16
BMI (kg m−2)	24.1 ± 3.4	27.0 ± 6.4
Cholesterol (mg/dl)	212 ± 36	181 ± 29
Triglycerides (mg/dl)	108 ± 72	85 ± 34
HDL (mg/dl)	55 ± 9	59 ± 14
LDL (mg/dl)	131 ± 24	105 ± 31
Glucose (mg/dl)	87 ± 5	101 ± 14*
Hemoglobin (g/dl)	13 ± 1	14 ± 1
Hematocrit (%)	40 ± 3	44 ± 3*
HbA1C (%)	5.3 ± 0.3	5.6 ± 0.3
RAPA (au)	7.6 ± 1.9	8.3 ± 1.9

Values are presented as means ± SD. BMI, body mass index. HDL, high-density lipoprotein. LDL, low-density lipoprotein. HbA1C, hemoglobin A1C. RAPA, The Rapid Assessment of Physical Activity.

^*P < 0.05 vs. sham

Table 2.

Participant medication usage

	Sham	Heat Therapy
Hypothyroidism	1	1
Hypercholesterolemia	0	5
Osteoporosis	2	2
Antibiotic	1	0
Corticosteroid	1	0
Ophthalmic Lubricant	1	0
Acid Reflux	1	0
Anti-Inflammatory	2	2
Migraine	2	0
Topical Estrogen	0	1
Allergy	2	0
Multivitamin	7	4

Values are the number of participants per medication category. One participant in the sham group started an antibiotic, corticosteroid, and ophthalmic lubricant during the intervention and continued through post-testing as prescribed for cataract surgery.

Experimental Approach.

We utilized a single-blind, sham-controlled experimental design. Participants were randomly assigned (stratified block, two levels: < 70 and ≥ 70 yrs of age) to sham or heat therapy at a 1:1 ratio. These levels of stratification were chosen to ensure that the age distribution was balanced across sham and heat therapy groups. Participants were provided with a pair of tube-lined pants (Med-Eng, Ottawa, ON, Canada) that connect to a portable water circulator (Polyscience 7L Heated Circulator, Niles, IL) that controls water temperature within ± 0.07 °C of set-point (Figure 1). Water temperature was set to 31 °C for the sham group and 51 °C for the heat therapy group, to effectively clamp skin temperature at ~33 °C and ~40 °C, respectively. The latter target skin temperature increases body core temperature by ~0.8°C over a 60 min exposure in older adults (13). Participants were instructed to wear the pants in the Fowler’s position for 60 min, 4 days per week, for a total of 8 weeks. In addition, participants were required to record blood pressure and heart rate before, every 20 min during, and 5–10 min after each session using a log book and automated oscillometric blood pressure device (A&D Medical, Ann Arbor, MI). These data were reviewed electronically on a weekly basis to ensure participant adherence and safety Participants were instructed to maintain their current diet and physical activities throughout the study. Cardiovascular function was assessed before (pre) the first heat therapy session and within 24–72 hours after the last session (post). If testing within 72 hours of the last session was not feasible due to scheduling conflicts, participants were required to perform several “maintenance sessions” until post-testing was completed. All study personnel, except for the individual monitoring participant adherence and safety, were blinded to the intervention assignment.

Figure 1.

Shown is a pair of tube-lined pants connected to a portable water circulator, which participants used during each intervention. Figure created with BioRender.

Measurements.

Participants reported for laboratory testing at ~8:30 AM after an overnight fast. In addition, participants were required to abstain from caffeine, alcohol, supplements, over-the-counter medication, and exercise for 24 h before the study. Participants were provided a standardized breakfast (Clif bar: 260 cal, 8 g fat, 11 g protein; Boost nutritional drink: 240 cal, 6 g fat, 10 g protein) ~1 hr before experimentation. Measurements were performed after a ~30 min resting period while participants were in the supine position. Laboratory temperature was maintained at ~21 °C during experimentation.

Ambulatory Blood Pressure and Heart Rate.

Blood pressure was measured over a 24-hr period via ambulatory monitoring on a day separate from laboratory testing. An ambulatory blood pressure monitor (Oscar 2, SunTech, Morrisville, NC) was placed on the non-dominant arm. Blood pressure and heart rate were then measured every 30 min during waking hours and every 60 min during sleep, in accordance with recent guidelines (18, 19). Participants were instructed to go about their daily routine while avoiding vigorous physical activity.

Laboratory Blood Pressure and Heart Rate.

Heart rate was measured using a five-lead electrocardiogram (Solar 8000M, GE Healthcare, Chicago, IL). Arterial blood pressure was measured using an automated sphygmomanometer (Tango M2, SunTech Medical, Morrisville, NC). To avoid white-coat syndrome, blood pressure was recorded as the final measurement following 1 or more consecutive readings.

Vasodilator Function.

Endothelium-dependent vasodilation was assessed via flow-mediated dilation of the superficial femoral artery in accordance with established guidelines (20, 21). Microvascular function was assessed simultaneously via leg reactive hyperemia (peak and area under the curve). Briefly, a pneumatic cuff (SC12D, Hokanson, Bellevue, WA) was placed on the lower leg immediately distal to the patella. Arterial inflow to the lower limb was occluded by rapidly inflating the cuff to 220 mmHg for 5 min (E20 Rapid Cuff Inflator, Hokanson, Bellevue, WA). Prior to cuff inflation, superficial femoral artery diameter and blood velocity were recorded during a 1-min baseline period and resumed 20 s before cuff deflation and continued for 3 min thereafter. Endothelium-independent vasodilation was assessed via glyceryl trinitrate-mediated dilation. Superficial femoral artery diameter and blood velocity were recorded during a 1 min baseline period and continued for 10 min after lingual administration of 0.4 mg glyceryl trinitrate (Nitroglycerin Lingual Spray, Perrigo Pharmaceuticals, Allegan MI). To prevent a hypotensive response, glyceryl trinitrate was not administered to participants with a systolic blood pressure of ~100 mmHg, when measured immediately beforehand.

Superficial femoral artery diameter and blood velocity were measured via duplex ultrasonography (11 MHz, Phillips iE33, Andover, MA), ~2–3 cm distal to the common femoral bifurcation using a linear array transducer and an insonation angle of 60°. The ultrasound was interfaced with a computer running custom software to capture blood velocity (DUC²) (22). Care was taken to match ultrasound settings (e.g., sample volume and depth) and anatomical landmarks to ensure consistent probe placement from pre- to post-testing. All measures of vasodilator function were performed in the right leg.

Arterial Stiffness.

Doppler waveforms (Vascular Minilab 1052 and 1059, Parks Medical Electronics, Aloha, OR) were recorded from the carotid, femoral, and dorsalis pedis arteries at 1000 Hz using a commercially available data acquisition and analysis system (PowerLab and Lab Chart, ADInstruments, Colorado Springs, CO). Distances between recording sites (carotid to femoral; femoral to dorsalis pedis) were measured as a straight line using a fabric tape measure.

Data and Statistical Analyses.

Blood velocity was measured from Doppler ultrasound audio recordings using an intensity-weighted algorithm (custom software), subsequent to demodulation of forward and reverse Doppler frequencies (22–25). Blood velocities were then thin-beam corrected using an average correction factor of 0.847 ± 0.028 (22). Correction factors were based on measured ultrasound probe beam-width of 3.67 mm and a vessel depth of 2.0 ± 0.3 cm. Vessel diameter was determined using custom edge-detection and wall-tracking software (26, 27). Leg blood flow was calculated by multiplying the cross-sectional area of the superficial femoral artery by mean blood velocity (reported in ml min⁻¹). Vascular conductance was calculated by dividing blood flow by mean arterial pressure (expressed as ml min⁻¹ mmHg⁻¹). Shear rate was calculated by multiplying 8 by the quotient of mean blood velocity and vessel diameter (expressed as s⁻¹).

Peak diameter measured during flow-mediated dilation and glyceryl trinitrate-mediated dilation was determined using an algorithm previously described by Black and colleagues (26). Reactive hyperemia was determined by averaging blood flow (determined via simultaneously acquired diameter and velocity) across 4 s bins for the initial 20 s subsequent to release of arterial occlusion and averaged across 10 s bins thereafter (14, 25). Vascular conductance was then determined for each bin to account for changes in perfusion pressure. Reactive hyperemia area under the curve was calculated by summing the product of each bin multiplied by its duration in minutes and was normalized for baseline conductance. Peak reactive hyperemia was recorded as the highest conductance measured over a single bin. Central and peripheral pulse wave velocity, an index of arterial stiffness, was calculated across 20 cardiac cycles using the “foot-to-foot” method and applied in conjunction with the measured distance between sampling sites (28).

Absolute data were analyzed using a two-way (group × time) mixed model analysis of variance (ANOVA) with repeated measures (JMP Pro 18; SAS Institute Inc., Cary, NC). General interactions were explored further using Tukey’s post hoc procedure. Planned comparisons were used to examine specific group-time interactions. Relative changes across time were analyzed via a one-tailed Student’s t-test. Flow-mediated dilation was assessed using the allometric modeling solution proposed by Atkinson et al (29, 30) subsequent to verification of the presence of inadequate scaling by examining the slope of the relation between logarithmically transformed baseline and peak diameter. Additionally, shear rate area under the curve summed through peak diameter was also entered into the model as a covariate to account for changes in shear stimulus. We performed a power analysis using an α = 0.05, a β = 0.8, and a partial η² = 0.14 and determined a sample size of N = 10 per group provided sufficient power (G*power; a priori F-test: within-between interaction for repeated measures ANOVA). All data are reported as means ± standard deviation.

Results

Adherence.

Participant adherence, verified via log book documentation and remote monitoring of heart rate and blood pressure, was 100% for both groups. The acute change in heart rate and mean arterial pressure averaged across each intervention (≥ 32 sessions) is shown in Figure 2. As expected, heart rate increased during heat therapy (Δ 5 ± 2 beats min⁻¹) when compared to sham (Δ −4 ± 1 beats min⁻¹; P < 0.01). Mean arterial pressure decreased during heat therapy (Δ −8 ± 5 mmHg), whereas there was no change during sham sessions (Δ 0 ± 2 mmHg; P < 0.01). No adverse events were reported over the course of both interventions.

Figure 2.

The acute change in heart rate (top panel) and mean arterial pressure (bottom panel) were averaged across each intervention (≥32 sessions). Change values were calculated as the difference between the measurements taken at the 60-min time point and those taken immediately before each session. Data were analyzed using a one-tailed Student’s t-test. The horizontal black line denotes the mean *P < 0.01 vs. sham.

Blood Pressure.

Across all participants, a total of 29 ± 3 blood pressure measurements were recorded during the ambulatory daytime period and 7 ± 1 measurements were recorded at nighttime. The change in daytime ambulatory blood pressure measured from pre to post intervention is shown in Figure 3. Absolute ambulatory and laboratory blood pressures are shown for both groups and across time in Table 3. Heat therapy reduced ambulatory daytime systolic blood pressure by Δ −5 ± 8 mmHg, whereas there was no change for the sham group (Δ 1 ± 6 mmHg; P = 0.04). Ambulatory daytime diastolic and mean arterial pressures did not change across time for either group (both P ≥ 0.2). Likewise, ambulatory nighttime blood pressures did not differ between groups or across time (all P ≥ 0.1). Interestingly, heat therapy reduced laboratory systolic (P = 0.02), diastolic (P = 0.02), and mean (P = 0.01) arterial pressures, whereas there was no change across time for the sham group (all P ≥ 0.6).

Figure 3.

Ambulatory daytime systolic (top), diastolic (middle), and mean (bottom) arterial blood pressures are shown for each group. Delta pressure was calculated as post-intervention minus pre-intervention pressure. Data were analyzed using a one-tailed Student’s t-test. The horizontal black line denotes the mean. *P = 0.04 vs. sham.

Table 3.

Hemodynamics

	Sham		Heat Therapy
	Pre	Post	Pre	Post
	Ambulatory Daytime
Systolic BP (mmHg)	117 ± 12	119 ± 10	128 ± 12*	123 ± 9†
Diastolic BP (mmHg)	70 ± 7	70 ± 8	71 ± 8	70 ± 5
Mean BP (mmHg)	86 ± 8	86 ± 8	90 ± 8	88 ± 5
Heart Rate (beats min−1)	69 ± 4	69 ± 3	74 ± 6	73 ± 8
	Ambulatory Nighttime
Systolic BP (mmHg)	105 ± 13	108 ± 14	116 ± 17	114 ± 12
Diastolic BP (mmHg)	62 ± 8	61 ± 10	63 ± 11	63 ± 5
Mean BP (mmHg)	76 ± 9	77 ± 11	81 ± 13	80 ± 7
Heart Rate (beats min−1)	63 ± 4	62 ± 4	67 ± 6	66 ± 7
	Laboratory
Systolic BP (mmHg)	120 ± 12	118 ± 12	132 ± 15	124 ± 16‡
Diastolic BP (mmHg)	74 ± 7	73 ± 12	79 ± 12	71 ± 9‡
Mean BP (mmHg)	89 ± 8	88 ± 12	97 ± 12	88 ± 9‡
Heart Rate (beats min−1)	64 ± 5	60 ± 4	65 ± 5	65 ± 9
	Pulse Wave Velocity
Central (m s−1)	8.0 ± 1.2	7.7 ± 1.1	8.0 ± 1.7	8.1 ± 1.5
Peripheral (m s−1)	11.4 ± 1.2	11.4 ± 1.8	13.2 ± 1.6*	12.4 ± 1.9

Values are presented as mean ± SD.

^*P ≤ 0.06 vs. sham at the indicated time point

^†P = 0.06 vs. pre, within group

^‡P ≤ 0.02 vs. pre, within group

Vasodilator Function.

Endothelium-dependent vasodilation, assessed via ANCOVA-adjusted flow-mediated dilation, is shown in Figure 4. Superficial femoral artery hemodynamics during the assessment of flow-mediated dilation and reactive hyperemia are shown in Table 4. Heat therapy increased flow-mediated dilation (P = 0.02), whereas there was no change across time for the sham group (P = 0.5). Additionally, reactive hyperemia area under the curve (P = 0.08 for interaction) and peak reactive hyperemia (P = 0.1 for interaction) did not differ between groups or across time. Endothelium-independent vasodilation, assessed via glyceryl trinitrate-mediated dilation, did not differ across time for the heat therapy group (pre, 4.8 ± 2.7 % vs. post, 4.9 ± 3.5 %) nor the sham group (pre, 6.1 ± 2.9 % vs post, 6.1 ± 3.2 %; P = 0.8 for interaction). Glyceryl trinitrate was not administered to N = 4 participants to avoid certain adverse reactions (i.e., hypotension or headache).

Figure 4.

Endothelium-dependent vasodilation, assessed via ANCOVA adjusted flow-mediated dilation, is shown for each group at pre (open circles) and post time points (graphite circles). Data were analyzed using a two-way (group × time) mixed model analysis of variance with repeated measures. Logarithmically transformed baseline diameter and shear rate area under the curve summed through peak diameter were also entered into the model as covariates. The horizontal black line denotes the mean and is positioned adjacent to the individual data points. *P = 0.02 vs. pre, within group.

Table 4.

Superficial femoral artery hemodynamics during assessment of flow-mediated dilation and reactive hyperemia

	Sham		Heat Therapy
	Pre	Post	Pre	Post
Baseline diameter, cm	0.616 ± 0.069	0.617 ± 0.056	0.606 ± 0.092	0.605 ± 0.086
Peak diameter, cm	0.627 ± 0.070	0.627 ± 0.060	0.616 ± 0.090	0.620 ± 0.082
Δ Diameter, cm	0.011 ± 0.005	0.010 ± 0.005	0.010 ± 0.007	0.015 ± 0.006*
Time to peak diameter, s	110 ± 37	77 ± 47	78 ± 40	71 ± 48
Shear rate AUC	22,002 ± 9,427	15,649 ± 6,310*	19,344 ± 5,052	17,202 ± 5,454*
Baseline blood flow, ml min−1	73 ± 16	62 ± 12*	80 ± 36	71 ± 35*
Baseline vascular conductance, ml min−1 mmHg−1	0.85 ± 0.20	0.70 ± 0.16	0.85 ± 0.41	0.79 ± 0.40
Reactive hyperemia AUC, ml min−1 mmHg−1	3.16 ± 1.20	2.72 ± 1.03	2.86 ± 1.08	3.11 ± 1.61
Peak reactive hyperemia, ml mmHg−1	6.62 ± 1.22	6.43 ± 1.16	6.32 ± 1.78	6.60 ± 1.61

Values are presented as mean ± SD. Shear rate AUC, shear rate area under the curve through peak diameter. Reactive hyperemia AUC, reactive hyperemia area under the curve.

^*P ≤ 0.04 vs. pre, within group.

Arterial Stiffness.

Arterial stiffness is shown in Table 3. Central pulse wave velocity did not differ from pre- to post-testing for either group (both P ≥ 0.4). Likewise, peripheral pulse wave velocity did not differ across time for either group (both P ≥ 0.1).

Discussion

The purpose of this study was to examine the extent to which 8 weeks of home-based lower body heat therapy alters cardiovascular function in older adults. In support of our hypothesis, we found that 8 weeks of home-based lower body heat therapy reduced ambulatory and laboratory blood pressures and improved endothelium-dependent vasodilation. Notably, these physiological outcomes were accompanied by a 100% adherence rate. Taken together, our results suggest that home-based lower body heat therapy improves several measures of cardiovascular function in older adults.

Blood Pressure: Clinical Implications and Mechanistic Underpinnings.

A reduction of 5 mmHg in systolic blood pressure is considered clinically meaningful as it is associated with a 10% reduction in major cardiovascular event risk (31). Prior studies have shown that whole-body heat therapy induces a blood pressure lowering effect in various populations. For example, Brunt and colleagues demonstrated that 8 weeks of hot tub immersion reduced laboratory systolic blood pressure by 4 mmHg in young, sedentary adults (11). Similar results have been found in clinical populations such as polycystic ovary syndrome (32) and patients with heart failure with reduced ejection fraction (33). Notably, we observed that lower-body heat therapy reduced ambulatory daytime systolic blood pressure by 5 mmHg in older adults. This finding suggests that a profound heat exposure (i.e., hot tub immersion) is not a requisite to induce a blood pressure lowering effect in this population, and that a more modest approach could be equally efficacious. In addition, based on their RAPA scores, our participants were classified as physically active. This underscores the intervention’s efficacy in a population with a favorable health profile and highlights its potential benefits in traditional clinical populations.

The change in ambulatory daytime systolic blood pressure measured after heat therapy was similar to that measured in-laboratory. Interestingly, diastolic and mean arterial pressures did not differ across time when measured via daytime ambulatory monitoring, but were reduced when measured in-laboratory. These findings highlight the importance of ambulatory blood pressure monitoring for an accurate assessment of blood pressure outside of the clinic. That is, the blood pressure measured in clinic or laboratory may not always reflect those measured in individuals as they perform their activities of daily living. Indeed, when compared with clinic measures, ambulatory blood pressure monitoring is superior in predicting future cardiovascular disease/events (34, 35).

The mechanisms mediating the blood pressure lowering effect induced by lower body heat therapy are unclear. The finding that microvascular function did not differ from pre- to post-heat therapy suggests that the mechanisms may be neural in origin. Along these lines, we recently demonstrated that the blood pressure lowering effect induced by acute heat exposure in older adults is mediated by sympathoinhibition that likely occurred secondary to resetting of the arterial baroreflex (13). It is possible that heat therapy could induce a similar adaptive response that persists beyond the initial exposure. Further research is needed to confirm the mechanisms by which lower body heat therapy lowers blood pressure in older adults.

Endothelium-dependent Vasodilation.

Whole-body heat therapy has been shown to consistently improve conduit artery endothelial function in healthy and clinical populations (32, 33, 36, 37). Considerably less is known about the impact that lower body heat therapy may have on endothelial function. Our group previously demonstrated that acute lower leg heat exposure improved superficial femoral artery endothelium-dependent vasodilation in older adults, whereas there was no effect in young adults (14). Cheng and colleagues recently extended these observations by demonstrating that lower leg heat therapy did not improve brachial artery endothelium-dependent vasodilation in young adults (38). However, these results could be explained by limb differences rather than age-related factors. Nevertheless, these studies combined with the results reported herein suggest that the ability to improve endothelial function via targeted heating of the legs or lower body may be dependent on age and/or the presence of overt endothelial dysfunction.

The endothelium expresses a diverse array of receptors and ion channels that sense shear stress (i.e., the frictional drag of red blood cells along the endothelium) and respond by activating signaling pathways that produce relaxing/hyperpolarizing factors, such as nitric oxide (39). Shear stress has been implicated as one of the principal mechanisms by which heat therapy improves endothelium-dependent vasodilation (16, 40–43). Therefore, it is reasonable to suggest that elevations in shear stress that occur during repeated lower body heat exposures contribute to the improvement in endothelium-dependent vasodilation observed in older adults. It is also possible that endothelial function is improved as a result of, or in combination with, increased body core and blood temperatures. To that end, transient receptor potential channels (e.g., TRPV3 and TRPV4) are heat sensitive and can increase calcium current in endothelial cells (44, 45). Of note, calcium influx activates several vasodilatory signaling pathways (e.g., nitric oxide) within endothelial cells. Though speculative, it is possible that repeated increases in body core and blood temperature may contribute to the improvement in endothelium-dependent vasodilation secondary to activation of transient receptor potential channels and the upregulation of endothelial nitric oxide synthase. Further work is necessary to determine the precise mechanisms mediating the improvement in endothelium-dependent vasodilation that occurs with lower body heat therapy.

Arterial Stiffness.

Currently, it is unclear why arterial stiffness was unchanged following heat therapy. It is possible that our intervention lacked sufficient magnitude to alter conduit artery structure. In this context, Brunt and colleagues found that 8 weeks of chest-down hot tub immersion (40 °C) reduced central arterial stiffness in young, sedentary adults (11). Additionally, Ganio and colleagues demonstrated that the extent to which acute passive heat exposure reduces arterial stiffness may depend on baseline stiffness (46). Thus, given that baseline central pulse wave velocity was normal in our participants (i.e., < 10 m/s), a more intense heat stimulus may be necessary to induce similar changes in older adults (47).

Experimental Considerations

A number of experimental considerations warrant discussion. First, participants in the heat therapy group would be categorized as having elevated blood pressure, based on the recent American College of Cardiology/American Heart Association Guidelines (34). Indeed, individuals with higher blood pressures stand to benefit more from therapeutic interventions, relative to those with lower blood pressure (48). Therefore, the blood pressure lowering effect induced by lower body heat therapy may differ in normotensive older adults. Second, participants were not truly blinded to their assigned intervention. However, we did utilize pseudo-blinding in that participants were informed that we were testing the efficacy of two temperatures. Despite the sham intervention being considered thermoneutral, a target skin temperature of 33 °C is warm relative to air temperature which is ~23 °C. Thus, participants perceived the sham intervention as being warm despite body core temperature remaining unchanged. Third, we did not measure skin or body core temperature during each session. Thus, it is possible that our target temperatures were not achieved in all participants across all sessions. Fourth, the majority of participants included in this study were women. As such, the results may be more broadly applicable to women. However, the Blood Pressure Lowering Treatment Trialist’ Collaboration suggests that men and women do not differ in their cardiovascular risk protection achieved from blood pressure lowering treatment (49). That being said, the prevalence of cardiovascular disease risk factors increases in women as they age (2, 50, 51), highlighting the benefit of this intervention in a population that is typically understudied. Finally, we are slightly underpowered for the sham group (N = 8). However, results for this group were highly consistent across time. Thus, including two additional participants in the sham group would likely not have affected the results reported herein.

Perspectives and Conclusions

The human lifespan in the twenty-first century is ~70 years of age and is expected to increase. However, a gap remains between lifespan and healthspan (i.e., the number of years lived without disease) (52, 53). Thus, novel approaches are needed to fill this gap and ultimately reduce cardiovascular morbidity and mortality. According to American Heart Association/American College of Sports Medicine position statements, exercise training remains a strong nonpharmacological intervention to promote healthy aging and reduce cardiovascular disease risk (4, 5). However, implementation of exercise training and adherence in older adults may be challenging, particularly in those who are unwilling or unable to exercise. Over the past decade, whole-body heat therapy has emerged as a novel therapeutic strategy to improve cardiovascular health in a number of populations (8–11, 15). Notably, our findings suggest that home-based lower body therapy can leverage the demonstrated benefits of whole-body heat therapy while managing safety and convenience. Importantly, the 100% adherence rate reported herein is greater than that reported for home-based exercise interventions in older adults, which can range between 60–95% adherence (54–56). In addition, investigating further the mechanisms mediating these improvements may facilitate the further optimization of heat therapy in this population and others.

In summary, our results combined with a strong adherence rate suggest that home-based lower body heat therapy could be an alternative nonpharmacological intervention to reduce blood pressure and improve vascular function, ultimately reducing long-term cardiovascular disease risk in older adults.

New and Noteworthy.

Advancing age is associated with vascular dysfunction and hypertension, both of which increase cardiovascular event risk. This study determined that 8 weeks of home-based leg therapy reduced ambulatory daytime systolic blood pressure and increased flow-mediated dilation of the superficial femoral artery, outcomes not observed in the sham group. These improvements, coupled with 100% adherence among participants, suggest that home-based heat therapy is a pragmatic and effective strategy for improving cardiovascular health in older adults.

Data Availability Statement

All datasets generated during and/or analyzed within the current study are available from the corresponding authors upon request.