Sex-specific microvascular and hemodynamic responses to passive limb heating in young adults.

OBJECTIVE: We examined sex-specific microvascular reactivity and hemodynamic responses under conditions of augmented resting blood flow induced by passive heating compared to normal blood flow. METHODS: Thirty-eight adults (19 females) completed a vascular occlusion test (VOT) on two occasions preceded by rest with or without passive heating in a randomized, counterbalanced order. Skeletal muscle tissue oxygenation (StO2, %) was assessed with near-infrared spectroscopy (NIRS), and the rate of desaturation and resaturation as well as maximal StO2 (StO2max) and prolonged hypersaturation (area under the curve, StO2AUC) were quantified. Before the VOT, brachial artery blood flow (BABF), vascular conductance, and relative BABF (BABF normalized to forearm lean mass) were determined. Sex × condition ANOVAs were used. A p-value ≤.05 was considered statistically significant. RESULTS: Twenty minutes of heating increased BABF compared to the control (102.9 ± 28.3 vs. 36.0 ± 20.9 mL min-1; p < .01). Males demonstrated greater BABF than females (91.9 ± 34.0 vs. 47.0 ± 19.1 mL min-1; p < .01). There was no sex difference in normalized BABF. There were no significant interactions for NIRS-VOT outcomes, but heat did increase the rate of desaturation (-0.140 ± 0.02 vs. -0.119 ± 0.03% s-1; p < .01), whereas regardless of condition, males exhibited greater rates of resaturation and StO2max than females. CONCLUSIONS: These results suggest that blood flow is not the primary factor causing sex differences in NIRS-VOT outcomes.

Blood, Sweat, and Tears: Implications for Hydration Testing in Combat Sports-Investigating Body Mass Loss and Biomarker Changes.

Combat sports athletes often undergo rapid body mass loss (BML), which presents health risks. Hydration testing has been proposed as a possible solution to reduce or eliminate rapid BML. However, combat sports athletes may exhibit distinct physiological characteristics due to repeated exposure to BML. Thus, traditional and emerging hydration biomarkers should be investigated to determine their potential suitability for field use in this cohort. This study examined whether BML can explain changes in serum and urine osmolality (SosmΔ, UosmΔ), tear osmolarity (TosmΔ), hematocrit (HctΔ), and urine-specific gravity (USGΔ) after mild-moderate passive dehydration. Biomarker reliability was also assessed across two trials. Fifteen male and female combat sports athletes (age: 26.3 ± 5.3 years, body mass: 67.7 ± 9.9 kg) underwent a sauna protocol twice (5-28 days apart) aiming for 4% BML. The average BML in Trials 1 and 2 was 3.0 ± 0.7%. Regression analysis revealed that BML explained HctΔ (R2 = 0.22, p = 0.009) but not SosmΔ (R2 = 0.11, p = 0.079) or other biomarkers. Intraclass correlation coefficients (ICCs) were significant for all biomarkers except TosmΔ (ICC = 0.06, p = 0.37) and post-Tosm (ICC = 0.04, p = 0.42); post-Hct performed best (ICC = 0.82, p < 0.001). Contingency tables with post-Sosm (295 mOsm/kg) and post-USG (1.020) cutoffs revealed an 80% true negative rate (TNR) and a 62% true positive rate (TPR). Increasing the Sosm cutoff to 301 mOsm/kg decreased the TNR to 52% but increased the TPR to 83%. Although blood parameters were most sensitive to BML, they could only explain 11%-22% of biomarker variation. The typical USG cutoff misclassified 42% of athletes postdehydration, and reliability was generally poor-moderate. Alternative strategies should be pursued to manage rapid BML in combat sports.

Post exercise hot water immersion and hot water immersion in isolation enhance vascular, blood marker, and perceptual responses when compared to exercise alone.

Exercise and passive heating induce some similar vascular hemodynamic, circulating blood marker, and perceptual responses. However, it remains unknown whether post exercise hot water immersion can synergise exercise derived responses and if they differ from hot water immersion alone. This study investigated the acute responses to post moderate-intensity exercise hot water immersion (EX+HWI) when compared to exercise (EX+REST) and hot water immersion (HWI+HWI) alone. Sixteen physically inactive middle-aged adults (nine males and seven females) completed a randomized cross-over counterbalanced design. Each condition consisted of two 30-min bouts separated by 10 min of rest. Cycling was set at a power output equivalent to 50% V̇o2 peak . Water temperature was controlled at 40°C up to the mid sternum with arms not submerged. Venous blood samples and artery ultrasound scans were assessed at 0 (baseline), 30 (immediately post stressor one), 70 (immediately post stressor two), and 100 min (recovery). Additional physiological and perceptual measures were assessed at 10-min intervals. Brachial and superficial femoral artery shear rates were higher after EX+HWI and HWI+HWI when compared with EX+REST (p < 0.001). Plasma nitrite was higher immediately following EX+HWI and HWI+HWI than EX+REST (p < 0.01). Serum interleukin-6 was higher immediately after EX+HWI compared to EX+REST (p = 0.046). Serum cortisol was lower at 30 min in the HWI+HWI condition in contrast to EX+REST (p = 0.026). EX+HWI and HWI+HWI were more enjoyable than EX+REST (p < 0.05). Irrespective of whether hot water immersion proceeded exercise or heating, hot water immersion enhanced vascular and blood marker responses, while also being more enjoyable than exercise alone.

Physiological mechanisms associated with the use of a passive heat intervention: positive implications for soccer substitutes.

PURPOSE: Soccer substitutes are exposed to periods of limited activity before entering match-play, likely negating benefits of active warm-ups. This study aimed to determine the effects of using a passive heat intervention following a pre-match, and half-time warm-up, on muscle and core temperature in soccer players during ambient (18 °C) and cold (2 °C) conditions. METHODS: On four occasions, 8 male players, completed a pre-match warm-up, followed by 45 min of rest. Following this, participants completed a half-time re-warm-up followed by an additional 45 min of rest, simulating a full match for an unplaying substitute. During periods of rest, participants wore either standardised tracksuit bottoms (CON), or heated trousers (HEAT), over typical soccer attire. RESULTS: Vastus lateralis temperature declined less in HEAT compared to CON following the 1st half in 2 °C (Δ - 4.39 ± 0.81 vs. - 6.21 ± 1.32 °C, P = 0.002) and 18 °C (Δ - 2.48 ± 0.71 vs. - 3.54 ± 0.88 °C, P = 0.003). These findings were also observed in the 2nd half for the 2 °C (Δ - 4.36 ± 1.03 vs. - 6.26 ± 1.04 °C, P = 0.002) and 18 °C (Δ - 2.85 ± 0.57 vs. - 4.06 ± 1 °C, P = 0.018) conditions. In addition, core temperature declined less in HEAT compared to CON following the 1st (Δ - 0.41 ± 0.25 vs. - 0.84 ± 0.41 °C, P = 0.037) and 2nd (Δ - 0.25 ± 0.33 vs. - 0.64 ± 0.34 °C, P = 0.028) halves of passive rest in 2 °C, with no differences in the 18 °C condition. Perceptual data confirmed that participants were more comfortable in HEAT vs. CON in 2 °C (P < 0.01). CONCLUSIONS: Following active warm-ups, heated trousers attenuate the decline in muscle temperature in ambient and cold environments.

The effect of underwater massage during hot water immersion on acute cardiovascular and mood responses.

PURPOSE: There is emerging evidence that demonstrates the health benefits of hot water immersion including improvements to cardiovascular health and reductions in stress and anxiety. Many commercially available hot tubs offer underwater massage systems which purport to enhance many benefits of hot water immersion, however, these claims have yet to be studied. METHODS: Twenty participants (4 females) completed three, 30-min sessions of hot-water immersion (beginning at 39 °C) in a crossover randomized design: with air massage (Air Jet), water massage (Hydro Jet) or no massage (Control). Cardiovascular responses comprising; heart rate, blood pressure and superficial femoral artery blood flow and shear rate were measured. State trait anxiety, basic affect, and salivary cortisol were recorded before and after each trial. Data were analysed using a mixed effects model. RESULTS: Post immersion, heart rate increased (Δ31bpm, P < 0.001, d = 1.38), mean arterial blood pressure decreased (Δ16 mmHg, P < 0.001, d = -0.66), with no difference between conditions. Blood flow and mean shear rate increased following immersion (P < 0.001, Δ362 ml/min, d = 1.20 and Δ108 s-1, d = 1.00), but these increases were blunted in the Air Jet condition (P < 0.001,Δ171 ml/min, d = 0.43 and Δ52 s-1, d = 0.52). Anxiety and salivary cortisol were reduced (P = 0.003, d = -0.20, P = 0.014, d = -0.11), but did not vary between conditions. Enjoyment did not vary between conditions. CONCLUSION: These data demonstrate positive acute responses to hot water immersion on markers of cardiovascular function, anxiety, and stress. There was no additional benefit of water-based massage, while air-based massage blunted some positive vascular responses due to lower heat conservation of the water.

Skeletal muscle angiogenic, regulatory, and heat shock protein responses to prolonged passive hyperthermia of the human lower limb.

Passive hyperthermia induces a range of physiological responses including augmenting skeletal muscle mRNA expression. This experiment aimed to examine gene and protein responses to prolonged passive leg hyperthermia. Seven young participants underwent 3 h of resting unilateral leg heating (HEAT) followed by a further 3 h of rest, with the contralateral leg serving as an unheated control (CONT). Muscle biopsies were taken at baseline (0 h), and at 1.5, 3, 4, and 6 h in HEAT and 0 and 6 h in CONT to assess changes in selected mRNA expression via qRT-PCR, and HSP72 and VEGFα concentration via ELISA. Muscle temperature (Tm) increased in HEAT plateauing from 1.5 to 3 h (+3.5 ± 1.5°C from 34.2 ± 1.2°C baseline value; P < 0.001), returning to baseline at 6 h. No change occurred in CONT. Endothelial nitric oxide synthase (eNOS), Forkhead box O1 (FOXO-1), Hsp72, and VEGFα mRNA increased in HEAT (P < 0.05); however, post hoc analysis identified that only Hsp72 mRNA statistically increased (at 4 h vs. baseline). When peak change during HEAT was calculated angiopoietin 2 (ANGPT-2) decreased (-0.4 ± 0.2-fold), and C-C motif chemokine ligand 2 (CCL2) (+2.9 ± 1.6-fold), FOXO-1 (+6.2 ± 4.4-fold), Hsp27 (+2.9 ± 1.7-fold), Hsp72 (+8.5 ± 3.5-fold), Hsp90α (+4.6 ± 3.7-fold), and VEGFα (+5.9 ± 3.1-fold) increased from baseline (all P < 0.05). At 6 h Tm were not different between limbs (P = 0.582; CONT = 32.5 ± 1.6°C, HEAT = 34.3 ± 1.2°C), and only ANGPT-2 (P = 0.031; -1.3 ± 1.4-fold) and VEGFα (P = 0.030; 1.1 ± 1.2-fold) differed between HEAT and CONT. No change in VEGFα or HSP72 protein concentration were observed over time; however, peak change in VEGFα did increase (P < 0.05) in HEAT (+140 ± 184 pg·mL-1) versus CONT (+7 ± 86 pg·mL-1). Passive hyperthermia transiently augmented ANGPT-2, CCL2, eNOS, FOXO-1, Hsp27, Hsp72, Hsp90α and VEGFα mRNA, and VEGFα protein.

Increases in muscle temperature by hot water improve muscle contractile function and reduce motor unit discharge rates.

PURPOSE: Examine the effects of 42°C hot-water immersion on muscle contraction function and motor unit discharge rates. Voluntary and evoked contraction assessments were examined first with a concomitant increase in the core and muscle temperature, and thereafter with increased muscle temperature but cooled core temperature. METHODS: Fifteen participants (24.9 ± 5.6 years) performed neuromuscular assessments before, after, and ~15-min after either 90-min of 42°C (hot) or 36°C (control) water immersion. Maximal voluntary contraction (MVC) assessment of knee extension was performed along with surface electromyography (sEMG) (vastus lateralis and medialis [VL, VM]) and voluntary activation level (VAL). Resting evoked twitch was elicited for peak torque and time to peak torque analysis. In addition, the VL and VM motor unit discharge rates (MUDR) were measured. RESULTS: After hot-water immersion (core temperature ↑1°C; muscle temperature ↑2.4°C), MVC torque and VAL decreased (p < 0.05). The sEMG (VL and VM) and peak twitch torque did not change (p > 0.05), while time to peak torque decreased (p = 0.007). The VL and VM MUDR decreased, showing a time effect, after both water immersion conditions (36 and 42°C) (p > 0.001). Fifteen minutes after the hot-water immersion (core temperature at baseline; muscle temperature ↑1.4°C), MVC torque returned to baseline, but VAL remained lower. The sEMG (VL and VM) remained unchanged. Peak twitch torque increased (p < 0.002) and time to peak torque remained lower (p = 0.028). The MUDR remained lower after both water immersion conditions (p < 0.05). CONCLUSION: Increased core temperature evoked by 42°C hot-water immersion decreases MVC torque and VAL. However, a passive increase in muscle temperature improved evoked muscle contractile function (i.e., time to peak torque [after] and peak twitch torque [~15 min after]). Moreover, a passive increase in muscle temperature reduced the required MUDR to attain the same torque.

The reliability of a portable steam sauna pod for the whole-body passive heating of humans.

INTRODUCTION: Passive heating is receiving increasing attention within human performance and health contexts. A low-cost, portable steam sauna pod may offer an additional tool for those seeking to manipulate physiological (cardiovascular, thermoregulatory and sudomotor) and perceptual responses for improving sporting or health profiles. This study aimed to 1) report the different levels of heat stress and determine the pods' inter-unit reliability, and 2) quantify the reliability of physiological and perceptual responses to passive heating. METHOD: In part 1, five pods were assessed for temperature and relative humidity (RH) every 5 min across 70 min of heating for each of the 9 settings. In part 2, twelve males (age: 24 ± 4 years) completed two 60 min trials of passive heating (3 × 20 min at 44 °C/99% RH, separated by 1 week). Heart rate (HR), rectal (Trectal) and tympanic temperature (Ttympanic) were recorded every 5 min, thermal comfort (Tcomfort) and sensation (Tsensation) every 10 min, mean arterial pressure (MAP) at each break period and sweat rate (SR) after exiting the pod. RESULTS: In part 1, setting 9 provided the highest temperature (44.3 ± 0.2 °C) and longest time RH remained stable at 99% (51±7 min). Inter-unit reliability data demonstrated agreement between pods for settings 5-9 (intra-class correlation [ICC] >0.9), but not for settings 1-4 (ICC <0.9). In part 2, between-visits, high correlations, and low typical error of measurement (TEM) and coefficient of variation (CV) were found for Trectal, HR, MAP, SR, and Tcomfort, but not for Ttympanic or Tsensation. A peak Trectal of 38.09 ± 0.30 °C, HR of 124 ± 15 b min-1 and a sweat loss of 0.73 ± 0.33 L were reported. No between-visit differences (p > 0.05) were observed for Trectal, Ttympanic, Tsensation or Tcomfort, however HR (+3 b.min-1) and MAP (+4 mmHg) were greater in visit 1 vs. 2 (p < 0.05). CONCLUSION: Portable steam sauna pods generate reliable heat stress between-units. The highest setting (44 °C/99% RH) also provides reliable but modest adjustments in physiological and perceptual responses.

Endothelial HSP72 is not reduced in type 2 diabetes nor is it a key determinant of endothelial insulin sensitivity.

Impaired endothelial insulin signaling and consequent blunting of insulin-induced vasodilation is a feature of type 2 diabetes (T2D) that contributes to vascular disease and glycemic dysregulation. However, the molecular mechanisms underlying endothelial insulin resistance remain poorly known. Herein, we tested the hypothesis that endothelial insulin resistance in T2D is attributed to reduced expression of heat shock protein 72 (HSP72). HSP72 is a cytoprotective chaperone protein that can be upregulated with heating and is reported to promote insulin sensitivity in metabolically active tissues, in part via inhibition of JNK activity. Accordingly, we further hypothesized that, in individuals with T2D, 7 days of passive heat treatment via hot water immersion to waist level would improve leg blood flow responses to an oral glucose load (i.e., endogenous insulin stimulation) via induction of endothelial HSP72. In contrast, we found that: 1) endothelial insulin resistance in T2D mice and humans was not associated with reduced HSP72 in aortas and venous endothelial cells, respectively; 2) after passive heat treatment, improved leg blood flow responses to an oral glucose load did not parallel with increased endothelial HSP72; and 3) downregulation of HSP72 (via small-interfering RNA) or upregulation of HSP72 (via heating) in cultured endothelial cells did not impair or enhance insulin signaling, respectively, nor was JNK activity altered. Collectively, these findings do not support the hypothesis that reduced HSP72 is a key driver of endothelial insulin resistance in T2D but provide novel evidence that lower-body heating may be an effective strategy for improving leg blood flow responses to glucose ingestion-induced hyperinsulinemia.

The acute effects of passive heating on endothelial function, muscle microvascular oxygen delivery, and expression of serum HSP90α.

Passive heating has been a therapeutic tool used to elevate core temperature and induce increases in cardiac output, blood flow, and shear stress. We aimed to determine the effects of a single bout of passive heating on endothelial function and serum heat shock protein 90α (HSP90α) levels in young, healthy subjects. 8 healthy subjects were recruited to participate in one bout of whole-body passive heating via immersion in a 40 °C hot tub to maintain a 1 °C increase in rectal temperature for 60 min. Twenty-four hours after heating, shear-rate corrected endothelium-dependent dilation increased (pre: 0.004 ± 0.002%SRAUC; post: 0.006 ± 0.003%SRAUC; p = 0.034) but serum [HSP90α] was not changed (pre: 36.7 ± 10.3 ng/mL; post: 40.6 ± 15.9 ng/mL; p = 0.39). Neither resting muscle O2 utilization (pre: 0.17 ± 0.11 mL O2 min-1 (100 g)-1; post: 0.14 ± 0.09 mL O2 min-1 (100 g)-1); p = 0.28) nor mean arterial pressure (pre: 74 ± 11 mmHg; post: 73 ± 11 mmHg; p = 0.79) were influenced by the heating intervention. Finally, time to peak after cuff release was significantly delayed for % O2 sat (TTPpre = 39 ± 8.9 s and TTPpost = 43.5 ± 8.2 s; p = 0.007) and deoxy-[heme] (TTPpre = 41.3 ± 18.1 s and TTPpost = 51.4 ± 16.3 s; p = 0.018), with no effect on oxy-[heme] (p = 0.19) and total-[heme] (p = 0.41). One bout of passive heating improved endothelium-dependent dilation 24 h later in young, healthy subjects. This data suggests that passive heat treatments may provide a simple intervention for improving vascular health.

Potential role of passively increased muscle temperature on contractile function.

Declines in muscle force, power, and contractile function can be observed in older adults, clinical populations, inactive individuals, and injured athletes. Passive heating exposure (e.g., hot baths, sauna, or heated garments) has been used for health purposes, including skeletal muscle treatment. An acute increase in muscle temperature by passive heating can increase the voluntary rate of force development and electrically evoked contraction properties (i.e., time to peak twitch torque, half-relation time, and electromechanical delay). The improvements in the rate of force development and evoked contraction assessments with increased muscle temperature after passive heating reveal peripheral mechanisms' potential role in enhancing muscle contraction. This review aimed to summarise, discuss, and highlight the potential role of an acute passive heating stimulus on skeletal muscle cells to improve contractile function. These mechanisms include increased calcium kinetics (release/reuptake), calcium sensitivity, and increased intramuscular fluid.

Taking the plunge: When is best for hot water immersion to complement exercise in heat and hypoxia.

This investigation assessed the psycho-physiological and performance effects of hot water immersion (HWI) implemented either before or after a repeated-sprint training in hypoxia (RSH) session conducted in the heat. Ten participants completed three RSH trials (3 × 10 × 5-s sprints), conducted at 40°C and simulated altitude of 3000 m. A 30-min monitoring period preceded and followed all exercise sessions. In PRE, the pre-exercise period was HWI, and the post-exercise period was seated rest in temperate conditions. This combination was reversed in POST. In CON, participants were seated in temperate conditions for both periods. Compared to CON, PRE elicited a reduction in power output during each repeated-sprint set (14.8-16.2%, all p < 0.001), and a significantly higher core temperature (Tc) during the pre-exercise period and throughout the exercise session (p < 0.001 and p = 0.025, respectively). In POST, power output and Tc until the end of exercise were similar to CON, with Tc higher at the conclusion of the post-exercise period (p < 0.001). Time across the entire protocol spent ≥38.5°C Tc was significantly longer in PRE (48.1 ± 22.5 min) than POST (31.0 ± 11.3 min, p = 0.05) and CON (15.8 ± 16.3 min, p < 0.001). Employing HWI following RSH conducted in the heat provides effective outcomes regarding physiological strain and cycling performance when compared to pre-exercise or no HWI.

The metabolic upper critical temperature of the human thermoneutral zone.

INTRODUCTION: The thermoneutral zone (TNZ) defines the range of ambient temperatures at which resting metabolic rate is at a minimum without sensible dry heat loss; the body not needing to defend its core temperature. The TNZ has been defined in a number of species yet surprisingly, in humans only its lower limit has been well characterised; indeed, it is not yet clear if there is an upper limit at which metabolic rate increases. AIM: To evaluate the evidence for a metabolic upper critical temperature to the thermoneutral zone in humans. METHODS: We synthesised current evidence about an upper limit to the human TNZ, highlighting the contradictions in the literature, and then discussed likely explanations for those contradictions. RESULTS: The data from relevant studies differ in terms of whether they indicate that the TNZ has an upper limit, and this was related to the fundamental type of heat exposure protocol employed. Those studies showing evidence for an upper limit associated that limit with a wide range of temperatures. CONCLUSIONS: We offer suggestions for future studies that should clarify the presence/absence of an upper limit to the TNZ and if present, where it lies.

The effect of heat therapy on blood pressure and peripheral vascular function: A systematic review and meta-analysis.

NEW FINDINGS: What is the topic of this review? We have conducted a systematic review and meta-analysis on the current evidence for the effect of heat therapy on blood pressure and vascular function. What advances does it highlight? We found that heat therapy reduced mean arterial, systolic and diastolic blood pressure. We also observed that heat therapy improved vascular function, as assessed via brachial artery flow-mediated dilatation. Our results suggest that heat therapy is a promising therapeutic tool that should be optimized further, via mode and dose, for the prevention and treatment of cardiovascular disease risk factors. ABSTRACT: Lifelong sauna exposure is associated with reduced cardiovascular disease risk. Recent studies have investigated the effect of heat therapy on markers of cardiovascular health. We aimed to conduct a systematic review with meta-analysis to determine the effects of heat therapy on blood pressure and indices of vascular function in healthy and clinical populations. Four databases were searched up to September 2020 for studies investigating heat therapy on outcomes including blood pressure and vascular function. Grading of Recommendations, Assessment, Development and Evaluations (GRADE) was used to assess the certainty of evidence. A total of 4522 titles were screened, and 15 studies were included. Healthy and clinical populations were included. Heat exposure was for 30-90 min, over 10-36 sessions. Compared with control conditions, heat therapy reduced mean arterial pressure [n = 4 studies; mean difference (MD): -5.86 mmHg, 95% confidence interval (CI): -8.63, -3.10; P < 0.0001], systolic blood pressure (n = 10; MD: -3.94 mmHg, 95% CI: -7.22, -0.67; P = 0.02) and diastolic blood pressure (n = 9; MD: -3.88 mmHg, 95% CI: -6.13, -1.63; P = 0.0007) and improved flow-mediated dilatation (n = 5; MD: 1.95%, 95% CI: 0.14, 3.76; P = 0.03). Resting heart rate was unchanged (n = 10; MD: -1.25 beats/min; 95% CI: -3.20, 0.70; P = 0.21). Early evidence also suggests benefits for arterial stiffness and cutaneous microvascular function. The certainty of evidence was moderate for the effect of heat therapy on systolic and diastolic blood pressure and heart rate and low for the effect of heat therapy on mean arterial pressure and flow-mediated dilatation. Heat therapy is an effective therapeutic tool to reduce blood pressure and improve macrovascular function. Future research should aim to optimize heat therapy, including the mode and dose, for the prevention and management of cardiovascular disease.

The sweat glands' maximum ion reabsorption rates following heat acclimation in healthy older adults.

NEW FINDINGS: What is the central question to this study? Do the sweat glands' maximum ion reabsorption rates increase following heat acclimation in healthy older individuals and is this associated with elevated aldosterone concentrations? What is the main finding and its importance? Sweat gland maximum ion reabsorption rates improved heterogeneously across body sites, which occurred without any changes in aldosterone concentration following a controlled hyperthermic heat acclimation protocol in healthy older individuals. ABSTRACT: We examined whether the eccrine sweat glands' ion reabsorption rates improved following heat acclimation (HA) in older individuals. Ten healthy older adults (>65 years) completed a controlled hyperthermic (+0.9°C rectal temperature, Tre ) HA protocol for nine non-consecutive days. Participants completed a passive heat stress test (lower leg 42°C water submersion) pre-HA and post-HA to assess physiological regulation of sweat gland ion reabsorption at the chest, forearm and thigh. The maximum ion reabsorption rate was defined as the inflection point in the slope of the relation between galvanic skin conductance and sweat rate (SR). We explored the responses again after a 7-day decay. During passive heating, the Tb thresholds for sweat onset on the chest and forearm were lowered after HA (P < 0.05). However, sweat sensitivity (i.e. the slope), the SR at a given Tre and gross sweat loss did not improve after HA (P > 0.05). Any changes observed were lost during the decay. Pilocarpine-induced sudomotor responses to iontophoresis did not change after HA (P ≥ 0.801). Maximum ion reabsorption rate was only enhanced at the chest (P = 0.001) despite unaltered aldosterone concentration after HA. The data suggest that this adaptation is lost after 7 days' decay. The HA protocol employed in the present study induced partial adaptive sudomotor responses. Eccrine sweat gland ion reabsorption rates improved heterogeneously across the skin sites. It is likely that aldosterone secretion did not alter the chest sweat ion reabsorption rates observed in the older adults.

Eccrine sweat glands' maximum ion reabsorption rates during passive heating in older adults (50-84 years).

PURPOSE: We examined whether eccrine sweat glands ion reabsorption rate declined with age in 35 adults aged 50-84 years. Aerobic fitness (VO2max) and salivary aldosterone were measured to see if they modulated ion reabsorption rates. METHODS: During a passive heating protocol (lower leg 42 °C water submersion) the maximum ion reabsorption rates from the chest, forearm and thigh were measured, alongside other thermophysiological responses. The maximum ion reabsorption rate was defined as the inflection point in the slope of the relation between galvanic skin conductance and sweat rate. RESULTS: The maximum ion reabsorption rate at the forearm, chest and thigh (0.29 ± 0.16, 0.33 ± 0.15, 0.18 ± 0.16 mg/cm2/min, respectively) were weakly correlated with age (r ≤ - 0.232, P ≥ 0.05) and salivary aldosterone concentrations (r ≤ - 0.180, P ≥ 0.179). A moderate positive correlation was observed between maximum ion reabsorption rate at the thigh and VO2max (r = 0.384, P = 0.015). Salivary aldosterone concentration moderately declined with age (r = - 0.342, P = 0.021). Whole body sweat rate and pilocarpine-induced sudomotor responses to iontophoresis increased with VO2max (r ≥ 0.323, P ≤ 0.027) but only moderate (r = - 0.326, P = 0.032) or no relations (r ≤ - 0.113, P ≥ 0.256) were observed with age. CONCLUSION: The eccrine sweat glands' maximum ion reabsorption rate is not affected by age, spanning 50-84 years. Aldosterone concentration in an aged cohort does not appear to modulate the ion reabsorption rate. We provide further support for maintaining cardiorespiratory fitness to attenuate any decline in sudomotor function.

Thermoregulation in the Aging Population and Practical Strategies to Overcome a Warmer Tomorrow.

As global temperatures continue to rise, improving thermal tolerance in the aged population is crucial to counteract age-associated impairments in thermoregulatory function. Impairments in reflex cutaneous vasodilation and sweating response can augment the vulnerability of older adults to heat-related injuries following exposure to heat stress. Mechanisms underlying a compromised cutaneous vasodilation are suggested to include reduced sympathetic neural drive, diminished cholinergic co-transmitter contribution, and altered second messenger signaling events. On the other hand, impairments in sweating response are ascribed to reduced sweat gland cholinergic sensitivity and altered cyclooxygenase and nitric oxide signaling. Several practical mitigation strategies such as exercise, passive heating, and behavioral adaptations are proposed as means to overcome heat stress and improve thermal tolerance in the aged. Aerobic exercise training is shown to be amongst the most effective ways to enhance thermoregulatory function. However, in elderly with limited exercise capability due to chronic diseases and mobility issues, passive heating can serve as a functional alternative as it has been shown to confer similar benefits to that of exercise training. Supplementary to exercise training and passive heating, behavioral adaptations can be applied to further enhance the heat-preparedness of the aged.

Elevating body termperature to reduce low-grade inflammation: a welcome strategy for those unable to exercise?

Chronic low-grade inflammation is increasingly recognized in the aetiology of a range of chronic diseases, including type 2 diabetes mellitus and cardiovascular disease, and may therefore serve as a promising target in their prevention or treatment. An acute inflammatory response can be induced by exercise; this is characterised by the acute increase in proinflammatory markers that subsequently stimulate the production of anti-inflammatory proteins. This may help explain the reduction in basal concentrations of pro-inflammatory markers following chronic exercise training. For sedentary populations, such as people with a disability, wheelchair users, or the elderly, the prevalence of chronic low-grade inflammation- related disease is further increased above that of individuals with a greater capacity to be physically active. Performing regular exercise with its proposed anti-inflammatory potential may not be feasible for these individuals due to a low physical capacity or other barriers to exercise. Therefore, alternatives to exercise that induce a transient acute inflammatory response may benefit their health. Manipulating body temperature may be such an alternative. Indeed, exercising in the heat results in a larger acute increase in inflammatory markers such as interleukin-6 and heat shock protein 72 when compared with exercising in thermoneutral conditions. Moreover, similar to exercise, passive elevation of body temperature can induce acute increases and chronic reductions in inflammatory markers and positively affect markers of glycaemic control. Here we discuss the potential benefits and mechanisms of active (i.e., exercise) and passive heating methods (e.g., hot water immersion, sauna therapy) to reduce chronic low-grade inflammation and improve metabolic health, with a focus on people who are restricted from being physically active.

Local knee heating increases spinal and supraspinal excitability and enhances plantar flexion and dorsiflexion torque production of the ankle in older adults.

PURPOSE: Aging is associated with progressive loss of active muscle mass and consequent decreases in resting metabolic rate and body temperature, and slowing of nerve conduction velocities and muscle contractility. These effectors compromise the ability of the elderly to maintain an upright posture during sudden balance perturbation, increase the risk of falls, and lead to self-imposed reduction in physical activity. Short-term superficial acute heating can modulate the neural drive transmission to exercising muscles without any marked change in deep-muscle temperature. METHODS: To determine whether the short-term (5 min) application of local passive knee-surface heating (next-to-skin temperature, ~ 44 °C) in healthy older subjects of both sexes (64-74 years; eight men/eight women) enhances reflex excitability, we compared the voluntarily and electrically induced ankle muscle torque production and contractile properties with those of healthy younger subjects of both sexes (21-35 years, 10 men/10 women). RESULTS: The application of local heating (vs. control) increased the maximal Hoffman reflex (Hmax), the maximal volitional wave (Vsup) amplitude, and the Hmax/Mmax amplitude ratio, and decreased Vsup latency only in older adults. In the older adults (vs. younger adults), the application of local heating (vs. control trial) was accompanied by a significant increase in maximal voluntary peak torque, rate of torque development, and isokinetic peak torque of plantar flexion/dorsiflexion muscle contraction. CONCLUSION: The spinal and supraspinal reflex excitability of older adults increased during local knee-heating application. The improved motor drive transmission observed in older adults was accompanied by increased voluntarily induced torque production of the ankle muscles during isometric/isokinetic contractions.

Muscle temperature kinetics and thermoregulatory responses to 42 °C hot-water immersion in healthy males and females.

PURPOSE: To determine the vastus lateralis muscle temperature kinetics during and after passive heating, to exam the effect of sex on thermoregulatory responses, and the thermal safety and tolerance of the 42 °C hot-water immersion protocol. METHODS: Thirty participants (15 males, 15 females) underwent a 2 h 42 ºC hot-water immersion to the waist level. Vastus lateralis, rectal and skin temperature, thermal sensation, heart rate and blood pressure (BP) were measured during the passive heating and recovery period. Participant recovery was monitored until muscle temperature returned to baseline. RESULTS: Vastus lateralis temperature increased to a maximal value of 39.0 ± 0.11 °C (P < 0.001), reaching a plateau after ~ 83.5 min of hot-water immersion and returning to baseline after ~ 115.8 min of recovery. Despite the anthropometric differences between males and females (e.g., height, body mass, body fat %, and fat thickness; P < 0.05), thermoregulatory responses showed no differences between sexes (P > 0.05). No change was found in systolic BP (~ 117 mmHg; P = 0.061). Peak rectal temperature (38.8 ± 0.14 °C; P < 0.001), heart rate (~ 100 bpm; P < 0.001), and diastolic BP (↓ ~ 13 mmHg; P < 0.001) during the hot-water immersion indicated the safety of the protocol. While skin temperature (~ 35.4 °C; P < 0.001) and thermal sensation (~ 5.95 AU; P < 0.001) confirmed protocol tolerance. CONCLUSION: These data demonstrate lower-body 42 °C hot-water immersion to increase vastus lateralis temperature and plateau ~ 2.8 °C above baseline. This amplitude of muscle temperature change aligns with reported cellular adaptation and muscle growth. Thermal strain incurred from this protocol appears safe and tolerable, positioning it well for health-related prescription.