Exercise-heat Acclimation Research Articles

Nutritional Considerations in Exercise-Based Heat Acclimation: A Narrative Review.

In addition to its established thermoregulatory and cardiovascular effects, heat stress provokes alterations in macronutrient metabolism, gastrointestinal integrity, and appetite. Inadequate energy, carbohydrate, and protein intake have been implicated in reduced exercise and heat tolerance. Classic exercise heat acclimation (HA) protocols employ low-to-moderate-intensity exercise for 5-14days, while recent studies have evolved the practice by implementing high-intensity and task-specific exercise during HA, which potentially results in impaired post-HA physical performance despite adequate heat adaptations. While there is robust literature demonstrating the performance benefit of various nutritional interventions during intensive training and competition, most HA studies implement few nutritional controls. This review summarizes the relationships between heat stress, HA, and intense exercise in connection with substrate metabolism, gastrointestinal function, and the potential consequences of reduced energy availability. We discuss the potential influence of macronutrient manipulations on HA study outcomes and suggest best practices to implement nutritional controls.

Impact of Exercise Heat Acclimation on Performance in Hot, Cool and Hypoxic Conditions

PurposeThe aim of this study was to confirm the impact of heat acclimation on aerobic performance in hot conditions and elucidate the transfer of heat adaptations to cool and hypoxic environments.MethodsTen males (VO2peak: 4.50 ± 0.50 L/min) completed two three-week interventions consisting of heat acclimation (HA: 36°C and 59% RH) and temperate training (TEMP: 18°C and 60% RH) in a counter-balanced crossover design. Training weeks consisted of four work-matched controlled heart rate sessions interspersed with one intermittent sprint session, and two rest days. Before and after the interventions VO2peak and 20-min time trial performance were evaluated in COOL (18°C), HOT (35°C) and hypoxic (HYP: 18°C and FiO2: 15.4%) conditions.ResultsFollowing HA, VO2peak increased significantly in HOT (0.24 L/min [0.01, 0.47], P = 0.040) but not COOL (P = 0.431) or HYP (P = 0.411), whereas TEMP had no influence on VO2peak (P ≥ 0.424). Mean time trial power output increased significantly in HOT (20 W [11, 28], P < 0.001) and COOL (12 W [4, 21], P = 0.004), but not HYP (7 W [−1, 16], P = 0.075) after HA, whereas TEMP had no influence on mean power output (P ≥ 0.110). Rectal (−0.13°C [−0.23, −0.03], P = 0.009) and skin (−0.7°C [−1.2, −0.3], P < 0.001) temperature were lower during the time trial in HOT after HA, whereas mean heart rate did not differ (P = 0.339).ConclusionsHA improved aerobic performance in HOT in conjunction with lower thermal strain and enhanced cardiovascular stability (similar heart rate for higher workload), whereas the mechanistic pathways improving performance in COOL and HYP remain unclear.

Recovery During Exercise Heat Acclimation: Will Post-Exercise Cooling Enhance or Interfere with Adaptation?

Recovery During Exercise Heat Acclimation: Will Post-Exercise Cooling Enhance or Interfere with Adaptation?

Auditing the Representation of Females Versus Males in Heat Adaptation Research.

The aim of this audit was to quantify female representation in research on heat adaptation. Using a standardized audit tool, the PubMed database was searched for heat adaptation literature from inception to February 2023. Studies were included if they investigated heat adaptation among female and male adults (≥18-50years) who were free from noncommunicable diseases, with heat adaptation the primary or secondary outcome of interest. The number and sex of participants, athletic caliber, menstrual status, research theme, journal impact factor, Altmetric score, Field-Weighted Citation Impact, and type of heat exposure were extracted. A total of 477 studies were identified in this audit, including 7,707 participants with ∼13% of these being female. Most studies investigated male-only cohorts (∼74%, n = 5,672 males), with ∼5% (n = 360 females) including female-only cohorts. Of the 126 studies that included females, only 10% provided some evidence of appropriate methodological control to account for ovarian hormone status, with no study meeting best-practice recommendations. Of the included female participants, 40% were able to be classified to an athletic caliber, with 67% of these being allocated to Tier 2 (i.e.,trained/developmental) or below. Exercise heat acclimation was the dominant method of heat exposure (437 interventions), with 21 studies investigating sex differences in exercise heat acclimation interventions. We recommend that future research on heat adaptation in female participants use methodological approaches that consider the potential impact of sexual dimorphism on study outcomes to provide evidence-based guidelines for female athletes preparing for exercise or competition in hot conditions.

Influence of exercise-heat acclimation protocol characteristics on adaptation kinetics: A systematic review with meta-analysis

Influence of exercise-heat acclimation protocol characteristics on adaptation kinetics: A systematic review with meta-analysis

A comparison of medium-term heat acclimation by post-exercise hot water immersion or exercise in the heat: adaptations, overreaching, and thyroid hormones.

This research compared thermal and perceptual adaptations, endurance capacity, and overreaching markers in men after 3, 6, and 12 days of post-exercise hot water immersion (HWI) or exercise heat acclimation (EHA) with a temperate exercise control (CON), and examined thyroid hormones as a mechanism for the reduction in resting and exercising core temperature (Tre) after HWI. HWI involved a treadmill run at 65% V̇o2peak at 19°C followed by a 40°C bath. EHA and CON involved a work-matched treadmill run at 65% V̇o2peak at 33°C or 19°C, respectively. Compared with CON, resting mean body temperature (Tb), resting and end-exercise Tre, Tre at sweating onset, thermal sensation, and perceived exertion were lower and whole-body sweat rate (WBSR) was higher after 12 days of HWI (all P ≤ 0.049, resting Tb: CON -0.11 ± 0.15°C, HWI -0.41 ± 0.15°C). Moreover, resting Tb and Tre at sweating onset were lower after HWI than EHA (P ≤ 0.015, resting Tb: EHA -0.14 ± 0.14°C). No differences were identified between EHA and CON (P ≥ 0.157) except WBSR that was greater after EHA (P = 0.013). No differences were observed between interventions for endurance capacity or overreaching markers (mood, sleep, Stroop, P ≥ 0.190). Thermal adaptations observed after HWI were not related to changes in thyroid hormone concentrations (P ≥ 0.086). In conclusion, 12 days of post-exercise hot water immersion conferred more complete heat acclimation than exercise heat acclimation without increasing overreaching risk, and changes in thyroid hormones are not related to thermal adaptations after post-exercise hot water immersion.

Different dehydration levels and their impact on blood ammonia, cognitive-motor performance, and muscle damage in acclimated runners.

Prolonged exercise in the heat can promote dehydration, which could impair ammonia metabolism, cognitive-motor performance, and muscle damage. However, exercise heat acclimation induces physiological adaptations that improve performance, metabolism, and cellular protection. This study aimed to evaluate different dehydration levels and their impact on blood ammonia, cognitive-motor performance, and muscle damage after a race in the heat in acclimated runners. Sixteen male amateur endurance runners performed a half marathon race. After the race, the runners were divided into two groups according to their percentage body mass change (Δ% BM): Δ% BM less than 3% (G1%; N.=8) and Δ% BM greater than or equal to 3% (G3%; N.=8). Hydration status, biochemical parameters, and cognitive-motor performance were assessed before and after the race. Blood ammonia concentrations were increased in both G1% (before: 46±26 µmol/L; after: 118±22 µmol/L) and G3% (before: 41±15 µmol/L; after: 108±15 µmol/L) groups. There was an early increase in all markers of muscle damage (creatine kinase [CK], lactate dehydrogenase [LDH], aspartate aminotransferase [AST], and alanine aminotransferase [ALT]) in both groups, but only LDH was greater in the G3% group than in the G1% group. Cognitive-motor performance did not differ between groups. Dehydration up to ~4% BM loss does not affect blood ammonia concentrations and cognitive-motor performance in acclimated runners. The results also suggest that exercising in the heat induces the early appearance of several markers of muscle damage in acclimated runners regardless of hydration status.

Exercise Heat Acclimation With Dehydration Does Not Affect Vascular and Cardiac Volumes or Systemic Hemodynamics During Endurance Exercise.

Permissive dehydration during exercise heat acclimation (HA) may enhance hematological and cardiovascular adaptations and thus acute responses to prolonged exercise. However, the independent role of permissive dehydration on vascular and cardiac volumes, ventricular-arterial (VA) coupling and systemic hemodynamics has not been systematically investigated. Seven males completed two 10-day exercise HA interventions with controlled heart rate (HR) where euhydration was maintained or permissive dehydration (-2.9 ± 0.5% body mass) occurred. Two experimental trials were conducted before and after each HA intervention where euhydration was maintained (-0.5 ± 0.4%) or dehydration was induced (-3.6 ± 0.6%) via prescribed fluid intakes. Rectal (Tre) and skin temperatures, HR, blood (BV) and left ventricular (LV) volumes, and systemic hemodynamics were measured at rest and during bouts of semi-recumbent cycling (55% V̇O2peak) in 33°C at 20, 100, and 180 min. Throughout HA sweat rate (12 ± 9%) and power output (18 ± 7 W) increased (P < 0.05), whereas Tre was 38.4 ± 0.2°C during the 75 min of HR controlled exercise (P = 1.00). Neither HA intervention altered resting and euhydrated exercising Tre, BV, LV diastolic and systolic volumes, systemic hemodynamics, and VA coupling (P > 0.05). Furthermore, the thermal and cardiovascular strain during exercise with acute dehydration post-HA was not influenced by HA hydration strategy. Instead, elevations in Tre and HR and reductions in BV and cardiac output matched pre-HA levels (P > 0.05). These findings indicate that permissive dehydration during exercise HA with controlled HR and maintained thermal stimulus does not affect hematological or cardiovascular responses during acute endurance exercise under moderate heat stress with maintained euhydration or moderate dehydration.

Exercise heat acclimation causes human responses and safety performance improvements.

Heat acclimation (HA) is a widely recognized physiological phenomenon of human body in hot environments. HA has many benefits, such aspreventing hyperthermia responses, and is an efficient way to improve human responses to hyperthermal environments. However, it is not known whether HA is dependent on the environmental conditions. Moreover, its mechanism and effect on the safety performance remain unexplored. In this study, we created a climate chamber to simulate a hyperthermal environment. Thirty healthy males were recruited for this study, who were then trained under the same ambient conditions (temperature of 38°C and relative humidity (RH) of 40%). The training involved running on treadmills (at 5km/h) to simulate heavy manual labor, and performing heat stress tests (HST) under six different conditions (32°C/40% RH, 35°C/40%, 38°C/40%, 32°C/70%, 35°C/70%, and 38°C/70%). Their physiological indices (rectal temperature, heart rate, sweat loss and skin temperature) and one psychological index (thermal sensation) were measured. Furthermore, a hazard avoidance test device (HATD) was designed to evaluate the individual safety performance by detecting human errors. The results show that training and environmental conditions have different effects on HA. After HA, the physiological and psychological strain were significantly improved. More importantly, HA also helped improve the participants' awareness of the dangers and required emergency responses to face potential hazards. Overall, a reasonable HA training under proper conditions is helpful to ensure the safety of human beings. More research is needed to study the role of HA on safety performance.

Exercise heat acclimation and post-exercise hot water immersion improve resting and exercise responses to heat stress in the elderly

ObjectivesTo investigate the efficacy of heat acclimation (HA) in the young (YEX) and elderly (EEX) following exercise-HA, and the elderly utilising post-exercise hot water immersion HA (EHWI). DesignCross-sectional study. MethodTwenty-six participants (YEX: n = 11 aged 22 ± 2 years, EEX:n = 8 aged 68 ± 3 years, EHWI: n = 7 aged 73 ± 3 years) completed two pre-/post-tests, separated by five intervention days. YEX and EEX exercised in hot conditions to raise rectal temperature (Trec) ≥38.5 °C within 60 min, with this increase maintained for a further 60 min. EHWI completed 30 min of cycling in temperate conditions, then 30 min of HWI (40 °C), followed by 30 min seated blanket wrap. Pre- and post-testing comprised 30 min rest, followed by 30 min of cycling exercise (3.5 W·kg−1 Ḣprod), and a six-minute walk test (6MWT), all in 35 °C, 50% RH. ResultsThe HA protocols did not elicit different mean heart rate (HR), Trec, and duration Trec ≥ 38.5 °C (p > 0.05) between YEX, EEX, and EHWI groups. Resting Trec, peak skin temperature, systolic and mean arterial pressure, perceived exertion and thermal sensation decreased, and 6MWT distance increased pre- to post-HA (p < 0.05), with no difference between groups. YEX also demonstrated a reduction in resting HR (p < 0.05). No change was observed in peak Trec or HR, vascular conductance, sweat rate, or thermal comfort in any group (p > 0.05). ConclusionsIrrespective of age or intervention, HA induced thermoregulatory, perceptual and exercise performance improvements. Both exercise-HA (EEX), and post-exercise HWI (EHWI) are considered viable interventions to prepare the elderly for heat stress.

A comparison of heat acclimation by post-exercise hot water immersion and exercise in the heat

ObjectivesTo compare heat acclimation adaptations after three and six days of either post-exercise hot water immersion (HWI) or exercise-heat-acclimation (EHA) in recreationally active individuals. DesignRandomised, mixed model, repeated measures. MethodsPost-exercise HWI involved a daily 40-min treadmill-run at 65% V̇O2peak in temperate conditions (19 °C, 45% RH) followed by HWI (≤40 min, 40 °C water; n = 9). Daily EHA involved a ≤60-min treadmill-run in the heat (65% V̇O2peak; 33 °C, 40% RH; n = 9), chosen to elicit a similar endogenous thermal stimulus to HWI. A thermoneutral exercise intervention (TNE, 19 °C, 45% RH; n = 9), work-matched to EHA, was also included to determine thermoregulatory adaptations to daily exercise in temperate conditions. An exercise-heat-stress-test was performed before and after three and six intervention days and involved a 40-min treadmill-run and time-to-exhaustion (TTE) at 65% V̇O2peak in the heat (33 °C, 40% RH). ResultsANCOVA, using baseline values as the covariate, revealed no interaction effects but significant group effects demonstrated that compared to EHA, HWI elicited larger reductions in resting rectal temperature (Tre; p = 0.021), Tre at sweating onset (p = 0.011), and end-exercise Tre during exercise-heat-stress (−0.47 °C; p = 0.042). Despite a similar endogenous thermal stimulus to HWI, EHA elicited a modest reduction in end-exercise Tre (−0.26 °C), which was not different from TNE (−0.25 °C, p = 1.000). There were no main effects or interaction effects for end-exercise Tsk, heart rate, physiological strain index, RPE, thermal sensation, plasma volume, or TTE (all p ≥ 0.154). ConclusionsCompared with conventional short-term exercise heat acclimation, short-term post-exercise hot water immersion elicited larger thermal adaptations.

Effects of short-term heat acclimation on whole-body heat exchange and local nitric oxide synthase- and cyclooxygenase-dependent heat loss responses in exercising older men.

What is the central question of this study? Does short-term heat acclimation enhance whole-body evaporative heat loss and augment nitric oxide synthase (NOS)-dependent cutaneous vasodilatation and NOS- and cyclooxygenase (COX)-dependent sweating, in exercising older men? What is the main finding and its importance? Our preliminary data (n=8) demonstrated that short-term heat acclimation improved whole-body evaporative heat loss, but it did not influence the effects of NOS and/or COX inhibition on cutaneous vasodilatation or sweating in older men during an exercise-heat stress. These outcomes might imply that although short-term heat acclimation enhances heat dissipation in older men, it does not modulate NOS- and COX-dependent control of cutaneous vasodilatation or sweating on the forearm. Ageing is associated with decrements in whole-body heat loss (evaporative+dry heat exchange), which might stem from alterations in nitric oxide synthase (NOS)- and cyclooxygenase (COX)-dependent cutaneous vasodilatation and sweating. We evaluated whether short-term heat acclimation would (i) enhance whole-body heat loss primarily by increasing evaporative heat loss, and (ii) augment NOS-dependent cutaneous vasodilatation and NOS- and COX-dependent sweating, in exercising older men. Eight older men [mean (SD) age, 59(8)years] completed a calorimetry and microdialysis trial before and after 7days of exercise-heat acclimation. For the calorimetry trials, whole-body evaporative and dry heat exchange were assessed using direct calorimetry during 30min bouts of cycling at light, moderate and vigorous metabolic heat productions (150, 200 and 250W/m2 , respectively) in dry heat (40°C, 20% relative humidity). For the microdialysis trials, local cutaneous vascular conductance and sweat rate were assessed during 60min exercise in the heat (35°C, 20% relative humidity) at four dorsal forearm skin sites treated with lactated Ringer solution (control), NOS inhibitor, COX inhibitor or combined NOS and COX inhibitors, via microdialysis. Evaporative heat loss during moderate (P=0.036) and vigorous (P=0.021) exercise increased after acclimation. Inhibition of NOS alone reduced cutaneous vascular conductance to a similar extent before and after acclimation (P<0.040), whereas separate and combined NOS and COX inhibition had no significant effects on sweating relative to the control site (P=0.745). Our preliminary results might suggest that short-term heat acclimation improves evaporative heat loss, but does not significantly modulate the contributions of NOS or COX to cutaneous vasodilatation or sweating on the forearm in older men during an exercise-heat stress.

Effect of exercise-heat acclimation on cardiac autonomic modulation in type 2 diabetes: a pilot study.

The effects of exercise-heat acclimation on heart rate variability (HRV) in individuals with type 2 diabetes (T2D) remains unclear. We assessed electrocardiogram recordings during exercise-heat stress in middle-aged-to-older individuals (50-70 years) with (n= 6) and without (control; n= 8;) T2D, before and after 7 days of exercise-heat acclimation. Exercising heart rate was reduced (control, -9 ± 5 bpm; T2D, -14 ± 9 bpm) yet HRV was not significantly different. Given the negative correlations between diminished HRV and cardiac risk observed in the scientific literature, further research is warranted. Novelty: Our observations indicate that 7 days exercise-heat acclimation may not effectively attenuate the deviation toward reduced overall HRV and unfavourable cardiac autonomic modulation in individuals with T2D.

Exercise heat acclimation has minimal effects on left ventricular volumes, function and systemic hemodynamics in euhydrated and dehydrated trained humans.

Heat acclimation (HA) may improve the regulation of cardiac output (Q̇) through increased blood volume (BV) and left ventricular (LV) diastolic filling and attenuate reductions in Q̇ during exercise-induced dehydration; however, these hypotheses have never been directly tested. Before and following 10-days exercise HA, eight males completed two trials of submaximal exercise in 33°C and 50% relative humidity while maintaining preexercise euhydrated body mass (EUH; -0.6 ± 0.4%) or becoming progressively dehydrated (DEH; -3.6 ± 0.7%). Rectal (Tre) and skin (Tsk) temperatures, heart rate (HR), LV volumes and function, systemic hemodynamics and BV were measured at rest and during bouts of semirecumbent cycling (55% V̇o2max) at 20, 100 and 180 min, interspersed by periods of upright exercise. Tre, BV, HR, LV volumes, LV systolic and diastolic function, and systemic hemodynamics were similar between trials at rest and during the first 20 min of exercise (all P > 0.05). These responses were largely unaffected by HA at 180 min in either hydration state. However, DEH induced higher Tre (0.6 ± 0.3°C) and HR (16 ± 7 beats/min) and lower end-diastolic volume (29 ± 16 mL), stroke volume (26 ± 16 mL), and Q̇ (2.1 ± 0.8 L/min) compared with EUH at 180 min (all P < 0.05), yet LV twist and untwisting rate were increased or maintained (P = 0.028 and 0.52, respectively). Findings indicate HA has minimal effects on LV volumes, LV mechanical function, and systemic hemodynamics during submaximal exercise in moderate heat, where HR and BV are similar. In contrast, DEH evokes greater hyperthermia and tachycardia, reduces BV, and impairs diastolic LV filling, lowering Q̇, regardless of HA state.NEW & NOTEWORTHY This study demonstrates that 10 days of exercise heat acclimation has minimal effects on left ventricular volumes, intrinsic cardiac function, and systemic hemodynamics during prolonged, repeated semirecumbent exercise in moderate heat, where heart rate and blood volume are similar to preacclimation levels. However, progressive dehydration is consistently associated with similar degrees of hyperthermia and tachycardia and reductions in blood volume, diastolic filling of the left ventricle, stroke volume, and cardiac output, regardless of acclimation state.

Inter-individual Variability In Rate Of Heat Acclimation Using A Standard, Fixed Intensity Protocol

In combination with increases in core temperature (Tc) during acute exercise in the heat, progressive increases in heart rate (HR) contribute to increased cardiovascular strain as compared to the same exercise performed in cooler conditions. It is well-established that heat acclimation (HA), defined by both thermal and cardiovascular adaptations (lower Tc and HR), is achieved within ~7 to 10 days of repeated exercise for 60-120 min or more in the heat. More recent research indicates that HA can be achieved in <7 days, also referred to as short-term heat acclimation (STHA). PURPOSE: To quantify the occurrence and magnitude of STHA in a group of young healthy males participating in a standard, 8-day military HA protocol. We hypothesized that some but not all volunteers would achieve STHA. METHODS: Thirteen healthy male volunteers (age 21 ± 3 yrs, ht: 173 ± 8 cm, wt: 75.1 ± 12.2 kg) participated in an 8 day exercise-heat acclimation protocol (120 minutes of treadmill walking: 3.1 mi·hr-1, 2% grade, in 40°C, 40% RH). Tc and HR were recorded every 5 minutes. Pre-and post-exercise nude body-weight (corrected for urine output) were used to calculate total body sweat rate (SR). Individual and group mean (ANOVA) changes in final Tc, HR, and SR were compared across Days 1, 5, and 8 of HA. The criteria for achievement of HA were ΔTc during exercise ≤ 0.9 °C and ΔHR ≤ 33 bpm, which were based on average values attained at Day 8. RESULTS: Group mean Tc (Day 1: 38.1 ± 0.34 vs. Day 5: 37.9 ± 0.3 vs. Day 8: 37.8 ± 0.3°C) and HR (Day 1: 134 ± 17 vs. Day 5: 122 ± 13 vs. Day 8: 121 ± 13 bpm) were significantly decreased by Day 5 (p<0.05) and did not decrease further by Day 8 (p>0.05). Using our criteria for achieving HA, 31% (4/13) of the volunteers achieved HA on Day 5. SR was not different across time points (Day 1: 860 ± 148 vs. Day 5: 908 ± 210 vs. Day 8: 873 ± 203 ml·hr-1; p>0.05). CONCLUSIONS: These data suggest that during a standard fixed-intensity heat acclimation protocol, about one third of the volunteers will achieve STHA with no further change in Tc or HR responses beyond Day 5. Future research should evaluate the mechanisms contributing to the variability of achieving STHA. Supported by USAMRDC; author views not official US Army or DoD policy.

Effect of 8 days of exercise-heat acclimation on aerobic exercise performance of men in hypobaric hypoxia.

Exercise-heat acclimation (EHA) induces adaptations that improve tolerance to heat exposure. Whether adaptations from EHA can also alter responses to hypobaric hypoxia (HH) conditions remains unclear. This study assessed whether EHA can alter time-trial performance and/or incidence of acute mountain sickness (AMS) during HH exposure. Thirteen sea-level (SL) resident men [SL peak oxygen consumption (V̇o2peak) 3.19 ± 0.43 L/min] completed steady-state exercise, followed by a 15-min cycle time trial and assessment of AMS before (HH1; 3,500 m) and after (HH2) an 8-day EHA protocol [120 min; 5 km/h; 2% incline; 40°C and 40% relative humidity (RH)]. EHA induced lower heart rate (HR) and core temperature and plasma volume expansion. Time-trial performance was not different between HH1 and HH2 after 2 h (106.3 ± 23.8 vs. 101.4 ± 23.0 kJ, P = 0.71) or 24 h (107.3 ± 23.4 vs. 106.3 ± 20.8 kJ, P > 0.9). From HH1 to HH2, HR and oxygen saturation, at the end of steady-state exercise and time-trial tests at 2 h and 24 h, were not different (P > 0.05). Three of 13 volunteers developed AMS during HH1 but not during HH2, whereas a fourth volunteer only developed AMS during HH2. Heat shock protein 70 was not different from HH1 to HH2 at SL [1.9 ± 0.7 vs. 1.8 ± 0.6 normalized integrated intensities (NII), P = 0.97] or after 23 h (1.8 ± 0.4 vs. 1.7 ± 0.5 NII, P = 0.78) at HH. Our results indicate that this EHA protocol had little to no effect-neither beneficial nor detrimental-on exercise performance in HH. EHA may reduce AMS in those who initially developed AMS; however, studies at higher elevations, having higher incidence rates, are needed to confirm our findings.

Heat acclimation does not modify autonomic responses to core cooling and the skin thermal comfort zone.

Exercise heat acclimation (HA) is known to magnify the sweating response by virtue of a lower threshold as well as increased gain and maximal capacity of sweating. However, HA has been shown to potentiate the shivering response in a cold-air environment. We investigated whether HA would alter heat loss and heat production responses during water immersion. Twelve healthy male participants underwent a 10-day HA protocol comprising daily 90-min controlled-hyperthermia (target rectal temperature, Tre 38.5°C) exercise sessions. Preceding and following HA, the participants performed a maximal exercise test in thermoneutral conditions (ambient temperature 23°C, relative humidity 50%) and were, following exercise, immersed in 28°C water for 60min. Thermal comfort zone (TCZ) was also assessed with participants regulating the temperature of a water-perfused suit during heating and cooling. Baseline pre-immersion Tre was similar pre- and post-HA (pre: 38.33±0.33°C vs post: 38.12±0.36°C, p=0.092). The Tre cooling rate was identical pre-to post-HA (-0.03±0.01°C·min-1, p=0.31), as was the vasomotor response reflected in the forearm-fingertip temperature difference. Shivering thresholds (p=0.43) and gains (p=0.61) were not affected by HA. TCZ was established at similar temperatures, with the magnitude in regulated water temperature being 7.6 (16.3) °C pre-HA and 5.1 (24.7) °C post-HA (p=0.65). The present findings suggest that heat production and heat loss responses during whole body cooling as well as the skin thermal comfort zone remained unaltered by a controlled-hyperthermia HA protocol.

Hematological Adaptations to Prolonged Heat Acclimation in Endurance-Trained Males.

Heat acclimation is associated with plasma volume (PV) expansion that occurs within the first week of exposure. However, prolonged effects on hemoglobin mass (Hbmass) are unclear as intervention periods in previous studies have not allowed sufficient time for erythropoiesis to manifest. Therefore, Hbmass, intravascular volumes, and blood volume (BV)-regulating hormones were assessed with 5½ weeks of exercise-heat acclimation (HEAT) or matched training in cold conditions (CON) in 21 male cyclists [(mean ± SD) age: 38 ± 9 years, body weight: 80.4 ± 7.9 kg, VO2peak: 59.1 ± 5.2 ml/min/kg]. HEAT (n = 12) consisted of 1 h cycling at 60% VO2peak in 40°C for 5 days/week in addition to regular training, whereas CON (n = 9) trained exclusively in cold conditions (<15°C). Before and after the intervention, Hbmass and intravascular volumes were assessed by carbon monoxide rebreathing, while reticulocyte count and BV-regulating hormones were measured before, after 2 weeks and post intervention. Total training volume during the intervention was similar (p = 0.282) between HEAT (509 ± 173 min/week) and CON (576 ± 143 min/week). PV increased (p = 0.004) in both groups, by 303 ± 345 ml in HEAT and 188 ± 286 ml in CON. There was also a main effect of time (p = 0.038) for Hbmass with +34 ± 36 g in HEAT and +2 ± 33 g in CON and a tendency toward a higher increase in Hbmass in HEAT compared to CON (time × group interaction: p = 0.061). The Hbmass changes were weakly correlated to alterations in PV (r = 0.493, p = 0.023). Reticulocyte count and BV-regulating hormones remained unchanged for both groups. In conclusion, Hbmass was slightly increased following prolonged training in the heat and although the mechanistic link remains to be revealed, the increase could represent a compensatory response in erythropoiesis secondary to PV expansion.

Exercise heat acclimation causes post-exercise hypotension and favorable improvements in lipid and immune profiles: A crossover randomized controlled trial

Passive hyperthermic exposure causes an acute hypotensive response following the cessation of heat stress. Chronic heat stress is well documented in animal studies to instigate metabolic and lipid alterations. However, it is unknown if exercise-heat acclimation also causes favorable chronic blood pressure, lipid, and immune responses in humans. This project tested the hypothesis that 10-day exercise-heat acclimation (HA) would cause greater post-exercise reductions in arterial blood pressure and favorable metabolic, lipid, and immune responses compared to 10-day exercise under neutral conditions (CON). Thirteen healthy sedentary participants (8M/5F, 28 ± 6y, 78 ± 17 kg), completed a 10-day (90 min/day exercise bout) clamped hyperthermia HA (increase internal temperature 1.5 °C, in 42 °C, 28% Rh) and control (CON: 23 °C, 42% Rh) protocols in a counterbalanced design with a 2 month washout. Pre- and post-exercise HA/CON blood pressures were taken 1-h post-exercise on exercise days 1 and 10. Metabolic, lipid and immune panels were taken pre-post HA/CON. Exercise under heat stress had greater post-exercise hypotension (systolic; -6 mmHg, diastolic; -8 mmHg; and mean arterial pressure; -7 mmHg) on both days 1 and 10 compared to exercise under neutral conditions (main effect for condition, P ≤ 0.004). Only from pre-to-post HA, total cholesterol (168 ± 19 to 157 ± 15; P < 0.03) and triglycerides (137 ± 45 to 111 ± 30; P < 0.03) were reduced, while absolute lymphocytes (-26%), monocytes (-22%), and basophils (-49%) significantly decreased (each P ≤ 0.04). Relative values of neutrophils increased (18%) and lymphocytes decreased (-20%) only after HA (P ≤ 0.04). These data indicate that exercise in the heat (regardless of acclimation status) causes a profound post-exercise hypotensive response, while HA causes favorable lipid, and immune profile changes. Further examination of exercise-heat acclimation on vascular, metabolic, and immune responses will offer insight for benefits in other clinical populations with vascular, metabolic and immune dysfunction.

High-intensity Interval Training In The Heat: A "hotter" Alternative For Promoting Cardiovascular Health And Performance?

Chronic heat exposure during exercise, exercise heat acclimation (EHA), and high-intensity interval training (HIIT) both promote positive physiological and performance adaptations; however, it remains unknown if HIIT acts synergistically with EHA compounding the performance benefit of HIIT. PURPOSE: To investigate the effects of HIIT and EHA (HIIT+Heat) on cardiovascular function (CV), endurance running performance, and muscle function vs. HIIT alone. METHODS: Using a randomized controlled parallel-design, 10 young healthy males and females completed 6 sessions of HIIT (8 x 30s on, 90s off) performed either in the heat (HIIT+Heat, 30°C, 50% RH) or thermoneutral (HIIT, ~20°C, 15% RH) condition. Measures of cardiovascular and muscle function, running performance and economy were measured prior to, and >72hr post, training in a thermoneutral environment. A 5 km time-trial and graded treadmill protocol were conducted to assess for running performance and economy, while power and velocity during maximal vertical jump were used to assess muscle function. CV function was assessed via, heart rate (HR), HR variability (HRV; root mean square of successive differences; RMSSD, and standard deviation of N-N intervals; SDNN), central (cBP), peripheral blood pressure (pBP), and pulse wave velocity (PWV). RESULTS: No baseline differences were observed between groups. No differences in performance improvement (-4 ± 2 vs. -4 ± 4%∆ in 5km time) or running economy were observed between groups (p>0.05). Resting HR (-2 ± 3 vs. -2 ± 2 %∆) and HRV (SDNN 5 ±2 vs. 11 ±4%) were improved in both groups but were not different between conditions (HIIT vs. HIIT+Heat, p>0.05). However, cSBP (1 ± 2 vs. -7 ± 3 %∆), pSBP (-2 ± 2 vs. -8 ± 2%∆), and PWV (0 ± 1 vs. -6 ±3%∆) only decreased in the HIIT+Heat (HIIT vs. HIIT+heat, respectively, all p<0.05). Improvements in jump velocity (-3 ± 5 vs. 8 ± 5%∆) and power (-2 ± 5 vs. 9 ± 6%∆) tended be greater in HIIT+heat (p=0.08-0.10). CONCLUSION: Short term HIIT combined with heat stress did not improve running performance or economy more than HIIT alone, but did significantly improve blood pressure, vascular stiffness, and tended to improve muscle function in thermoneutral conditions. Further work exploring longer training and/or greater heat stress in larger populations, or those with vascular dysfunction, is warranted.