Heat-related changes in the velocity and kinetic energy of flowing blood influence the human heart's output during hyperthermia.

Passive whole-body hyperthermia increases limb blood flow and cardiac output ( Q ̇ $\dot Q$ ), but the interplay between peripheral and central thermo-haemodynamic mechanisms remains unclear. Here we tested the hypothesis that local hyperthermia-induced alterations in peripheral blood flow and blood kinetic energy modulate flow to the heart and Q ̇ $\dot Q$ . Body temperatures, regional (leg, arm, head) and systemic haemodynamics, and left ventricular (LV) volumes and functions were assessed in eight healthy males during: (1) 3 h control (normothermic condition); (2) 3 h of single-leg heating; (3) 3 h of two-leg heating; and (4) 2.5 h of whole-body heating. Leg, forearm, and extracranial blood flow increased in close association with local rises in temperature while brain perfusion remained unchanged. Increases in blood velocity with small to no changes in the conduit artery diameter underpinned the augmented limb and extracranial perfusion. In all heating conditions, Q ̇ $\dot Q$ increased in association with proportional elevations in systemic vascular conductance, related to enhanced blood flow, blood velocity, vascular conductance and kinetic energy in the limbs and head (all R2 ≥ 0.803; P < 0.001), but not in the brain. LV systolic (end-systolic elastance and twist) and diastolic functional profiles (untwisting rate), pulmonary ventilation and systemic aerobic metabolism were only altered in whole-body heating. These findings substantiate the idea that local hyperthermia-induced selective alterations in peripheral blood flow modulate the magnitude of flow to the heart and Q ̇ $\dot Q$ through changes in blood velocity and kinetic energy. Localised heat-activated events in the peripheral circulation therefore affect the human heart's output. KEY POINTS: Local and whole-body hyperthermia increases limb and systemic perfusion, but the underlying peripheral and central heat-sensitive mechanisms are not fully established. Here we investigated the regional (leg, arm and head) and systemic haemodynamics (cardiac output: Q ̇ $\dot Q$ ) during passive single-leg, two-leg and whole-body hyperthermia to determine the contribution of peripheral and central thermosensitive factors in the control of human circulation. Single-leg, two-leg, and whole-body hyperthermia induced graded increases in leg blood flow and Q ̇ $\dot Q$ . Brain blood flow, however, remained unchanged in all conditions. Ventilation, extracranial blood flow and cardiac systolic and diastolic functions only increased during whole-body hyperthermia. The augmented Q ̇ $\dot Q$ with hyperthermia was tightly related to increased limb and head blood velocity, flow and kinetic energy. The findings indicate that local thermosensitive mechanisms modulate regional blood velocity, flow and kinetic energy, thereby controlling the magnitude of flow to the heart and thus the coupling of peripheral and central circulation during hyperthermia.

Cross-adaptation from heat stress to hypoxia: A systematic review and exploratory meta-analysis.

Cross-adaptation (CA) refers to the successful induction of physiological adaptation under one environmental stressor (e.g., heat), to enable subsequent benefit in another (e.g., hypoxia). This systematic review and exploratory meta-analysis investigated the effect of heat acclimation (HA) on physiological, perceptual and physical performance outcome measures during rest, and submaximal and maximal intensity exercise in hypoxia. Database searches in Scopus and MEDLINE were performed. Studies were included when they met the Population, Intervention, Comparison, and Outcome criteria, were of English-language, peer-reviewed, full-text original articles, using human participants. Risk of bias and study quality were assessed using the COnsensus based Standards for the selection of health status Measurement INstruments checklist. Nine studies were included, totalling 79 participants (100 % recreationally trained males). The most common method of HA included fixed-intensity exercise comprising 9 ± 3 sessions, 89 ± 24-min in duration and occurred within 39 ± 2 °C and 32 ± 13 % relative humidity. CA induced a moderate, beneficial effect on physiological measures at rest (oxygen saturation: g = 0.60) and during submaximal exercise (heart rate: g = -0.65, core temperature: g = -0.68 and skin temperature: g = -0.72). A small effect was found for ventilation (g = 0.24) and performance measures (peak power: g = 0.32 and time trial time: g = -0.43) during maximal intensity exercise. No effect was observed for perceptual outcome measures. CA may be appropriate for individuals, such as occupational or military workers, whose access to altitude exposure prior to undertaking submaximal activity in hypoxic conditions is restricted. Methodological variances exist within the current literature, and females and well-trained individuals have yet to be investigated. Future research should focus on these cohorts and explore the mechanistic underpinnings of CA.

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.

Changes in gastrointestinal cell integrity after marathon running and exercise-associated collapse.

PURPOSE: Endurance exercise and hyperthermia are associated with compromised intestinal permeability and endotoxaemia. The presence of intestinal fatty acid-binding protein (I-FABP) in the systemic circulation suggests intestinal wall damage, but this marker has not previously been used to investigate intestinal integrity after marathon running. METHODS: Twenty-four runners were recruited as controls prior to completing a standard marathon and had sequential I-FABP measurements before and on completion of the marathon, then at four and 24 h later. Eight runners incapacitated with exercise-associated collapse (EAC) with hyperthermia had I-FABP measured at the time of collapse and 1 hour later. RESULTS: I-FABP was increased immediately on completing the marathon (T0; 2593 ± 1373 ng·l-1) compared with baseline (1129 ± 493 ng·l-1; p < 0.01) in the controls, but there was no significant difference between baseline and the levels at four hours (1419 ± 1124 ng·l-1; p = 0.7), or at 24 h (1086 ± 302 ng·l-1; p = 0.5). At T0, EAC cases had a significantly higher I-FABP concentration (15,389 ± 8547 ng.l-1) compared with controls at T0 (p < 0.01), and remained higher at 1 hour after collapse (13,951 ± 10,476 ng.l-1) than the pre-race control baseline (p < 0.05). CONCLUSION: I-FABP is a recently described biomarker whose presence in the circulation is associated with intestinal wall damage. I-FABP levels increase after marathon running and increase further if the endurance exercise is associated with EAC and hyperthermia. After EAC, I-FABP remains high in the circulation for an extended period, suggesting ongoing intestinal wall stress.

Short-Term Heat Acclimation and Precooling, Independently and Combined, Improve 5-km Time Trial Performance in the Heat.

James, CA, Richardson, AJ, Watt, PW, Willmott, AGB, Gibson, OR, and Maxwell, NS. Short-term heat acclimation and precooling, independently and combined, improve 5-km time trial performance in the heat. J Strength Cond Res 32(5): 1366-1375, 2018-Following heat acclimation (HA), endurance running performance remains impaired in hot vs. temperate conditions. Combining HA with precooling (PC) demonstrates no additive benefit in intermittent sprint, or continuous cycling exercise protocols, during which heat strain may be less severe compared to endurance running. This study investigated the effect of short-term HA (STHA) combined with mixed methods PC, on endurance running performance and directly compared PC and HA. Nine amateur trained runners completed 5-km treadmill time trials (TTs) in the heat (32° C, 60% relative humidity) under 4 conditions; no intervention (CON), PC, short-term HA (5 days-HA) and STHA with PC (HA + PC). Mean (±SD) performance times were; CON 1,476 (173) seconds, PC 1,421 (146) seconds, HA 1,378 (116) seconds and HA + PC 1,373 (121) seconds. This equated to the following improvements versus CON; PC -3.7%, HA -6.6% and HA + PC -7.0%. Statistical differences were only observed between HA and CON (p = 0.004, d = 0.68, 95% CI [-0.27 to 1.63]) however, similar effect sizes were observed for HA + PC vs. CON (d = 0.70, 95% CI [-0.25 to 1.65]), with smaller effects between PC vs. CON (d = 0.34, 95% CI [-0.59 to 1.27]), HA vs. PC (d = 0.33, 95% CI [-0.60 to 1.26]) and HA + PC vs. PC (d = 0.36, 95% CI [-0.57 to 1.29]). Pilot testing revealed a TT typical error of 16 seconds (1.2%). Precooling offered no further benefit to performance in the acclimated individual, despite modest alleviation of physiological strain. Maintenance of running speed in HA + PC, despite reduced physiological strain, may indicate an inappropriate pacing strategy therefore, further familiarization is recommended to optimize a combined strategy. Finally, these data indicate HA, achieved through cycle training, yields a larger ergogenic effect than PC on 5-km running performance in the heat, although PC remains beneficial when HA is not possible.

Short-term heat acclimation prior to a multi-day desert ultra-marathon improves physiological and psychological responses without compromising immune status.

Multistage, ultra-endurance events in hot, humid conditions necessitate thermal adaptation, often achieved through short term heat acclimation (STHA), to improve performance by reducing thermoregulatory strain and perceptions of heat stress. This study investigated the physiological, perceptual and immunological responses to STHA prior to the Marathon des Sables. Eight athletes (age 42 ± 4 years and body mass 81.9 ± 15.0 kg) completed 4 days of controlled hyperthermia STHA (60 min·day‒1, 45°C and 30% relative humidity). Pre, during and post sessions, physiological and perceptual measures were recorded. Immunological measures were recorded pre-post sessions 1 and 4. STHA improved thermal comfort (P = 0.02), sensation (P = 0.03) and perceived exertion (P = 0.04). A dissociated relationship between perceptual fatigue and Tre was evident after STHA, with reductions in perceived Physical (P = 0.04) and General (P = 0.04) fatigue. Exercising Tre and HR did not change (P > 0.05) however, sweat rate increased 14% (P = 0.02). No changes were found in white blood cell counts or content (P > 0.05). Four days of STHA facilitates effective perceptual adaptations, without compromising immune status prior to an ultra-endurance race in heat stress. A greater physiological strain is required to confer optimal physiological adaptations.

Power Relative to Body Mass Best Predicts Change in Core Temperature During Exercise-Heat Stress.

Gibson, OR, Willmott, AGB, James, CA, Hayes, M, and Maxwell, NS. Power relative to body mass best predicts change in core temperature during exercise-heat stress. J Strength Cond Res 31(2): 403-414, 2017-Controlling internal temperature is crucial when prescribing exercise-heat stress, particularly during interventions designed to induce thermoregulatory adaptations. This study aimed to determine the relationship between the rate of rectal temperature (Trec) increase, and various methods for prescribing exercise-heat stress, to identify the most efficient method of prescribing isothermic heat acclimation (HA) training. Thirty-five men cycled in hot conditions (40° C, 39% R.H.) for 29 ± 2 minutes. Subjects exercised at 60 ± 9% V[Combining Dot Above]O2peak, with methods for prescribing exercise retrospectively observed for each participant. Pearson product moment correlations were calculated for each prescriptive variable against the rate of change in Trec (° C·h), with stepwise multiple regressions performed on statistically significant variables (p ≤ 0.05). Linear regression identified the predicted intensity required to increase Trec by 1.0-2.0° C between 20- and 45-minute periods and the duration taken to increase Trec by 1.5° C in response to incremental intensities to guide prescription. Significant (p ≤ 0.05) relationships with the rate of change in Trec were observed for prescriptions based on relative power (W·kg; r = 0.764), power (%Powermax; r = 0.679), rating of perceived exertion (RPE) (r = 0.577), V[Combining Dot Above]O2 (%V[Combining Dot Above]O2peak; r = 0.562), heart rate (HR) (%HRmax; r = 0.534), and thermal sensation (r = 0.311). Stepwise multiple regressions observed relative power and RPE as variables to improve the model (r = 0.791), with no improvement after inclusion of any anthropometric variable. Prescription of exercise under heat stress using power (W·kg or %Powermax) has the strongest relationship with the rate of change in Trec with no additional requirement to correct for body composition within a normal range. Practitioners should therefore prescribe exercise intensity using relative power during isothermic HA training to increase Trec efficiently and maximize adaptation.

Effective microorganism - X attenuates circulating superoxide dismutase following an acute bout of intermittent running in hot, humid conditions.

This study determined the effectiveness of antioxidant supplementation on high-intensity exercise-heat stress. Six males completed a high-intensity running protocol twice in temperate conditions (TEMP; 20.4°C), and twice in hot conditions (HOT; 34.7°C). Trials were completed following7 days supplementation with 70 ml·day(-1) effective microorganism-X (EM-X; TEMPEMX or HOTEMX) or placebo (TEMPPLA or HOTPLA). Plasma extracellular Hsp72 (eHsp72) and superoxide dismutase (SOD) were measured by ELISA. eHsp72 and SOD increased pre-post exercise (p < 0.001), with greater eHsp72 (p < 0.001) increases observed in HOT (+1.5 ng·ml(-1)) compared to TEMP (+0.8 ng·ml(-1)). EM-X did not influence eHsp72 (p > 0.05). Greater (p < 0.001) SOD increases were observed in HOT (+0.22 U·ml(-1)) versus TEMP (+0.10 U·ml(-1)) with SOD reduced in HOTEMX versus HOTPLA (p = 0.001). Physiological and perceptual responses were all greater (p < 0.001) in HOT versus TEMP conditions, with no difference followed EM-X (p > 0.05). EM-X supplementation attenuated the SOD increases following HOT, potentiating its application as an ergogenic aid to ameliorate oxidative stress.

Isothermic and fixed intensity heat acclimation methods induce similar heat adaptation following short and long-term timescales.

Heat acclimation requires the interaction between hot environments and exercise to elicit thermoregulatory adaptations. Optimal synergism between these parameters is unknown. Common practise involves utilising a fixed workload model where exercise prescription is controlled and core temperature is uncontrolled, or an isothermic model where core temperature is controlled and work rate is manipulated to control core temperature. Following a baseline heat stress test; 24 males performed a between groups experimental design performing short term heat acclimation (STHA; five 90 min sessions) and long term heat acclimation (LTHA; STHA plus further five 90 min sessions) utilising either fixed intensity (50% VO2peak), continuous isothermic (target rectal temperature 38.5 °C for STHA and LTHA), or progressive isothermic heat acclimation (target rectal temperature 38.5 °C for STHA, and 39.0 °C for LTHA). Identical heat stress tests followed STHA and LTHA to determine the magnitude of adaptation. All methods induced equal adaptation from baseline however isothermic methods induced adaptation and reduced exercise durations (STHA = -66% and LTHA = -72%) and mean session intensity (STHA = -13% VO2peak and LTHA = -9% VO2peak) in comparison to fixed (p < 0.05). STHA decreased exercising heart rate (-10 b min(-1)), core (-0.2 °C) and skin temperature (-0.51 °C), with sweat losses increasing (+0.36 Lh(-1)) (p<0.05). No difference between heat acclimation methods, and no further benefit of LTHA was observed (p > 0.05). Only thermal sensation improved from baseline to STHA (-0.2), and then between STHA and LTHA (-0.5) (p<0.05). Both the continuous and progressive isothermic methods elicited exercise duration, mean session intensity, and mean T(rec) analogous to more efficient administration for maximising adaptation. Short term isothermic methods are therefore optimal for individuals aiming to achieve heat adaptation most economically, i.e. when integrating heat acclimation into a pre-competition taper. Fixed methods may be optimal for military and occupational applications due to lower exercise intensity and simplified administration.

Prediction of physiological responses and performance at altitude using the 6-minute walk test in normoxia and hypoxia.

OBJECTIVE: The 6-minute walk test (6MWT) is a reliable and valid tool for determining an individual's functional capacity, and has been used to predict summit success. The primary aim of the study was to evaluate whether a 6MWT in normobaric hypoxia could predict physiological responses and exercise performance at altitude. The secondary aim was to determine construct validity of the 6MWT for monitoring acclimatization to 3400 m (Cuzco, Peru). METHODS: Twenty-nine participants performed six 6MWTs in four conditions: normoxic outdoor (NO), normoxic treadmill (NT), and hypoxic treadmill (HT) were each performed once; and hypoxic outdoor (HO) was performed three times, at 42 hours (HO1), 138 hours (HO2), and 210 hours (HO3) after arrival at Cuzco. RESULTS: One-way analysis of variance revealed no difference (P>.05) between NO and HO1 for 6MWT distance. HT and HO protocols were comparable for the measurement of delta heart rate (HR) and post-test peripheral oxygen saturation (%Spo2; P>.05). Acclimatization was evidenced by reductions (P<.05) in resting HR and respiratory rate (RR) between HO1, HO2, and HO3, and preservation of Spo2 between HO1 and HO2. Postexercise HR and RR were not different (P>.05) with acclimatization. The duration to ascend to 4215 m on a trek was moderately correlated (P<.05) to HR during the trek and the 6MWT distance during HT; no other physiological markers predicted performance. CONCLUSIONS: The 6MWT is a simple, time-efficient tool for predicting physiological responses to simulated and actual altitude, which are comparable. The 6MWT is effective at monitoring elements of acclimatization to moderate altitude.

Increased air temperature decreases high-speed, but not total distance, in international field hockey.

This study investigated the effect of heat stress on locomotor activity within international field hockey at team, positional and playing-quarter levels. Analysis was conducted on 71 matches played by the Malaysia national men's team against 24 opponents. Fixtures were assigned to match conditions, based on air temperature [COOL (14 ± 3°C), WARM (24 ± 1°C), HOT (27 ± 1°C), or VHOT (32 ± 2°C), p < 0.001]. Relationships between locomotor metrics and air temperature (AIR), absolute and relative humidity, and wet bulb globe temperature (WBGT) were investigated further using correlation and regression analyses. Increased AIR and WBGT revealed similar correlations (p < 0.01) with intensity metrics; high-speed running (AIR r = -0.51, WBGT r = -0.45), average speed (AIR r = -0.48, WBGT r = -0.46), decelerations (AIR r = -0.41, WBGT r = -0.41), sprinting efforts (AIR r = -0.40, WBGT r = -0.36), and sprinting distance (AIR r = -0.37, WBGT r = -0.29). In comparison to COOL, HOT, and VHOT matches demonstrated reduced high-speed running intensity (-14-17%; p < 0.001), average speed (-5-6%; p < 0.001), sprinting efforts (-17%; p = 0.010) and decelerations per min (-12%; p = 0.008). Interactions were found between match conditions and playing quarter for average speed (+4-7%; p = 0.002) and sprinting distance (+16-36%; p < 0.001), both of which were higher in the fourth quarter in COOL versus WARM, HOT and VHOT. There was an interaction for "low-speed" (p < 0.001), but not for "high-speed" running (p = 0.076) demonstrating the modulating effect of air temperature (particularly >25°C) on pacing within international hockey. These are the first data demonstrating the effect of air temperature on locomotor activity within international men's hockey, notably that increased air temperature impairs high-intensity activities by 5-15%. Higher air temperatures compromise high-speed running distances between matches in hockey.

Regional thermal hyperemia in the human leg: Evidence of the importance of thermosensitive mechanisms in the control of the peripheral circulation.

Hyperthermia is thought to increase limb blood flow through the activation of thermosensitive mechanisms within the limb vasculature, but the precise vascular locus in which hyperthermia modulates perfusion remains elusive. We tested the hypothesis that local temperature-sensitive mechanisms alter limb hemodynamics by regulating microvascular blood flow. Temperature and oxygenation profiles and leg hemodynamics of the common (CFA), superficial (SFA) and profunda (PFA) femoral arteries, and popliteal artery (POA) of the experimental and control legs were measured in healthy participants during: (1) 3 h of whole leg heating (WLH) followed by 3 h of recovery (n = 9); (2) 1 h of upper leg heating (ULH) followed by 30 min of cooling and 1 h ULH bout (n = 8); and (3) 1 h of lower leg heating (LLH) (n = 8). WLH increased experimental leg temperature by 4.2 ± 1.2ºC and blood flow in CFA, SFA, PFA, and POA by ≥3-fold, while the core temperature essentially remained stable. Upper and lower leg blood flow increased exponentially in response to leg temperature and then declined during recovery. ULH and LLH similarly increased the corresponding segmental leg temperature, blood flow, and tissue oxygenation without affecting these responses in the non-heated leg segment, or perfusion pressure and conduit artery diameter across all vessels. Findings demonstrate that whole leg hyperthermia induces profound and sustained elevations in upper and lower limb blood flow and that segmental hyperthermia matches the regional thermal hyperemia without causing thermal or hemodynamic alterations in the non-heated limb segment. These observations support the notion that heat-activated thermosensitive mechanisms in microcirculation regulate limb tissue perfusion during hyperthermia.

Volume and Intensity of Locomotor Activity in International Men's Field Hockey Matches Over a 2-Year Period.

The locomotor demands of international men's field hockey matches were investigated across positions (DEF, MID, FWD) and playing quarters. Volume (i.e., total values) and intensity (i.e., relative to playing time) data were collected using 10-Hz GPS/100-Hz accelerometer units from the #11 world-ranked (WR) team, during 71 matches, against 24 opponents [WR 12 ± 11 (range, 1-60)]. Mean ± SD team total distance (TD) was 4,861 ± 871 m, with 25% (1,193 ± 329 m) "high-speed running" (>14.5 km h-1) and 8% (402 ± 144 m) "sprinting" (>19.0 km h-1). Reduced TD (range, -3 to 4%) and average speed (range, -3.4 to 4.7%) occurred through subsequent quarters, vs. Q1 (p < 0.05). A "large" negative relationship (r = -0.64) was found between playing duration and average speed. Positional differences (p < 0.05) were identified for all volume metrics including; playing duration (DEF, 45:50 ± 8:00 min; MID, 37:37 ± 7:12 min; FWD, 33:32 ± 6:22 min), TD (DEF, 5,223 ± 851 m; MID, 4,945 ± 827 m; FWD, 4,453 ± 741 m), sprinting distance (DEF, 315 ± 121 m; MID, 437 ± 144 m; FWD, 445 ± 129 m), and acceleration efforts (>2 m s-2; DEF, 48 ± 12; MID, 51 ± 11; FWD, 50 ± 14). Intensity variables similarly revealed positional differences (p < 0.05) but with a different pattern between positions; average speed (DEF, 115 ± 10 m min-1; MID, 132 ± 10 m min-1; FWD, 134 ± 15 m min-1), sprinting (DEF, 7 ± 3 m min-1; MID, 12 ± 4 m min-1; FWD, 14 ± 4 m min-1), and accelerations (DEF, 1.1 ± 0.3 n min-1; MID, 1.4 ± 0.2 n min-1; FWD, 1.5 ± 0.3 n min-1). Physical outputs reduced across playing quarters, despite unlimited substitutions, demonstrating the importance of optimizing physical preparation prior to international competition. Volume and intensity data highlight specific positional requirements, with forwards displaying shorter playing durations but greater high-intensity activities than defenders.

Systemic but not local rehydration restores dehydration-induced changes in pulmonary function in healthy adults.

Water transport and local (airway) hydration are critical for the normal functioning of lungs and airways. Currently, there is uncertainty regarding the effects of systemic dehydration on pulmonary function. Our aims were 1) to clarify the impact of exercise- or fluid restriction-induced dehydration on pulmonary function in healthy adults; and 2) to establish whether systemic or local rehydration can reverse dehydration-induced alterations in pulmonary function. Ten healthy participants performed four experimental trials in a randomized order (2 h exercise in the heat twice and 28 h fluid restriction twice). Pulmonary function was assessed using spirometry and whole body plethysmography in the euhydrated, dehydrated, and rehydrated states. Oral fluid consumption was used for systemic rehydration and nebulized isotonic saline inhalation for local rehydration. Both exercise and fluid restriction induced mild dehydration (2.7 ± 0.7% and 2.5 ± 0.4% body mass loss, respectively; P < 0.001) and elevated plasma osmolality (P < 0.001). Dehydration across all four trials was accompanied by a reduction in forced vital capacity (152 ± 143 mL, P < 0.01) and concomitant increases in residual volume (216 ± 177 mL, P < 0.01) and functional residual capacity (130 ± 144 mL, P < 0.01), with no statistical differences between modes of dehydration. These changes were normalized by fluid consumption but not nebulization. Our results suggest that, in healthy adults: 1) mild systemic dehydration induced by exercise or fluid restriction leads to pulmonary function impairment, primarily localized to small airways; and 2) systemic, but not local, rehydration reverses these potentially deleterious alterations.NEW & NOTEWORTHY This study demonstrates that, in healthy adults, mild systemic dehydration induced by exercise in the heat or a prolonged period of fluid restriction leads to negative alterations in pulmonary function, primarily localized to small airways. Oral rehydration, but not nebulized isotonic saline, is able to restore pulmonary function in dehydrated individuals. Our findings highlight the importance of maintaining an adequate systemic fluid balance to preserve pulmonary function.

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

OBJECTIVES: To 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). DESIGN: Cross-sectional study. METHOD: Twenty-six participants (YEX: n = 11 aged 22 ±â€¯2 years, EEX:n = 8 aged 68 ±â€¯3 years, EHWI: n = 7 aged 73 ±â€¯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 Hprod), and a six-minute walk test (6MWT), all in 35 °C, 50% RH. RESULTS: The 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). CONCLUSIONS: Irrespective 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.

Exercise hyperthermia induces greater changes in gastrointestinal permeability than equivalent passive hyperthermia.

Hyperthermia and exertional heat illness increase gastrointestinal (GI) permeability, although whether the latter is only via hyperthermia is unclear. The aim of this pilot study was to determine whether different changes in GI permeability, characterized by an increased plasma lactulose:rhamnose concentration ratio ([L:R]), occurred in exercise hyperthermia in comparison to equivalent passive hyperthermia. Six healthy adult male participants (age 25 ± 5 years, mass 77.0 ± 6.7 kg, height 181 ± 6 cm, peak oxygen uptake [ V·O2peak ] 48 ± 8 ml.kg-1 .min-1 ) underwent exercise under hot conditions (Ex-Heat) and passive heating during hot water immersion (HWI). Heart rate (HR), rectal temperature (TCORE ), rating of perceived exertion (RPE), and whole-body sweat loss (WBSL) were recorded throughout the trials. The L:R ratio, peak HR, change in HR, and change in RPE were higher in Ex-Heat than HWI, despite no differences in trial duration, peak core temperature or WBSL. L:R was strongly correlated (p < 0.05) with HR peak (r = 0.626) and change in HR (r = 0.615) but no other variable. The greater L:R in Ex-Heat, despite equal TCORE responses to HWI, indicates that increased cardiovascular strain occurred during exercise, and exacerbates hyperthermia-induced GI permeability at the same absolute temperature.

The efficacy of steroids in reducing morbidity and mortality from extreme hyperthermia and heatstroke-A systematic review.

Severe hyperthermia from classical or exertional heatstroke, or from drug ingestion or other noninfective pyrogens, is associated with a high mortality and morbidity. A systemic pro-inflammatory response occurs during heatstroke, characterized by elevated cytokines with endotoxemia from elevated lipopolysaccharide (LPS) levels. Corticosteroids reduce LPS and cytokine levels, suggesting that they may improve outcome. A systematic review searching Embase, MEDLINE, and PubMed from the earliest date available until September 2019 was conducted, according to the PRISMA guidelines, with five papers identified. In four studies, systemic steroids administered before or at the onset of heat stress improved mortality or reduced organ dysfunction. Survival time was greatest when steroid administration preceded heat stress. In one study, a nonsignificant increase in mortality was seen. A dose response was observed, with higher doses extending survival time. Animal studies suggest that steroids improve mortality and/or organ dysfunction after an episode of heat stress or extreme hyperthermia.

Heat alleviation strategies for athletic performance: A review and practitioner guidelines.

International competition inevitably presents logistical challenges for athletes. Events such as the Tokyo 2020 Olympic Games require further consideration given historical climate data suggest athletes will experience significant heat stress. Given the expected climate, athletes face major challenges to health and performance. With this in mind, heat alleviation strategies should be a fundamental consideration. This review provides a focused perspective of the relevant literature describing how practitioners can structure male and female athlete preparations for performance in hot, humid conditions. Whilst scientific literature commonly describes experimental work, with a primary focus on maximizing magnitudes of adaptive responses, this may sacrifice ecological validity, particularly for athletes whom must balance logistical considerations aligned with integrating environmental preparation around training, tapering and travel plans. Additionally, opportunities for sophisticated interventions may not be possible in the constrained environment of the athlete village or event arenas. This review therefore takes knowledge gained from robust experimental work, interprets it and provides direction on how practitioners/coaches can optimize their athletes' heat alleviation strategies. This review identifies two distinct heat alleviation themes that should be considered to form an individualized strategy for the athlete to enhance thermoregulatory/performance physiology. First, chronic heat alleviation techniques are outlined, these describe interventions such as heat acclimation, which are implemented pre, during and post-training to prepare for the increased heat stress. Second, acute heat alleviation techniques that are implemented immediately prior to, and sometimes during the event are discussed. Abbreviations: CWI: Cold water immersion; HA: Heat acclimation; HR: Heart rate; HSP: Heat shock protein; HWI: Hot water immersion; LTHA: Long-term heat acclimation; MTHA: Medium-term heat acclimation; ODHA: Once-daily heat acclimation; RH: Relative humidity; RPE: Rating of perceived exertion; STHA: Short-term heat acclimation; TCORE: Core temperature; TDHA: Twice-daily heat acclimation; TS: Thermal sensation; TSKIN: Skin temperature; V̇O2max: Maximal oxygen uptake; WGBT: Wet bulb globe temperature.

Heat acclimation attenuates the increased sensations of fatigue reported during acute exercise-heat stress.

Athletes exercising in heat stress experience increased perceived fatigue acutely, however it is unknown whether heat acclimation (HA) reduces the magnitude of this perceptual response and whether different HA protocols influence the response. This study investigated sensations of fatigue following; acute exercise-heat stress; short- (5-sessions) and medium-term (10-sessions) HA; and between once- (ODHA) and twice-daily HA (TDHA) protocols. Twenty male participants (peak oxygen uptake: 3.75 ± 0.47 L·min-1) completed 10 sessions (60-min cycling at ~2 W·kg-1, 45°C/20% relative humidity) of ODHA (n = 10) or non-consecutive TDHA (n = 10). Sensations of fatigue (General, Physical, Emotional, Mental, Vigor and Total Fatigue) were assessed using the multi-dimensional fatigue scale inventory-short form pre and post session 1, 5 and 10. Heat adaptation was induced following ODHA and TDHA, with reductions in resting rectal temperature and heart rate, and increased plasma volume and sweat rate (P < 0.05). General, Physical and Total Fatigue increased from pre-to-post for session 1 within both groups (P < 0.05). Increases in General, Physical and Total Fatigue were attenuated in session 5 and 10 vs. session 1 of ODHA (P < 0.05). This change only occurred at session 10 of TDHA (P < 0.05). Whilst comparative heat adaptations followed ODHA and TDHA, perceived fatigue is prolonged within TDHA. ABBREVIATIONS: ∆: Change; ANOVA: Analysis of variance; HA: Heat acclimation; HR: Heart rate; IL-6: Interleukin-6; MFS-SF: Multi-dimensional fatigue symptom inventory-short form (MFSI-SF); MTHA: Medium-term heat acclimation; Na+: Sodium; ODHA: Once daily heat acclimation; PV: Plasma volume; RH: Relative humidity; RPE: Rating of perceived exertion; SD: Standard deviation; SE: Standard error of the slope coefficient or intercept; SEE : Standard error of the estimate for the regression equation; STHA: Short-term heat acclimation; TDHA: Twice daily heat acclimation; TC: Thermal Comfort; Tre: Rectal temperature; TSS: Thermal sensation; V̇O2peak: Peak oxygen uptake; WBSL: whole-body sweat loss.

Could Heat Therapy Be an Effective Treatment for Alzheimer's and Parkinson's Diseases? A Narrative Review.

Neurodegenerative diseases involve the progressive deterioration of structures within the central nervous system responsible for motor control, cognition, and autonomic function. Alzheimer's disease and Parkinson's disease are among the most common neurodegenerative disease and have an increasing prevalence over the age of 50. Central in the pathophysiology of these neurodegenerative diseases is the loss of protein homeostasis, resulting in misfolding and aggregation of damaged proteins. An element of the protein homeostasis network that prevents the dysregulation associated with neurodegeneration is the role of molecular chaperones. Heat shock proteins (HSPs) are chaperones that regulate the aggregation and disaggregation of proteins in intracellular and extracellular spaces, and evidence supports their protective effect against protein aggregation common to neurodegenerative diseases. Consequently, upregulation of HSPs, such as HSP70, may be a target for therapeutic intervention for protection against neurodegeneration. A novel therapeutic intervention to increase the expression of HSP may be found in heat therapy and/or heat acclimation. In healthy populations, these interventions have been shown to increase HSP expression. Elevated HSP may have central therapeutic effects, preventing or reducing the toxicity of protein aggregation, and/or peripherally by enhancing neuromuscular function. Broader physiological responses to heat therapy have also been identified and include improvements in muscle function, cerebral blood flow, and markers of metabolic health. These outcomes may also have a significant benefit for people with neurodegenerative disease. While there is limited research into body warming in patient populations, regular passive heating (sauna bathing) has been associated with a reduced risk of developing neurodegenerative disease. Therefore, the emerging evidence is compelling and warrants further investigation of the potential benefits of heat acclimation and passive heat therapy for sufferers of neurodegenerative diseases.