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To determine the effects of heat acclimation on gastrointestinal (GI) damage and the gastric emptying (GE) rate following endurance exercise in a hot environment. Fifteen healthy men were divided into two groups: endurance training in hot (HOT, 35 °C, n = 8) or cool (COOL, 18 °C, n = 7) environment. All subjects completed 10 days of endurance training (eight sessions of 60 min continuous exercise at 50% of the maximal oxygen uptake (V·O2max). Subjects completed a heat stress exercise tests (HST, 60 min exercise at 60% V·O2max) to evaluate the plasma intestinal fatty acid-binding protein (I-FABP) level and the GE rate following endurance exercise in a hot environment (35 °C) before (pre-HST) and after (post-HST) the training period. We assessed the GE rate using the 13C-sodium acetate breath test. The core temperature during post-HST exercise decreased significantly in the HOT group compared to the pre-HST (p = 0.004) but not in the COOL group. Both the HOT and COOL groups showed exercise-induced plasma I-FABP elevations in the pre-HST (p = 0.002). Both groups had significantly attenuated exercise-induced I-FABP elevation in the post-HST. However, the reduction of exercise-induced I-FABP elevation was not different significantly between both groups. GE rate following HST did not change between pre- and post-HST in both groups, with no significant difference between two groups in the post-HST. Ten days of endurance training in a hot environment improved thermoregulation, whereas exercise-induced GI damage and delay of GE rate were not further attenuated compared with training in a cool environment.

Background While active heat acclimation strategies have been robustly explored, not many studies highlighted passive heat acclimation strategies. Particularly, little evidence demonstrated advantages of utilizing a water-perfused suit as a passive heating strategy. This study aimed to explore heat adaptive changes in physiological and perceptual responses during 10-day heat acclimation training using a water-perfused suit. Methods Nineteen young males were divided into three experimental groups: exercise condition ( N = 6, HA EXE , 1-h exercise at 6 km h −1 followed by 1-h rest in a sitting position), exercise and passive heating condition ( N = 6, HA EXE+SUIT , 1-h exercise at 6 km h −1 followed 1-h passive heating in a sitting position), and passive heating condition ( N = 7, HA SUIT , 2-h passive heating in a sitting position). All heating programs were conducted for 10 consecutive days in a climatic chamber maintained at 33 °C with 60% relative humidity. The passive heating was conducted using a newly developed water-perfused suit with 44 °C water. Results Greater whole-body sweat rate and alleviated perceptual strain were found in HA SUIT and HA EXE+SUIT after 5 and/or 10 days ( P < 0.05) but not in the exercise-only condition (HA EXE ). Lower rectal temperature and heart rate were found in all conditions after the training ( P < 0.05). Heat adaptive changes appeared earlier in HA SUIT except for sweat responses. Conclusions For heat acclimation in hot humid environments, passive and post-exercise heat acclimation training using the suit (water inflow temperature 44 °C) were more effective than the mild exercise (1-h walking at 6 km h −1 ). This form of passive heating (HA SUIT ) may be an especially effective strategy for the elderly and the disabled who are not able to exercise in hot environments.

Compared with the induction of heat acclimation (HA), studies investigating the decay and re-induction of HA (RA) are relatively sparse and have yielded conflicting results. Therefore, 16 semi-nude men were acclimated to dry-heat by undertaking an exercise protocol in a hot chamber (dry-bulb temperature 46.1 +/- 0.1 degrees C; relative humidity 17.9 +/- 0.1%) on 10 consecutive days (HA1-10) in winter UK. Thereafter, the subjects were divided into two groups and re-exposed to the work-in-heat tests after 12 and 26 days until RA was attained (RA(12), n = 8; RA(26), n = 8). The exercise protocol consisted of 60 min of treadmill walking (1.53 m s(-1)) at an incline individually set to induce a rectal temperature (T (re)) of approximately 38.5 degrees C during HA1 (equating to 45 +/- 4% peak oxygen uptake), followed by 10 min of rest and 40 min of further treadmill exercise, the intensity of which was increased across HA to maintain T(re )at approximately 38.5 degrees C. T(re), mean skin temperature, heart rate and rate of total water loss measured at 60 min did not change after HA7, and HA was taken as the mean of the responses during HA8-10. For both groups, there was no decay in T(re) and for all measured variables RA was attained after 2 and 4 days in RA(12) and RA(26), respectively. It is concluded that once adaptation to heat has been attained, the time that individuals may spend in cooler conditions before returning to a hot environment could be as long as one month, without the need for extensive re-adaptation to heat.

The effects of early age thermal conditioning (ETC), vinegar supplementation (VS) of drinking water, broilers’ gender, and their interactions on respiratory rate, body temperature, and blood parameters (biochemical, hematological, and thyroid hormones) of broiler chickens reared under high ambient temperatures were determined. A total of 1100 1-day-old chicks were divided into four treatments: the “control” which were non-conditioned and non-supplemented; “heat-conditioned” which were exposed to 38 ± 1 °C for 24 h at 5 days of age; “vinegar supplemented” which were given drinking water supplemented with 0.2% of commercial vinegar from 28 to 49 days of age; and “combined” which were both heat conditioned and vinegar supplemented. All groups were exposed to the natural fluctuations of summer ambient temperature (average diurnal ambient temperature of about 30 ± 1 °C and average relative humidity of 58 ± 5%). ETC and broiler gender did not affect the respiratory rate or body temperature of chronic heat-exposed chickens. VS changed the body temperature across time (d35, d42, d49) (linear and quadratic effects, P < 0.05) without changing respiratory rate. Heat-conditioned chickens exhibited lower levels of glycemia (P < 0.0001) and higher hematocrit and red blood cell counts (P < 0.05). Furthermore, the greatest effects of VS, alone or associated with ETC, were the lowering of cholesterol and triglyceride blood concentrations. A significant (P < 0.05) effect of ETC, gender, and ETC×gender on T3:T4 ratio was observed. Finally, some beneficial physiological responses induced by ETC and VS, separately or in association, on chronically heat-stressed chickens were observed. However, the expected cumulative positive responses when the two treatments were combined were not evident.

In order to pinpoint phytohormone changes associated with enhanced heat stress tolerance, the complex phytohormone profiles [cytokinins, auxin, abscisic acid (ABA), jasmonic acid (JA), salicylic acid and ethylene precursor 1-aminocyclopropane-1-carboxylic acid (ACC)] were compared in after direct heat shock (45°C, 3 h) and in heat-stressed pre-acclimated plants (1 h at 37°C followed by 2 h at optimal temperature 20°C). Organ-specific responses were followed in shoot apices, leaves, and roots immediately after heat shock and after 24-h recovery at 20°C. The stress strength was evaluated membrane ion leakage and the activity of nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (NOX) and antioxidant enzymes [superoxide dismutases, guaiacol peroxidases (POD), catalases, ascorbate peroxidases (APX)]. Heat acclimation diminished negative effects of heat stress, especially in apices and roots, no significant differences being observed in leaves. Low NOX1-3 activities indicated diminished production of reactive oxygen species. Higher activity of APX, POD1, and the occurrence of POD3-4 reflected acclimation-stimulated readiness of the antioxidant system. Acclimation diminished heat shock-induced changes of ABA, JA, cytokinin, and auxin levels in apices. Excess of ABA catabolites suggested an early stress response. The strong up-regulation of ABA and ACC in roots indicated defense boost in roots of acclimated plants compared to the non-acclimated ones. To evaluate the possibility to enhance stress tolerance by cytokinin pool modulation, INCYDE-F, an inhibitor of cytokinin oxidase/dehydrogenase, was applied. As cytokinin effects on stress tolerance may depend on timing of their regulation, INCYDE was applied at several time-points. In combination with acclimation, INCYDE treatment had a slight positive effect on heat stress tolerance, mainly when applied after 2-h period of the optimal temperature. INCYDE increased contents of cytokinins -zeatin and -zeatin in roots and auxin in all tissues after heat shock. INCYDE also helped to suppress the content of ABA in leaves, and ethylene in apices and roots. INCYDE application to non-acclimated plants (applied before or after heat shock) strengthened negative stress effects, probably by delaying of the repair processes. In conclusion, pre-treatment with moderately elevated temperature enhanced heat stress tolerance and accelerated recovery after stress. Inhibition of cytokinin degradation by INCYDE slightly improved recovery of acclimated plants.

Over the last few decades, females have significantly increased their participation in athletic competitions and occupations (e.g. military, firefighters) in hot and thermally challenging environments. Heat acclimation, which involves repeated passive or active heat exposures that lead to physiological adaptations, is a tool commonly used to optimize performance in the heat. However, the scientific community’s understanding of adaptations to heat acclimation are largely based on male data, complicating the generalizability to female populations. Though limited, current evidence suggests that females may require a greater number of heat acclimation sessions or greater thermal stress to achieve the same magnitude of physiological adaptations as males. The underlying mechanisms explaining the temporal sex differences in the physiological adaptations to heat acclimation are currently unclear. Therefore, the aims of this state-of-the-art review are to: (i) present a brief yet comprehensive synthesis of the current female and sex difference literature, (ii) highlight sex-dependent (e.g. anthropometric, menstrual cycle) and sex-independent factors (e.g. environmental conditions, fitness) influencing the physiological and performance adaptations to heat acclimation, and (iii) address key avenues for future research.

High‐altitude training is widely adopted by endurance athletes with the aim of increasing total haemoglobin mass (tHb mass ) and thereby endurance exercise performance. However, divergent effects on tHb mass and exercise performance have been reported in athletes commencing altitude camps with initial high baseline levels for tHb mass , questioning the efficacy of in‐season interventions in elite athletes. Therefore, haematological adaptations and exercise performance were evaluated in 12 elite cyclists completing an in‐season ‘Live High–Train High’ (LHTH) altitude camp (21 days at 3000 m) immediately after participating in the national championships. Additionally, for seven participants, we compared haematological and exercise performance effects with an off‐season heat acclimation training (HEAT) intervention (six 1‐h sessions per week for 5 weeks). The LHTH resulted in a 3.5 ± 2.0% ( P  < 0.001, n  = 12) increase in tHb mass , with decay to Pre levels 10 days after returning to sea‐level. For participants followed for 9 months, the tHb mass effect was comparable to that of the off‐season HEAT intervention (5.4 ± 3.9% for HEAT, LHTH vs. HEAT: P  = 0.801, n  = 7) and baseline levels prior to the interventions were almost identical (965 g Pre‐HEAT vs. 960 g Pre‐LHTH). Exercise performance and maximal oxygen uptake, tested immediately (2–3 days) and 10 days after LHTH, were not improved, and individual changes were not correlated to any of the haematological parameters assessed. In conclusion, the in‐season LHTH training camp effectively increased tHb mass in elite cyclists; however, there was a rapid decay in tHb mass upon return to sea‐level and no effect on exercise performance. What is the central question of this study? What is the effectiveness of an in‐season ‘Live High–Train High’ (LHTH) altitude camp on haematological adaptations and sea‐level exercise performance compared to off‐season heat acclimation training (HEAT) in elite male cyclists? What is the main finding and its importance? The 3.5% elevation in total haemoglobin mass (tHb mass ) following LHTH did not translate into improved exercise performance or maximal oxygen uptake at sea‐level and displayed a rapid decay after return to sea‐level. Although the boost in tHb mass was similar to off‐season HEAT for participants tracked across the competitive season, the absence of an exercise performance effect is noteworthy and should be considered for athletes preparing for competitions at sea‐level.

Heat tolerance of plants related to cell membrane thermostability is commonly estimated via the measurement of ion leakage from plant segments after defined heat treatment. To compare heat tolerance of various plants, it is crucial to select suitable heating conditions. This selection is time-consuming and optimizing the conditions for all investigated plants may even be impossible. Another problem of the method is its tendency to overestimate basal heat tolerance. Here we present an improved ion leakage method, which does not suffer from these drawbacks. It is based on gradual heating of plant segments in a water bath or algal suspensions from room temperature up to 70–75°C. The electrical conductivity of the bath/suspension, which is measured continuously during heating, abruptly increases at a certain temperature T COND (within 55–70°C). The T COND value can be taken as a measure of cell membrane thermostability, representing the heat tolerance of plants/organisms. Higher T COND corresponds to higher heat tolerance (basal or acquired) connected to higher thermostability of the cell membrane, as evidenced by the common ion leakage method. The new method also enables determination of the thermostability of photochemical reactions in photosynthetic samples via the simultaneous measurement of Chl fluorescence.

Plants can obtain superinduction of defense against unpredictable challenges based on prior acclimation, but the mechanisms involved in the acclimation memory are little known. The objective of this study was to characterize mechanisms of heat acclimation memory in Rhododendron hainanense , a thermotolerant wild species of azalea. Pretreatment of a 2-d recovery (25/18°C, day/night) after heat acclimation (37°C, 1 h) (AR-pt) did not weaken but enhanced acquired thermotolerance in R. hainanense with less damaged phenotype, net photosynthetic rate, and membrane stability than non-acclimation pretreated (NA-pt) plants. Combined transcriptome and proteome analysis revealed that a lot of heat-responsive genes still maintained high protein abundance rather than transcript level after the 2-d recovery. Photosynthesis-related genes were highly enriched and most decreased under heat stress (HS: 42°C, 1 h) with a less degree in AR-pt plants compared to NA-pt. Sustainably accumulated chloroplast-localized heat shock proteins (HSPs), Rubisco activase 1 (RCA1), beta-subunit of chaperonin-60 (CPN60β), and plastid transcriptionally active chromosome 5 (pTAC5) in the recovery period probably provided equipped protection of AR-pt plants against the subsequent HS, with less damaged photochemical efficiency and chloroplast structure. In addition, significant higher levels of RCA1 transcripts in AR-pt compared to NA-pt plants in early stage of HS showed a more important role of RCA1 than other chaperonins in heat acclimation memory. The novel heat-induced RCA1, rather than constitutively expressed RCA2 and RCA3, showed excellent thermostability after long-term HS (LHS: 42/35°C, 7 d) and maintained balanced Rubisco activation state in photosynthetic acclimation. This study provides new insights into plant heat acclimation memory and indicates candidate genes for genetic modification and molecular breeding in thermotolerance improvement.

PurposeThis study investigated whether intermittent post-exercise sauna bathing across three-weeks endurance training improves exercise heat tolerance and exercise performance markers in temperate conditions, compared to endurance training alone. The subsidiary aim was to determine whether exercise-heat tolerance would further improve following 7-Weeks post-exercise sauna bathing.MethodsTwenty middle-distance runners (13 female; mean ± SD, age 20 ± 2 years, VO2max 56.1 ± 8.7 ml kg−1 min−1) performed a running heat tolerance test (30-min, 9 km h−1/2% gradient, 40 °C/40%RH; HTT) and temperate (18 °C) exercise tests (maximal aerobic capacity [VO2max], speed at 4 mmol L−1 blood lactate concentration ([La−]) before (Pre) and following three-weeks (3-Weeks) normal training (CON; n = 8) or normal training with 28 ± 2 min post-exercise sauna bathing (101–108 °C, 5–10%RH) 3 ± 1 times per week (SAUNA; n = 12). Changes from Pre to 3-Weeks were compared between-groups using an analysis of co-variance. Six SAUNA participants continued the intervention for 7 weeks, completing an additional HTT (7-Weeks; data compared using a one-way repeated-measures analysis of variance).ResultsDuring the HTT, SAUNA reduced peak rectal temperature (Trec; − 0.2 °C), skin temperature (− 0.8 °C), and heart rate (− 11 beats min−1) more than CON at 3-Weeks compared to Pre (all p < 0.05). SAUNA also improved VO2max (+ 0.27 L−1 min−1; p = 0.02) and speed at 4 mmol L−1 [La−] (+ 0.6 km h−1; p = 0.01) more than CON at 3-Weeks compared to Pre. Only peak Trec (− 0.1 °C; p = 0.03 decreased further from 3-Weeks to 7-Weeks in SAUNA (other physiological variables p > 0.05).ConclusionsThree-weeks post-exercise sauna bathing is an effective and pragmatic method of heat acclimation, and an effective ergogenic aid. Extending the intervention to seven weeks only marginally improved Trec.