280 research outputs found

    Prescribing workload administration to optimise isothermic heat acclimation

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    Repeated exercise-heat exposures, known as heat acclimation (HA), are often implemented as an intervention to attenuate decrements in physiological strain and exercise tolerance prior to work in normothermic and hot, humid conditions. The fundamental potentiating stimuli for thermoregulatory adaptation are repeated, significant rises in core temperature. Targeting of a specific core temperature is known as isothermic, or controlled hyperthermic HA. Different methods of modulating the exercise component of isothermic HA have been implemented, with prescription previously based upon either peak oxygen uptake (VO2peak), power, or subjective ratings of perceived exertion or thermal sensation. Interestingly, metabolic heat production, a measure to determine changes in core temperature, has not been used to prescribe isothermic HA. The aim of this study was to determine the relationship between the rate of rectal (core) temperature (Trec) increase, and different methods for prescribing workload during an acute exercise-heat exposure, with the objective of trying to refine the prescription of isothermic HA workloads

    Oxygen Cost of Recreational Horse-Riding in Females

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    Version: as accepted for publication.BACKGROUND: The purpose of this study was to characterize the physiological demands of a riding session comprising different types of recreational horse riding in females. METHODS: Sixteen female recreational riders (aged 17 to 54 years) completed an incremental cycle ergometer exercise test to determine peak oxygen consumption (VO₂peak) and a 45-minute riding session based upon a British Horse Society Stage 2 riding lesson (including walking, trotting, cantering and work without stirrups). Oxygen consumption (VO₂), from which metabolic equivalent (MET) and energy expenditure values were derived, was measured throughout. RESULTS: The mean VO₂ requirement for trotting/cantering (18.4 ± 5.1 ml·kg⁻¹·min⁻¹; 52 ± 12% VO₂peak; 5.3 ± 1.1 METs) was similar to walking/trotting (17.4 ± 5.1 ml·kg⁻¹·min⁻¹; 48 ± 13% VO₂peak; 5.0 ± 1.5 METs) and significantly higher than for work without stirrups (14.2 ± 2.9 ml·kg⁻¹·min⁻¹; 41 ± 12% VO₂peak; 4.2 ± 0.8 METs) (P = .001). CONCLUSIONS: The oxygen cost of different activities typically performed in a recreational horse riding session meets the criteria for moderate intensity exercise (3-6 METs) in females, and trotting combined with cantering imposes the highest metabolic demand. Regular riding could contribute to the achievement of the public health recommendations for physical activity in this population

    Editorial: Heat acclimation for special populations

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    Editorial on the Research Topic: Heat Acclimation for Special Populations: This heat acclimation for special population's Research Topic questions the "one size fits all" approach for heat adaptation and that it may not be appropriate for all populations. Therefore, to highlight these differences we endeavored to collect a set of studies on how heat acclimation may benefit a wide range of special populations who have specific needs. We have published 12 articles in this Research Topic and defined four main areas of research. (a) an epidemiological approach and the aging process; (b) understanding physiological mechanisms and a novel heat acclimation method; (c) adaptation to the heat for special populations including males, females, military personnel and Paralympic athletes; and (d) the use of heat therapy for special populations. We have summarized the most noteworthy evidence of each study in these research areas

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

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    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 90min sessions) and long term heat acclimation (LTHA; STHA plus further five 90min sessions) utilising either fixed intensity (50%), 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%and LTHA=−9%) in comparison to fixed (p0.05). 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 meanTrecanalogous 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

    Defining the determinants of endurance running performance in the heat

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    In cool conditions, physiological markers accurately predict endurance performance, but it is unclear whether thermal strain and perceived thermal strain modify the strength of these relationships. This study examined the relationships between traditional determinants of endurance performance and time to complete a 5 km time trial in the heat. Seventeen club runners completed graded exercise tests (GXT) in hot (GXTHOT; 32°C, 60% RH, 27.2°C WBGT) and cool conditions (GXTCOOL; 13°C, 50% RH, 9.3°C WBGT) to determine maximal oxygen uptake (V̇O2max), running economy (RE), velocity at V̇O2max (vV̇O2max), and running speeds corresponding to the lactate threshold (LT, 2 mmol.l-1) and lactate turnpoint (LTP, 4 mmol.l-1). Simultaneous multiple linear regression was used to predict 5 km time, using these determinants, indicating neither GXTHOT (R2=0.72) or GXTCOOL (R2=0.86) predicted performance in the heat as strongly has previously been reported in cool conditions. vV̇O2max was the strongest individual predictor of performance, both when assessed in GXTHOT (r=-0.83) and GXTCOOL (r=-0.90). The GXTs revealed the following correlations for individual predictors in GXTHOT; V̇O2max r=-0.7, RE r=0.36, LT r=-0.77, LTP r=-0.78 and in GXTCOOL; V̇O2max r=-0.67, RE r=0.62, LT r=-0.79, LTP r=-0.8. These data indicate: (i) GXTHOT does not predict 5 km running performance in the heat as strongly as a GXTCOOL, (ii) as in cool conditions, vV̇O2max may best predict running performance in the heat.

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

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    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 [urn:x-wiley:2051817X:media:phy214945:phy214945-math-0001] 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

    Mouse models for preeclampsia: disruption of redox-regulated signaling

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    The concept that oxidative stress contributes to the development of human preeclampsia has never been tested in genetically-defined animal models. Homozygous deletion of catechol-Omethyl transferase (Comt-/-) in pregnant mice leads to human preeclampsia-like symptoms (high blood pressure, albuminurea and preterm birth) resulting from extensive vasculo-endothelial pathology, primarily at the utero-fetal interface where maternal cardiac output is dramatically increased during pregnancy. Comt converts estradiol to 2-methoxyestradiol 2 (2ME2) which counters angiogenesis by depleting hypoxia inducible factor-1 alpha (HIF-1 alpha) at late pregnancy. We propose that in wild type (Comt++) pregnant mice, 2ME2 destabilizes HIF-1 alpha by inhibiting mitochondrial superoxide dismutase (MnSOD). Thus, 2ME2 acts as a pro-oxidant, disrupting redox-regulated signaling which blocks angiogenesis in wild type (WT) animals in physiological pregnancy. Further, we suggest that a lack of this inhibition under normoxic conditions in mutant animals (Comt-/-) stabilises HIF-1 alpha by inactivating prolyl hydroxlases (PHD). We predict that a lack of inhibition of MnSOD, leading to persistent accumulation of HIF-1 alpha, would trigger inflammatory infiltration and endothelial damage in mutant animals. Critical tests of this hypothesis would be to recreate preeclampsia symptoms by inducing oxidative stress in WT animals or to ameliorate by treating mutant mice with Mn-SOD-catalase mimetics or activators of PHD
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