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Epidemiological evidence has highlighted a strong relationship between cardiorespiratory fitness and surgical outcomes; specifically, fitter patients possess heightened resilience to withstand the surgical stress response. This narrative review draws on exercise and surgical physiology research to discuss and hypothesise the potential mechanisms by which higher fitness affords perioperative benefit. A higher fitness, as indicated by higher peak rate of oxygen consumption and ability to sustain metabolic homeostasis (i.e. higher anaerobic threshold) is beneficial postoperatively when metabolic demands are increased. However, the associated adaptations with higher fitness, and the related participation in regular exercise or physical activity, might also underpin the observed perioperative benefit through a process of hormesis, a protective adaptive response to the moderate and intermittent stress of exercise. Potential mediators discussed include greater antioxidant capacity, metabolic flexibility, glycaemic control, lean body mass, and improved mood.

Physical activity is the most common source of heat strain for humans. The thermal strain of physical activity causes overbreathing (hyperventilation) and this has adverse physiological repercussions. The mechanisms underlying heat-induced hyperventilation during exercise are unknown, but recent evidence supports a primary role of carotid body hyperexcitability (increased tonic activity and sensitivity) underpinning hyperventilation in passively heated humans. In a repeated-measures crossover design, 12 healthy participants (6 female) completed two low-intensity cycling exercise conditions (25% maximal aerobic power) in randomized order, one with core temperature (T

Endurance exercise induces cardiovascular adaptations; the athletic phenotypes of the heart and arteries are well characterised, but few studies have investigated the effects of chronic exercise on the venous system. The aim of this study was to describe the anatomy and function of lower limb deep and superficial veins in athletes compared to controls. Endurance-trained athletes and untrained controls (13 males, 7 females per group) were examined utilising ultrasound to measure vein diameter and flow, and air plethysmography to assess calf venous volume dynamics and muscle pump function at rest, during a single step, ambulation (10 steps) and after acute treadmill exercise (30 min ~80% age-predicted heart rate maximum). Diameters of 3 of the 7 deep veins assessed were larger in athletes (P≤0.0167) and more medial calf perforators were detectable (5 vs. 3, P=0.0039). Calf venous volume was 22% larger in athletes (P=0.0057), calf muscle pump ejection volume and ambulatory venous volume after 10 steps were both greater in athletes (20 and 46% respectively, P≤0.0482). Following acute exercise, flow recovery profiles in deep and superficial veins draining the leg were not different between groups, despite athletes performing ~four times more work. After exercise, venous volume and ejection volume were reduced by ~20% in athletes with no change in controls (interaction P≤0.0372) and while ambulatory venous volume reduced, this remained greater in athletes. These findings highlight venous adaptations that compensate for the demands of regular endurance exercise, all of which are suited to enhance flow through the lower limb venous system.

What is the central question of this study? What are the profiles of acute physiological and psychophysical strain during and in recovery from different modes of heating, and to what extent do these diminish after repeated exposure? What is the main finding and its importance? Mode of heating affects the strain profiles during heat stress and recovery. Exercise in the heat incurred the greatest cardiovascular strain during heating and recovery. Humid heat was poorly tolerated despite heat strain being no greater than in other heating modes, and tolerance did not improve with multiple exposures.Heat stress is common and arises endogenously and exogenously. It can be acutely hazardous while also increasingly advocated to drive health and performance-related adaptations. Yet, the nature of strain (deviation in regulated variables) imposed by different heating modes is not well established, despite the potential for important differences. We, therefore, compared three modes of heat stress for thermal, cardiovascular and perceptual strain profiles during exposure and recovery when experienced as a novel stimulus and an accustomed stimulus. In a crossover design, 13 physically active participants (five females) underwent 5 days of 60-min exposures to hot water immersion (40°C), sauna (55°C, 54% relative humidity) and exercise in the heat (40°C, 52% relative humidity), and a thermoneutral water immersion control (36.5°C), each separated by ≥4 weeks. Physiological (thermal, cardiovascular, haemodynamic) and psychophysical strain responses were assessed on days 1 and 5. Sauna evoked the warmest skin (40°C; P 0.001) but exercise in the heat caused the largest increase in core temperature, sweat rate, heart rate (post hoc comparisons all P 0.001) and systolic blood pressure (P ≤ 0.002), and possibly decrease in diastolic blood pressures (P ≤ 0.130), regardless of day. Thermal sensation and feeling state were more favourable on day 5 than on day 1 (P ≤ 0.021), with all modes of heat being equivalently uncomfortable (P ≥ 0.215). Plasma volume expanded the largest extent during immersions (P 0.001). The current data highlight that exercising in the heat generates a more complex strain profile, while passive heat stress in humid heat has lower tolerance and more cardiovascular strain than hot water immersion.

What is the central question of this study? What are the independent effects of air temperature and humidity on performance, physiological and perceptual responses during endurance exercise? What is the main finding and its importance? When examined independently, elevated air temperature increased heat strain and impaired aerobic exercise performance, but to a lesser extent than has been reported previously. These findings highlight the importance of absolute humidity relative to temperature when exercising or working under severe heat stress.Many studies have reported that ambient heat stress increases physiological and perceptual strain and impairs endurance exercise, but effects of air temperature per se remain almost unexamined. Most studies have used matched relative humidity, thereby exponentially increasing absolute humidity (water content in air) concurrently with temperature. Absolute (not relative) humidity governs evaporative rate and is more important at higher work rates and air temperatures. Therefore, we examined the independent effects of air temperature and humidity on performance, thermal, cardiovascular and perceptual measures during endurance exercise. Utilizing a crossover design, 14 trained participants (7 females) completed 45 min fixed-intensity cycling (70%

Purpose Cognition can be impaired during exercise in the heat, potentially contributing to military casualties. To our knowledge, the independent role of elevated core temperature during exercise has not been determined. The aim of the current study was to evaluate effects of elevated core temperature on cognition during physically encumbering, heated exercise, and to determine whether the perceptual cooling effects of menthol preserves cognition. Methods Eight participants complete three trials in randomised order: one normothermic (CON) and two with elevated (38.5°C) core temperature, induced by prior immersion in neutral versus hot water The CON trial and one hot trial (HOT) used a water mouth-rinse following each cognitive task of the trial, (HOT) while the other used a menthol mouth-rinse (MENT). Participants walked in humid heat (33°C, 75% relative humidity) in military clothing, completing a cognitive battery of reaction time, perceptual processing, working memory, executive function, cognitive flexibility, vigilance, and declarative memory. Results No differences in cognitive performance were observed between any conditions. Near-infrared spectroscopy showed greater oxygenated haemoglobin tissue content in HOT and MENT compared to CON (ΔO2Hb-deO2Hb: 2.3 ± 4.5 µM, p

Teaching traditionally asserts that the arterial pressure pulse is dampened across the capillary bed to the extent that pulsatility is nonexistent in the venous circulation of the lower limbs. Herein, we present evidence of transmission of arterial pulsations across the capillary network into perforator veins in the lower limbs of healthy, heat-stressed humans. Perforator veins are connections from the superficial veins that drain into the deep veins. When assessed using ultrasound at rest, they infrequently demonstrate flow, and a pulsatile flow waveform is not described. We investigated perforator vein pulsatility in 10 young, healthy volunteers who underwent passive heating by +2°C core body temperature via a hot-water-perfused suit, and 5 who also underwent active heating by +2°C via low-intensity cycling while wearing the hot-water-perfused suit. At +0.5°C increments in temperature, blood velocity in an ankle perforator vein was measured using duplex ultrasound. In all perforators with heating, sustained flow was demonstrated, with a pulsatile waveform that was synchronous with the cardiac cycle. The maximum velocity was 30 ± 13 cm/s with passive heating and approximately half with active heating ( P = 0.04). The small veins of the skin at the ankle also demonstrated increased perfusion with pulsatility, seen with low-velocity microvascular imaging technology. We consider explanations for this pulsatility and conclude that it is propagated from the arterial inflow through the skin microcirculation as a result of increased dilatation and flow volume and that this is a normal response to increased skin blood flow.

KEY POINTS Cognitive function depends on adequate cerebrovascular perfusion and control. However, it is unknown whether acutely-reduced cerebral blood flow (CBF) impairs cognition in healthy adults. In the present study, we used a placebo-controlled, single-blinded, randomized cross-over design to test the hypothesis that acutely-reduced CBF (using a pharmacological aid; indomethacin) would impair cognition in young and older healthy adults. At baseline, older adults had lower cognitive performance and CBF, but similar cerebrovascular reactivity to CO2 and dynamic cerebral autoregulation compared to young adults. In both young and older adults, cognitive performance on a mental switching task was slightly (7%) reduced after indomethacin, but not significantly associated with reductions in CBF (∼31%). These results indicate that cognitive performance is broadly resilient against a ∼31% reduction in CBF per se in healthy young and older adults. ABSTRACT Cognitive function depends on adequate cerebrovascular perfusion and control. However, it is unknown whether acutely-reduced cerebral blood flow (CBF) impairs cognition in healthy adults. Using a placebo-controlled, single-blinded, randomized cross-over design, we tested the hypothesis that acutely-reduced CBF (using indomethacin [1.2 mg kg-1 oral dose]) would impair cognition in young (n = 13; 25 ± 4 years) and older (n = 12; 58 ± 6 years) healthy adults. CBF and cerebrovascular control were measured using middle cerebral artery blood velocity (MCAvmean ) and its reactivity to hypercapnia (CVRHYPER ) and hypocapnia (CVRHYPO ), respectively. Cognitive function was assessed using a computerized battery including response time tasks. Baseline comparisons revealed that older adults had 14% lower MCAvmean and 15% lower cognitive performance (all P ≤ 0.048), but not lower CVRHYPER/HYPO (P ≥ 0.26). Linear and rank-based mixed models revealed that indomethacin decreased MCAvmean by 31% (95% confidence interval = -35 to -26), CVRHYPER by 68% [interquartile range (IQR) = -94 to -44] and CVRHYPO by 50% (IQR = -83 to -33) (treatment-effect; all P

New findings What is the central question of this study? How does resistance exercise affect peripheral haemodynamics in the active and inactive limb? What is the main finding and its importance? Preliminary data indicate that resistance exercise increases flow and shear rate in the active limb transiently. The same exercise has minimal, short-lasting influence on peripheral haemodynamics in the inactive limb, but further research is required to elaborate on resistance exercise-mediated changes in vascular function in active and inactive limbs. Abstract Current evidence indicates that to achieve maximum health benefits, regular resistance exercise should be a key component of structured physical activity. Several studies have revealed that regular resistance exercise may be associated with impaired vascular function, although this finding is inconsistent. Proposed explanations for impairment include substantial increases in blood pressure and increased retrograde blood flow in active limbs promoted by resistance exercise. However, few studies have examined the acute haemodynamics of resistance exercise in active - and even fewer in inactive - limbs. The purpose of this study was to characterise the haemodynamic responses in peripheral arteries in active and inactive limbs in response to resistance exercise using upper and lower limbs. Ten participants (five male, five female) familiar with resistance training performed three sets of 10 isotonic repetitions of right-sided bicep curls or knee extensions on separate days. Blood flow, shear rate and muscle oxygenation in the active and inactive limb, and blood pressure were measured before and for 3 min after each set. Blood flow increased in response to resistance exercise in the active limb (∼8-fold and ∼6-fold for the upper and lower limb respectively), with concurrent significant increases in mean and antegrade shear rate. In the inactive limb, blood flow more than doubled for both upper and lower limb exercise, transiently, with no significant change in retrograde shear rate. These acute blood flow profiles following resistance exercise are not indicative of long-term vessel impairment based on current understanding of blood flow and shear stress patterns.

Cardiopulmonary exercise testing is performed increasingly for cardiorespiratory fitness assessment and pre-operative risk stratification. Lower limb osteoarthritis is a common comorbidity in surgical patients, meaning traditional cycle ergometry-based cardiopulmonary exercise testing is difficult. The purpose of this study was to compare cardiopulmonary exercise testing variables and subjective responses in four different exercise modalities. In this crossover study, 15 patients with osteoarthritis scheduled for total hip or knee arthroplasty (mean (SD) age 68 (7) years; body mass index 31.4 (4.1) kg.m-2 ) completed cardiopulmonary exercise testing on a treadmill, elliptical cross-trainer, cycle and arm ergometer. Mean (SD) peak oxygen consumption was 20-30% greater on the lower limb modalities (treadmill 21.5 (4.6) (p < 0.001); elliptical cross-trainer (21.2 (4.1) (p < 0.001); and cycle ergometer (19.4 (4.2) ml.min-1 .kg-1 (p = 0.001), respectively) than on the arm ergometer (15.7 (3.7) ml.min-1 .kg-1 ). Anaerobic threshold was 25-50% greater on the lower limb modalities (treadmill 13.5 (3.1) (p < 0.001); elliptical cross-trainer 14.6 (3.0) (p < 0.001); and cycle ergometer 10.7 (2.9) (p = 0.003)) compared with the arm ergometer (8.4 (1.7) ml.min-1 .kg-1 ). The median (95%CI) difference between pre-exercise and peak-exercise pain scores was greater for tests on the treadmill (2.0 (0.0-5.0) (p = 0.001); elliptical cross-trainer (3.0 (2.0-4.0) (p = 0.001); and cycle ergometer (3.0 (1.0-5.0) (p = 0.001)), compared with the arm ergometer (0.0 (0.0-1.0) (p = 0.406)). Despite greater peak exercise pain, cardiopulmonary exercise testing modalities utilising the lower limbs affected by osteoarthritis elicited higher peak oxygen consumption and anaerobic threshold values compared with arm ergometry.

International audience; The increasing number of older adults has seen a corresponding growth in those affected by neurovascular diseases, including stroke and dementia. Since cures are currently unavailable, major efforts in improving brain health need to focus on prevention, with emphasis on modifiable risk factors such as promoting physical activity. Moderate-intensity continuous training (MICT) paradigms have been shown to confer vascular benefits translating into improved musculoskeletal, cardiopulmonary and cerebrovascular function. However, the time commitment associated with MICT is a potential barrier to participation, and high-intensity interval training (HIIT) has since emerged as a more time-efficient mode of exercise that can promote similar if not indeed superior improvements in cardiorespiratory fitness for a given training volume and further promote vascular adaptation. However, randomised controlled trials (RCTs) investigating the impact of HIIT on the brain are surprisingly limited. The present review outlines how the HIIT paradigm has evolved from a historical perspective and describes the established physiological changes including its mechanistic bases. Given the dearth of RCTs, the vascular benefits of MICT are discussed with a focus on the translational neuroprotective benefits including their mechanistic bases that could be further potentiated through HIIT. Safety implications are highlighted and components of an optimal HIIT intervention are discussed including practical recommendations. Finally, statistical effect sizes have been calculated to allow prospective research to be appropriately powered and optimise the potential for detecting treatment effects. Future RCTs that focus on the potential clinical benefits of HIIT are encouraged given the prevalence of cognitive decline in an ever-ageing population.

Cognition, cerebral blood flow (CBF) and its major regulator (i.e., arterial CO2), increase with submaximal exercise and decline with severe exercise. These responses may depend on fitness. We investigated whether exercise-related changes in cognition are mediated in part by concomitant changes in CBF and CO2, in ten active (26 ± 3 years) and ten inactive (24 ± 6 years) healthy adults. Participants completed two randomised sessions; exercise and a resting CO2-control—wherein end-tidal CO2 (PETCO2) was matched between sessions and clamped across conditions at exercise-associated increases (+ 3 mmHg) and hypercapnia (+ 10 mmHg). Exercise comprised inclined walking at submaximal and severe intensities. CBF was indexed using right middle cerebral artery blood velocity (MCAv). Cognition (visuomotor, switching and inhibitory response time) was measured before, during, and after exercise. MCAv and its inverted-U response to exercise were comparable between groups, whereas visuomotor performance improved during submaximal exercise in the active group only (p = 0.046). Submaximal, but not severe (p = 0.33), exercise increased MCAv (p ≤ 0.03). Hypercapnia increased MCAv during the CO2-control (27 ± 12%) and during submaximal exercise (39 ± 17%; p

Recent studies have determined that ambient humidity plays a more important role in aerobic performance than dry-bulb temperature does in warm environments; however, no studies have kept humidity constant and independently manipulated temperature. Therefore, the purpose of this study was to determine the contribution of dry-bulb temperature, when vapor pressure was matched, on the thermoregulatory, perceptual and performance responses to a 30-min cycling work trial. Fourteen trained male cyclists (age: 32 ± 12 year; height: 178 ± 6 cm; mass: 76 ± 9 kg; $$\dot{V}{\text{O}}_{{{2}\,{\max}}}$$: 59 ± 9 mL kg−1 min−1; body surface area: 1.93 ± 0.12 m2; peak power output: 393 ± 53 W) volunteered, and underwent 1 exercise bout in moderate heat (MOD: 34.9 ± 0.2 °C, 50.1 ± 1.1% relative humidity) and 1 in mild heat (MILD: 29.2 ± 0.2 °C, 69.4 ± 0.9% relative humidity) matched for vapor pressure (2.8 ± 0.1 kPa), with trials counterbalanced. Despite a higher weighted mean skin temperature during MOD (36.3 ± 0.5 vs. 34.5 ± 0.6 °C, p

Humans hyperventilate under heat and cold strain. This hyperventilatory response has detrimental consequences including acid-base dysregulation, dyspnoea, decreased cerebral blood flow and accelerated brain heating. The ventilatory response to hypoxia is exaggerated under whole-body heating and cooling, indicating that altered carotid body function might contribute to thermally mediated hyperventilation. To address whether the carotid body might contribute to heat- and cold-induced hyperventilation, we indirectly measured carotid body tonic activity via hyperoxia, and carotid body sensitivity via hypoxia, under graded heat and cold strain in 13 healthy participants in a repeated-measures design. We hypothesised that carotid body tonic activity and sensitivity would be elevated in a dose-dependent manner under graded heat and cold strain, thereby supporting its role in driving thermally mediated hyperventilation. Carotid body tonic activity was increased in a dose-dependent manner with heating, reaching 175% above baseline (P 0.0005), and carotid body suppression with hyperoxia removed all of the heat-induced increase in ventilation (P = 0.9297). Core cooling increased carotid body activity by up to 250% (P 0.0001), but maximal values were reached with mild cooling and thereafter plateaued. Carotid body sensitivity to hypoxia was profoundly increased by up to 180% with heat stress (P = 0.0097), whereas cooling had no detectable effect on hypoxic sensitivity. In summary, cold stress increased carotid body tonic activity and this effect was saturated with mild cooling, whereas heating had clear dose-dependent effects on carotid body tonic activity and sensitivity. These dose-dependent effects with heat strain indicate that the carotid body probably plays a primary role in driving heat-induced hyperventilation. KEY POINTS: Humans over-breathe (hyperventilate) when under heat and cold stress, and though this has detrimental physiological repercussions, the mechanisms underlying this response are unknown. The carotid body, a small organ that is responsible for driving hyperventilation in hypoxia, was assessed under incremental heat and cold strain. The carotid body drive to breathe, as indirectly assessed by transient hyperoxia, increased in a dose-dependent manner with heating, reaching 175% above baseline; cold stress similarly increased the carotid body drive to breathe, but did not show dose-dependency. Carotid body sensitivity, as indirectly assessed by hypoxic ventilatory responses, was profoundly increased by 70-180% with mild and severe heat strain, whereas cooling had no detectable effect. Carotid body hyperactivity and hypersensitivity are two interrelated mechanisms that probably underlie the increased drive to breathe with heat strain, whereas carotid body hyperactivity during mild cooling may play a subsidiary role in cold-induced hyperventilation.

We investigated whether substituting the final half within 60-min bouts of exercise with passive warm or cold water immersion would provide similar or greater benefits for cardiometabolic health. Thirty healthy participants were randomized to two of three short-term training interventions in a partial crossover (12 sessions over 14–16 days, 4 week washout): (i) EXS: 60 min cycling 70% maximum heart rate (HRmax), (ii) WWI: 30 min cycling then 30 min warm water (38–40°C) immersion, and/or (iii) CWI: 30 min cycling then 30 min cold water (10–12°C) immersion. Before and after, participants completed a 20 min cycle work trial, V.O2max test, and an Oral Glucose Tolerance Test during which indirect calorimetry was used to measure substrate oxidation and metabolic flexibility (slope of fasting to post-prandial carbohydrate oxidation). Data from twenty two participants (25 ± 5 year, BMI 23 ± 3 kg/m2, Female = 11) were analyzed using a fixed-effects linear mixed model. V.O2max increased more in EXS (interaction p = 0.004) than CWI (95% CI: 1.1, 5.3 mL/kg/min, Cohen’s d = 1.35), but not WWI (CI: −0.4, 3.9 mL/kg/min, d = 0.72). Work trial distance and power increased 383 ± 223 m and 20 ± 6 W, respectively, without differences between interventions (interaction both p > 0.68). WWI lowered post-prandial glucose ∼9% (CI −1.9, −0.5 mmol/L; d = 0.63), with no difference between interventions (interaction p = 0.469). Substituting the second half of exercise with WWI provides similar cardiometabolic health benefits to time matched exercise, however, substituting with CWI does not.

BackgroundMilitary personnel often deploy into hot environments that impose substantial strain on physical and cognitive performance. Hot environments can present as arid or humid and occur in different terrains, requiring different operational approaches. The aim of this study was to characterise the physiological, cognitive and perceptual strain experienced by military personnel during typical operations in arid and humid environments. MethodsNine pack-fit military personnel participated in two heat-stress tests to exhaustion, one in an arid environment (44°C, 21% humidity) and the other in a humid environment (33°C, 78% humidity). Participants walked at 5 km.h-1 while physiological, cognitive and perceptual measures were recorded. Tests were terminated volitionally, or by excessive core temperature or heart rate. Results The operational environments induced similar physiological stress, resulting in no difference in time to exhaustion (p = .155). The humid environment saw a greater elevation in core temperature (+0.3°C, p < .001) and heart rate (+5 b.min-1, p < .001). Skin temperature was greater in the arid environment (+0.4, p < .001) as was sweat evaporation (+0.3 L.h1, p = .045). Baseline performance predictors only provided moderate predictions of performance, whereas changes in perceptual measures provided the best performance predictors during the exercise, specifically perceptions relating to thermal sensation (β = -.65 - -.80) and sleepiness (β = -.79 - -.87). While no differences in cognitive performance were observed, greater cognitive stress was reported by participants over time, regardless of environment (all p < .011). ConclusionsThe humid operational environment elicited a greater thermal strain that may threaten safety, and impair performance, to a greater degree than the arid environment. Perceptual measures of thermal sensation and sleepiness were the best predictors of test termination and could likely be used to monitor thermal tolerance in field settings.

NEW FINDINGS What is the central question of this study? Does habitual resistance and endurance exercise modify dynamic cerebral autoregulation? What is the main finding and its importance? To the authors' knowledge, this is the first study to directly assess dynamic cerebral autoregulation in resistance-trained individuals, and potential differences between exercise training modalities. Forced oscillations in blood pressure were induced by repeated squat-stands, from which dynamic cerebral autoregulation was assessed using transfer function analysis. These data indicate that dynamic cerebral autoregulatory function is largely unaffected by habitual exercise type, and further document the systemic circulatory effects of regular exercise. ABSTRACT Regular endurance and resistance exercise produce differential but desirable physiological adaptations in both healthy and clinical populations. The chronic effect of these different exercise modalities on cerebral vessels' ability to respond to rapid changes in blood pressure (BP) had not been examined. We examined dynamic cerebral autoregulation (dCA) in 12 resistance-trained (mean ± SD, 25 ± 6 years), 12 endurance-trained (28 ± 9 years) and 12 sedentary (26 ± 6 years) volunteers. The dCA was assessed using transfer function analysis of forced oscillations in BP vs. middle cerebral artery blood velocity (MCAv), induced via repeated squat-stands at 0.05 and 0.10 Hz. Resting BP and MCAv were similar between groups (interaction: both P ≥ 0.544). The partial pressure of end-tidal carbon dioxide ( PETCO2 ) was unchanged (P = 0.561) across squat-stand manoeuvres (grouped mean for absolute change +0.6 ± 2.3 mmHg). Gain and normalized gain were similar between groups across all frequencies (both P ≥ 0.261). Phase showed a frequency-specific effect between groups (P = 0.043), tending to be lower in resistance-trained (0.63 ± 0.21 radians) than in endurance-trained (0.90 ± 0.41, P = 0.052) and -untrained (0.85 ± 0.38, P = 0.081) groups at slower frequency (0.05 Hz) oscillations. Squat-stands induced mean arterial pressure perturbations differed between groups (interaction: P = 0.031), with greater changes in the resistance (P

Tokyo 2020 will likely be the most heat stressful Olympics to date, so preparation to mitigate the effects of humid heat will be essential for performance in several of the 33 sports. One key consideration is heat acclimation (HA); the repeated exposure to heat to elicit physiological and psychophysical adaptations that improve tolerance and exercise performance in the heat. Heat can be imposed in various ways, including exercise in the heat, hot water immersion, or passive exposure to hot air (e.g., sauna). The physical requirements of each sport will determine the impact that the heat has on performance, and the adaptations required from HA to mitigate these effects. This review focuses on one key adaptation, plasma volume expansion (PVE), and how the mode of HA may affect the kinetics of adaptation. PVE constitutes a primary HA-mediated adaptation and contributes to functional adaptations (e.g., lower heart rate and increased heat loss capacity), which may be particularly important in athletes of “sub-elite” cardiorespiratory fitness (e.g., team sports), alongside athletes of prolonged endurance events. This review: i) highlights the ability of exercise in the heat, hot-water immersion, and passive hot air to expand PV, providing the first quantitative assessment of the efficacy of different heating modes; ii) discusses how this may apply to athletes at Tokyo 2020; and iii) provides recommendations regarding the protocol of HA and the prospect for achieving PVE (and the related outcomes).

A growing body of evidence indicates regular physical activity benefits older adults’ cognitive functioning, particularly when a high level of cognitive control is required. Recent research has pointed to improved cerebrovascular function as one mechanism through which such benefits might arise. This study built on previous research by investigating in 51 healthy older adults aged 60–72 years relationships between habitual physical activity, cerebrovascular function (indicated by resting cerebral blood flow velocity in the middle cerebral artery [n = 42], and its responsiveness to hypercapnia [n = 26] and hypocapnia [n = 25]), and cognitive control (inhibition and switching). Linear regression analyses showed moderate positive associations between physical activity and inhibitory control, but not cerebrovascular function. There were also no significant relationships between the cerebrovascular measures and cognitive control. These results indicate that regular engagement in physical activity is associated with superior inhibitory control in older adulthood, but cerebrovascular function was not found to explain those relationships. Taken together, the current findings reinforce reports of positive links between habitual physical activity and cognition in healthy older adults, but also signal that interrelationships with cerebrovascular function may be more complex than currently indicated by the literature, necessitating further research to elucidate the role cerebrovascular function might play in accounting for physical activity-cognition links in healthy older adults.

KEY POINTS The human brain is particularly vulnerable to heat stress; this manifests as impaired cognition, orthostatic tolerance, work capacity and eventually, brain death. The brain's limitation in the heat is often ascribed to inadequate cerebral blood flow (CBF), but elevated intracranial pressure is commonly observed in mammalian models of heat stroke and can on its own cause functional impairment. The CBF response to incremental heat strain was dependent on the mode of heating, decreasing by 30% when exposed passively to hot, humid air (sauna), while remaining unchanged or increasing with passive hot-water immersion (spa) and exercising in a hot environment. Non-invasive intracranial pressure estimates (nICP) were increased universally by 18% at volitional thermal tolerance across all modes of heat stress, and therefore may play a contributing role in eliciting thermal tolerance. The sauna, more so than the spa or exercise, poses a greater challenge to the brain under mild to severe heating due to lower blood flow but similarly increased nICP. ABSTRACT The human brain is particularly vulnerable to heat stress; this manifests as impaired cognitive function, orthostatic tolerance, work capacity, and eventually, brain death. This vulnerability is often ascribed to inadequate cerebral blood flow (CBF); however, elevated intracranial pressure (ICP) is also observed in mammalian models of heat stroke. We investigated the changes in CBF with incremental heat strain under three fundamentally different modes of heating, and assessed whether heating per se increased ICP. Fourteen fit participants (seven female) were heated to thermal tolerance or 40°C core temperature (Tc ; oesophageal) via passive hot-water immersion (spa), passive hot, humid air exposure (sauna), cycling exercise, and cycling exercise with CO2 inhalation to prevent heat-induced hypocapnia. CBF was measured with duplex ultrasound at each 0.5°C increment in Tc and ICP was estimated non-invasively (nICP) from optic nerve sheath diameter at thermal tolerance. At thermal tolerance, CBF was decreased by 30% in the sauna (P

Background Attenuated increases in ventricular stroke volume during exercise are common in type 2 diabetes and contribute to reduced aerobic capacity. The purpose of this study was to determine whether impaired ventricular filling or reduced systolic ejection were responsible for the attenuated stroke volume reserve in people with uncomplicated type 2 diabetes. Methods Peak aerobic capacity and total blood volume were measured in 17 people with diabetes and 16 non-diabetic controls with no evidence of cardiovascular disease. Left ventricular volumes and other systolic and diastolic functional parameters were measured with echocardiography at rest and during semi-recumbent cycle ergometry at 40 and 60% of maximal aerobic power and compared between groups. Results People with diabetes had reduced peak aerobic capacity and heart rate reserve, and worked at lower workloads than non-diabetic controls. Cardiac output, stroke volume and ejection fraction were not different at rest, but increased less in people with diabetes during exercise. Left ventricular end systolic volume was not different between groups in any condition but end diastolic volume, although not different at rest, was smaller in people with diabetes during exercise. Total blood volume was not different between the groups, and was only moderately associated with left ventricular volumes. Conclusions People with type 2 diabetes exhibit an attenuated increase in stroke volume during exercise attributed to an inability to maintain/increase left ventricular filling volumes at higher heart rates. This study is the first to determine the role of filling in the blunted cardiac reserve in adults with type 2 diabetes. Electronic supplementary material The online version of this article (10.1186/s12933-017-0644-1) contains supplementary material, which is available to authorized users.

The aim of this meta-analysis was to determine the effectiveness of spinal manipulation in influencing various biochemical markers in healthy and or symptomatic population. Electronic databases (n = 10) were searched (from inception till September 2016) and eight trials (325 participants) that met the inclusion criteria were included in the meta-analysis. Two authors independently extracted and assessed the risk of bias in included studies. Standardised mean differences for outcome measures were used to calculate effect sizes. The Grading of Recommendations, Assessment, Development and Evaluation (GRADE) tool was used for assessing the quality of the body of evidence for each outcome of interest. There was moderate quality evidence that spinal manipulation influenced biochemical markers. There was moderate quality evidence of significant difference that spinal manipulation is better (SMD -0.46, 95% CI - 0.93 to 0) than control in eliciting changes in cortisol levels immediately after intervention. There was also a low quality evidence that spinal manipulation is better than control at post-intervention in increasing substance-P (SMD -0.48,95%CI-0.87 to −0.1), neurotensin (SMD -1.8,95%CI-2.56 to −1.04) and oxytocin levels (SMD -2.61,95%CI-3.5to-1.72). However, low quality evidence indicated that spinal manipulation did not influence epinephrine (SMD 0.1,95%CI- 0.56to0.75) or nor-epinephrine levels (SMD -0.06,95%CI-0.71to0.6). The current review found that spinal manipulation can increase substance-p, neurotensin, oxytocin and interleukin levels and may influence cortisol levels post-intervention. However, future trials targeting symptomatic populations are required to understand the clinical importance of such changes.

Passive heat induces beneficial perfusion profiles, provides substantive cardiovascular strain, and reduces blood pressure, thereby holding potential for healthy and cardiovascular disease populations. The aim of this study was to assess acute responses to passive heat via lower-limb, hot-water immersion in patients with peripheral arterial disease (PAD) and healthy, elderly controls. Eleven patients with PAD (age 71 ± 6 yr, 7 male, 4 female) and 10 controls (age 72 ± 7 yr, 8 male, 2 female) underwent hot-water immersion (30-min waist-level immersion in 42.1 ± 0.6°C water). Before, during, and following immersion, brachial and popliteal artery diameter, blood flow, and shear stress were assessed using duplex ultrasound. Lower-limb perfusion was measured also using venous occlusion plethysmography and near-infrared spectroscopy. During immersion, shear rate increased ( P < 0.0001) comparably between groups in the popliteal artery (controls: +183 ± 26%; PAD: +258 ± 54%) and brachial artery (controls: +117 ± 24%; PAD: +107 ± 32%). Lower-limb blood flow increased significantly in both groups, as measured from duplex ultrasound (>200%), plethysmography (>100%), and spectroscopy, while central and peripheral pulse-wave velocity decreased in both groups. Mean arterial blood pressure was reduced by 22 ± 9 mmHg (main effect P < 0.0001, interaction P = 0.60) during immersion, and remained 7 ± 7 mmHg lower 3 h afterward. In PAD, popliteal shear profiles and claudication both compared favorably with those measured immediately following symptom-limited walking. A 30-min hot-water immersion is a practical means of delivering heat therapy to PAD patients and healthy, elderly individuals to induce appreciable systemic (chronotropic and blood pressure lowering) and hemodynamic (upper and lower-limb perfusion and shear rate increases) responses.

Key points Despite an attenuated fluctuation in ovarian hormone concentrations in well-trained women, one in two of such women believe their menstrual cycle negatively impacts training and performance. Forthcoming large international events will expose female athletes to hot environments, and studies evaluating aerobic exercise performance in such environments across the menstrual cycle are sparse, with mixed findings. We have identified that autonomic heat loss responses at rest and during fixed-intensity exercise in well-trained women are not affected by menstrual cycle phase, but differ between dry and humid heat. Furthermore, exercise performance is not different across the menstrual cycle, yet is lower in humid heat, in conjunction with reduced evaporative cooling. Menstrual cycle phase does not appear to affect exercise performance in the heat in well-trained women, but humidity impairs performance, probably due to reduced evaporative power. Abstract We studied thermoregulatory responses of ten well-trained [VO2 max , 57 (7) ml min−1 kg−1] eumenorrheic women exercising in dry and humid heat, across their menstrual cycle. They completed four trials, each of resting and cycling at fixed intensities (125 and 150 W), to assess autonomic regulation, then self-paced intensity (30 min work trial), to assess behavioural regulation. Trials were in early-follicular (EF) and mid-luteal (ML) phases in dry (DRY) and humid (HUM) heat matched for wet bulb globe temperature (WBGT, 27°C). During rest and fixed-intensity exercise, rectal temperature was ∼0.2°C higher in ML than EF (P

Cognition, cerebral blood flow (CBF) and its major regulator (i.e., arterial COParticipants completed two randomised sessions; exercise and a resting COMCAv and its inverted-U response to exercise were comparable between groups, whereas visuomotor performance improved during submaximal exercise in the active group only (p = 0.046). Submaximal, but not severe (p = 0.33), exercise increased MCAv (p ≤ 0.03). Hypercapnia increased MCAv during the COAcute increases in PETCO

To examine the interactive effects of VM and isometric resistance exercise on cerebral haemodynamics. Eleven healthy participants (mean ± SD 28 ± 9 years; 2 females) completed 20-s bilateral isometric leg extension at 50% of maximal voluntary contraction with continued ventilation (RE), a 20-s VM at mouth pressure of 40 mmHg (VM), and a combination (RE + VM), in randomised order. Mean beat-to-beat blood velocity in the posterior (PCAvmean) and middle cerebral arteries (MCAvmean), vertebral artery blood flow, end-tidal partial pressure of CO2 and mean arterial pressure (MAP) were measured. RE data were time aligned to RE + VM and analysed according to standard VM phases. Interaction effects (VM phase × condition) were observed for MCAvmean, PCAvmean, vertebral artery blood flow and MAP (all ≤ 0.010). Phase I MCAvmean was greatest for RE [88 ± 19, vs. 71 ± 11 and 78 ± 12 cm s−1 for VM (P = 0.008) and RE + VM (P = 0.021), respectively]. Greater increases in MCAvmean than PCAvmean occurred in phase I of RE only (24 ± 15% vs. 16 ± 16%, post hoc P = 0.044). In phase IIb, MAP was lower in RE than RE + VM (115 ± 15 vs. 138 ± 21 mmHg, P = 0.004), but did not reduce MCAvmean (78 ± 8 vs. 79 ± 9 cm s−1, P = 0.579) or PCAvmean (45 ± 11 vs .46 ± 11 cm s−1, P = 0.617). Phase IIb MCAvmean and PCAvmean was lowest in VM (66 ± 6 and 39 ± 8 cm s−1, respectively, all P

The purpose of the present study was to determine the neuroendocrine response after a thoracic spinal manipulation in people with Achilles tendinopathy.This was a randomized 2-sequence, 2-period crossover trial. A total of 24 participants, mean (standard deviation) age of 48 (7) years, with a diagnosis of Achilles tendinopathy (3 mo) were randomly assigned into sequence 1 (sham intervention and then thoracic spinal manipulation) or sequence 2 (thoracic spinal manipulation and then sham intervention). The trial was conducted at a university laboratory with a washout period of 1 week. The primary outcome measure was the testosterone/cortisol (T/C) ratio (salivary samples). The secondary outcome measures included heart rate variability (measured with electrocardiography) and total oxygenation index (nmol/L) of calf muscle and Achilles tendon (measured with near-infrared spectroscopy). A 2-way mixed-model analysis of variance was performed. The statistic of interest was the condition by time interaction.A statistically significant condition by time interaction was found for the T/C ratio (mean difference: -0.16; confidence interval: -0.33 to 0.006; interaction: P.05) and the total oxygenation index (mean difference: 1.35; confidence interval: -1.3 to 4.1; interaction: P.05) of calf muscle but not for Achilles tendon (P = .6); however, no difference was found for heart rate variability (P = .5).In people with Achilles tendinopathy, thoracic spinal manipulation resulted in immediate increase in the total oxygenation index in the calf muscle followed by an increase in the T/C ratio 6 hours post-intervention.

NEW FINDINGS What is the central question of the study? What are the effects of acute mental stress on the mechanisms regulating cerebral blood flow? What is the main finding and its importance? The major new findings are as follows: (i) high mental stress and hypercapnia had an interactive effect on mean middle cerebral artery blood velocity; (ii) high mental stress altered the regulation of cerebral blood flow; (iii) the increased cerebrovascular hypercapnic reactivity was not driven by changes in mean arterial pressure alone; and (iv) this increased perfusion with mental stress appeared not to be justified functionally by an increase in oxygen demand (as determined by near-infrared spectroscopy-derived measures). ABSTRACT In this study, we examined the effects of acute mental stress on cerebrovascular function. Sixteen participants (aged 23 ± 4 years; five female) were exposed to low and high mental stress using simple arithmetic (counting backwards from 1000) and more complex arithmetic (serial subtraction of 13 from a rapidly changing four-digit number), respectively. During consecutive conditions of baseline, low stress and high stress, end-tidal partial pressure of CO2 ( PET,CO2 ) was recorded at normocapnia (37 ± 3 mmHg) and clamped at two elevated levels (P

Peripheral arterial disease (PAD) is characterized by lower limb atherosclerosis impairing blood supply and causing walking-induced leg pain or claudication. Adherence to traditional exercise training programs is poor due to these symptoms despite exercise being a mainstay of conservative treatment. Heat therapy improves many cardiovascular health outcomes, so this study tested if this was a viable alternative cardiovascular therapy for PAD patients. Volunteers with PAD were randomized to 12 wk of heat ( n = 11; mean age 76 ± 8 yr, BMI 28.7 ± 3.5 kg/m2, 4 females) or exercise ( n = 11; 74 ± 10 yr, 28.5 ± 6.8 kg/m2, 3 females). Heat involved spa bathing at ∼39°C, 3–5 days/wk for ≤30 min, followed by ≤30 min of callisthenics. Exercise involved ≤90 min of supervised walking and gym-based exercise, 1–2 days/wk. Following the interventions, total walking distance during a 6-min walk test increased (from ∼350 m) by 41 m (95% CI: [13, 69], P = 0.006) regardless of group, and pain-free walking distance increased (from ∼170 m) by 43 m ([22, 63], P < 0.001). Systolic blood pressure was reduced more following heat (−7 mmHg, [−4, −10], P < 0.001) than following exercise (−3 mmHg, [0, −6], P = 0.078), and diastolic and mean arterial pressure decreased by 4 mmHg in both groups ( P = 0.002). There were no significant changes in blood volume, ankle-brachial index, or measures of vascular health. There were no differences in the improvement in functional or blood pressure outcomes between heat and exercise in individuals with PAD. NEW & NOTEWORTHY Heat therapy via hot-water immersion and supervised exercise both improved walking distance and resting blood pressure in peripheral arterial disease (PAD) patients over 12 wk. Adherence to heat therapy was excellent, and the heat intervention was well tolerated. The results of the current study indicate that heat therapy can improve functional ability and has potential as an effective cardiovascular conditioning tool for individuals with PAD. Listen to this article's corresponding podcast at https://ajpheart.podbean.com/e/heat-therapy-vs-exercise-in-peripheral-arterial-disease/ .

Type 2 diabetes is associated with reduced left ventricular reserve. It is unclear whether exercise training improves left ventricular function in people with type 2 diabetes.This study aimed to determine whether 3 months of high-intensity interval training (HIIT) improves left ventricular function during exercise in adults with type 2 diabetes.Participants performed a V˙O2peak test and received a DXA scan and total blood volume measurement at baseline. Left ventricular end-diastolic volume (LVEDV), left ventricular end-systolic volume (LVESV), and left ventricular stroke volume (LVSV) were then measured at rest and during low- and moderate-intensity semirecumbent exercise in adults with type 2 diabetes before and after 3 months of HIIT (n = 11) or no training (control) (n = 5). The effects of HIIT were determined using repeated-measures ANOVA.HIIT increased V˙O2peak by approximately 15% (P0.002) but did not change body composition or total blood volume. LVESV decreased and LVEDV and LVSV increased from rest to moderate-intensity exercise in both groups at baseline (all P0.01). Three months of HIIT increased LVEDV (P = 0.008) and LVSV (P = 0.02) at all conditions, but there was no difference in controls (all P0.05). HIIT augmented the reduction in LVESV from rest to moderate-intensity exercise (P0.04), but LVESV was unchanged in controls. Increased LVEDV explained 51% of the change in LVSV after HIIT intervention. Mitral inflow parameters and mitral annular velocities were unaffected by HIIT (all P0.05).HIIT training increased the LVSV response to exercise in adults with type 2 diabetes. These data suggest that HIIT can improve LV filling and emptying during exercise and reverse early cardiac consequences of type 2 diabetes.

Human physiological responses to heat, cold, hypoxia, microgravity, hyperbaria, hypobaria and fasting are well studied in isolation. However, in the natural world these stressors are often combined or experienced sequentially (Tipton, 2012). Studies examining human responses to these more realistic, yet relatively complex, circumstances remain sparse, but could provide important insights into an emerging area within human physiology: cross-adaptation (Figure 1)(Lunt et al., 2010; Gibson et al., 2017). Much of the current state of knowledge involves data demonstrating benefits of exercising in hot conditions, prior to performance in hypoxia (Gibson et al., 2015; Heled et al., 2012; Lee et al., 2014a, 2014b, 2016; Salgado et al., 2017; White et al., 2016), with cold to hypoxia (Lunt et al., 2010), hypoxia to heat (Sotiridis et al., 2018), combined stressors (Neal et al., 2017; Takeno et al., 2001), and more mechanistic (signalling) data from animal models exposed to substantive volumes of stress (Maloyan & Horowitz, 2002, 2005). The role of nutrient availability and the nutrient-exercise interactions which drive phenotypic adaptations to skeletal muscle exposed to a multitude of stressors is also a growing field of interest (Hawley, Lundby, Cotter, & Burke, 2018). This research topic includes publications which address both clinical and exercise-centric aspects allied to Cross-adaptation and Cross-tolerance in Human Health and Disease.

Open-water swimming (OWS) is undertaken in diverse bodies of water and climatic locations, over distances mostly between 1.5 and 88 km. OWS provides a unique and potentially hazardous thermoregulatory challenge for multiple reasons, but the lack of information on physiological, performance and health effects is conspicuous and surprising. At least one heat-related death and numerous cold-related deaths provide sobering testament to these challenges. Net effects are difficult to predict because of large and typically opposing influences of the exercise medium, temperature, posture, arm-based mode and the individual differences in fitness and anthropometry. For example, evaporative power is essentially nullified but is counteracted by the high convective power of water immersion. Immersion and exercise have opposing effects on blood volume but dehydration-induced hypovolaemia will typically develop for physical, physiological and practical reasons. Competition between metabolic and thermoregulatory demands for cardiac output is lessened by the posture, immersion effects and location of active musculature, but increased by the reliance on convective heat loss. Behavioural thermoregulation may be more important than in terrestrial exercise but concomitantly impaired for practical and potentially also physiological (thermo-afferent) reasons. This chapter addresses such issues and provides resultant advice on potential countermeasures including those discussed in detail but generic contexts in preceding chapters.

Exercise-associated hyponatremia can be life-threatening. Excessive hypotonic fluid ingestion is the primary etiological factor but does not explain all variability. Possible effects of chronic sodium intake are unknown. The aim of this study was to determine whether dietary sodium affects plasma sodium concentration [Na+] during exercise in the heat, when water intake nearly matches mass loss. Endurance-trained men (n = 9) participated in this crossover experiment. Each followed a low-sodium (lowNa) or high-sodium (highNa) diet for 9 days with 24-h fluid intakes and urine outputs measured before experimental trials (day 10). The trials were ≥2 week apart. Trials comprised 3 h (or if not possible to complete, to exhaustion) cycling (55% VO2max; 34 °C, 65% RH) with water intake approximating mass loss. Plasma [Na+], hematocrit, sweat and urine [Na+], heart rate, core temperature, and subjective perceptions were monitored. Urine [Na+] was lower on lowNa 24 h prior to (31 ± 24, 76 ± 30 mmol/L, P = 0.027) and during trials (10 ± 10, 52 ± 32 mmol/L, P = 0.004). Body mass was lower on lowNa (79.6 ± 8.5, 80.5 ± 8.9, P = 0.03). Plasma [Na+] was lower on lowNa before (137 ± 2, 140 ± 3, P = 0.007) and throughout exercise (P = 0.001). Sweat [Na+] was unaffected by diet (54.5 ± 40, 54.5 ± 23 mmol/L, P = 0.99). Heart rate and core temperature were higher on lowNa (P ≤ 0.001). Despite decreased urinary sodium losses, plasma sodium was lower on lowNa, with decreased mass indicating (extracellular) water may have been less, explaining greater heart rate and core temperature. General population health recommendations to lower salt intake may not be appropriate for endurance athletes, particularly those training in the heat.

Purpose: To examine the retention and re-acclimation responses during a periodized heat acclimation (HA) protocol in elite sailors preparing for the 2013 World Championships in Muscat, Oman (∼27–30°C, 40–60% RH). Methods: Two elite male Laser class sailors completed 5 consecutive days of HA (60 min per day in 35°C, 60% RH). Heat response tests (HRT) were performed on day 1 and 5 of HA, then 1 (decay 1, D1) and 2 (D2) weeks following HA. Participants were then re-acclimated (RA) for 2 days, within the next week, before a final HRT ∼72 h post-RA. Rectal temperature, plasma volume, heart rate, sweat rate, as well as thermal discomfort and rating of perceived exertion were measured during each HRT. Results: Rectal temperature decreased with HA (0.46 ± 0.05°C), while individual responses following D1, D2 and RA varied. Heart rate (14 ± 7 bpm), thermal discomfort (0.6 ± 0.1 AU) and rating of perceived exertion (1.8 ± 0.6 AU) decreased across HA, and adaptations were retained by D2. Plasma volume steadily increased over the decay period (D2 = 8.0 ± 1.3%) and after RA (15.5 ± 1.1%) compared with baseline. RA resulted in further thermoregulatory improvements in each Athlete, although individual adjustments varied. Conclusion: Heat strain was reduced in elite Laser sailors following HA and most thermoregulatory adaptations were retained for 2 weeks afterwards. RA may ‘top up’ adaptations after 2 weeks of HA decay.

Alongside age-related brain deterioration, cognitive functioning declines, particularly for more demanding tasks. Past research indicates that, to offset this decline, older adults exhibit hemodynamic changes consistent with recruitment of more anterior brain regions. However, the nature of the hemodynamic changes remains unclear. To address this knowledge gap, we used near-infrared spectroscopy in 36 young adults (aged 18-30 years) and 36 older adults (aged 60-72 years) to assess anterior frontal hemodynamic responses to engagement in three cognitive tasks of increasing difficulty. Behavioral results for all three tasks confirmed aging deficits (evidenced by slower reaction times and reduced accuracy rates) that progressively increased with task difficulty. Hemodynamic results showed opposing effects in young versus older adults, with oxygenated and total hemoglobin decreasing in young but increasing in older adults, particularly during the harder tasks. Also, tissue oxygenation increased only in older adults during the harder tasks. Among the older adults only, anterior frontal hemodynamic changes correlated with better cognitive performance, indicating that they were compensatory in nature. These findings provide novel evidence of age-related anterior frontal hemodynamic changes that intensify with cognitive demands and compensate for performance deficits.

Exercise induces arterial flow patterns that promote functional and structural adaptations, improving functional capacity and reducing cardiovascular risk. While heat is produced by exercise, local and whole-body passive heating have recently been shown to generate favorable flow profiles and associated vascular adaptations in the upper limb. Flow responses to acute heating in the lower limbs have not yet been assessed, or directly compared to exercise, and other cardiovascular effects of lower-limb heating have not been fully characterized. Lower-limb heating by hot-water immersion (30 min at 42°C, to the waist) was compared to matched-duration treadmill running (65-75% age-predicted heart rate maximum) in 10 healthy, young adult volunteers. Superficial femoral artery shear rate assessed immediately upon completion was increased to a greater extent following immersion (mean ± SD: immersion +252 ± 137% vs. exercise +155 ± 69%, interaction: p = 0.032), while superficial femoral artery flow-mediated dilation was unchanged in either intervention. Immersion increased heart rate to a lower peak than during exercise (immersion +38 ± 3 beats·min-1 vs. exercise +87 ± 3 beats·min-1, interaction: p < 0.001), whereas only immersion reduced mean arterial pressure after exposure (−8 ± 3 mmHg, p = 0.012). Core temperature increased twice as much during immersion as exercise (+1.3 ± 0.4°C vs. +0.6 ± 0.4°C, p < 0.001). These data indicate that acute lower-limb hot-water immersion has potential to induce favorable shear stress patterns and cardiovascular responses within vessels prone to atherosclerosis. Whether repetition of lower-limb heating has long-term beneficial effects in such vasculature remains unexplored.

The application of molecular techniques to exercise biology has provided novel insight into the complexity and breadth of intracellular signaling networks involved in response to endurance-based exercise. Here we discuss several strategies that have high uptake by athletes and, on mechanistic grounds, have the potential to promote cellular adaptation to endurance training in skeletal muscle. Such approaches are based on the underlying premise that imposing a greater metabolic load and provoking extreme perturbations in cellular homeostasis will augment acute exercise responses that, when repeated over months and years, will amplify training adaptation.

KEY POINTS: One in two female athletes chronically take a combined, monophasic oral contraceptive pill (OCP). Previous thermoregulatory investigations proposed that an endogenous rhythm of the menstrual cycle still occurs with OCP usage. Forthcoming large international sporting events will expose female athletes to hot environments differing in their thermal profile, yet few data exist on how trained women will respond from both a thermoregulatory and performance stand‐point. In the present study, we have demonstrated that a small endogenous rhythm of the menstrual cycle still affects T (core) and also that chronic OCP use attenuates the sweating response, whereas behavioural thermoregulation is maintained. Furthermore, humid heat affects both performance and thermoregulatory responses to a greater extent than OCP usage and the menstrual cycle does. ABSTRACT: We studied thermoregulatory responses of ten well‐trained ([Formula: see text] , 57 ± 7 mL min(−1) kg(−1)) women taking a combined, monophasic oral contraceptive pill (OCP) (≥12 months) during exercise in dry and humid heat, across their active OCP cycle. They completed four trials, each of resting and cycling at fixed intensities (125 and 150 W), aiming to assess autonomic regulation, and then a self‐paced intensity (30‐min work trial) to assess behavioural regulation. Trials were conducted in quasi‐follicular (qF) and quasi‐luteal (qL) phases in dry (DRY) and humid (HUM) heat matched for wet bulb globe temperature (WBGT) (27°C). During rest and exercise at 125 W, rectal temperature was 0.15°C higher in qL than qF (P = 0.05) independent of environment (P = 0.17). The onset threshold and thermosensitivity of local sweat rate and forearm blood flow relative to mean body temperature was unaffected by the OCP cycle (both P > 0.30). Exercise performance did not differ between quasi‐phases (qF: 268 ± 31 kJ, qL: 263 ± 26 kJ, P = 0.31) but was 5 ± 7% higher during DRY than during HUM (273 ± 29 kJ, 258 ± 28 kJ; P = 0.03). Compared to matched eumenorrhoeic athletes, chronic OCP use impaired the sweating onset threshold and thermosensitivity (both P < 0.01). In well‐trained, OCP‐using women exercising in the heat: (i) a performance‐thermoregulatory trade‐off occurred that required behavioural adjustment; (ii) humidity impaired performance as a result of reduced evaporative power despite matched WBGT; and (iii) the sudomotor but not behavioural thermoregulatory responses were impaired compared to matched eumenorrhoeic athletes.