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Background Heat-related illness, including heat exhaustion and heat stroke, is seen as a major risk for athletes with a physical impairment. Objective Primary: To survey the illness statistics during the 2015 Para Athletics World Championships and report on any cases of significant heat-related illnesses. Secondary: To document the heat countermeasures taken on behalf of the organizing committee. Design Retrospective audit. Setting Medical records collected at medical centers during the 2015 Para Athletics World Championships. Participants Athletes participating in the 2015 Para Athletics World Championships. Methods Illness statistics and records of hospitalizations of athletes participating in the championships were recorded by the medical officials during the precompetition (3 days) and competition (10 days) periods. Furthermore, wet-bulb globe temperatures (WBGTs) were measured at the competition venues. Main outcome measurements Incidence rates of illness during the precompetition and competition periods. Results WBGTs ranged from 24.6°C to 36.0°C, regularly exceeding the American College of Sports Medicine (ACSM) and International Association of Athletics Federations (IAAF) guidelines for cancelation in the morning both during the competition (ACSM, 52%; IAAF, 97%) and precompetition periods (ACSM, 75%; IAAF, 100%). These guidelines were not exceeded as regularly during the evening and noon for both the precompetition and competition periods (ACSM, 0%-5%; IAAF, 0%-58%). The illness incidence rate was 2.89 per 1000 athlete-days (incidence proportion = 3.76%; confidence interval = 2.69%-4.83%). Only seven cases of heat-related illness were recorded, of which three required hospitalization. Conclusion This study indicates low rates of illness, including hospitalization and intravenous administration for heat-related illness among athletes participating in the 2015 Para Athletics World Championships. Level of evidence III.

The aim of this study was to determine the time course of physiological adaptations and their relationship with performance improvements during 2 weeks of heat acclimatization. Nine trained cyclists completed 2 weeks of training in naturally hot environment (34 ± 3 °C; 18 ± 5% relative humidity). On days 1, 6, and 13, they performed standardized heat response tests (HRT-1, 2, 3), and 43.4-km time trials in the heat (TTH-1, 2, 3) were completed on days 2, 7, and 14. Within the first 5–6 days, sweat sodium concentration decreased from 75 ± 22 mmol/L to 52 ± 24 mmol/L, sweat rate increased (+20 ± 15%), and resting hematocrit decreased (−5.6 ± 5.4%), with no further changes during the remaining period. In contrast, power output during TTHs gradually improved from TTH-1 to TTH-2 (+11 ± 8%), and from TTH-2 to TTH-3 (+5 ± 4%). Individual improvements in performance from TTH-1 to TTH-2 correlated with individual changes in hematocrit (assessed after the corresponding HRT; r = −0.79, P

This study examined the influence of hyperthermia on middle cerebral artery mean blood velocity (MCA Vmean). Eleven cyclists undertook a 750 kJ self-paced time trial in HOT (35 °C) and COOL (20 °C) conditions. Exercise time was longer in HOT (56 min) compared with COOL (49 min; P

This study investigated if well-trained cyclists improve and performance in cool conditions following heat acclimatization through natural outdoor training in hot conditions. Eighteen trained male cyclists were tested for physiological adaptations, , peak aerobic power output, exercise efficiency, and outdoor time trial (TT) performance (43.4 km in cool environment, ∼5–13 °C) before and after 2 weeks of training in a cool (CON, n = 9) or hot (∼35 °C, HA, n = 9) environment. After heat acclimatization, TT performance in the heat was improved by 16%; however, there was no change in the HA group in (4.79 ± 0.21 L/min vs 4.82 ± 0.35 L/min), peak aerobic power output (417 ± 16 W vs 422 ± 17 W), and outdoor TT performance in cool conditions (300 ± 14 W/69 ± 3 min vs 302 ± 9 W/69 ± 4 min). The present study shows that 2 weeks of heat acclimatization was associated with marked improvements in TT performance in the heat. However, for the well-trained endurance athletes, this did not transfer to an improved aerobic exercise capacity or outdoor TT performance in cool conditions.

Exercise heat acclimation induces physiological adaptations that improve thermoregulation, attenuate physiological strain, reduce the risk of serious heat illness, and improve aerobic performance in warm-hot environments and potentially in temperate environments. The adaptations include improved sweating, improved skin blood flow, lowered body temperatures, reduced cardiovascular strain, improved fluid balance, altered metabolism, and enhanced cellular protection. The magnitudes of adaptations are determined by the intensity, duration, frequency, and number of heat exposures, as well as the environmental conditions (i.e., dry or humid heat). Evidence is emerging that controlled hyperthermia regimens where a target core temperature is maintained, enable more rapid and complete adaptations relative to the traditional constant work rate exercise heat acclimation regimens. Furthermore, inducing heat acclimation outdoors in a natural field setting may provide more specific adaptations based on direct exposure to the exact environmental and exercise conditions to be encountered during competition. This review initially examines the physiological adaptations associated with heat acclimation induction regimens, and subsequently emphasizes their application to competitive athletes and sports.

We assessed neuromuscular fatigue and recovery of the plantar flexors after playing football with or without severe heat stress. Neuromuscular characteristics of the plantar flexors were assessed in 17 male players at baseline and ∼30 min, 24, and 48 h after two 90-min football matches in temperate (∼20 °C and 55% rH) and hot (∼43 °C and 20% rH) environments. Measurements included maximal voluntary strength, muscle activation, twitch contractile properties, and rate of torque development and soleus EMG (i.e., root mean square activity) rise from 0 to 30, -50, -100, and -200 ms during maximal isometric contractions for plantar flexors. Voluntary activation and peak twitch torque were equally reduced (-1.5% and -16.5%, respectively; P

Introduction: We examined the extent to which fatiguing cycling exercise in the heat influences contractile function in modulating the force–frequency relationship. Methods: Before (∽37.0°C) and after (∽38.5°C) exercise (ExH) and passive (PaH) hyperthermia, an 8-s train of stimulation at 10, 20, 50, and 100 Hz (2 s per frequency) and a potentiated twitch were evoked on the relaxed knee extensors using percutaneous stimulation. Results: ExH and PaH produced a decrease in the 20:50 Hz force ratio, indicative of low-frequency fatigue (P

New findings • What is the central question of this study? We examined whether passive hyperthermia exacerbates central fatigue due to an increase in peak muscle relaxation rate, and whether exercise-induced hyperthermia attenuates this response because of a reduction in contractile speed related to peripheral fatigue. • What is the main finding and its importance? Exercise and passive hyperthermia increase muscle relaxation rate. An increase from moderate to severe passive hyperthermia enhances this rate, but without exacerbating force loss or voluntary muscle and cortical activation, relative to exercise. The centrally mediated rate of activation appears sufficient to overcome the increase in peak muscle relaxation. This study examined whether central fatigue was exacerbated by an increase in muscle contractile speed caused by passive hyperthermia (PaH) and whether exercise-induced hyperthermia (ExH) combined with related peripheral fatigue influenced this response. The ExH was induced by cycling at 60% of maximal oxygen uptake in 38°C conditions and the PaH by sitting in a 48°C climate chamber. Ten men performed brief (∼5 s) and sustained (30 s) maximal voluntary isometric contractions (MVCs) of the knee extensors at baseline (CON, ∼37.1°C) and during moderate (MOD, ∼38.5°C) and severe (SEV, ∼39.5°C) hyperthermia. Motor nerve and transcranial magnetic stimulation were used to assess voluntary muscle and cortical activation level, along with contractile properties. Brief MVC force decreased to a similar extent during SEV-ExH (−8%) and SEV-PaH (−6%; P < 0.05 versus CON). Sustained MVC force also decreased during MOD-ExH (−10%), SEV-ExH (−13%) and SEV-PaH (−7%; P < 0.01 versus CON). Motor nerve and cortical activation were reduced on reaching MOD (∼3%) and SEV (∼5%) ExH and PaH during the brief and sustained MVCs (P < 0.01 versus CON). Peak twitch force decreased on reaching SEV-ExH and SEV-PaH (P < 0.05 versus CON). Following transcranial magnetic stimulation, during the brief and sustained MVCs the peak muscle relaxation rate increased in ExH and PaH (P < 0.01 versus CON). The increase was greatest during the sustained contraction in SEV-PaH (P < 0.01), but this did not exacerbate central fatigue relative to ExH. These results indicate that during fatiguing cycling exercise in the heat, quadriceps peak relaxation rate increases. However, the centrally mediated rate of activation appears sufficient to overcome even the largest increase in muscle relaxation rate, seen during SEV-PaH.

Baseline, postexercise (20 min cycling) and postexhaustion (incremental test) neuromuscular function was assessed in control (24°C) and hot (40°C) conditions. Heat affects the plantar flexors and knee extensors differently, but most of the effects of heat (e.g., M-wave decrement) and fatigue (e.g., voluntary activation and H-reflex decrement) were independent of each other. However, peripheral fatigue of the knee extensors was lower at exhaustion in hot than neutral environment (peak twitch decrement from baseline to exhaustion: -19% vs. -33%, p < .05). In addition, heat had no negative effect on transcranial magnetic stimulation responses during cycling, and neuromuscular failure is unlikely to explain the early exercise cessation in the heat (13 min 50 s vs. 17 min 9 s) that occurred when participants reached maximal perceived exertion (19.2 vs. 19.1, ns) with higher core temperature (38.7°C vs. 38.2°C, p < .05) and heart rate (184 bpm vs. 179 bpm, p < .05). Descriptors: Temperature, Thermoregulation, Voluntary muscle activation, Cycling exercise, Perceived exertion (RPE)

The aim of the present study was to examine the associations between adaptive responses to an in-season soccer training camp in the heat and changes in submaximal exercising heart rate (HRex, 5-min run at 9 km/h), postexercise HR recovery (HRR) and HR variability (HRV). Fifteen well-trained but non-heat-acclimatized male adult players performed a training week in Qatar (34.6 ± 1.9°C wet bulb globe temperature). HRex, HRR, HRV (i.e. the standard deviation of instantaneous beat-to-beat R–R interval variability measured from Poincare plots SD1, a vagal-related index), creatine kinase (CK) activity, plasma volume (PV) changes, and post-5-min run rate of perceived exertion (RPE) were collected at six occasions in temperate environmental conditions (22°C). Players also performed the yo-yo intermittent recovery test level 1 (Yo-Yo IR1) in the same environmental conditions (22°C), both at the beginning and at the end of the training week. Throughout the intervention, HRex and HRV showed decreasing (P

This review focuses on the effects of different environmental temperatures on the neuromuscular system. During short duration exercise, performance improves from 2% to 5% with a 1 °C increase in muscle temperature. However, if central temperature increases (i.e., hyperthermia), this positive relation ceases and performance becomes impaired. Performance impairments in both cold and hot environment are related to a modification in neural drive due to protective adaptations, central and peripheral failures. This review highlights, to some extent, the different effects of hot and cold environments on the supraspinal, spinal and peripheral components of the neural drive involved in the up- and down-regulation of neuromuscular function and shows that temperature also affects the neural drive transmission to the muscle and the excitation-contraction coupling.

Independent of environmental conditions, rectal temperature follows a circadian rhythm with an acrophase in the late afternoon. In neutral environment, this diurnal increase in temperature is believed to have a passive warm-up effect improving muscle contractility, and in turn, muscle force, power and performance. However, a hot environment blunts the diurnal variation in muscle function by only improving muscle contractility, and in turn, muscle force, power and performance in the morning, when body temperature is at its lowest. Despite this diurnal variation in muscle function, long-duration exercise is only slightly affected by the time-of-day in neutral environment. However, higher afternoon body temperatures can reduce the heat storage capacity and result in a reduction in exercise capacity in hot environments. In addition, in parallel to the circadian variations in muscle contractility and central temperature, exercise capacity in hot environment may also be affected by the diurnal variations in melatonin concentration and in the onset of peripheral vasodilatation and sweating.

To examine the time course of alteration in neural process (spinal loop properties) during prolonged tennis playing, 12 competitive players performed a series of neuromuscular tests every 30 min during a 3-h match protocol. Muscle activation (twitch interpolation) and normalized EMG activity were assessed during maximal voluntary contraction (MVC) of plantar flexors. Spinal reflexes and M-waves were evoked at rest (i.e., H(max) and M(max) , respectively) and during MVC (i.e., H(sup) , V-wave, M(sup) , respectively). MVC torque declined significantly (P

The aims of this study were to determine (i) the effect of passive hyperthermia on motor drive and cognitive function, and (ii) whether head cooling can limit the hyperthermia-induced alterations. Sixteen subjects were randomly exposed for 2 h to three different conditions: control (Con, 20°C), hot (Hot, 50°C) and hot head cool (HHC – where cold packs were applied to the head under Hot conditions). Three cognitive tests measuring attention and two measuring memory were performed. Neuromuscular testing included electrically evoked muscle action potentials (M-waves) and reflex waves (H-reflex) at rest and during brief (4–5 s) and sustained (120 s) maximal voluntary contractions (MVC) of the plantar flexors. All the tests were performed in the environmental room. During brief MVC, torque was significantly lower in both Hot and HHC as compared to Con (P < 0.05). The decrease in muscle activation was significant in Hot (P < 0.05) but not in HBC (P= 0.07). This was accompanied by peripheral failures in the transmission of the neural drive at both spinal (significant decrements in H-reflexes and V-waves, P < 0.05) and neuromuscular junction (significant decrements in M-waves, P < 0.05) levels. During sustained MVC, muscle activation was further depressed (P < 0.05) without any concomitant failures in M-waves, suggesting neural activation adjustments occurring probably at the supraspinal level. Cerebral perturbations were confirmed by significant decrements in both memory tests in Hot as compared with Con (P < 0.05) but not in simple tests (attention tests) that were not affected by hyperthermia. The decrement in memory capacity suggested the existence of frontal lobe activity impairments. Thus, HHC preserved memory capacity but not the visual memory.

Aim Heat stress and hypoxia independently influence cerebrocortical activity and impair prolonged exercise performance. This study examined the relationship between electroencephalography (EEG) activity and self-paced exercise performance in control (CON, 18°C, 40% RH), hot (HOT, 35°C, 60%RH) and hypoxic (HYP, 18°C, 40%RH FiO2: 0.145) conditions. Methods Eleven well-trained cyclists completed a 750 kJ cycling time trial in each condition on separate days in a counter-balanced order. EEG activity was recorded with α and β activity evaluated in the frontal (F3 and F4) and central (C3 and C4) areas. Standardised low-resolution brain electromagnetic tomography (sLORETA) was also utilised to localise changes in cerebrocortical activity. Results Both α and β activity decreased in the frontal and central areas during exercise in HOT relative to CON (P

This study aimed to determine the effect of hyperthermia on transmission efficacy of the Ia-afferent spinal pathway. Recruitment curves of the Hoffman reflex (H-reflex) and compound motor potential (M-wave), and homo-synaptic post-activation depression (HPAD) recovery curves were obtained in 14 volunteers during normothermia (CON, ~37.3oC) and hyperthermia (HOT, core temperature clamped at ~39.0oC). Electromyographic responses were obtained from the soleus (SOL) and medial gastrocnemius (MG) muscles following electrical stimulation of the tibial nerve at varying intensities and paired-pulse frequencies (0.07 Hz to 10 Hz). Results showed that maximal amplitude of the H-reflex was reached at a similar intensity of stimulation in CON and HOT (p > 0.47), with a similar associated M-wave (p > 0.69). However, maximal H-reflex amplitude was significantly lower in HOT than CON (p 0.23). In summary, hyperthermia alters neuromuscular and Ia-afferent pathway transmission, albeit the latter without an increase in HPAD.

This study aimed to determinate the effect of hyperthermia on transmission efficacy of the Ia-afferent spinal pathway. Recruitment curves of the Hoffman reflex (H-reflex) and compound motor potential (M-wave) along with homosynaptic postactivation depression (HPAD) recovery curves were obtained in 14 volunteers in two controlled ambient temperatures that resulted in significantly different core temperatures (CON, core temperature ∼37.3°C; and HOT, core temperature ∼39.0°C). Electromyographic responses were obtained from the soleus (SOL) and medial gastrocnemius (MG) muscles following electrical stimulation of the tibial nerve at varying intensities and paired pulse frequencies (0.07–10 Hz). Results showed that maximal amplitude of the H-reflex was reached for a similar intensity of stimulation in CON and HOT (both muscles P > 0.47), with a similar associated M-wave (both muscles P > 0.69) but was significantly decreased in HOT as compared to CON (all P < 0.05), whether expressed in absolute terms (−50% in SOL, −32% in MG) or when normalized to the maximum M-wave (−23% in SOL, −32% in MG). The HPAD recovery curve was not affected by the elevated core temperature (both muscles P > 0.23). Taken together, these results suggest that hyperthermia can alter neuromuscular transmission across the neuromuscular junction and/or muscle membrane as well as transmission efficacy of the Ia-afferent pathway, albeit the latter not via an increase in HPAD.