Sex Differences in Sympathetic Responses to Lower-Body Negative Pressure.

INTRODUCTION: Trauma-induced hemorrhage is a leading cause of death in prehospital settings. Experimental data demonstrate that females have a lower tolerance to simulated hemorrhage (i.e., central hypovolemia). However, the mechanism(s) underpinning these responses are unknown. Therefore, this study aimed to compare autonomic cardiovascular responses during central hypovolemia between the sexes. We hypothesized that females would have a lower tolerance and smaller increase in muscle sympathetic nerve activity (MSNA) to simulated hemorrhage. METHODS: Data from 17 females and 19 males, aged 19-45 yr, were retrospectively analyzed. Participants completed a progressive lower-body negative pressure (LBNP) protocol to presyncope to simulate hemorrhagic tolerance with continuous measures of MSNA and beat-to-beat hemodynamic variables. We compared responses at baseline, at two LBNP stages (-40 and -50 mmHg), and at immediately before presyncope. In addition, we compared responses at relative percentages (33%, 66%, and 100%) of hemorrhagic tolerance, calculated via the cumulative stress index (i.e., the sum of the product of time and pressure at each LBNP stage). RESULTS: Females had lower tolerance to central hypovolemia (female: 561 ± 309 vs male: 894 ± 304 min·mmHg [time·LBNP]; P = 0.003). At LBNP -40 and -50 mmHg, females had lower diastolic blood pressures (main effect of sex: P = 0.010). For the relative LBNP analysis, females exhibited lower MSNA burst frequency (main effect of sex: P = 0.016) accompanied by a lower total vascular conductance (sex: P = 0.028; main effect of sex). CONCLUSIONS: Females have a lower tolerance to central hypovolemia, which was accompanied by lower diastolic blood pressure at -40 and -50 mmHg LBNP. Notably, females had attenuated MSNA responses when assessed as relative LBNP tolerance time.

Burn size and environmental conditions modify thermoregulatory responses to exercise in burn survivors.

This project tested the hypothesis that burn survivors can perform mild/moderate-intensity exercise in temperate and hot environments without excessive elevations in core body temperature. Burn survivors with low (23 ± 5%TBSA; N = 11), moderate (40 ± 5%TBSA; N = 9), and high (60 ± 8%TBSA; N = 9) burn injuries performed 60 minutes of cycle ergometry exercise (72 ± 15 watts) in a 25°C and 23% relative humidity environment (ie, temperate) and in a 40°C and 21% relative humidity environment (ie, hot). Absolute gastrointestinal temperatures (TGI) and changes in TGI (ΔTGI) were obtained. Participants with an absolute TGI of >38.5°C and/or a ΔTGI of >1.5°C were categorized as being at risk for hyperthermia. For the temperate environment, exercise increased ΔTGI in all groups (low: 0.72 ± 0.21°C, moderate: 0.42 ± 0.22°C, and high: 0.77 ± 0.25°C; all P < .01 from pre-exercise baselines), resulting in similar absolute end-exercise TGI values (P = .19). Importantly, no participant was categorized as being at risk for hyperthermia, based upon the aforementioned criteria. For the hot environment, ΔTGI at the end of the exercise bout was greater for the high group when compared to the low group (P = .049). Notably, 33% of the moderate cohort and 56% of the high cohort reached or exceeded a core temperature of 38.5°C, while none in the low cohort exceeded this threshold. These data suggest that individuals with a substantial %TBSA burned can perform mild/moderate intensity exercise for 60 minutes in temperate environmental conditions without risk of excessive elevations in TGI. Conversely, the risk of excessive elevations in TGI during mild/moderate intensity exercise in a hot environment increases with the %TBSA burned.

Exertional Heat Stroke Survival at the Falmouth Road Race: 180 New Cases With Expanded Analysis.

CONTEXT: A high number of exertional heat stroke (EHS) cases occur during the Falmouth Road Race. OBJECTIVES: To extend previous analyses of EHS cases during the Falmouth Road Race by assessing or describing (1) EHS and heat exhaustion (HE) incidence rates, (2) EHS outcomes as they relate to survival, (3) the effect of the environment on these outcomes, and (4) how this influences medical provider planning and preparedness. DESIGN: Descriptive epidemiologic study. SETTING: Falmouth Road Race. PATIENTS OR OTHER PARTICIPANTS: Patients with EHS or HE admitted to the medical tent. MAIN OUTCOME MEASURE(S): We obtained 8 years (2012 to 2019) of Falmouth Road Race anonymous EHS and HE medical records. Meteorologic data were collected and analyzed to evaluate the effect of environmental conditions on the heat illness incidence (exertional heat illness [EHI] = EHS + HE). The EHS treatment and outcomes (ie, cooling time, survival, and discharge outcome), number of HE patients, and wet bulb globe temperature (WBGT) for each race were analyzed. RESULTS: A total of 180 EHS and 239 HE cases were identified. Overall incidence rates per 1000 participants were 2.07 for EHS and 2.76 for HE. The EHI incidence rate was 4.83 per 1000 participants. Of the 180 EHS cases, 100% survived, and 20% were transported to the emergency department. The WBGT was strongly correlated with the incidence of both EHS (r2 = 0.904, P = .026) and EHI (r2 = 0.912, P = .023). CONCLUSIONS: This is the second-largest civilian database of EHS cases reported. When combined with the previous dataset of EHS survivors from this race, it amounts to 454 EHS cases resulting in 100% survival. The WBGT remained a strong predictor of EHS and EHI cases. These findings support 100% survival from EHS when patients over a wide range of ages and sexes are treated with cold-water immersion.

Age alters the thermoregulatory responses to extreme heat exposure with accompanying activities of daily living.

Older adults are at greater risk for heat-related morbidity and mortality, due in part to age-related reductions in heat dissipating capabilities. Previous studies investigating the impact of age on responses to heat stress used approaches that lack activities of daily living and therefore may not accurately depict the thermal/physiological strain that would occur during actual heatwaves. We sought to compare the responses of young (18-39 yr) and older (≥65 yr) adults exposed to two extreme heat simulations. Healthy young (n = 20) and older (n = 20) participants underwent two 3-h extreme heat exposures on different days: 1) DRY (47°C and 15% humidity) and 2) HUMID (41°C and 40% humidity). To mimic heat generation comparable with activities of daily living, participants performed 5-min bouts of light physical activity dispersed throughout the heat exposure. Measurements included core and skin temperatures, heart rate, blood pressure, local and whole body sweat rate, forearm blood flow, and perceptual responses. Δ core temperature (Young: 0.68 ± 0.27°C vs. Older: 1.37 ± 0.42°C; P < 0.001) and ending core temperature (Young: 37.81 ± 0.26°C vs. Older: 38.15 ± 0.43°C; P = 0.005) were greater in the older cohort during the DRY condition. Δ core temperature (Young: 0.58 ± 0.25°C vs. Older: 1.02 ± 0.32°C; P < 0.001), but not ending core temperature (Young: 37.67 ± 0.34°C vs. Older: 37.83 ± 0.35°C; P = 0.151), was higher in the older cohort during the HUMID condition. We demonstrated that older adults have diminished thermoregulatory responses to heat stress with accompanying activities of daily living. These findings corroborate previous reports and confirm epidemiological data showing that older adults are at a greater risk for hyperthermia.NEW & NOTEWORTHY Using an experimental model of extreme heat exposure that incorporates brief periods of light physical activity to simulate activities of daily living, the extent of thermal strain reported herein more accurately represents what would occur during actual heatwave conditions. Despite matching metabolic heat generation and environmental conditions, we show that older adults have augmented core temperature responses, likely due to age-related reductions in heat dissipating mechanisms.

Inhibiting regional sweat evaporation modifies the ventilatory response to exercise: interactions between core and skin temperature.

In humans, elevated body temperatures can markedly increase the ventilatory response to exercise. However, the impact of changing the effective body surface area (BSA) for sweat evaporation (BSAeff) on such responses is unclear. Ten healthy adults (9 males, 1 female) performed eight exercise trials cycling at 6 W/kg of metabolic heat production for 60 min. Four conditions were used where BSAeff corresponded to 100%, 80%, 60%, and 40% of BSA using vapor-impermeable material. Four trials (one at each BSAeff) were performed at 25°C air temperature, and four trials (one at each BSAeff) at 40°C air temperature, each with 20% humidity. The slope of the relation between minute ventilation and carbon dioxide elimination (V̇E/V̇co2 slope) assessed the ventilatory response. At 25°C, the V̇E/V̇co2 slope was elevated by 1.9 and 2.6 units when decreasing BSAeff from 100 to 80 and to 40% (P = 0.033 and 0.004, respectively). At 40°C, V̇E/V̇co2 slope was elevated by 3.3 and 4.7 units, when decreasing BSAeff from 100 to 60 and to 40% (P = 0.016 and P < 0.001, respectively). Linear regression analyses using group average data from each condition demonstrated that end-exercise mean body temperature (integration of core and mean skin temperature) was better associated with the end-exercise ventilatory response, compared with core temperature alone. Overall, we show that impeding regional sweat evaporation increases the ventilatory response to exercise in temperate and hot environmental conditions, and the effect is mediated primarily by increases in mean body temperature.NEW & NOTEWORTHY Exercise in the heat increases the slope of the relation between minute ventilation and carbon dioxide elimination (V̇E/V̇co2 slope) in young healthy adults. An indispensable role for skin temperature in modulating the ventilatory response to exercise is noted, contradicting common belief that internal/core temperature acts independently as a controller of ventilation during hyperthermia.

Prospective Validation of 2B-Cool : Integrating Wearables and Individualized Predictive Analytics to Reduce Heat Injuries.

INTRODUCTION: An uncontrollably rising core body temperature (T C ) is an indicator of an impending exertional heat illness. However, measuring T C invasively in field settings is challenging. By contrast, wearable sensors combined with machine-learning algorithms can continuously monitor T C nonintrusively. Here, we prospectively validated 2B-Cool , a hardware/software system that automatically learns how individuals respond to heat stress and provides individualized estimates of T C , 20-min ahead predictions, and early warning of a rising T C . METHODS: We performed a crossover heat stress study in an environmental chamber, involving 11 men and 11 women (mean ± SD age = 20 ± 2 yr) who performed three bouts of varying physical activities on a treadmill over a 7.5-h trial, each under four different clothing and environmental conditions. Subjects wore the 2B-Cool system, consisting of a smartwatch, which collected vital signs, and a paired smartphone, which housed machine-learning algorithms and used the vital sign data to make individualized real-time forecasts. Subjects also wore a chest strap heart rate sensor and a rectal probe for comparison purposes. RESULTS: We observed very good agreement between the 2B-Cool forecasts and the measured T C , with a mean bias of 0.16°C for T C estimates and nearly 75% of measurements falling within the 95% prediction intervals of ±0.62°C for the 20-min predictions. The early-warning system results for a 38.50°C threshold yielded a 98% sensitivity, an 81% specificity, a prediction horizon of 35 min, and a false alarm rate of 0.12 events per hour. We observed no sex differences in the measured or predicted peak T C . CONCLUSION: 2B-Cool provides early warning of a rising T C with a sufficient lead time to enable clinical interventions and to help reduce the risk of exertional heat illness.

Low-dose morphine reduces pain perception and blood pressure, but not muscle sympathetic outflow, responses during the cold pressor test.

Our knowledge about how low-dose (analgesic) morphine affects autonomic cardiovascular regulation is primarily limited to animal experiments. Notably, it is unknown if low-dose morphine affects human autonomic cardiovascular responses during painful stimuli in conscious humans. Therefore, we tested the hypothesis that low-dose morphine reduces perceived pain and subsequent sympathetic and cardiovascular responses in humans during an experimental noxious stimulus. Twenty-nine participants (14 females/15 males; 29 ± 6 yr; 26 ± 4 kg·m-2, means ± SD) completed this randomized, crossover, placebo-controlled trial during two laboratory visits. During each visit, participants completed a cold pressor test (CPT; hand in ∼0.4°C ice bath for 2 min) before and ∼35 min after drug/placebo administration (5 mg iv morphine or saline). We compared pain perception (100 mm visual analog scale), muscle sympathetic nerve activity (MSNA; microneurography; 14 paired recordings), and beat-to-beat blood pressure (BP; photoplethysmography) between trials (at both pre- and postdrug/placebo time points) using paired, two-tailed t tests. Before drug/placebo infusion, perceived pain (P = 0.92), ΔMSNA burst frequency (n = 14, P = 0.21), and Δmean BP (P = 0.39) during the CPT were not different between trials. After the drug/placebo infusion, morphine versus placebo attenuated perceived pain (morphine: 43 ± 20 vs. placebo: 57 ± 24 mm, P < 0.001) and Δmean BP (morphine: 10 ± 7 vs. placebo: 13 ± 8 mmHg, P = 0.003), but not ΔMSNA burst frequency (morphine: 10 ± 11 vs. placebo: 13 ± 11 bursts·min-1, P = 0.12), during the CPT. Reductions in pain perception and Δmean BP were only weakly related (r = 0.34, P = 0.07; postmorphine CPT minus postplacebo CPT). These data provide valuable information regarding how low-dose morphine affects autonomic cardiovascular responses during an experimental painful stimulus.NEW & NOTEWORTHY In this randomized, crossover, placebo-controlled trial, we found that low-dose morphine administration reduced pain perception and blood pressure responses during the cold pressor test via attenuated increases in heart rate and cardiac output. We also determined that muscle sympathetic outflow responses during the cold pressor test seem to be unaffected by low-dose morphine administration. Finally, our exploratory analysis suggests that biological sex does not influence morphine-induced antinociception in healthy adults.

Low-dose morphine reduces tolerance to central hypovolemia in healthy adults without affecting muscle sympathetic outflow.

Hemorrhage is a leading cause of preventable battlefield and civilian trauma deaths. Low-dose (i.e., an analgesic dose) morphine is recommended for use in the prehospital (i.e., field) setting. Morphine administration reduces hemorrhagic tolerance in rodents. However, it is unknown whether morphine impairs autonomic cardiovascular regulation and consequently reduces hemorrhagic tolerance in humans. Thus, the purpose of this study was to test the hypothesis that low-dose morphine reduces hemorrhagic tolerance in conscious humans. Thirty adults (15 women/15 men; 29 ± 6 yr; 26 ± 4 kg·m-2, means ± SD) completed this randomized, crossover, double-blinded, placebo-controlled trial. One minute after intravenous administration of morphine (5 mg) or placebo (saline), we used a presyncopal limited progressive lower-body negative pressure (LBNP) protocol to determine hemorrhagic tolerance. Hemorrhagic tolerance was quantified as a cumulative stress index (mmHg·min), which was compared between trials using a Wilcoxon matched-pairs signed-rank test. We also compared muscle sympathetic nerve activity (MSNA; microneurography) and beat-to-beat blood pressure (photoplethysmography) during the LBNP test using mixed-effects analyses [time (LBNP stage) × trial]. Median LBNP tolerance was lower during morphine trials (placebo: 692 [473-997] vs. morphine: 385 [251-728] mmHg·min, P < 0.001, CI: -394 to -128). Systolic blood pressure was 8 mmHg lower during moderate central hypovolemia during morphine trials (post hoc P = 0.02; time: P < 0.001, trial: P = 0.13, interaction: P = 0.006). MSNA burst frequency responses were not different between trials (time: P < 0.001, trial: P = 0.80, interaction: P = 0.51). These data demonstrate that low-dose morphine reduces hemorrhagic tolerance in conscious humans. Thus, morphine is not an ideal analgesic for a hemorrhaging individual in the prehospital setting.NEW & NOTEWORTHY In this randomized, crossover, placebo-controlled trial, we found that tolerance to simulated hemorrhage was lower after low-dose morphine administration. Such reductions in hemorrhagic tolerance were observed without differences in MSNA burst frequency responses between morphine and placebo trials. These data, the first to be obtained in conscious humans, demonstrate that low-dose morphine reduces hemorrhagic tolerance. Thus, morphine is not an ideal analgesic for a hemorrhaging individual in the prehospital setting.

Low-dose fentanyl reduces pain perception, muscle sympathetic nerve activity responses, and blood pressure responses during the cold pressor test.

Our knowledge about how low-dose (analgesic) fentanyl affects autonomic cardiovascular regulation is primarily limited to animal experiments. Notably, it is unknown if low-dose fentanyl influences human autonomic cardiovascular responses during painful stimuli in humans. Therefore, we tested the hypothesis that low-dose fentanyl reduces perceived pain and subsequent sympathetic and cardiovascular responses in humans during an experimental noxious stimulus. Twenty-three adults (10 females/13 males; 27 ± 7 yr; 26 ± 3 kg·m-2, means ± SD) completed this randomized, crossover, placebo-controlled trial during two laboratory visits. During each visit, participants completed a cold pressor test (CPT; hand in ∼0.4°C ice bath for 2 min) before and 5 min after drug/placebo administration (75 µg fentanyl or saline). We compared pain perception (100-mm visual analog scale), muscle sympathetic nerve activity (MSNA; microneurography, 11 paired recordings), and beat-to-beat blood pressure (BP; photoplethysmography) between trials (at both pre- and postdrug/placebo timepoints) using paired, two-tailed t tests. Before drug/placebo administration, perceived pain (P = 0.8287), ΔMSNA burst frequency (P = 0.7587), and Δmean BP (P = 0.8649) during the CPT were not different between trials. After the drug/placebo administration, fentanyl attenuated perceived pain (36 vs. 66 mm, P < 0.0001), ΔMSNA burst frequency (9 vs. 17 bursts/min, P = 0.0054), and Δmean BP (7 vs. 13 mmHg, P = 0.0174) during the CPT compared with placebo. Fentanyl-induced reductions in pain perception and Δmean BP were moderately related (r = 0.40, P = 0.0641). These data provide valuable information regarding how low-dose fentanyl reduces autonomic cardiovascular responses during an experimental painful stimulus.

Low-dose fentanyl does not alter muscle sympathetic nerve activity, blood pressure, or tolerance during progressive central hypovolemia.

Hemorrhage is a leading cause of battlefield and civilian trauma deaths. Several pain medications, including fentanyl, are recommended for use in the prehospital (i.e., field setting) for a hemorrhaging solider. However, it is unknown whether fentanyl impairs arterial blood pressure (BP) regulation, which would compromise hemorrhagic tolerance. Thus, the purpose of this study was to test the hypothesis that an analgesic dose of fentanyl impairs hemorrhagic tolerance in conscious humans. Twenty-eight volunteers (13 females) participated in this double-blinded, randomized, placebo-controlled trial. We conducted a presyncopal limited progressive lower body negative pressure test (LBNP; a validated model to simulate hemorrhage) following intravenous administration of fentanyl (75 µg) or placebo (saline). We quantified tolerance as a cumulative stress index (mmHg·min), which was compared between trials using a paired, two-tailed t test. We also compared muscle sympathetic nerve activity (MSNA; microneurography) and beat-to-beat BP (photoplethysmography) during the LBNP test using a mixed effects model [time (LBNP stage) × trial]. LBNP tolerance was not different between trials (fentanyl: 647 ± 386 vs. placebo: 676 ± 295 mmHg·min, P = 0.61, Cohen's d = 0.08). Increases in MSNA burst frequency (time: P < 0.01, trial: P = 0.29, interaction: P = 0.94) and reductions in mean BP (time: P < 0.01, trial: P = 0.50, interaction: P = 0.16) during LBNP were not different between trials. These data, the first to be obtained in conscious humans, demonstrate that administration of an analgesic dose of fentanyl does not alter MSNA or BP during profound central hypovolemia, nor does it impair tolerance to this simulated hemorrhagic insult.

A 3-D virtual human thermoregulatory model to predict whole-body and organ-specific heat-stress responses.

OBJECTIVE: This study aimed at assessing the risks associated with human exposure to heat-stress conditions by predicting organ- and tissue-level heat-stress responses under different exertional activities, environmental conditions, and clothing. METHODS: In this study, we developed an anatomically detailed three-dimensional thermoregulatory finite element model of a 50th percentile U.S. male, to predict the spatiotemporal temperature distribution throughout the body. The model accounts for the major heat transfer and thermoregulatory mechanisms, and circadian-rhythm effects. We validated our model by comparing its temperature predictions of various organs (brain, liver, stomach, bladder, and esophagus), and muscles (vastus medialis and triceps brachii) under normal resting conditions (errors between 0.0 and 0.5 °C), and of rectum under different heat-stress conditions (errors between 0.1 and 0.3 °C), with experimental measurements from multiple studies. RESULTS: Our simulations showed that the rise in the rectal temperature was primarily driven by the activity level (~ 94%) and, to a much lesser extent, environmental conditions or clothing considered in our study. The peak temperature in the heart, liver, and kidney were consistently higher than in the rectum (by ~ 0.6 °C), and the entire heart and liver recorded higher temperatures than in the rectum, indicating that these organs may be more susceptible to heat injury. CONCLUSION: Our model can help assess the impact of exertional and environmental heat stressors at the organ level and, in the future, evaluate the efficacy of different whole-body or localized cooling strategies in preserving organ integrity.

Roundtable on Preseason Heat Safety in Secondary School Athletics: Heat Acclimatization.

OBJECTIVE: To provide best-practice recommendations for developing and implementing heat-acclimatization strategies in secondary school athletics. DATA SOURCES: An extensive literature review on topics related to heat acclimatization and heat acclimation was conducted by a group of content experts. Using the Delphi method, action-oriented recommendations were developed. CONCLUSIONS: A period of heat acclimatization consisting of ≥14 consecutive days should be implemented at the start of fall preseason training or practices for all secondary school athletes to mitigate the risk of exertional heat illness. The heat-acclimatization guidelines should outline specific actions for secondary school athletics personnel to use, including the duration of training, the number of training sessions permitted per day, and adequate rest periods in a cool environment. Further, these guidelines should include sport-specific and athlete-specific recommendations, such as phasing in protective equipment and reintroducing heat acclimatization after periods of inactivity. Heat-acclimatization guidelines should be clearly detailed in the secondary school's policy and procedures manual and disseminated to all stakeholders. Heat-acclimatization guidelines, when used in conjunction with current best practices surrounding the prevention, management, and care of secondary school student-athletes with exertional heat stroke, will optimize their health and safety.

Movement Technique and Standing Balance After Graded Exercise-Induced Dehydration.

CONTEXT: Hypohydration has been shown to alter neuromuscular function. However, the longevity of these impairments remains unclear. OBJECTIVE: To examine the effects of graded exercise-induced dehydration on neuromuscular control 24 hours after exercise-induced hypohydration. DESIGN: Crossover study. SETTING: Laboratory. PATIENTS OR OTHER PARTICIPANTS: A total of 23 men (age = 21 ± 2 years, height = 179.8 ± 6.4 cm, mass = 75.24 ± 7.93 kg, maximal oxygen uptake [VO2max] = 51.7 ± 5.5 mL·kg-1·min-1, body fat = 14.2% ± 4.6%). INTERVENTION(S): Participants completed 3 randomized exercise trials: euhydrated arrival plus fluid replacement (EUR), euhydrated arrival plus no fluid (EUD), and hypohydrated arrival plus no fluid (HYD) in hot conditions (ambient temperature = 35.2°C ± 0.6°C, relative humidity = 31.3% ± 2.5%). Each trial consisted of 180 minutes of exercise (six 30-minute cycles: 8 minutes at 40% VO2max; 8 minutes, 60% VO2max; 8 minutes, 40% VO2max; 6 minutes, passive rest) followed by 60 minutes of passive recovery. MAIN OUTCOME MEASURE(S): We used the Landing Error Scoring System and Balance Error Scoring System (BESS) to measure movement technique and postural control at pre-exercise, postexercise and passive rest (POSTEX), and 24 hours postexercise (POST24). Differences were assessed using separate mixed-design (trial × time) repeated-measures analyses of variance. RESULTS: The magnitude of hypohydration at POSTEX was different among EUR, EUD, and HYD trials (0.2% ± 1%, 3.5% ± 1%, and 5% ± 0.9%, respectively; P < .05). We observed no differences in Landing Error Scoring System scores at pre-exercise (2.9 ± 1.6, 3.0 ± 2.1, 3.0 ± 2.0), POSTEX (3.3 ± 1.5, 3.0 ± 2.0, 3.1 ± 1.9), or POST24 (3.3 ± 1.9, 3.2 ± 1.4, 3.3 ± 1.6) among the EUD, EUR, and HYD trials, respectively (P = .90). Hydration status did not affect BESS scores (P = .11), but BESS scores at POSTEX (10.4 ± 1.1) were greater than at POST24 (7.7 ± 0.9; P = .03). CONCLUSIONS: Whereas exercise-induced dehydration up to 5% body mass did not impair movement technique or postural control 24 hours after a prolonged bout of exercise in a hot environment, postural control was impaired at 60 minutes after prolonged exercise in the heat. Consideration of the length of recovery time between bouts of exercise in hot environments is warranted.

Interaction of Exercise Intensity and Simulated Burn Injury Size on Thermoregulation.

PURPOSE: This study aimed to test the hypothesis that the elevation in internal body temperature during exercise in a hot environment is influenced by the combination of exercise intensity and BSA burned. METHODS: Ten healthy participants (8 males, 2 females; 32 ± 9 yr; 75.3 ± 11.7 kg) completed eight exercise trials on a cycle ergometer, each with different combinations of metabolic heat productions (low, 4 W·kg-1; moderate, 6 W·kg-1) and simulated BSA burn in a hot environmental chamber (39.9°C ± 0.3°C, 20.1% ± 1.5% RH). Burns were simulated by covering 0%, 20%, 40%, or 60% of participants' BSA with a highly absorbent, vapor-impermeable material. Gastrointestinal temperature (TGI) was recorded, with the primary analysis being the increase in TGI after 60 min of exercise. RESULTS: We identified an interaction effect for the increase in TGI (P < 0.01), suggesting TGI was influenced by both intensity and simulated burn BSA. Regardless of the percentage BSA burn simulated, the increase in TGI was similar across low-intensity trials (0.70°C ± 0.26°C, P > 0.11 for all). However, during moderate-intensity exercise, the increase in TGI was greater for the 60% (1.78°C ± 0.38°C, P < 0.01) and 40% BSA coverage trials (1.33°C ± 0.44°C, P = 0.04), relative to 0% (0.82°C ± 0.36°C). There were no differences in TGI responses between 0% and 20% trials. CONCLUSION: These data suggest that exercise intensity influences the relationship between burn injury size and thermoregulatory responses in a hot environment.

Adoption of Lightning Safety Best-Practices Policies in the Secondary School Setting.

CONTEXT: Lightning-related injuries are among the top 10 causes of sport-related death at all levels of sport, including the nearly 8 million athletes participating in US secondary school sports. OBJECTIVE: To investigate the adoption of lightning safety policies and the factors that influence the development of comprehensive lightning safety policies in United States secondary schools. DESIGN: Cross-sectional study. SETTING: Secondary school. PATIENTS OR OTHER PARTICIPANTS: Athletic trainers (ATs). MAIN OUTCOME MEASURE(S): An online questionnaire was developed based on the "National Athletic Trainers' Association Position Statement: Lightning Safety for Athletics and Recreation" using a health behavior model, the precaution adoption process model, along with facilitators of and barriers to the current adoption of lightning-related policies and factors that influence the adoption of lightning policies. Precaution adoption process model stage (unaware for need, unaware if have, unengaged, undecided, decided not to act, decided to act, acting, maintaining) responses are presented as frequencies. Chi-square tests of associations and prevalence ratios with 95% CIs were calculated to compare respondents in higher and lower vulnerability states, based on data regarding lightning-related deaths. RESULTS: The response rate for this questionnaire was 13.43% (n = 365), with additional questionnaires completed via social media (n = 56). A majority of ATs reported maintaining (69%, n = 287) and acting (6.5%, n = 27) a comprehensive lightning safety policy. Approximately 1 in 4 ATs (25.1%, n = 106) described using flash to bang as an evacuation criterion. Athletic trainers practicing in more vulnerable states were more likely to adopt a lightning policy than those in less vulnerable states (57.4% versus 42.6%, prevalence ratio [95% CI] = 1.16 [1.03, 1.30]; P = .009). The most commonly cited facilitator and barrier were a requirement from a state high school athletics association and financial limitations, respectively. CONCLUSIONS: A majority of ATs related adopting (eg, maintaining and acting) the best practices for lightning safety. However, many ATs also indicated continued use of outdated methods (eg, flash to bang).

Low dose ketamine reduces pain perception and blood pressure, but not muscle sympathetic nerve activity, responses during a cold pressor test.

KEY POINTS: Low dose ketamine is a leading medication used to provide analgesia in pre-hospital and hospital settings. Low dose ketamine is increasingly used off-label to treat conditions such as depression. In animals, ketamine stimulates the sympathetic nervous system and increases blood pressure, but these physiological consequences have not been studied in conscious humans. Our data suggest that low dose ketamine administration blunts pain perception and reduces blood pressure, but not muscle sympathetic nerve activity burst frequency, responses during a cold pressor test in healthy humans. These mechanistic, physiological results inform risk-benefit analysis for clinicians administering low dose ketamine in humans. ABSTRACT: Low dose ketamine is an effective analgesic medication. However, our knowledge of the effects of ketamine on autonomic cardiovascular regulation is primarily limited to animal experiments. Notably, it is unknown if low dose ketamine influences autonomic cardiovascular responses during painful stimuli in humans. We tested the hypothesis that low dose ketamine blunts perceived pain, and blunts subsequent sympathetic and cardiovascular responses during an experimental noxious stimulus. Twenty-two adults (10F/12M; 27 ± 6 years; 26 ± 3 kg m-2 , mean ± SD) completed this randomized, crossover, placebo-controlled trial during two laboratory visits. During each visit, participants completed cold pressor tests (CPT; hand in ∼0.4°C ice bath for 2 min) pre- and 5 min post-drug administration (20 mg ketamine or saline). We compared pain perception (100 mm visual analogue scale), muscle sympathetic nerve activity (MSNA; microneurography, 12 paired recordings), and beat-to-beat blood pressure (BP; photoplethysmography) during the pre- and post-drug CPTs separately using paired, two-tailed t tests. For the pre-drug CPT, perceived pain (P = 0.4378), MSNA burst frequency responses (P = 0.7375), and mean BP responses (P = 0.6457) were not different between trials. For the post-drug CPT, ketamine compared to placebo administration attenuated perceived pain (P < 0.0001) and mean BP responses (P = 0.0047), but did not attenuate MSNA burst frequency responses (P = 0.3662). Finally, during the post-drug CPT, there was a moderate relation between cardiac output and BP responses after placebo administration (r = 0.53, P = 0.0121), but this relation was effectively absent after ketamine administration (r = -0.12, P = 0.5885). These data suggest that low dose ketamine administration attenuates perceived pain and pressor, but not MSNA burst frequency, responses during a CPT.

Incidence of Recurrent Exertional Heat Stroke in a Warm-Weather Road Race.

Background and Objectives: Exertional heat stroke (EHS) survivors may be more susceptible to subsequent EHS; however, the occurrence of survivors with subsequent EHS episodes is limited. Therefore, the purpose of this study was to evaluate the incidence of participants with repeated EHS (EHS-2+) cases in a warm-weather road race across participation years compared to those who experienced 1 EHS (EHS-1). Materials and Methods: A retrospective observational case series design was utilized. Medical record data from 17-years at the Falmouth Road Race between 2003-2019 were examined for EHS cases. Incidence of EHS-2+ cases per race and average EHS cases per EHS-2+ participant were calculated (mean ± SD) and descriptive factors (rectal temperature (TRE), finish time (FT), Wet Bulb Globe Temperature (WBGT), age, race year) for each EHS was collected. Results: A total of 333 EHS patients from 174,853 finishers were identified. Sixteen EHS-2+ participants (11 males, 5 females, age = 39 ± 16 year) accounted for 11% of the total EHS cases (n = 37/333). EHS-2+ participants had an average of 2.3 EHS cases per person (range = 2-4) and had an incidence rate of 2.6 EHS per 10 races. EHS-2+ participants finished 93 races following initial EHS, with 72 of the races (77%) completed without EHS incident. Initial EHS TRE was not statistically different than subsequent EHS initial TRE (+0.3 ± 0.9 °C, p > 0.050). Initial EHS-2+ participant FT was not statistically different than subsequent EHS FT (-4.2 ± 7.0 min, p > 0.050). The years between first and second EHS was 3.6 ± 3.5 year (Mode: 1, Range: 1-12). Relative risk ratios revealed that EHS patients were at a significantly elevated risk for subsequent EHS episodes 2 years following their initial EHS (relative risk ratio = 3.32, p = 0.050); however, the risk from 3-5 years post initial EHS was not statistically elevated, though the relative risk ratio values remained above 1.26. Conclusions: These results demonstrate that 11% of all EHS cases at the Falmouth Road Race are EHS-2+ cases and that future risk for a second EHS episode at this race is most likely to occur within the first 2 years following the initial EHS incident. After this initial 2-year period, risk for another EHS episode is not significantly elevated. Future research should examine factors to explain individuals who are susceptible to multiple EHS cases, incidence at other races and corresponding prevention strategies both before and after initial EHS.