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.

Six Months of Exercise Training Improves Ventilatory Responses during Exercise in Adults with Well-Healed Burn Injuries.

INTRODUCTION: Pulmonary function is lower after a severe burn injury, which could influence ventilatory responses during exercise. It is unclear whether exercise training improves pulmonary function or ventilatory responses during exercise in adults with well-healed burn injuries. Therefore, we tested the hypothesis that exercise training improves pulmonary function and ventilatory responses during exercise in adults with well-healed burn injuries. METHODS: Thirty-nine adults (28 with well-healed burn injuries and 11 non-burn-injured controls) completed 6 months of unsupervised, progressive exercise training including endurance, resistance, and high-intensity interval components. Before and after exercise training, we performed comprehensive pulmonary function testing and measured ventilatory responses during cycling exercise. We compared variables using two-way ANOVA (group-time; i.e., preexercise/postexercise training (repeated factor)). RESULTS: Exercise training did not increase percent predicted spirometry, lung diffusing capacity, or airway resistance measures (time: P ≥ 0.14 for all variables). However, exercise training reduced minute ventilation ( V̇E ; time: P ≤ 0.05 for 50 and 75 W) and the ventilatory equivalent for oxygen ( V̇E /V̇O 2 ; time: P < 0.001 for 75 W) during fixed-load exercise for both groups. The ventilatory equivalent for carbon dioxide ( V̇E /V̇CO 2 ) during exercise at 75 W was reduced after exercise training (time: P = 0.04). The percentage of age-predicted maximum heart rate at the ventilatory threshold was lower in adults with well-healed burn injuries before ( P = 0.002), but not after ( P = 0.22), exercise training. Lastly, exercise training increased V̇E and reduced V̇E /V̇O 2 during maximal exercise (time: P = 0.005 for both variables). CONCLUSIONS: These novel findings demonstrate that exercise training can improve ventilatory responses during exercise in adults with well-healed burn injuries.

Thermoregulatory Responses with Size-matched Simulated Torso or Limb Skin Grafts.

PURPOSE: This study aimed to test the hypothesis that a simulated burn injury on the torso will be no more or less detrimental to core temperature control than on the limbs during uncompensable exercise-heat stress. METHODS: Nine nonburned individuals (7 men, 2 women) completed the protocol. On separate occasions, burn injuries of identical surface area (0.45 ± 0.08 m2 or 24.4% ± 4.4% of total body surface area) were simulated on the torso or the arms/legs using an absorbent, vapor-impermeable material that impedes sweat evaporation in those regions. Participants performed 60 min of treadmill walking at 5.3 km·h-1 and a 4.1% ± 0.8% grade, targeting 6 W·kg-1 of metabolic heat production in 40.1°C ± 0.2°C and 19.6% ± 0.6% relative humidity conditions. Rectal temperature, heart rate, and perceptual responses were measured. RESULTS: Rectal temperature increased to a similar extent with simulated injuries on the torso and limbs (condition-by-time interaction, P = 0.86), with a final rectal temperature 0.9°C ± 0.3°C above baseline in both conditions. No differences in heart rate, perceived exertion, or thermal sensation were observed between conditions (condition-by-time interactions, P ≥ 0.50). CONCLUSIONS: During uncompensable exercise-heat stress, sized-matched simulated burn injuries on the torso or limbs evoke comparable core temperature, heart rate, and perceptual responses, suggesting that the risk of exertional heat illness in such environmental conditions is independent of injury location.

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.

Exercise Training Improves Microvascular Function in Burn Injury Survivors.

INTRODUCTION: Vasodilator function is impaired in individuals with well-healed burn injuries; however, therapeutic interventions that lessen or reverse this maladaptation are lacking. The purpose of this study was to test the hypothesis that a 6-month community-based exercise training program would increase microvascular dilator function in individuals with well-healed burn injuries, irrespective of the magnitude of the injured body surface area. Further, we hypothesize that macrovascular dilator function would remain unchanged posttraining. METHODS: Microvascular function (forearm reactive hyperemia), macrovascular function (brachial artery flow-mediated dilation), and the maximal vasodilatory response after ischemic handgrip exercise (an estimate of microvascular remodeling) were assessed before and after exercise training in nonburned control subjects (n = 11) and individuals with burn injuries covering a moderate body surface area (26% ± 7%; n = 13) and a high body surface area (59% ± 15%; n = 19). RESULTS: Peak vascular conductance and area under the curve during postocclusive reactive hyperemia increased from pretraining to posttraining in control and burn injury groups (both P < 0.05), the magnitude of which did not differ between groups (both P = 0.6). Likewise, the maximal vasodilatory response after ischemic handgrip exercise increased in all groups after exercise training (P < 0.05). Macrovascular dilator function did not differ across time or between groups (P = 0.8). CONCLUSIONS: These data suggest that a community-based exercise training program improves microvascular function in individuals with well-healed burn injuries, which may be due in part to vascular remodeling.

Burn Injury Does Not Exacerbate Heat Strain during Exercise while Wearing Body Armor.

INTRODUCTION: Although evaporative heat loss capacity is reduced in burn-injured individuals with extensive skin grafts, the thermoregulatory strain due to a prior burn injury during exercise-heat stress may be negligible if the burn is located underneath protective clothing with low vapor permeability. PURPOSE: This study aimed to test the hypothesis that heat strain during exercise in a hot-dry environment while wearing protective clothing would be similar with and without a simulated torso burn injury. METHODS: Ten healthy individuals (8 men/2 women) underwent three trials wearing: uniform (combat uniform, tactical vest, and replica torso armor plates), uniform with a 20% total body surface area simulated torso burn (uniform + burn), or shorts (and sports bra) only (control). Exercise consisted of treadmill walking (5.3 km·h; 3.7% ± 0.9% grade) for 60 min at a target heat production of 6.0 W·kg in 40.0°C ± 0.1°C and 20.0% ± 0.6% relative humidity conditions. Measurements included rectal temperature, heart rate, ratings of perceived exertion (RPE), and thermal sensation. RESULTS: No differences in rectal temperature (P ≥ 0.85), heart rate (P ≥ 0.99), thermal sensation (P ≥ 0.73), or RPE (P ≥ 0.13) occurred between uniform + burn and uniform trials. In the control trial, however, core temperature, heart rate, thermal sensation, and RPE were lower compared with the uniform and uniform + burn trials (P ≤ 0.04 for all). CONCLUSIONS: A 20% total body surface area simulated torso burn injury does not further exacerbate heat strain when wearing a combat uniform. These findings suggest that the physiological strain associated with torso burn injuries is not different from noninjured individuals when wearing protective clothing during an acute exercise-heat stress.

Exercise Core Temperature Response with a Simulated Burn Injury: Effect of Body Size.

Although the severity of a burn injury is often associated with the percentage of total body surface area burned (%TBSA), the thermoregulatory consequences of a given %TBSA injury do not account for the interactive effects of body morphology and metabolic heat production (Hprod). PURPOSE: Using a simulated burn injury model to mimic the detrimental effect of a 40% TBSA injury on whole-body evaporative heat dissipation, core temperature response to exercise in physiologically uncompensable conditions between morphologically disparate groups were examined at (i) an absolute Hprod (W), and (ii) a mass-specific Hprod (W·kg). METHODS: Healthy, young, nonburned individuals of small (SM, n = 11) or large (LG, n = 11) body size cycled for 60 min at 500 W or 5.3 W·kg of Hprod in 39°C and 20% relative humidity conditions. A 40% burn injury was simulated by affixing a highly absorbent, vapor-impermeable material across the torso (20% TBSA), arms (10% TBSA), and legs (10% TBSA) to impede evaporative heat loss in those regions. RESULTS: Although the elevation in core temperature was greater in SM compared with LG at an Hprod of 500 W (SM, 1.69°C ± 0.26°C; LG, 1.05°C ± 0.26°C; P < 0.01), elevations in core temperature were not different at an Hprod of 5.3 W·kg between groups (SM, 0.99°C ± 0.32°C; LG, 1.05°C ± 0.26°C; P = 0.66). CONCLUSIONS: These data suggest that among individuals with a 40% TBSA burn injury, a smaller body size leads to exacerbated elevations in core temperature during physical activities eliciting the same absolute Hprod (non-weight-bearing tasks) but not activities eliciting the same mass-specific Hprod (weight-bearing tasks).

Exercise Thermoregulation with a Simulated Burn Injury: Impact of Air Temperature.

The U.S. Army's Standards of Medical Fitness (AR 40-501) states: "Prior burn injury (to include donor sites) involving a total body surface area of 40% or more does not meet the standard." However, the standard does not account for the interactive effect of burn injury size and air temperature on exercise thermoregulation. PURPOSE: To evaluate whether the detrimental effect of a simulated burn injury on exercise thermoregulation is dependent on air temperature. METHODS: On eight occasions, nine males cycled for 60 min at a fixed metabolic heat production (6 W·kg) in air temperatures of 40°C or 25°C with simulated burn injuries of 0% (Control), 20%, 40%, or 60% of total body surface area (TBSA). Burn injuries were simulated by covering the skin with an absorbent, vapor-impermeable material to impede evaporation from the covered areas. Core temperature was measured in the gastrointestinal tract via telemetric pill. RESULTS: In 40°C conditions, greater elevations in core temperature were observed with 40% and 60% TBSA simulated burn injuries versus Control (P < 0.01). However, at 25°C, core temperature responses were not different versus Control with 20%, 40%, and 60% TBSA simulated injuries (P = 0.97). The elevation in core temperature at the end of exercise was greater in the 40°C environment with 20%, 40%, and 60% TBSA simulated burn injuries (P ≤ 0.04). CONCLUSIONS: Simulated burn injuries ≥20% TBSA exacerbate core temperature responses in hot, but not temperate, air temperatures. These findings suggest that the U.S. Army's standard for inclusion of burned soldiers is appropriate for hot conditions, but could lead to the needless discharge of soldiers who could safely perform their duties in cooler training/operational settings.

Impaired Thermoregulatory Function during Dynamic Exercise in Multiple Sclerosis.

INTRODUCTION: Impairments in sudomotor function during passive whole-body heating have been reported in multiple sclerosis (MS), a demyelinating disease of the CNS that disrupts autonomic function. However, the capability of the thermoregulatory system to control body temperature during exercise has never been assessed in MS. Thus, the aim of the present study was to test the hypothesis that thermoregulatory function is impaired in MS patients compared with healthy controls (CON) exercising at similar rates of metabolic heat production. METHODS: Sweating and skin blood flow responses were compared between 12 individuals diagnosed with relapsing-remitting MS (9 females, 3 males) and 12 sex-, age-, mass-, and BSA-matched CON during a single bout of cycling exercise (rate of metabolic heat production: ∼4.5 W·kg) for 60 min in a climate-controlled room (25°C, 30% RH). RESULTS: Individuals with MS exhibited an attenuated increase in cumulative whole-body sweat loss after 30 min (MS, 72 ± 51 g; CON, 104 ± 37 g; P = 0.04) and 60 min (MS, 209 ± 94 g; CON, 285 ± 62 g; P = 0.02), as well as lower sweating thermosensitivity (MS, 0.49 ± 0.26 mg·cm·min·°C; CON, 0.86 ± 0.30 mg·cm·min·°C; P = 0.049). Despite evidence for thermoregulatory dysfunction, there were no differences between MS and CON in esophageal or rectal temperatures at 30- or 60-min time points (P > 0.05). Cutaneous vasculature responses were also not different in MS compared with CON (P > 0.05). CONCLUSION: Taken together, MS blunts sweating responses during exercise while cutaneous vasculature responses are preserved. Altered mechanisms of body temperature regulation in persons with MS may lead to temporary worsening of disease symptoms and limit exercise tolerance under more thermally challenging conditions.

No Thermoregulatory Impairment in Skin Graft Donor Sites during Exercise-Heat Stress.

The US Army's Standards of Medical Fitness, AR 40-501, state that "Prior burn injury (to include donor sites) involving a total body surface area of 40% or more does not meet the standard." Inclusion of donor sites (sites harvested for skin grafts) in this standard implies that thermoregulatory function is impaired within donor sites during exercise-heat stress; however, supporting evidence is currently lacking. PURPOSE: To test the hypothesis that well-healed donor and noninjured sites demonstrate similar elevations in skin blood flow and sweating during exercise-induced hyperthermia. METHODS: Twenty burn survivors (>1 yr postinjury; four females) cycled for 60 min in a 39.7°C ± 0.3°C and 21.1% ± 3.3% relative humidity environment at approximately 50% of maximal aerobic capacity. Core and mean skin temperatures were recorded throughout exercise. Skin blood flow (laser-Doppler imaging) was measured at baseline and after exercise within donor (LDFDON) and adjacent noninjured control (LDFCON) sites. At 45 min of exercise, local sweat rates (Technical Absorbents) were measured within the same donor (LSRDON) and noninjured (LSRCON) areas. RESULTS: After 60 min of exercise, core and skin temperatures reached 38.2°C ± 0.4°C and 35.5°C ± 1.2°C, respectively. The increase in skin blood flow from baseline to end-exercise (LDFDON, 91.6 ± 44.5 AU; LDFCON, 106.0 ± 61.6 AU; P = 0.17) and local sweat rates (LSRDON, 0.46 ± 0.26 mg·cm·min; LSRCON, 0.53 ± 0.25 mg·cm·min; P = 0.14) were not different between donor and noninjured control sites. CONCLUSIONS: Well-healed donor sites retain the ability to increase skin blood flow and sweating during exercise heat stress, providing evidence against the inclusion of donor sites when determining whether a burn injury meets the Army's Standards of Medical Fitness.