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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.

Compared with younger adults, passive heating induced increases in cardiac output are attenuated by ∼50% in older adults. This attenuated response may be associated with older individuals’ inability to maintain stroke volume through ionotropic mechanisms and/or through altered chronotropic mechanisms. The purpose of this study was to identify the interactive effect of age and hyperthermia on cardiac responsiveness to dobutamine-induced cardiac stimulation. Eleven young (26 ± 4 yr) and 8 older (68 ± 5 yr) participants underwent a normothermic and a hyperthermic (baseline core temperature +1.2°C) trial on the same day. In both thermal conditions, after baseline measurements, intravenous dobutamine was administered for 12 min at 5 µg/kg/min, followed by 12 min at 15 µg/kg/min. Primary measurements included echocardiography-based assessments of cardiac function, gastrointestinal and skin temperatures, heart rate, and mean arterial pressure. Heart rate responses to dobutamine were similar between groups in both thermal conditions ( P > 0.05). The peak systolic mitral annular velocity (S′), i.e., an index of left ventricular longitudinal systolic function, was similar between groups for both thermal conditions at baseline. While normothermic, the increase in S′ between groups was similar with dobutamine administration. However, while hyperthermic, the increase in S′ was attenuated in the older participants with dobutamine ( P < 0.001). Healthy, older individuals show attenuated inotropic, but maintained chronotropic responsiveness to dobutamine administration during hyperthermia. These data suggest that older individuals have a reduced capacity to increase cardiomyocyte contractility, estimated by changes in S′, via β1-adrenergic mechanisms while hyperthermic.

Aerobic exercise is important in the rehabilitation of individuals with prior burn injuries, but no studies have examined whether adult burn survivors demonstrate cardiac remodeling to long-term aerobic exercise training. In this study, we tested the hypothesis that 6 months of progressive exercise training would improve cardiac magnetic resonance imaging-based measures of cardiac structure and function in well-healed burn survivors. Our findings highlight the ability of exercise training to modify cardiac structure and function in well-healed burn survivors and nonburned sedentary controls alike.

The human body constantly exchanges heat with the environment. Temperature regulation is a homeostatic feedback control system that ensures deep body temperature is maintained within narrow limits despite wide variations in environmental conditions and activity-related elevations in metabolic heat production. Extensive research has been performed to study the physiological regulation of deep body temperature. This review focuses on healthy and disordered human temperature regulation during heat stress. Central to this discussion is the notion that various morphological features, intrinsic factors, diseases, and injuries independently and interactively influence deep body temperature during exercise and/or exposure to hot ambient temperatures. The first sections review fundamental aspects of the human heat stress response, including the biophysical principles governing heat balance and the autonomic control of heat loss thermoeffectors. Next, we discuss the effects of different intrinsic factors (morphology, heat adaptation, biological sex, and age), diseases (neurological, cardiovascular, metabolic, and genetic), and injuries (spinal cord injury, deep burns, and heat stroke), with emphasis on the mechanisms by which these factors enhance or disturb the regulation of deep body temperature during heat stress. We conclude with key unanswered questions in this field of research.

Exercise training reduces cardiovascular disease risk, partly due to arterial blood pressure (BP) lowering at rest and during fixed-load exercise. However, it is unclear whether exercise training can reduce BP at rest and during exercise in adults with well-healed burn injuries. Therefore, the purpose of this investigation was to test the hypothesis that 6 mo of unsupervised exercise training reduces BP at rest and during lower-body cycle ergometry in adults with well-healed burn injuries. Thirty-nine adults (28 with well-healed burn injuries and 11 controls) completed 6 mo of unsupervised, progressive exercise training including endurance, resistance, and high-intensity interval components. Before and after exercise training, we measured BP at rest, during fixed-load submaximal exercise (50 and 75 W), during fixed-intensity submaximal exercise (40% and 70% of V̇o

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.

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.

The purpose of this study was to evaluate whether burn survivors have lower adherence compared to non-burned control individuals during a 6-month community-based exercise program. In burn survivors we sought to answer if there was a relation between the size of the burn injury and dropout frequency. Fifty-two burn survivors and 15 non-burned controls (n=67) were recruited for a 6-month community-based (i.e., non-supervised), progressive, exercise training program. During the exercise program, 27% (i.e., 4 of 15 enrolled) of the non-burned individuals dropped out of the study, while 37% (i.e., 19 of 52) of the burn survivors dropped out from the study. There was no difference in the percentage of individuals who dropped out between groups (p = 0.552). There was no difference in size of the burn injury, expressed as percent body surface area burned (%BSA) between the burn-survivors that dropped out versus those who completed the exercise regimen (p = 0.951). We did not observe a relation between %BSA burned and dropouts (log odds = -0.15-0.01(%BSA), B= -0.01, SE = 0.015, p = 0.541). There was no effect of %BSA burned on the probability of dropout [Exp (B) = 0.991, 95% CI (0.961, 1.020)] and there were no differences in the percentage of individuals who dropped out of the study based on %BSA burned (χ2(1) = 0.44, p = 0.51). These data demonstrate that burn survivors have similar exercise adherence relative to a non-burned group and the extent of a burn injury does not affect exercise program adherence.

The Innocor® device utilizes an insoluble gas (SF6) to estimate lung volume and the rate of disappearance of a soluble gas (N2O) to measure pulmonary blood flow (PBF), which approximates cardiac output assuming no shunt. We sought to identify error in the measurement of the insoluble gas in an effort to reduce variation in Innocor® measurement.We enrolled 28 participants from the Dallas Heart Study (mean age 63 years; 57% male; 43% white). Stroke volume was measured at rest and at submaximal (20 and 40 W) exercise using both echocardiography (Philips iE33) and the Innocor® device. We defined a priori peak and equilibrium SF6 measurement errors as greater or less than 20% of the mean observed value. Three Innocor measurements were obtained at rest (N = 27) for a total of 81 measurements. Of these, 22 % had SF6 measurements that fell outside of the priori range.Resting Innocor® stroke volume measures with peak SF6 measured above a priori range (0.12%) was associated with larger stroke volumes compared to stroke volume measures without peak SF6 error [101.4 (26.8) vs. 64.9 (8.7) mL, p = 0.006] and overestimated stroke volume when compared to stroke volume by echo [101.4 (26.8) vs. 59.9 (16.3) mL, p = 0.017]. A similar pattern was observed at submaximal exercise. In contrast, there was no consistent association between variation in equilibrium SF6 concentrations and measured stroke volume.Variability in peak SF6 concentration is common while using the Innocor® device and results in overestimated stroke volume. These findings have implications for research protocols using this device.

Skin grafting following a burn injury attenuates/abolishes sweat production within grafted areas. It is presently unknown whether the thermoregulatory consequences of skin grafting depend on anatomical location.Purpose: 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 non-burned individuals (7 males, 2 females) 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 ± 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).Conclusion: 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.

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

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: 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 (8M/2F) underwent three trials wearing: Uniform (combat uniform, tactical vest, and replica torso armor plates), Uniform with a 20% total body surface area (TBSA) simulated torso burn (Uniform + Burn), or shorts (and sports bra) only (Control). Exercise consisted of treadmill walking (5.3 km·h(–1); 3.7 ± 0.9% grade) for 60 min at a target heat production of 6.0 W·kg(−1) in 40.0 ± 0.1°C; 20.0 ± 0.6% relative humidity conditions. Measurements included rectal temperature, heart rate, rating of perceived exertion, and thermal sensation. RESULTS: No differences in rectal temperature (P ≥ 0.85), heart rate (P ≥ 0.99), thermal sensation (P ≥ 0.73), or rating of perceived exertion (P ≥ 0.13) occurred between Uniform + Burn and Uniform trials. In the Control trial, however, core temperature, heart rate, thermal sensation, and rating of perceived exertion were lower compared to the Uniform and Uniform + Burn trials (P ≤ 0.04 for all). CONCLUSION: A 20% TBSA 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 non-injured individuals when wearing protective clothing during an acute exercise-heat stress.

Due to various pathophysiological responses associated with a severe burn injury, we hypothesized that burn survivors exhibit chronotropic incompetence. To test this hypothesis, a graded peak oxygen consumption (V̇O2peak) test was performed in 94 adults (34 nonburned, 31 burn survivors with 14–35% body surface area grafted, and 29 burn survivors with >35% body surface area grafted). The threshold of 35% body surface area grafted was determined by receiver operating characteristic (ROC) curve analysis. Peak exercise heart rates (HRmax) were compared against age-predicted HRmax within each group. The proportion of individuals not meeting their age-predicted HRmax (within 5 b/min) were compared between groups. Age-predicted HRmax was not different from measured HRmax in the nonburned and moderate burn groups (P = .09 and .22, respectively). However, measured HRmax was 10 ± 6 b/min lower than the age-predicted HRmax in those with a large burn injury (P < .001). While 56 and 65% of individuals in the nonburned and moderate burn group achieved a measured HRmax within 5 b/min or greater of age-predicted HRmax, only 21% of those in the large burn group met this criterion (P < .001). These data provide preliminary evidence of chronotropic incompetence in individuals with severe burn injury covering >35% body surface area.

Purpose Upper-body exercise performed in a cold environment may increase cardiovascular strain, which could be detrimental to patients with coronary artery disease (CAD). This study compared cardiovascular responses of CAD patients during graded upper-body dynamic and static exercise in cold and neutral environments. Methods 20 patients with stable CAD performed 30 min of progressive dynamic (light, moderate, and heavy rating of perceived exertion) and static (10, 15, 20, 25 and 30% of maximal voluntary contraction) upper body exercise in cold (− 15 °C) and neutral (+ 22 °C) environments. Heart rate (HR), blood pressure (BP) and electrocardiographic (ECG) responses were recorded and rate pressure product (RPP) calculated. Results Dynamic-graded upper-body exercise in the cold increased HR by 2.3–4.8% (p = 0.002–0.040), MAP by 3.9–5.9% (p = 0.038–0.454) and RPP by 18.1–24.4% (p = 0.002–0.020) when compared to the neutral environment. Static graded upper-body exercise in the cold resulted in higher MAP (6.3–9.1%; p = 0.000–0.014), lower HR (4.1–7.2%; p = 0.009–0.033), but unaltered RPP compared to a neutral environment. Heavy dynamic exercise resulted in ST depression that was not related to temperature. Otherwise, ECG was largely unaltered during exercise in either thermal condition. Conclusions Dynamic- and static-graded upper-body exercise in the cold involves higher cardiovascular strain compared with a neutral environment among patients with stable CAD. However, no marked changes in electric cardiac function were observed. The results support the use of upper-body exercise in the cold in patients with stable CAD. Trial registration Clinical trial registration NCT02855905 August 2016.

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 pre-syncopal 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] x 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.

Each year, within the United States, tens of thousands of individuals are hospitalized for burn-related injuries. The treatment of deep burns often involves skin grafts to accelerate healing and reduce the risk of infection. The grafting procedure results in a physical disruption between the injured and subsequently debrided host site and the skin graft placed on top of that site. Both neural and vascular connections must occur between the host site and the graft for neural modulation of skin blood flow to take place. Furthermore, evaporative cooling from such burn injured areas is effectively absent, leading to greatly impaired thermoregulatory responses in individuals with large portions of their body surface area burned. Hospitalization following a burn injury can last weeks to months, with cardiovascular and metabolic consequences of such injuries having the potential to adversely affect the burn survivor for years postdischarge. With that background, the objectives of this article are to discuss 1) our current understanding of the physiology and associated consequences of skin grafting, 2) the effects of skin grafts on efferent thermoregulatory responses and the associated consequences pertaining to whole body thermoregulation, 3) approaches that may reduce the risk of excessive hyperthermia in burn survivors, 4) the long-term cardiovascular consequences of burn injuries, and 5) the extent to which burn survivors can “normalize” otherwise compromised cardiovascular responses. Our primary objective is to guide the reader toward an understanding that severe burn injuries result in significant physiological consequences that can persist for years after the injury.

Due to improvements in acute burn care over the last few decades, most patients with severe burns (up to 90% of the total body surface) survive. However, the metabolic and cardiovascular complications that accompany a severe burn can persist for up to 3 years post injury. Accordingly, there is now a greater appreciation of the need for strategies that can hasten recovery and reduce long-term morbidity post burn. Rehabilitation exercise training (RET) is a proven effective treatment to restore lean body mass, glucose and protein metabolism, cardiorespiratory fitness, and muscle strength in burn survivors. Despite this, very few hospitals incorporate RET in programs to aid the rehabilitation of patients with severe burns. Given that RET is a safe and efficacious treatment that restores function and reduces post-burn morbidity, we propose that a long-term exercise prescription plan should be considered for all patients with severe burns. In this literature review, we discuss the current understanding of burn trauma on major organ systems, and the positive benefits of incorporating RET as a part of the long-term rehabilitation of severely burned individuals. We also provide burn-specific exercise prescription guidelines for clinical exercise physiologists.

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 (H(prod)). 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 H(prod) (watts, W), and (ii) a mass-specific H(prod) (watts per kilogram of body mass, W·kg(−1)). METHODS: Healthy, young, non-burned 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(−1) of H(prod) 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: While the elevation in core temperature was greater in SM compared to LG at a H(prod) of 500 W (SM: 1.69 ± 0.26°C, LG: 1.05 ± 0.26°C, P < 0.01), elevations in core temperature were not different at a H(prod) of 5.3 W·kg(−1) between groups (SM: 0.99 ± 0.32°C, LG: 1.05 ± 0.26°C, P = 0.66). CONCLUSION: 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 H(prod) (non-weight-bearing tasks) but not activities eliciting the same mass-specific H(prod) (weight-bearing tasks).

There is considerable interindividual variability in the perception of pain. Given that pain management is a major public health problem, gaining insight into the underlying physiology of these perceptual differences is important. We tested the hypothesis that when interindividual variability in initial muscle sympathetic nerve activity (MSNA) responses to a cold pressor test (CPT) is identified, the divergent responses will be linked to differences in pain perception in healthy young men and women. In the supine position, blood pressure (BP) and MSNA were measured at baseline and during a 2-min CPT. Immediately following the CPT, pain was rated (range 0–10). Two groups were established: positive responders (Pos, n = 12) and negative responders (Neg, n = 12) based on the initial (first 30 s) MSNA response profiles (Pos: 12 ± 9, Neg: −3 ± 3 bursts/min, P

INTRODUCTION. Vasodilator function is impaired in individuals with well-healed burn injuries, but 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 post-training. METHODS. Microvascular function, (forearm reactive hyperemia), macrovascular function (brachial artery flow-mediated dilation), and the maximal vasodilatory response following ischemic handgrip exercise (an estimate of microvascular remodeling) were assessed before and after exercise training in non-burned 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 post-occlusive reactive hyperemia increased from pre- to post-training 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 following 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). CONCLUSION. 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.

New findings What is the central question of this study? Does dietary nitrate supplementation with beetroot juice attenuate thermoregulatory and cardiovascular strain in older adults during severe heat stress? What is the main finding and its importance? A 7-day nitrate supplementation regimen lowered resting mean arterial pressure in thermoneutral conditions. During heat stress, core and mean skin temperatures, vasodilatory responses, sweat loss, heart rate and left ventricular function were unchanged, and mean arterial pressure was only transiently reduced, post-supplementation. These data suggest nitrate supplementation with beetroot juice does not mitigate thermoregulatory or cardiovascular strain in heat-stressed older individuals. Abstract This study tested the hypothesis that dietary nitrate supplementation with concentrated beetroot juice attenuates thermoregulatory and cardiovascular strain in older individuals during environmental heat stress. Nine healthy older individuals (six females, three males; aged 67 ± 5 years) were exposed to 42.5 ± 0.1°C and 34.0 ± 0.5% relative humidity conditions for 120 min before (CON) and after 7 days of dietary nitrate supplementation with concentrated beetroot juice (BRJ; 280 ml, ∼16.8 mmol of nitrate daily). Core and skin temperatures, body mass changes (indicative of whole-body sweat loss), skin blood flow and cutaneous vascular conductance, forearm blood flow and vascular conductance, heart rate, arterial blood pressures and indices of cardiac function were measured. The 7-day beetroot juice regimen increased plasma nitrate/nitrite levels from 27.4 ± 15.2 to 477.0 ± 102.5 μmol l-1 (P 0.05). Mean arterial pressure was lower in BRJ vs. CON during heat stress (treatment-by-time interaction: P = 0.02). Overall, these findings suggest that dietary nitrate supplementation with concentrated beetroot juice does not attenuate thermoregulatory or cardiovascular strain in older individuals exposed to severe ambient heat stress.

KEY POINTS Haemorrhage is the leading cause of battlefield and civilian trauma deaths. Given that a haemorrhagic injury on the battlefield is almost always associated with pain, it is paramount that the administered pain medication does not disrupt the physiological mechanisms that are beneficial in defending against the haemorrhagic insult. Current guidelines from the US Army's Committee on Tactical Combat Casualty Care (CoTCCC) for the selection of pain medications administered to a haemorrhaging soldier are based upon limited scientific evidence, with the clear majority of supporting studies being conducted on anaesthetized animals. Specifically, the influence of low-dose ketamine, one of three analgesics employed in the pre-hospital setting by the US Army, on haemorrhagic tolerance in humans is unknown. For the first time in conscious males and females, the findings of the present study demonstrate that the administration of an analgesic dose of ketamine does not compromise tolerance to a simulated haemorrhagic insult. Increases in muscle sympathetic nerve activity during progressive lower-body negative pressure were not different between trials. Despite the lack of differences for muscle sympathetic nerve activity responses, mean blood pressure and heart rate were higher during moderate hypovolemia after ketamine vs. placebo administration. ABSTRACT Haemorrhage is the leading cause of battlefield and civilian trauma deaths. For a haemorrhaging soldier, there are several pain medications (e.g. ketamine) recommended for use in the prehospital, field setting. However, the data to support these recommendations are primarily limited to studies in animals. Therefore, it is unknown whether ketamine adversely affects physiological mechanisms responsible for maintenance of arterial blood pressure (BP) during haemorrhage in humans. In humans, ketamine has been demonstrated to raise resting BP, although it has not been studied with the concomitant central hypovolemia that occurs during haemorrhage. Thus, the present study aimed to test the hypothesis that ketamine does not impair haemorrhagic tolerance in humans. Thirty volunteers (15 females) participated in this double-blinded, randomized, placebo-controlled trial. A pre-syncopal limited progressive lower-body negative pressure (LBNP; a validated model for simulating haemorrhage) test was conducted following the administration of ketamine (20 mg) or placebo (saline). Tolerance was quantified as a cumulative stress index and compared between trials using a paired, two-tailed t test. We compared muscle sympathetic nerve activity (MSNA; microneurography), beat-to-beat BP (photoplethysmography) and heart rate (electrocardiogram) responses during the LBNP test using a mixed effects model (time [LBNP stage] × drug). Tolerance to the LBNP test was not different between trials (Ketamine: 635 ± 391 vs. Placebo: 652 ± 360 mmHg‧min, p = 0.77). Increases in MSNA burst frequency (time: P

We investigated that the effects of hypercapnia-induced elevations in cerebral perfusion during a heat stress on global cerebrovascular responses to an orthostatic challenge. Seven volunteers completed a progressive lower-body negative pressure (LBNP) challenge to presyncope during heat stress, with or without breathing a hypercapnic gas mixture. Administration of the hypercapnic gas mixture increased the partial pressure of end-tidal CO2 greater than pre-heat stress alone, and increased both internal carotid artery (ICA) and vertebral artery (VA) blood flows (P P

The present study evaluated whether wearing a water-soaked t-shirt, with or without electric fan use, mitigates thermal and cardiovascular strain in older individuals exposed to hot and moderately humid conditions. Nine healthy older individuals (68 ± 4 yr; five women) completed three 120-min heat exposures (42.4 ± 0.2°C, 34.2 ± 0.9% relative humidity) on separate days while wearing a dry t-shirt (CON), a t-shirt soaked with 500 ml of tap water (WET), or a t-shirt soaked with 500 ml of tap water while facing an electric fan (2.4 ± 0.4 m/s; WET+FAN). Measurements included core and skin temperatures, evaporative mass losses, heart rate, and blood pressure. In the WET condition, elevations in core temperature were attenuated compared with DRY from 30 to 120 min and compared with WET+FAN from 30 to 90 min ( P < 0.05). Evaporative mass losses (inclusive of sweat and water losses from the shirt) were greatest in WET+FAN, followed by WET, and then DRY ( P < 0.01). Sweat losses were lowest in WET, followed by DRY, and then WET+FAN ( P < 0.01). Heart rate was lower only at 60 min in WET versus DRY ( P = 0.01). No differences in mean arterial pressure were observed ( P = 0.51). In conclusion, wearing a water-soaked t-shirt without, but not with, electric fan use is an effective heat management strategy to mitigate thermal strain and lower sweat losses in older individuals exposed to hot and moderately humid conditions. NEW & NOTEWORTHY In older individuals exposed to hot and moderately humid environments, electric fan use coupled with a water-soaked t-shirt exacerbates sweat losses without mitigating heat strain compared with a dry t-shirt. However, wearing a water-soaked t-shirt without fan use reduces sweat losses and attenuates heat strain compared with a dry t-shirt and a fan/water-soaked t-shirt combination. These findings suggest wearing a water-soaked t-shirt is an effective heat-management strategy for older individuals during heat waves when air conditioning is inaccessible.

NEW FINDINGS What is the central question of this study? The venoarteriolar response (VAR) contributes substantially to the maintenance of orthostatic tolerance in humans. Despite its importance in haemodynamic homeostasis, the impact of ageing on the VAR remains understudied. What is the main finding and its importance? Older adults exhibit an augmented VAR in response to leg dependency. The age-related augmentation of the VAR might be linked with progressive increases of peripheral vascular resistance with ageing. We found a modest but significant correlation between the leg VAR and the morning blood pressure surge in older adults. Augmented leg VAR might contribute to the blood pressure elevation in the early morning. ABSTRACT The venoarteriolar response (VAR) is a non-adrenergic, non-baroreflex-mediated mechanism of vasoconstriction, which has been proposed to contribute ∼45% of the increase in total peripheral resistance during orthostasis. Despite its importance in human cardiovascular control during orthostatic stress, there is no information available regarding the impact of age and sex on the VAR or its role in diurnal blood pressure (BP) variation. We studied 33 (15 women) young (mean ± SD; 28 ± 4 years old) and 26 (12 women) older (71 ± 3 years old) healthy individuals. Brachial and femoral blood flow were measured using Doppler ultrasound. The percentage reduction in vascular conductance (blood flow/mean BP) during 4 min of limb dependency (35-40 cm below the heart level) was used to assess the VAR. The morning surge in BP was assessed using 24 h ambulatory BP monitoring. Peak VAR in the lower limb, but not in the upper limb, was significantly higher in the older than the younger adults (33 ± 4 versus 26 ± 6%, older versus young; P < 0.05). There was no sex difference in the VAR in either the young or the older group. A greater leg VAR was related to a greater morning surge in BP in older adults (r = -0.4, P = 0.02) but not in the young adults (r = -0.26, P = 0.1). Thus, advancing age enhances the VAR in the lower limb and is associated with the morning blood pressure surge in older adults. Sex does not affect this local axonal reflex in healthy humans.

Objective To determine if a healthy newborn's age in hours (3, 6, or 9 hours after birth) affects thermoregulatory status after the first bath as indicated by axillary and skin temperatures. Design Quasi-experimental, mixed-model (between subjects and within subjects) design with hours of age as the nonrepeated variable and prebath and postbath temperatures as the repeated variables. Setting Family-centered care unit at an urban hospital in the southwestern United States. Participants Healthy newborns (N = 75) 37 weeks or more completed gestation. Methods Mothers chose time of first bath based on available time slots (n = 25 newborns in each age group). Research nurses sponge bathed the newborns in the mothers' rooms. Axillary temperature, an index of core temperature, was measured with a digital thermometer, and skin temperature, an index of body surface temperature, was measured with a thermography camera. Temperatures were taken before the bath; immediately after the bath; and 5, 30, 60, and 120 minutes after the bath. Immediately after the bath, newborns were placed in skin-to-skin care (SSC) for 60 or more minutes. Results We found a difference (p = .0372) in axillary temperatures between the 3- and 9-hour age groups, although this difference was not clinically significant (0.18 °F [0.10 °C]). We found no statistically significant differences in skin temperatures among the three age groups. Regardless of age group, axillary and skin temperatures initially decreased and then recovered after the bath. Conclusion For up to 2 hours postbath, axillary and skin temperatures were not different between healthy newborns bathed at 3, 6, or 9 hours of age. Thermography holds promise for learning about thermoregulation, bathing, and SSC.

Following exercise, mean arterial pressure (MAP) is reduced ~5–10 mmHg from preexercise baseline. In nonendurance-trained males, postexercise hypotension results from peripheral vasodilation not offset by increased cardiac output (CO). By contrast, postexercise hypotension occurs through a reduction in CO from preexercise baseline in endurance-trained males. The reason(s) explaining these divergent responses remain unknown. Exercise at fixed percentage of peak oxygen consumption (V̇o2peak) is associated with a greater rate of metabolic heat production in trained individuals and therefore elevated sweat rates, both when compared with untrained individuals. We hypothesized that greater fluid loss would explain the postexercise reduction in CO of endurance-trained males. Twelve endurance-trained males (Trained: V̇o2peak, 64 ± 5 ml O2·kg−1·min−1) cycled for 60 min at 60% V̇o2peak (Trained60%). On separate days, 12 nonendurance trained males (Untrained: V̇o2peak, 49 ± 3 ml O2·kg−1·min−1) cycled at 1) 60% V̇o2peak (Untrained60%), and 2) a rate of heat production equivalent to that achieved by the Trained group (UntrainedMatched). Fluid loss was similar between Trained60% (−1.32 ± 0.20 kg) and UntrainedMatched (−1.32 ± 0.23 kg; P = 0.99) but was greater in these conditions relative to Untrained60% (−0.95 ± 0.11 kg; both P < 0.01). During the final 30 min of postexercise supine recovery, MAP was similarly reduced by 5 ± 2 mmHg in all three conditions ( P = 0.91). The reduction in MAP was mediated by a 0.5 ± 0.3 l/min reduction in CO from baseline in Trained60% ( P = 0.01). In contrast, CO returned to baseline following exercise during UntrainedMatched and Untrained60% (both P ≥ 0.30). These data demonstrate that greater fluid loss does not fully explain the divergent postexercise hemodynamic responses observed in trained relative to untrained males. NEW & NOTEWORTHY Even when matched for exercise-induced fluid loss, cardiac output was decreased in trained males but returned to baseline following exercise in their untrained counterparts. However, as per our hypothesis, reductions in stroke volume were similar between groups. This suggests that exercise-induced fluid loss is an important determinant of the stroke volume response during recovery but factors affecting heart rate such as exercise intensity and/or heat stress are also important determinants of postexercise hemodynamics.

Physical movement lasting any more than a few seconds (e.g., exercise), requires coordination of motor control with concomitant changes in the cardiovascular and respiratory support necessary to respond to the rapid increases in metabolic demand. Without such coordination, delivery of oxygen and removal of waste products become rate limiting and will restrict the duration, speed, and quality of movement. Fortunately, under healthy conditions, the central and peripheral nervous systems contribute importantly to this remarkable level of coordination via complex mechanisms that remain to be fully elucidated. The purposes of this review are to present the current state of knowledge regarding: (i) mechanisms by which the body maintains appropriate perfusion pressure to all organs during acute bouts of exercise, and (ii) alterations occurring in these mechanisms via central nervous system adaptations when exercise is performed or not performed on a regular basis (e.g., physically active versus sedentary lifestyle, respectively). Results from studies performed in humans and laboratory animals provide the reader a well-rounded knowledge base. They are intended to instill an appreciation of what is known, and not known, about how the brain regulates the cardiovascular system during acute bouts of exercise, and the adaptations that occur when individuals exercise regularly versus when chronically sedentary. Discussion of the latter is intended to provide novel mechanisms for the increased incidence of cardiovascular disease in sedentary individuals versus a reduced incidence in individuals who are regularly active. © 2018 American Physiological Society. Compr Physiol 8:103-151, 2018.

Purpose In 2014, ECRI recommended that blanket warming cabinets be set at a maximum temperature of 130°F because of safety concerns with warmed rolled and folded blankets. We could find no research to support this recommendation. The purpose of this study was to measure skin temperatures and thermal comfort in healthy volunteers before and after application of folded and rolled dry cotton blankets warmed in 130°F or 200°F cabinets. Design Randomized, descriptive, and comparative study. Methods Participants (n = 20) received two blankets (one rolled and one folded) from warming cabinets set at 130°F or 200°F. Folded blankets were applied to the back and rolled to the neck. Skin temperatures and thermal comfort were obtained at fixed time intervals. Findings Skin temperatures from blankets in the 200°F cabinet were greater than those in the 130°F cabinet. No skin temperatures reached temperature and/or duration thresholds for dermal injury. Conclusions This study provides supportive evidence that warming cabinets may be set at a maximum of 200°F without compromising patient safety.

Skeletal muscle blood flow is attenuated in aged humans performing dynamic exercise, which is due, in part, to impaired local vasodilatory mechanisms. Recent evidence suggests that folic acid improves cutaneous vasodilation during localized and whole body heating through nitric oxide-dependent mechanisms. However, it is unclear whether folic acid improves vasodilation in other vascular beds during conditions of increased metabolism (i.e., exercise). The purpose of this study was to test the hypothesis that folic acid ingestion improves skeletal muscle blood flow in aged adults performing graded handgrip and plantar flexion exercise via increased vascular conductance. Nine healthy, aged adults (two men and seven women; age: 68 ± 5 yr) performed graded handgrip and plantar flexion exercise before (control), 2 h after (acute, 5 mg), and after 6 wk (chronic, 5 mg/day) folic acid ingestion. Forearm (brachial artery) and leg (superficial femoral artery) blood velocity and diameter were measured via Duplex ultrasonography and used to calculate blood flow. Acute and chronic folic acid ingestion increased serum folate (both P < 0.05 vs. control). During handgrip exercise, acute and chronic folic acid ingestion increased forearm blood flow (both conditions P < 0.05 vs. control) and vascular conductance (both P < 0.05 vs. control). During plantar flexion exercise, acute and chronic folic acid ingestion increased leg blood flow (both P < 0.05 vs. control), but only acute folic acid ingestion increased vascular conductance ( P < 0.05 vs. control). Taken together, folic acid ingestion increases blood flow to active skeletal muscle primarily via improved local vasodilation in aged adults.NEW & NOTEWORTHY Our findings demonstrate that folic acid ingestion improves blood flow via enhanced vascular conductance in the exercising skeletal muscle of aged humans. These findings provide evidence for the therapeutic use of folic acid to improve skeletal muscle blood flow, and perhaps exercise and functional capacity, in human primary aging.Listen to this article’s corresponding podcast at http://ajpheart.podbean.com/e/folic-acid-and-exercise-hyperemia-in-aging/ .

Background Multiple sclerosis (MS) is a neurological disease marked by demyelination and axonal loss. Individuals with MS experience increases in clinical signs and symptoms during heat exposure. Objective To test the hypothesis that moderate heat exposure adversely affects postural sway in individuals with MS. Methods Ten individuals with relapsing-remitting MS (50 ± 8y) and nine controls (47 ± 10y) were examined under a Thermal and a Time Control trial. Following a 30 min thermoneutral baseline (25 °C, 30% relative humidity (RH)), stand tests randomized with eyes open and closed, were performed. For Thermal, subjects were first exposed to 60 min of heating (40 °C, 30%RH) followed by 60 min of cooling (20 °C, 30%RH). For Time Control, subjects remained in a thermoneutral environment throughout. Stand tests were repeated at consistent times in both trials. Results No difference in skin and core temperatures between groups were observed for any trial (P > 0.05). During heating, postural sway was higher in MS relative to control subjects (eyes open, P = 0.03; eyes closed, P = 0.011). No differences in postural sway, regardless of eye status, were observed during the Time Control trial for either group (P > 0.05). Conclusion These data demonstrate that exposure to a moderate heating environment increases postural sway in patients with MS.

Local heating of an extremity increases blood flow and vascular shear stress throughout the arterial tree. Local heating acutely improves macrovascular dilator function in the upper limbs of young healthy adults through a shear stress-dependent mechanism but has no such effect in the lower limbs of this age group. The effect of acute limb heating on dilator function within the atherosclerotic prone vasculature of the lower limbs of aged adults is unknown. Therefore, the purpose of this study was to test the hypothesis that acute lower limb heating improves macro- and microvascular dilator function within the leg vasculature of aged adults. Nine young and nine aged adults immersed their lower limbs at a depth of ~33 cm into a heated (~42°C) circulated water bath for 45 min. Before and 30 min after heating, macro (flow-mediated dilation)- and microvascular (reactive hyperemia) dilator functions were assessed in the lower limb, following 5 min of arterial occlusion, via Doppler ultrasound. Compared with preheat, macrovascular dilator function was unchanged following heating in young adults ( P = 0.6) but was improved in aged adults ( P = 0.04). Similarly, microvascular dilator function, as assessed by peak reactive hyperemia, was unchanged following heating in young adults ( P = 0.1) but was improved in aged adults ( P < 0.01). Taken together, these data suggest that acute lower limb heating improves both macro- and microvascular dilator function in an age dependent manner. NEW & NOTEWORTHY We demonstrate that lower limb heating acutely improves macro- and microvascular dilator function within the atherosclerotic prone vasculature of the leg in aged adults. These findings provide evidence for a potential therapeutic use of chronic lower limb heating to improve vascular health in primary aging and various disease conditions.

Introduction Excision of burned skin and subsequent grafting removes sweat glands and thereby impairs thermoregulation. Consequently, rehabilitation and associated exercise may be accompanied by a greater risk of hyperthermia, depending on exercise duration, intensity and environmental temperature. Current physical activity guidelines recommend adults perform at least 150 min of moderate-intensity exercise per week, which is often divided into 30-min daily sessions. This project tested the hypothesis that burn survivors could exercise for 30 min without excessive elevations in core body temperature, regardless of the total body surface area (%TBSA) burned or environmental temperature. Methods Ten subjects cycled for 60 min at 1) a moderate intensity (97±8 watts) in a thermoneutral environment (24°C, MOD_NEU), 2) a moderate intensity (100±17 watts) in a hot environment (39°C, MOD_HOT), and 3) a low intensity (65±10 watts) in a hot environment (39°C, LOW_HOT). Burn injuries were simulated by covering 0%, 20%, 40%, or 60% of the individual’s TBSA with an absorbent material that prevented sweat evaporation. Changes in gastrointestinal temperature (ΔTcore) were analyzed at 15-min increments throughout exercise. Results For the MOD_NEU trial, there were no differences in ΔTcore between the %TBSA coverage bouts at any time point during exercise. For the MOD_HOT trial, there were no differences in ΔTcore at 15 and 30 min of exercise regardless of the %TBSA coverage, while ΔTcore was appreciably elevated (P< 0.05) at 45 and 60 min of exercise for 20%+ TBSA bouts. For the MILD_HOT trial, there were no differences in ΔTcore at any time point between %TBSA bouts, with the sole exception of 60% simulated burn having a slightly greater ΔTcore (0.3±0.34°C; P< 0.05) at 60 min of exercise relative to the 0% TBSA bout. Conclusions These data indicate that individuals with up to 60% of their TBSA burned could exercise at a moderate intensity for 30 min, even in hot environmental conditions, without excessive elevations in body core temperature. Applicability of Research to Practice Individuals with significant burn injuries can benefit from exercise, without the risk of excessive hyperthermia, for up to 30 min in the heat or at least 60 min in an air conditioned space. Funding: DOD W81XWH-15-1-0647

BACKGROUND Regular long-term physical exercise has favourable effects on endothelial function in patients with coronary artery disease (CAD). However, the effects of an acute exercise bout in the cold on endothelial function are not known. METHODS At first, the effects of moderate-intensity aerobic lower-body exercise were assessed in CAD patients (n = 16) in a neutral [+22°C] and cold [-15°C] environment. Secondly, responses to static and dynamic upper-body exercise in a neutral [+22°C] and cold [-15°C] environment were investigated in CAD patients (n = 15). All experiments were performed in a random order. Endothelial function was measured by flow-mediated dilation (FMD) of the brachial artery in response to reactive hyperaemia, before and after the exposures in a neutral environment. RESULTS No significant temperature*exercise*condition (pre-post) interaction was observed in FMD% when comparing rest versus aerobic exercise or static versus dynamic upper-body exercise. Relative reactive hyperaemia during FMD protocol, measured by changes in shear rate, was elevated after rest compared to aerobic exercise (p = .001) and after static compared to dynamic upper-body exercise (p

Vast improvements in the survival rates following burn injuries has led to a greater number of patients living with a wide range of long-term impairments, activity limitations, and participation constraints. Therefore, long-term care is critical in this clinical population and necessitates appropriate rehabilitation strategies to maximize an individual's overall health. The purpose of this study was to test the hypothesis that the extent to which outcomes within the International Classification of Functioning, Disability, and Health (ICF) framework are improved following 6 months of unsupervised exercise training is influenced by the severity of a burn injury (i.e., percent body surface area injured). Outcome variables representing the dimensions of the ICF, body functions & structure, activity, and participation, were collected pre- and post- 6 months of exercise training in three groups of participants: non-injured control subjects (N = 11), subjects with moderate-level well-healed burn injuries (N = 13, 26 ± 6% body surface area burned), and subjects with high-level well-healed burn injuries (N = 20, 58 ± 15% body surface area burned). Exercise training improved lower extremity strength (changes in peak torque/kg body mass at 90 degrees/sec flexion: 30 ± 5% and extension: 36 ± 4%, p < 0.05) and functional activities (changes in sit to stand: -9 ± 4% and ascend stairs: -4 ± 1%; p < 0.05) in all groups. For outcome variables representing ICF levels of body functions & structure and activity, there were no differences at baseline or improvements made between the groups after training. That said, with the exception of the domain of functional activity (reported 17 ± 34% improvement in the high-level burn cohort, p < 0.05), no changes were revealed in the participation level of ICF indexed by health-related quality of life questionnaires. These findings support the utilization of a 6-month unsupervised exercise training program in the long-term rehabilitation of individuals with burn injuries; that is, improvements in body functions & structure and activity can be achieved with an exercise regimen regardless of the severity of burn injury.

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 percent 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 upon air temperature. METHODS: On eight occasions, nine males cycled for 60 min at a fixed metabolic heat production (6 W·kg(−1)) 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 vs. Control (P < 0.01). However, at 25°C, core temperature responses were not different vs. 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). CONCLUSION: 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.

Supine hypertension affects about half of patients with primary autonomic failure (AF), complicates the treatment of orthostatic hypotension (OH) and induces nocturnal polyuria, resulting in worsening of morning OH. We previously showed that short exposure to local passive heat (40-42°C applied for ≤2 hours over abdomen and pelvis with a heating pad) acutely decreased systolic blood pressure (BP) by -25±5 mmHg in AF patients with supine hypertension due to decreases in stroke volume (-29±5%) and cardiac output (-30±5%). In this study, we hypothesized that local passive heat therapy applied overnight would lower nocturnal BP and polyuria, and improve early morning OH in these patients. Ten AF patients with supine hypertension (age 76±2 years, 6 men, supine systolic BP 168±3 mmHg) received passive heat (38°C with a water-perfused heating pad placed under the torso) or placebo, in a 2-night crossover study. Supine BP was monitored every 2 hr from 8pm-8am. Heat therapy was applied from 10pm-6am. Morning orthostatic tolerance was assessed at 8 am. Systolic BP significantly decreased during overnight heat therapy compared to placebo (Figure; P