Assessing Injury Susceptibility at Marine Corps Recruit Depot, San Diego, California.

ABSTRACT: Poh, PYS, Sessoms, PH, Haluch, KS, and Trone, DW. Assessing injury susceptibility at Marine Corps Recruit Depot, San Diego, California. J Strength Cond Res 37(7): 1530-1536, 2023-Marine Corps Recruit Depot (MCRD) recruits undergo demanding training. Musculoskeletal injury (MSKI) accounts for attrition and graduation delays. Functional tests, such as Functional Movement Screen (FMS), Y-Balance Test-Lower Quarter (YBT-LQ), and ankle dorsiflexion range of motion (AD-ROM), may identify individuals at greater MSKI risk. This study tested the hypothesis that functional assessments may inform injury prediction. Male recruits ( N = 407; mean ± SD : age, 20 ± 2 years) performed baseline functional tests. Marine Corps Recruit Depot staff tracked MSKI and graduation outcomes. The chi-square test of independence (individual FMS exercises) and Mann-Whitney U (FMS composite score) test examined the relationship between FMS and MSKI incidence. One-way analysis of variance compared YBT-LQ and AD-ROM with MSKI incidence. Twelve recruits (3%) incurred a lower extremity MSKI and were dropped. Of those 12, 9 had a delayed graduation, and 3 separated from enlistment. The level of significance was set at p < 0.10 to identify between-group differences (yes-MSKI vs. no-MSKI). Functional movement screen composite score ( p = 0.064), hurdle step ( p = 0.059), and trunk stability ( p = 0.001) were lower in yes-MSKI. Y-Balance Test-Lower Quarter anterior direction difference between legs ( p = 0.011) and AD-ROM right side ( p = 0.055) was greater in yes-MSKI. Odds ratios (OR) were calculated using cut-off scores, with strong odds of sustaining MSKI with FMS trunk stability score <2 (OR: 7.56, 95% confidence interval [CI]: [2.32, 24.61]) and YBT-LQ anterior difference >6.25 cm (OR: 6.38, 95% CI: [1.98, 20.55]). Recruits who incurred MSKI had scores that indicated lesser mobility and stability of the lower extremity, providing preliminary evidence that when assessed together, FMS, YBT-LQ, and AD-ROM, may have predictive value for identifying those at MSKI risk.

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.

Folic acid supplementation does not attenuate thermoregulatory or cardiovascular strain of older adults exposed to extreme heat and humidity.

NEW FINDINGS: What is the central question of this study? Does folic acid supplementation alleviate thermoregulatory and cardiovascular strain of older adults during exposure to extreme heat and humidity? What is the main finding and its importance? Folic acid supplementation for 6 weeks did not affect whole-limb blood flow/vasodilatation, core and skin temperatures, heart rate, blood pressure and cardiac output. Thus, 6 weeks of folic acid supplementation does not alleviate thermoregulatory or cardiovascular strain of healthy older adults exposed to extreme heat and humidity. ABSTRACT: Folic acid supplementation reverses age-related reductions in cutaneous vasodilatation during passive heating. However, it is unknown if folic acid supplementation alleviates thermoregulatory and cardiovascular strain experienced by older adults during heat exposure. We evaluated the effect of folic acid supplementation on thermoregulatory and cardiovascular responses of nine healthy older adults (61-72 years, 3 males/6 females) exposed to extreme heat and humidity. Participants rested at 42°C while relative humidity was increased from 30% to 70% in 2% increments every 5 min. The protocol was performed before (CON) and after (FOLIC) 6 weeks of folic acid supplementation (5 mg day-1 ). Local cutaneous vascular conductance (CVC, laser-Doppler flowmetry), forearm vascular conductance (FVC, Doppler ultrasound), mean skin and oesophageal temperatures, heart rate, blood pressure and cardiac output were measured. Folic acid supplementation increased fasting serum folate concentrations (P < 0.01). Absolute CVC was greater throughout the protocol following supplementation (CON: 1.29 ± 0.16 units mmHg-1 vs. FOLIC: 1.65 ± 0.24 units mmHg-1 , P < 0.01). However, normalized CVC (CON: 54 ± 8% vs. FOLIC: 59 ± 7%, P = 0.22), FVC (CON: 3.47 ± 0.76 ml mmHg-1 vs. FOLIC: 3.40 ± 0.56 ml mmHg-1 , P = 0.93), mean skin (P = 0.81) and oesophageal (CON: 36.87 ± 0.28°C vs. folic: 36.90 ± 0.25°C, P = 0.98) temperatures, heart rate (CON: 83 ± 10 beats min-1 vs. FOLIC: 84 ± 8 beats min-1 , P = 0.64), blood pressure (P = 0.71) and cardiac output (P = 0.20) were unaffected by folic acid supplementation. These results demonstrate that 6 weeks of folic acid supplementation does not alleviate thermoregulatory or cardiovascular strain of healthy older adults exposed to extreme heat and humidity.

Volume loading augments cutaneous vasodilatation and cardiac output of heat stressed older adults.

KEY POINTS: Age-related changes in cutaneous microvascular and cardiac functions limit the extent of cutaneous vasodilatation and the increase in cardiac output that healthy older adults can achieve during passive heat stress. However, it is unclear if these age-related changes in microvascular and cardiac functions maximally restrain the levels of cutaneous vasodilatation and cardiac output that healthy older adults can achieve during heat stress. We observed that rapid volume loading, performed during passive heat stress, augments both cutaneous vasodilatation and cardiac output in healthy older humans. These findings demonstrate that the microcirculation of healthy aged skin can further dilate during passive heat exposure, despite peripheral limitations to vasodilatation. Furthermore, healthy older humans can augment cardiac output when cardiac pre-load is increased during heat stress. ABSTRACT: Primary ageing markedly attenuates cutaneous vasodilatation and the increase in cardiac output during passive heating. However, it remains unclear if these responses are maximally restrained by age-related changes in cutaneous microvascular and cardiac functions. We hypothesized that rapid volume loading performed during heat stress would increase cardiac output in older adults without parallel increases in cutaneous vasodilatation. Twelve young (Y: 26 ± 5 years) and ten older (O: 69 ± 3 years) healthy adults were passively heated until core temperature increased by 1.5°C. Cardiac output (thermodilution), forearm vascular conductance (FVC, venous occlusion plethysmography) and cutaneous vascular conductance (CVC, laser-Doppler) were measured before and after rapid infusion of warmed saline (15 mL kg-1 , ∼7 min). While heat stressed, but prior to saline infusion, cardiac output (O: 6.8 ± 0.4 vs. Y: 9.4 ± 0.6 L min-1 ), FVC (O: 0.08 ± 0.01 vs. Y: 0.17 ± 0.02 mL (100 mL min-1  mmHg-1 )-1 ), and CVC (O: 1.29 ± 0.34 vs. Y: 1.93 ± 0.30 units mmHg-1 ) were lower in older adults (all P < 0.01). Rapid saline infusion increased cardiac output (O: +1.9 ± 0.3, Y: +1.8 ± 0.7 L min-1 ), FVC (O: +0.015 ± 0.007, Y: +0.048 ± 0.013 mL (100 mL min-1  mmHg-1 )-1 ), and CVC (O: +0.28 ± 0.10, Y: +0.29 ± 0.16 units mmHg-1 ) in both groups (all P < 0.01). The absolute increase in cardiac output and CVC were similar between groups, whereas FVC increased to a greater extent in young adults (P < 0.01). These results demonstrate that healthy older adults can achieve greater levels of cutaneous vasodilatation and cardiac output during passive heating.

Age Modulates Physiological Responses during Fan Use under Extreme Heat and Humidity.

PURPOSE: We examined the effect of electric fan use on cardiovascular and thermoregulatory responses of nine young (26 ± 3 yr) and nine aged (68 ± 4 yr) adults exposed to extreme heat and humidity. METHODS: While resting at a temperature of 42°C, relative humidity increased from 30% to 70% in 2% increments every 5 min. On randomized days, the protocol was repeated without or with fan use. HR, core (Tcore) and mean skin (Tsk) temperatures were measured continuously. Whole-body sweat loss was measured from changes in nude body weight. Other measures of cardiovascular (cardiac output), thermoregulatory (local cutaneous and forearm vascular conductance, local sweat rate), and perceptual (thermal and thirst sensations) responses were also examined. RESULTS: When averaged over the entire protocol, fan use resulted in a small reduction of HR (-2 bpm, 95% confidence interval [CI], -8 to 3), and slightly greater Tcore (+0.05°C; 95% CI, -0.13 to 0.23) and Tsk (+0.03°C; 95% CI, -0.36 to 0.42) in young adults. In contrast, fan use resulted in greater HR (+5 bpm; 95% CI, 0-10), Tcore (+0.20°C; 95% CI, 0.00-0.41), and Tsk (+0.47°C; 95% CI, 0.18-0.76) in aged adults. A greater whole-body sweat loss during fan use was observed in young (+0.2 kg; 95% CI, -0.2 to 0.6) but not aged (0.0 kg; 95% CI, -0.2 to 0.2) adults. Greater local sweat rate and cutaneous vascular conductance were observed with fan use in aged adults. Other measures of cardiovascular, thermoregulatory, and perceptual responses were unaffected by fan use in both groups. CONCLUSIONS: During extreme heat and humidity, fan use elevates physiological strain in aged, but not young, adults.

Increased postural sway in persons with multiple sclerosis during short-term exposure to warm ambient temperatures.

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 30min 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 60min of heating (40°C, 30%RH) followed by 60min 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.

Plasma hyperosmolality improves tolerance to combined heat stress and central hypovolemia in humans.

Heat stress profoundly impairs tolerance to central hypovolemia in humans via a number of mechanisms including heat-induced hypovolemia. However, heat stress also elevates plasma osmolality; the effects of which on tolerance to central hypovolemia remain unknown. This study examined the effect of plasma hyperosmolality on tolerance to central hypovolemia in heat-stressed humans. With the use of a counterbalanced and crossover design, 12 subjects (1 female) received intravenous infusion of either 0.9% iso-osmotic (ISO) or 3.0% hyperosmotic (HYPER) saline. Subjects were subsequently heated until core temperature increased ~1.4°C, after which all subjects underwent progressive lower-body negative pressure (LBNP) to presyncope. Plasma hyperosmolality improved LBNP tolerance (ISO: 288 ± 193 vs. HYPER: 382 ± 145 mmHg × min, P = 0.04). However, no differences in mean arterial pressure (P = 0.10), heart rate (P = 0.09), or muscle sympathetic nerve activity (P = 0.60, n = 6) were observed between conditions. When individual data were assessed, LBNP tolerance improved ≥25% in eight subjects but remained unchanged in the remaining four subjects. In subjects who exhibited improved LBNP tolerance, plasma hyperosmolality resulted in elevated mean arterial pressure (ISO: 62 ± 10 vs. HYPER: 72 ± 9 mmHg, P < 0.01) and a greater increase in heart rate (ISO: +12 ± 24 vs. HYPER: +23 ± 17 beats/min, P = 0.05) before presyncope. No differences in these variables were observed between conditions in subjects that did not improve LBNP tolerance (all P ≥ 0.55). These results suggest that plasma hyperosmolality improves tolerance to central hypovolemia during heat stress in most, but not all, individuals.

Healthy aging does not compromise the augmentation of cardiac function during heat stress.

During heat stress, stroke volume is maintained in young adults despite reductions in cardiac filling pressures. This is achieved by a general augmentation of cardiac function, highlighted by a left and upward shift of the Frank-Starling relation. In contrast, healthy aged adults are unable to maintain stroke volume during heat stress. We hypothesized that this would be associated with a lack of shift in the Frank-Starling relation. Frank-Starling relations were examined in 11 aged [69 ± 4 (SD) yr, 4 men/7 women] and 12 young (26 ± 5 yr, 6 men/6 women) adults during normothermic and heat stress (1.5°C increase in core temperature) conditions. During heat stress, increases in cardiac output were attenuated in aged adults (+2.5 ± 0.3 (95% CI) vs. young: +4.5 ± 0.5 l/min, P < 0.01) because of an attenuated chronotropic response (+30 ± 4 vs. young: +42 ± 5 beats/min, P < 0.01). In contrast to our hypothesis, a leftward shift of the Frank-Starling relation maintained stroke volume during heat stress in aged adults (76 ± 8 vs. normothermic: 74 ± 8 ml, P = 0.38) despite reductions in cardiac filling pressure (6.6 ± 1.0 vs. normothermic: 8.9 ± 1.1 mmHg, P < 0.01). In a subset of participants, volume loading was used to return cardiac filling pressure during heat stress to normothermic values, which resulted in a greater stroke volume for a given cardiac filling pressure in both groups. These results demonstrate that the Frank-Starling relation shifts during heat stress in healthy young and aged adults, thereby preserving stroke volume despite reductions in cardiac filling pressures.

Hemodynamic Stability to Surface Warming and Cooling During Sustained and Continuous Simulated Hemorrhage in Humans.

One in 10 deaths worldwide is caused by traumatic injury, and 30% to 40% of those trauma-related deaths are due to hemorrhage. Currently, warming a bleeding victim is the standard of care due to the adverse effects of combined hemorrhage and hypothermia on survival. We tested the hypothesis that heating is detrimental to the maintenance of arterial pressure and cerebral perfusion during hemorrhage, while cooling is beneficial to victims who are otherwise normothermic. Twenty-one men (31 ±â€Š9 y) were examined under two separate protocols designed to produce central hypovolemia similar to hemorrhage. Following 15 min of supine rest, 10 min of 30 mm Hg of lower body negative pressure (LBNP) was applied. On separate randomized days, subjects were then exposed to skin surface cooling (COOL), warming (WARM), or remained thermoneutral (NEUT), while LBNP continued. Subjects remained in these thermal conditions for either 40 min of 30 mm Hg LBNP (N = 9), or underwent a continuous LBNP ramp until hemodynamic decompensation (N = 12). Arterial blood pressure during LBNP was dependent on the thermal perturbation as blood pressure was greater during COOL (P >0.001) relative to NEUT and WARM for both protocols. Middle cerebral artery blood velocity decreased (P <0.001) from baseline throughout sustained and continuous LBNP, but the magnitude of reduction did not differ between thermal conditions. Contrary to our hypothesis, WARM did not reduce cerebral blood velocity or LBNP tolerance relative to COOL and NEUT in normothermic individuals. While COOL increased blood pressure, cerebral perfusion and time to presyncope were not different relative to NEUT or WARM during sustained or continuous LBNP. Warming an otherwise normothermic hemorrhaging victim is not detrimental to hemodynamic stability, nor is this stability improved with cooling.

Plasma hyperosmolality attenuates skin sympathetic nerve activity during passive heat stress in humans.

KEY POINTS: Plasma hyperosmolality delays the onset for sweat production and cutaneous vasodilatation during heat stress in humans; however, the mechanism by which hyperosmolality exerts this effect remains unknown. This study examined if plasma hyperosmolality exerts a central and/or peripheral modulation of thermoregulatory function in humans. The main findings are that plasma hyperosmolality delays the increase in skin sympathetic nerve activity during whole-body passive heat stress in humans. In contrast, local intradermal infusion of hyperosmotic saline did not affect sweating or cutaneous vasodilatation. These results suggest that plasma hyperosmolality delays the onset threshold for sweating and cutaneous vasodilatation by inhibiting efferent thermoregulatory activity in humans. ABSTRACT: In humans, plasma hyperosmolality delays the onset of sweating and cutaneous vasodilatation during heat stress. However, it remains unknown if hyperosmolality exerts this effect through a central (i.e. CNS) and/or peripheral (i.e. effector organ) modulation of thermoregulatory activity. We examined if intravenous infusion of hyperosmotic saline affects skin sympathetic nerve activity (SSNA) during whole-body passive heating in healthy humans. Furthermore, we examined if local intradermal infusion of hyperosmotic saline affects sweating and cutaneous vasodilatation during passive heating. Following intravenous infusion of either 0.9% (ISO) or 3.0% (HYPER) NaCl saline, 12 subjects were passively heated until core temperature increased by ∼0.6°C. During each condition, sweating and cutaneous vascular conductance were measured over two intradermal microdialysis probes, one perfused with ISO saline and the other with HYPER saline. Intravenous infusion of HYPER saline increased plasma osmolality (294 ± 3 to 316 ± 5 mOsm kg(-1) H2O, P ≤ 0.01), which remained greater than ISO throughout heating. Plasma hyperosmolality delayed the mean body temperature onset of sweating (+1.24 ± 0.18 vs. +1.60 ± 0.18°C, P ≤ 0.01) and cutaneous vasodilatation (+1.15 ± 0.18 vs. +1.53 ± 0.22°C, P ≤ 0.01), and attenuated the increase in SSNA during heating (+147 ± 178 vs. +427 ± 281%, P ≤ 0.01). Intradermal infusion of HYPER saline increased baseline cutaneous vascular conductance (P ≤ 0.01), which did not increase further during the subsequent heating period (P = 0.11). In contrast, intradermal infusion of HYPER saline did not affect sweating (P = 0.99). These results provide direct evidence that plasma hyperosmolality exerts a central modulatory effect governing efferent thermoregulatory activity in humans.

Physiological, Perceptual and Psychological Responses of Career versus Volunteer Firefighters to Live-fire Training Drills.

A primary objective of the present study was to examine the effect of short-term live-fire firefighting activities on key physiological, perceptual and psychological variables and whether occupational status influenced these responses. It was also of interest to examine whether individual difference factors differentiated the occupational status groups and if so, whether such individual difference factors influenced perceptual and psychological responses to firefighting activities. Male firefighters (n = 52 career, n = 53 volunteer firefighters) participated in 18 min of simulated firefighting activity in a training structure that contained live fires. Measures of heart rate (HR) and Tcore were obtained before and after firefighting activities along with perceptions of thermal sensations, exertion, respiratory distress and affect. Firefighting activities resulted in significant elevations in HR and Tcore , whereas thermal sensations, respiratory distress, exertion and affect all showed significant and sizable changes reflecting greater distress and dysphoria. Occupational status and individual difference factors accounted for some of this negative change. The findings replicate and extend previous work by demonstrating the influence of occupational status and individual difference factors in the psychological responses to firefighting activity. Copyright © 2014 John Wiley & Sons, Ltd.

Respiratory pump contributes to increased physiological reserve for compensation during simulated haemorrhage.

Intrathoracic pressure regulation (IPR) represents a therapy for increasing systemic circulation through the creation of negative intrathoracic pressure. We hypothesized that using this 'respiratory pump' effect would slow the diminution of the physiological reserve to compensate during progressive reductions in central blood volume. The compensatory reserve index (CRI) algorithm was used to measure the proportion (from 100 to 0%) of reserve capacity that remained to compensate for central volume loss before the onset of cardiovascular decompensation. Continuous analog recordings of arterial waveforms were extracted from data files of seven healthy volunteers. Subjects had previously participated in experiments designed to induce haemodynamic decompensation (presyncope) by progressive reduction in central blood volume using graded lower-body negative pressure. The lower-body negative pressure protocol was completed while breathing spontaneously through a standard medical face mask without (placebo) and with a resistance (approximately -7 cmH2O; active IPR) applied during inspiration. At the onset of presyncope in the placebo conditions, CRI was smaller than the CRI observed at the same time point in the active IPR conditions. The CRI at the onset of presyncope during active IPR (0.08 ± 0.01) was similar to the CRI at presyncope with placebo. Kaplan-Meier and log rank tests indicated that CRI survival curves were shifted to the right by active IPR. Optimizing the respiratory pump contributed a small but significant effect of increasing tolerance to progressive reductions in central blood volume by extending the compensatory reserve.

Orthostatic hypotension after 10 days of exercise-heat acclimation and 28 hours of sleep loss.

INTRODUCTION: Orthostatic hypotension (OH) occurs among several populations; elevated temperatures increase an individual's susceptibility, whereas the effect of sleep loss (SL) remains inconclusive. The purpose was: 1) to evaluate the effects of 10 d of heat acclimation (HA) and 28 h of SL on OH; and 2) to determine the best measurements to assess OH in clinical and field settings. METHODS: There were 11 men (mean +/- SD; age, 20 +/- 1 yr; mass, 81.7 +/- 12.2 kg) who underwent a repeated measures research design. Before and after 90 min of HA, with the 11th day performed in conjunction with SL, subjects performed a lie-to-stand test where blood pressure (BP), heart rate (HR), and OH signs and symptoms were obtained. RESULTS: OH incidence and intensity, assessed via acute changes in post-exercise systolic BP (SBP), significantly decreased during HA from Day 2 (15 +/- 12 mmHg) to Day 8 (8 +/- 8 mmHg), while SL showed no effect. As OH responses decreased, concomitant HR increases diminished from Day 2 (113 +/- 15 bpm) to Day 8 (103 +/- 14 bpm). Post-exercise lightheadedness, dizziness, and nausea significantly decreased from Day 2 to Day 8, while no changes were associated with SL. CONCLUSIONS: During HA, BP control improved and cardiovascular strain was reduced, along with OH signs and symptoms; mild SL had no measurable effect. Acute HR changes may be explained by decreased cardiac output and increased stroke volume. In clinical settings, SBP delta may indicate the threshold at which OH signs and symptoms arise. In the absence of a sphygmomanometer, HR taken upon standing, or ratings of lightheadedness and dizziness may be used as alternative field expedient techniques.

Eleven days of moderate exercise and heat exposure induces acclimation without significant HSP70 and apoptosis responses of lymphocytes in college-aged males.

The purpose of this study was to assess whether a lymphocyte heat shock response and altered heat tolerance to ex vivo heat shock is evident during acclimation. We aimed to use flow cytometry to assess the CD3(+)CD4(+) T lymphocyte cell subset. We further aimed to induce acclimation using moderately stressful daily exercise-heat exposures to achieve acclimation. Eleven healthy males underwent 11 days of heat acclimation. Subjects walked for 90 min (50 ± 8% VO(2max)) on a treadmill (3.5 mph, 5% grade), in an environmental chamber (33°C, 30-50% relative humidity). Rectal temperature (°C), heart rate (in beats per minute), rating of perceived exertion , thermal ratings, hydration state, and sweat rate were measured during exercise and recovery. On days 1, 4, 7, 10, and 11, peripheral blood mononuclear cells were isolated from pre- and post-exercise blood samples. Intracellular and surface HSP70 (SPA-820PE, Stressgen, Assay Designs), and annexin V (ab14085, Abcam Inc.), as a marker of early apoptosis, were measured on CD3(+) and CD4(+) (sc-70624, sc-70670, Santa Cruz Biotechnology) gated lymphocytes. On day 10, subjects experienced 28 h of sleep loss. Heat acclimation was verified with decreased post-exercise rectal temperature, heart rate, and increased sweat rate on day 11, versus day 1. Heat acclimation was achieved in the absence of significant changes in intracellular HSP70 mean fluorescence intensity and percent of HSP70(+) lymphocytes during acclimation. Furthermore, there was no increased cellular heat tolerance during secondary ex vivo heat shock of the lymphocytes acquired from subjects during acclimation. There was no effect of a mild sleep loss on any variable. We conclude that our protocol successfully induced physiological acclimation without induction of cellular heat shock responses in lymphocytes and that added mild sleep loss is not sufficient to induce a heat shock response.