Nonfreezing cold-induced injuries.

Non-freezing cold injury (NFCI) is the Cinderella of thermal injuries and is a clinical syndrome that occurs when tissues are exposed to cold temperatures close to freezing point for sustained periods. NFCI is insidious in onset, often difficult to recognize and problematic to treat, and yet the condition accounts for significant morbidity in both military and civilians who work in cold conditions. Consequently recognition of those at risk, limiting their exposure and the appropriate and timely use of suitable protective equipment are essential steps in trying to reduce the impact of the condition. This review addresses the issues surrounding NFCI.

Effect of increased plasma osmolality on cold-induced thirst attenuation.

The effects of elevating plasma osmolality (P (osm)) on thirst ratings was studied in eight dehydrated males during exposure to 4 degrees C. On two occasions, subjects were dehydrated (DH; 3-4% body mass) via 90 min exercise-heat exposure and overnight fluid restriction (day 1). On a third occasion, subjects were exposed to heat but were given fluid (EU). On day 2, subjects consumed NaCl (NaCl; 0.1 g NaCl kg(-1) body mass in 500 ml H(2)O; DH only) or Placebo (P; 500 ml H(2)O; DH and EU). Subjects stood for 30 min at 24 degrees C and for 45 min at 4 degrees C (75 min post-dose). P (osm) was elevated (P < 0.05) 30 and 75 min after NaCl administration in DH + NaCl versus DH + P and EU + P treatments. Thirst ratings remained elevated (P < 0.05) in the DH + NaCl treatment 30 min after dosing and 45 min at 4 degrees C versus DH + P and EU + P. Attenuation of thirst when dehydrated in the cold can be over-ridden by increasing P (osm).

Rehydration with fluid of varying tonicities: effects on fluid regulatory hormones and exercise performance in the heat.

This study examined the effects of rehydration (Rehy) with fluids of varying tonicities and routes of administration after exercise-induced hypohydration on exercise performance, fluid regulatory hormone responses, and cardiovascular and thermoregulatory strain during subsequent exercise in the heat. On four occasions, eight men performed an exercise-dehydration protocol of approximately 185 min (33 degrees C) to establish a 4% reduction in body weight. Following dehydration, 2% of the fluid lost was replaced during the first 45 min of a 100-min rest period by one of three random Rehy treatments (0.9% saline intravenous; 0.45% saline intravenous; 0.45% saline oral) or no Rehy (no fluid) treatment. Subjects then stood for 20 min at 36 degrees C and then walked at 50% maximal oxygen consumption for 90 min. Subsequent to dehydration, plasma Na(+), osmolality, aldosterone, and arginine vasopressin concentrations were elevated (P < 0.05) in each trial, accompanied by a -4% hemoconcentration. Following Rehy, there were no differences (P > 0.05) in fluid volume restored, post-rehydration (Post-Rehy) body weight, or urine volume. Percent change in plasma volume was 5% above pre-Rehy values, and plasma Na(+), osmolality, and fluid regulatory hormones were lower compared with no fluid. During exercise, skin and core temperatures, heart rate, and exercise time were not different (P > 0.05) among the Rehy treatments. Plasma osmolality, Na(+), percent change in plasma volume, and fluid regulatory hormones responded similarly among all Rehy treatments. Neither a fluid of greater tonicity nor the route of administration resulted in a more rapid or greater fluid retention, nor did it enhance heat tolerance or diminish physiological strain during subsequent exercise in the heat.

Effect of hydration status on thirst, drinking, and related hormonal responses during low-intensity exercise in the heat.

During exercise-heat stress, ad libitum drinking frequently fails to match sweat output, resulting in deleterious changes in hormonal, circulatory, thermoregulatory, and psychological status. This condition, known as voluntary dehydration, is largely based on perceived thirst. To examine the role of preexercise dehydration on thirst and drinking during exercise-heat stress, 10 healthy men (21 +/- 1 yr, 57 +/- 1 ml x kg(-1) x min(-1) maximal aerobic power) performed four randomized walking trials (90 min, 5.6 km/h, 5% grade) in the heat (33 degrees C, 56% relative humidity). Trials differed in preexercise hydration status [euhydrated (Eu) or hypohydrated to -3.8 +/- 0.2% baseline body weight (Hy)] and water intake during exercise [no water (NW) or water ad libitum (W)]. Blood samples taken preexercise and immediately postexercise were analyzed for hematocrit, hemoglobin, serum aldosterone, plasma osmolality (P(osm)), plasma vasopressin (P(AVP)), and plasma renin activity (PRA). Thirst was evaluated at similar times using a subjective nine-point scale. Subjects were thirstier before (6.65 +/- 0.65) and drank more during Hy+W (1.65 +/- 0.18 liters) than Eu+W (1.59 +/- 0.41 and 0.31 +/- 0.11 liters, respectively). Postexercise measures of P(osm) and P(AVP) were significantly greater during Hy+NW and plasma volume lower [Hy+NW = -5.5 +/- 1.4% vs. Hy+W = +1.0 +/- 2.5% (P = 0.059), Eu+NW = -0.7 +/- 0.6% (P < 0.05), Eu+W = +0.5 +/- 1.6% (P < 0.05)] than all other trials. Except for thirst and drinking, however, no Hy+W values differed from Eu+NW or Eu+W values. In conclusion, dehydration preceding low-intensity exercise in the heat magnifies thirst-driven drinking during exercise-heat stress. Such changes result in similar fluid regulatory hormonal responses and comparable modifications in plasma volume regardless of preexercise hydration state.

Physiological responses to cold exposure in men: a disabled submarine study.

A disabled submarine (DISSUB) lacking power and/or environmental control will become cold, and the ambient air may become hypercapnic and hypoxic. This study examined if the combination of hypoxia, hypercapnia, and cold exposure would adversely affect thermoregulatory responses to acute cold exposure in survivors awaiting rescue. Seven male submariners (33 +/- 6 yrs) completed a series of cold-air tests (CAT) that consisted of 20-min at T(air) = 22 degrees C, followed by a linear decline (1 degrees C x min(-1)) in T(air) to 12 degrees C, which was then held constant for an additional 150-min. CAT were performed under normoxic, normocapnic conditions (D0), acute hypoxia (D1, 16.75% O2), after 4 days of chronic hypoxia, hypercapnia and cold (D5, 16.75% O2, 2.5% CO2, 4 degrees C), and hypoxia-only again (D8, 16.75% O2). The deltaTsk during CAT was larger (P < 0.05) on D0 (-5.2 degrees C), vs. D1 (-4.8 degrees C), D5 (-4.5 degrees C), and D8 (-4.4 degrees C). The change (relative to 0-min) in metabolic heat production (deltaM) at 20-min of CAT was lower (P < 0.05) on D1, D5, and D8, vs. D0, with no differences between D1, D5 and D8. DeltaM was not different among trials at any time point after 20-min. The mean body temperature threshold for the onset of shivering was lower on D1 (35.08 degrees C), D5 (34.85 degrees C), and D8 (34.69 degrees C), compared to D0 (36.01 degrees C). Changes in heat storage did not differ among trials and rectal temperature was not different in D0 vs. D1, D5, and D8. Thus, mild hypoxia (16.75% F1O2) impairs vasoconstrictor and initial shivering responses, but the addition of elevated F1CO2 and cold had no further effect. These thermoregulatory effector changes do not increase the risk for hypothermia in DISSUB survivors who are adequately clothed.

Effect of overhydration on time-trial swim performance.

The effect of hydration status on performance has not been adequately emphasized or examined in swimmers. Theoretically, moderate overhydration might reduce the proportionate fluid loss from the circulation during exercise of this nature. To explore this issue, 11 (5 women, 6 men) collegiate swimmers swam 2 183-m (200-yd) time trials (3 days apart) in alternate, randomized euhydrated (EUH) and overhydrated (OH) states. Pre-exercise plasma osmolality (EUH: 288.5 +/- 2.5 and OH: 284.6 +/- 3.3 mOsmol.kg(-1); p < 0.001), urine specific gravity (EUH: 1.022 +/- 0.003 and OH: 1.012 +/- 0.003; p < 0.001), and body weight (EUH: 72.1 +/- 9.3 and OH: 72.6 +/- 9.2 kg; p < 0.01) values distinguished the two hydration states of the swimmers. There was no difference (p > 0.05) between hydration states in postexercise plasma osmolality (EUH: 312.8 +/- 4.8 and OH: 307.2 +/- 9.9 mOsmol.kg(-1)), plasma volume (EUH: -16.5 +/- 10.0 and OH: -17.7 +/- 6.8 %Delta), plasma lactate (EUH: 18.6 +/- 3.6 and OH: 17.8 +/- 3.4 mmol.1(-1)), heart rate (EUH: 167 +/- 11 and OH: 166 +/- 16 beats.min(-1)), or perceived exertion (EUH: 16 +/- 1 and OH: 16 +/- 2) responses. Although performance time improved for 7 of the 11 swimmers during OH, there was not a statistically significant difference between the EUH (121.2 +/- 8.1 seconds) and OH (120.8 +/- 7.7 seconds) conditions. However, there was a modest bivariate correlation (r = -0.602; p < 0.05) between the change in body weight and change in performance time in going from the EUH to OH trials. These data demonstrated that overhydration provided no performance advantage for this group during a 183-m time-trial swim but emphasized the importance of adequate hydration in swim performance.

Cold strain index applied to exercising men in cold-wet conditions.

A cold strain index (CSI) based on rectal (T(re)) and mean skin temperatures ((sk)) using data from seminude resting subjects has been proposed (Moran DS, Castellani JW, O'Brien C, Young AJ, and Pandolf KB. Am J Physiol Regulatory Integrative Comp Physiol 277: R556-R564, 1999). The current study determined whether CSI could provide meaningful data for clothed subjects exercising in the cold with compromised insulation. Ten men exercised in cold-wet conditions (CW) for 6 h before (D0) and after 3 days of exhaustive exercise (D3). Each hour of CW consisted of 10 min of standing in rain (5.4 cm/h, 5 degrees C air) followed by 45 min of walking (1.34 m/s, 5.4 m/s wind, 5 degrees C air). The change in T(re) across time was greater (P < 0.05) on D3 than on D0, and the change in (sk) was less (P < 0.05) on D3 than on D0. Although CSI increased across time, the index at the end of both trials (D3 = 4.6 +/- 0.6; D0 = 4.2 +/- 0.8) was similar (P > 0.05). Thus, while (sk) was 1.3 degrees C higher (P < 0.05) and T(re) was 0.3 degrees C lower (P < 0.05) on D3 than on D0, CSI did not discriminate the greater heat loss that occurred on D3. These findings indicate that when vasoconstrictor responses to cold are altered, such as after exhaustive exercise, CSI does not adequately quantify the different physiological strain between treatments. CSI may be useful for indicating increased strain across time, but its utility as a marker of strain between different treatments or studies is uncertain because no independent measure of strain has been used to determine to what extent CSI is a valid and reliable measure of strain.

Intracellular monocyte and serum cytokine expression is modulated by exhausting exercise and cold exposure.

This study tested the hypothesis that exercise elicits monocytic cytokine expression and that prolonged cold exposure modulates such responses. Nine men (age, 24.6 +/- 3.8 y; VO(2 peak), 56.8 +/- 5.6 ml. kg(-1). min(-1)) completed 7 days of exhausting exercise (aerobic, anaerobic, resistive) and underwent three cold, wet exposures (CW). CW trials comprised

Cortisol and testosterone concentrations in wheelchair athletes during submaximal wheelchair ergometry.

It is yet unknown how upper body exercise combined with high ambient temperatures affects plasma testosterone and cortisol concentrations and furthermore, how these hormones respond to exercise in people suffering spinal cord injuries. The purpose of this study was to characterize plasma testosterone and cortisol responses to upper body exercise in wheelchair athletes (WA) compared to able-bodied individuals (AB) at two ambient temperatures. Four WA [mean age 36 (SEM 13) years, mean body mass 66.9 (SEM 11.8) kg, injury level T7-T11], matched with five AB [mean age 33.4 (SEM 8.9) years, mean body mass 72.5 (SEM 13.1) kg] exercised (cross-over design) for 20 min on a wheelchair ergometer (0.03 kg resistance.kg-1 body mass) at 25 degrees C and 32 degrees C. Blood samples were obtained before (PRE), at min 10 (MID), and min 20 (END) of exercise. No differences were found between results obtained at 25 degrees C and 32 degrees C for any physiological variable studied and therefore these data were combined. Pre-exercise testosterone concentration was lower (P < 0.05) in WA [18.3 (SEM 0.9) nmol.l-1] compared to AB [21.9 (SEM 3.6) nmol.l-1], and increased PRE to END only in WA. Cortisol concentrations were similar between groups before and during exercise, despite higher rectal temperatures in WA compared to AB, at MID [37.21 (SEM 0.14) and 37.02 (SEM 0.08) degrees C, respectively] and END [37.36 (SEM 0.16) and 37.19 (SEM 0.10) degrees C, respectively]. Plasma norepinephrine responses were similar between groups. In conclusion, there were no differences in plasma cortisol concentrations, which may have been due to the low relative exercise intensities employed. The greater exercise response in WA for plasma testosterone should be confirmed on a larger population. It could have been the result of the lower plasma testosterone concentrations at rest in our group.

Exertion-induced fatigue and thermoregulation in the cold.

Cold exposure facilitates body heat loss which can reduce body temperature, unless mitigated by enhanced heat conservation or increased heat production. When behavioral strategies inadequately defend body temperature, vasomotor and thermogenic responses are elicited, both of which are modulated if not mediated by sympathetic nervous activation. Both exercise and shivering increase metabolic heat production which helps offset body heat losses in the cold. However, exercise also increases peripheral blood flow, in turn facilitating heat loss, an effect that can persist for some time after exercise ceases. Whether exercise alleviates or exacerbates heat debt during cold exposure depends on the heat transfer coefficient of the environment, mode of activity and exercise intensity. Prolonged exhaustive exercise leading to energy substrate depletion could compromise maintenance of thermal balance in the cold simply by precluding continuation of further exercise and the associated thermogenesis. Hypoglycemia impairs shivering, but this appears to be centrally mediated, rather than a limitation to peripheral energy metabolism. Research is equivocal regarding the importance of muscle glycogen depletion in explaining shivering impairments. Recent research suggests that when acute exercise leads to fatigue without depleting energy stores, vasoconstrictor responses to cold are impaired, thus body heat conservation becomes degraded. Fatigue that was induced by chronic overexertion sustained over many weeks, appeared to delay the onset of shivering until body temperature fell lower than when subjects were rested, as well as impair vasoconstrictor responses. When heavy physical activity is coupled with underfeeding for prolonged periods, the resulting negative energy balance leads to loss of body mass, and the corresponding reduction in tissue insulation, in turn, compromises thermal balance by facilitating conductive transfer of body heat from core to shell. The possibility that impairments in thermoregulatory responses to cold associated with exertional fatigue are mediated by blunted sympathetic nervous responsiveness to cold is suggested by some experimental observations and merits further study.

Blood glucose responses to carbohydrate feeding prior to exercise in the heat: effects of hypohydration and rehydration.

This study assessed the plasma glucose (PG) and hormonal responses to carbohydrate ingestion, prior to exercise in the heat, in a hypohydrated state versus partial rehydration with intravenous solutions. On separate days, 8 subjects (21.0 +/- 1.8 years; 57.3 +/- 3.7 ml x kg(-1) x min(-1)) exercised at 50% VO2max in a 33 degree C environment until a 4% body weight loss was achieved. Following this, subjects were rehydrated (25 ml x kg(-1)) with either: 0.45% IV saline (45IV), 0.9% IV saline (9IV), or no fluid (NF). Subjects then ingested 1 g x kg(-1) of carbohydrate and underwent an exercise test (treadmill walking, 50% VO2max, 36 degrees C) for up to 90 min. Compared to pre-exercise level (294 mg x dl(-1)), PG increased significantly (>124 mg x dl(-1)) at 15 min of the exercise test in all trials and remained significantly elevated for 75 min in NF, 30 min more than in the 2 rehydration trials. Although serum Insulin increased significantly at 15 min of exercise in the 45IV trial (7.2 +/- 1.2 vs. 23.7 +/- 4.7 mIU x ml(-1)), no significant differences between trials were observed. Peak plasma norepinephrine was significantly higher in NF (640 +/- 66 pg x ml(-1)) compared to the 45IV and 9IV trials (472 +/- 55 and 474 +/- 52 pg x ml(-1), respectively). In conclusion, ingestion of a small solid carbohydrate load prior to exercise in the 4% hypohydration level resulted in prolonged high PG concentration compared to partial IV rehydration.

Thermoregulation during cold exposure after several days of exhaustive exercise.

This study examined the hypothesis that several days of exhaustive exercise would impair thermoregulatory effector responses to cold exposure, leading to an accentuated core temperature reduction compared with exposure of the same individual to cold in a rested condition. Thirteen men (10 experimental and 3 control) performed a cold-wet walk (CW) for up to 6 h (6 rest-work cycles, each 1 h in duration) in 5 degrees C air on three occasions. One cycle of CW consisted of 10 min of standing in the rain (5.4 cm/h) followed by 45 min of walking (1.34 m/s, 5.4 m/s wind). Clothing was water saturated at the start of each walking period (0.75 clo vs. 1.1 clo when dry). The initial CW trial (day 0) was performed (afternoon) with subjects rested before initiation of exercise-cold exposure. During the next 7 days, exhaustive exercise (aerobic, anaerobic, resistive) was performed for 4 h each morning. Two subsequent CW trials were performed on the afternoon of days 3 and 7, approximately 2.5 h after cessation of fatiguing exercise. For controls, no exhaustive exercise was performed on any day. Thermoregulatory responses and body temperature during CW were not different on days 0, 3, and 7 in the controls. In the experimental group, mean skin temperature was higher (P < 0.05) during CW on days 3 and 7 than on day 0. Rectal temperature was lower (P < 0.05) and the change in rectal temperature was greater (P < 0.05) during the 6th h of CW on day 3. Metabolic heat production during CW was similar among trials. Warmer skin temperatures during CW after days 3 and 7 indicate that vasoconstrictor responses to cold, but not shivering responses, are impaired after multiple days of severe physical exertion. These findings suggest that susceptibility to hypothermia is increased by exertional fatigue.

Plasma vasopressin and aldosterone responses to oral and intravenous saline rehydration.

This investigation examined plasma arginine vasopressin (AVP) and aldosterone (Ald) responses to 1) oral and intravenous (IV) methods of rehydration (Rh) and 2) different IV Rh osmotic loads. We hypothesized that AVP and Ald responses would be similar between IV and oral Rh and that the greater osmolality and sodium concentration of a 0.9% IV saline treatment would stimulate a greater AVP response compared with a 0.45% IV saline treatment. On four occasions, eight men (age: 22.1 +/- 0.8 yr; height: 179.6 +/- 1.5 cm; weight: 73.6 +/- 2.5 kg; maximum O(2) consumption: 57.9 +/- 1.6 ml. kg(-1). min(-1), body fat: 7.7 +/- 0.9%) performed a dehydration (Dh) protocol (33 degrees C) to establish a 4-5% reduction in body weight. After Dh, subjects underwent each of three randomly assigned Rh (back to -2% body wt) treatments (0.9 and 0.45% IV saline, 0.45% oral saline) and a no Rh treatment during the first 45 min of a 100-min rest period. Blood samples were obtained pre-Dh, immediately post-Dh, and at 15, 35, and 55 min post-Rh. Before Dh, plasma AVP and Ald were not different among treatments but were significantly elevated post-Dh. In general, at 15, 35, and 55 min post-Rh, AVP, Ald, osmolality, and plasma volume shifts did not differ between IV and oral fluid replacement. These results demonstrated that the manner in which plasma AVP and Ald responded to oral and IV Rh or to different sodium concentrations (0.9 vs. 0.45%) was not different given the degree of Dh (-4.5% body wt) and Rh and amount of time after Rh (55 min).

Evaluating physiological strain during cold exposure using a new cold strain index.

A cold strain index (CSI) based on core (T(core)) and mean skin temperatures (T(sk)) and capable of indicating cold strain in real time and analyzing existing databases has been developed. This index rates cold strain on a universal scale of 0-10 and is as follows: CSI = 6.67(T(core t) - T(core 0)). (35 - T(core 0))(-1) + 3.33(T(sk (t)) - T(sk 0)). (20 - T(sk 0))(-1), where T(core 0) and T(sk 0) are initial measurements and T(core t) and T(sk t) are simultaneous measurements taken at any time t; when T(core t) > T(core 0), then T(core t) - T(core 0) = 0. CSI was applied to three databases. The first database was obtained from nine men exposed to cold air (7 degrees C, 40% relative humidity) for 120 min during euhydration and two hypohydration conditions achieved by exercise-heat stress-induced sweating or by ingestion of furosemide 12 h before cold exposure. The second database was from eight men exposed to cold air (10 degrees C) immediately on completion of 61 days of strenuous outdoor military training, 48 h later, and after 109 days. The third database was from eight men repeatedly immersed in 20 degrees C water three times in 1 day and during control immersions. CSI significantly differentiated (P < 0.01) between the trials and individually categorized the strain of the subject for two of these three databases. This index has the potential to be widely accepted and used universally.

Immune changes in humans during cold exposure: effects of prior heating and exercise.

This study examined the immunological responses to cold exposure together with the effects of pretreatment with either passive heating or exercise (with and without a thermal clamp). On four separate occasions, seven healthy men [mean age 24.0 +/- 1.9 (SE) yr, peak oxygen consumption = 45.7 +/- 2.0 ml. kg(-1). min(-1)] sat for 2 h in a climatic chamber maintained at 5 degrees C. Before exposure, subjects participated in one of four pretreatment conditions. For the thermoneutral control condition, subjects remained seated for 1 h in a water bath at 35 degrees C. In another pretreatment, subjects were passively heated in a warm (38 degrees C) water bath for 1 h. In two other pretreatments, subjects exercised for 1 h at 55% peak oxygen consumption (once immersed in 18 degrees C water and once in 35 degrees C water). Core temperature rose by 1 degrees C during passive heating and during exercise in 35 degrees C water and remained stable during exercise in 18 degrees C water (thermal clamping). Subsequent cold exposure induced a leukocytosis and granulocytosis, an increase in natural killer cell count and activity, and a rise in circulating levels of interleukin-6. Pretreatment with exercise in 18 degrees C water augmented the leukocyte, granulocyte, and monocyte response. These results indicate that acute cold exposure has immunostimulating effects and that, with thermal clamping, pretreatment with physical exercise can enhance this response. Increases in levels of circulating norepinephrine may account for the changes observed during cold exposure and their modification by changes in initial status.

Thermoregulatory responses to cold water at different times of day.

This study examined how time of day affects thermoregulation during cold-water immersion (CWI). It was hypothesized that the shivering and vasoconstrictor responses to CWI would differ at 0700 vs. 1500 because of lower initial core temperatures (T(core)) at 0700. Nine men were immersed (20 degrees C, 2 h) at 0700 and 1500 on 2 days. No differences (P > 0.05) between times were observed for metabolic heat production (M, 150 W. m(-2)), heat flow (250 W. m(-2)), mean skin temperature (T(sk), 21 degrees C), and the mean body temperature-change in M (DeltaM) relationship. Rectal temperature (T(re)) was higher (P < 0.05) before (Delta = 0.4 degrees C) and throughout CWI during 1500. The change in T(re) was greater (P < 0. 05) at 1500 (-1.4 degrees C) vs. 0700 (-1.2 degrees C), likely because of the higher T(re)-T(sk) gradient (0.3 degrees C) at 1500. These data indicate that shivering and vasoconstriction are not affected by time of day. These observations raise the possibility that CWI may increase the risk of hypothermia in the early morning because of a lower initial T(core).

Thermoregulation during cold exposure: effects of prior exercise.

This study examined whether acute exercise would impair the body's capability to maintain thermal balance during a subsequent cold exposure. Ten men rested for 2 h during a standardized cold-air test (4.6 degrees C) after two treatments: 1) 60 min of cycle exercise (Ex) at 55% peak O(2) uptake and 2) passive heating (Heat). Ex was performed during a 35 degrees C water immersion (WI), and Heat was conducted during a 38.2 degrees C WI. The duration of Heat was individually adjusted (mean = 53 min) so that rectal temperature was similar at the end of WI in both Ex (38.2 degrees C) and Heat (38.1 degrees C). During the cold-air test after Ex, relative to Heat 1) rectal temperature was lower (P < 0.05) from minutes 40-120, 2) mean weighted heat flow was higher (P < 0.05), 3) insulation was lower (P < 0.05), and 4) metabolic heat production was not different. These results suggest that prior physical exercise may predispose a person to greater heat loss and to experience a larger decline in core temperature when subsequently exposed to cold air. The combination of exercise intensity and duration studied in these experiments did not fatigue the shivering response to cold exposure.

Immune deficits induced by strenuous exertion under adverse environmental conditions: manifestations and countermeasures.

A brief description is given of the various laboratory and clinical manifestations of immune suppression that arise when strenuous exertion must be carried out in the face of a negative energy balance, shifts of circadian rhythm, sleep deprivation, psychological stressors, and exposure to hostile environments (extremes of heat or cold, high or low ambient pressures, and hyper- or hypo-gravity conditions). From the operational viewpoint, immune suppression could impair both physical and mental performance by increasing susceptibility to opportunistic microorganisms. It is also likely to increase susceptibility to sepsis following trauma or extensive burns, and has occasionally predisposed to fatal myocarditis. The effects of such challenges are complex, in part because of interactions between the various stressors. It is thus important to investigate the impact and to devise appropriate countermeasures with the full physical and intellectual resources of a defense environmental research laboratory. Existing knowledge of the topic is reviewed, and suggestions are made for research that may lead to new and more effective countermeasures.

Exertional fatigue, sleep loss, and negative energy balance increase susceptibility to hypothermia.

The purpose of this study was to determine how chronic exertional fatigue and sleep deprivation coupled with negative energy balance affect thermoregulation during cold exposure. Eight men wearing only shorts and socks sat quietly during 4-h cold air exposure (10 degreesC) immediately after (<2 h, A) they completed 61 days of strenuous military training (energy expenditure approximately 4,150 kcal/day, energy intake approximately 3,300 kcal/day, sleep approximately 4 h/day) and again after short (48 h, SR) and long (109 days, LR) recovery. Body weight decreased 7.4 kg from before training to A, then increased 6.4 kg by SR, with an additional 6.4 kg increase by LR. Body fat averaged 12% during A and SR and increased to 21% during LR. Rectal temperature (Tre) was lower before and during cold air exposure for A than for SR and LR. Tre declined during cold exposure in A and SR but not LR. Mean weighted skin temperature (Tsk) during cold exposure was higher in A and SR than in LR. Metabolic rate increased during all cold exposures, but it was lower during A and LR than SR. The mean body temperature (0.67 Tre + 0.33 Tsk) threshold for increasing metabolism was lower during A than SR and LR. Thus chronic exertional fatigue and sleep loss, combined with underfeeding, reduced tissue insulation and blunted metabolic heat production, which compromised maintenance of body temperature. A short period of rest, sleep, and refeeding restored the thermogenic response to cold, but thermal balance in the cold remained compromised until after several weeks of recovery when tissue insulation had been restored.

Human thermoregulatory responses during serial cold-water immersions.

This study examined whether serial cold-water immersions over a 10-h period would lead to fatigue of shivering and vasoconstriction. Eight men were immersed (2 h) in 20 degrees C water three times (0700, 1100, and 1500) in 1 day (Repeat). This trial was compared with single immersions (Control) conducted at the same times of day. Before Repeat exposures at 1100 and 1500, rewarming was employed to standardize initial rectal temperature. The following observations were made in the Repeat relative to the Control trial: 1) rectal temperature was lower and heat debt was higher (P < 0.05) at 1100; 2) metabolic heat production was lower (P < 0.05) at 1100 and 1500; 3) subjects perceived the Repeat trial as warmer at 1100. These data suggest that repeated cold exposures may impair the ability to maintain normal body temperature because of a blunting of metabolic heat production, perhaps reflecting a fatigue mechanism. An alternative explanation is that shivering habituation develops rapidly during serially repeated cold exposures.