Effect of nifedipine on core cooling in rats during tail cold water immersion

Male rats (450 g, n=11/group) were heated at an ambient temperature of 42°C until a rectal temperature of 42.8°C was attained. Rats, then received either saline (30°C)+tail ice water immersion (F+I) or saline (30°C)+tail ice water immersion+Nifedipine, a peripheral vasodilator, (F+I+N) to determine cooling rate effectiveness and survivability. The time to reach a rectal temperature of 42.8°C averaged 172 min in both groups resulting in similar heating rates (0.029°C/min). The cooling rates in group F+I and F+I+N were not significantly different from each other. We conclude that since Nifedipine did not improve cooling rates when combined with fluid+tail ice water immersion, its use as a cooling adjunct does not seem warranted.     

Role of core temperature as a stimulus for cold acclimation during repeated immersion in 20 degrees C water.

The relative importance of skin vs. core temperature for stimulating cold acclimation (CA) was examined by 5 wk of daily 1-h water immersions (20 degrees C) in resting (RG) and exercising (EG) subjects. Rectal temperature fell (0.8 degrees C; P < 0.05) during immersion only in RG. Skin temperature fell (P < 0.05) similarly in both groups. Physiological responses during cold-air exposure (90 min, 5 degrees C) were assessed before and after CA. Body temperatures and metabolic heat production were similar in both groups with no change due to CA. Cardiac output was lower (P < 0.05) in both groups post-CA (10.4 +/- 1.2 l/min) than pre-CA (12.2 +/- 1. 0 l/min), but mean arterial pressure was unchanged (pre-CA 107 +/- 2 mmHg, post-CA 101 +/- 2 mmHg). The increase in norepinephrine was greater (P < 0.05) post-CA (954 +/- 358 pg/ml) compared with pre-CA (1,577 +/- 716 pg/ml) for RG, but CA had no effect on the increase in norepinephrine for EG (pre-CA 1,288 +/- 438 pg/ml, post-CA 1,074 +/- 279 pg/ml). Skin temperature reduction alone may be a sufficient stimulus during CA for increased vasoconstrictor response, but core temperature reduction appears necessary to enhance sympathetic activation during cold exposure.     

Effects of pyridostigmine bromide on human thermoregulation during cold water immersion

This study examined the effects of an oral 30-mg dose of pyridostigmine bromide (PYR) on thermoregulatory and physiological responses of men undergoing cold stress. Six men were immersed in cold water (20 degrees C) for up to 180 min on two occasions, once each 2 h after ingestion of PYR and 2 h after ingestion of a placebo. With PRY, erythrocyte cholinesterase inhibition was 33 +/- 12% (SD) 110 min postingestion (10 min preimmersion) and 30 +/- 7% at termination of exposure (mean 117 min). Percent cholinesterase inhibition was significantly related to lean body mass (r = -0.91, P less than 0.01). Abdominal discomfort caused termination in three of six PYR experiments but in none of the control experiments (mean exposure time 142 min). During immersion, metabolic rate, ventilatory volume, and respiratory rate increased significantly (P less than 0.05) over preimmersion levels and metabolic rate increased with duration of immersion (P less than 0.01) in both treatment but did not differ between conditions. PYR had no significant effect on rectal temperature, mean body temperature, thermal sensations, heart rate, plasma cortisol, or change in plasma volume. It was concluded that a 30-mg dose of PYR does not increase an individual's susceptibility to hypothermia during cold water immersion; however, in combination with cold stress, PYR may result in marked abdominal cramping and limit cold tolerance.     

Evaluation of two cold thermoregulatory models for prediction of core temperature during exercise in cold water.

Cold thermoregulatory models (CTM) have primarily been developed to predict core temperature (T(core)) responses during sedentary immersion. Few studies have examined their efficacy to predict T(core) during exercise cold exposure. The purpose of this study was to compare observed T(core) responses during exercise in cold water with the predicted T(core) from a three-cylinder (3-CTM) and a six-cylinder (6-CTM) model, adjusted to include heat production from exercise. A matrix of two metabolic rates (0.44 and 0.88 m/s walking), two water temperatures (10 and 15 degrees C), and two immersion depths (chest and waist) were used to elicit different rates of T(core) changes. Root mean square deviation (RMSD) and nonparametric Bland-Altman tests were used to test for acceptable model predictions. Using the RMSD criterion, the 3-CTM did not fit the observed data in any trial, whereas the 6-CTM fit the data (RMSD less than standard deviation) in four of eight trials. In general, the 3-CTM predicted a rapid decline in core temperature followed by a plateau. For the 6-CTM, the predicted T(core) appeared relatively tight during the early part of immersion, but was much lower during the latter portions of immersion, accounting for the nonagreement between RMSD and SD values. The 6-CTM was rerun with no adjustment for exercise metabolism, and core temperature and heat loss predictions were tighter. In summary, this study demonstrated that both thermoregulatory models designed for sedentary cold exposure, currently, cannot be extended for use during partial immersion exercise in cold water. Algorithms need to be developed to better predict heat loss during exercise in cold water.     

Critical water temperature during water immersion at various atmospheric pressures

The present work was undertaken to determine the effect of atmospheric pressure [ranging from a high altitude of 4,300 m above sea level or 0.6 atmospheres absolute (ATA) to depths of 10 m deep or 2 ATA] on the critical water temperature (Tcw), defined as the lowest water temperature a subject can tolerate at rest for 2 h without shivering, of the unprotected subject during water immersion. Nine healthy males wearing only shorts were subjected to immersion to the neck in water at 0.6, 1, and 2 ATA while resting for 2 h. Continuous measurements included esophageal (Tes) and skin (Tsk) temperatures, direct heat loss from the skin (Htissue), and insulation of the tissue (Itissue). The Tcw was significantly higher at 0.6 ATA than 1 and 2 ATA: however, Tcw at 1 ATA was identical to that at 2 ATA. The metabolic heat production remained unchanged among the pressures. During the 2-h immersion in Tcw, Tes was identical among all atmospheric pressures: however, Tsk was significantly higher (P less than 0.05) at 0.6 ATA and was identical between 1 and 2 ATA. The overall mean Itissue was near maximal during immersion in Tcw in each pressure, and no difference was detected among the pressures. However, Itissue at the acral extremities (arm, hand, and foot) decreased significantly at 0.6 ATA, and subsequently heat loss from these parts was increased, which elevated an extremity-to-trunk heat loss ratio to 1.4 at 0.6 ATA from 1.1 at 1 and 2 ATA.(ABSTRACT TRUNCATED AT 250 WORDS)     

Finite-element solution of thermal conductivity of muscle during cold water immersion

The in vivo or effective thermal conductivity (keff) of muscle tissue of the human forearm was determined through a finite-element (FE) model solution of the bioheat equation. Data were obtained from steady-state temperatures measured in the forearm after 3 h of immersion in water at temperatures (Tw) of 15 (n = 6), 20 (n = 5), and 30 degrees C (n = 5). Temperatures were measured every 0.5 cm from the longitudinal axis of the forearm to the skin approximately 9 cm distal from the elbow. Heat flux was measured at two sites on the skin adjacent to the temperature probe. The FE model is comprised of concentric annular compartments with boundaries defined by the location of temperature measurements. Through this approach, it was possible to include both the metabolic heat production and the convective heat transfer between blood and tissue at two levels of blood flow, one perfusing the compartment and the other passing through the compartment. Without heat exchange at the passing blood flow level, the arterial blood temperature would be assumed to have a constant value everywhere in the forearm muscles, leading to a solution of the bioheat equation that greatly underpredicts keff. The extent of convective heat exchange at the passing blood flow level is estimated to be approximately 60% of the total heat exchange between blood and tissue. Concurrent with this heat exchange is a decrease in the temperature of the arterial blood as it flows radially from the axis to the skin of the forearm, and this decrease is enhanced with a lowered Tw.(ABSTRACT TRUNCATED AT 250 WORDS)     

Heat balance precedes stabilization of body temperatures during cold water immersion.

Certain previous studies suggest, as hypothesized herein, that heat balance (i.e., when heat loss is matched by heat production) is attained before stabilization of body temperatures during cold exposure. This phenomenon is explained through a theoretical analysis of heat distribution in the body applied to an experiment involving cold water immersion. Six healthy and fit men (mean +/- SD of age = 37.5 +/- 6.5 yr, height = 1.79 +/- 0.07 m, mass = 81.8 +/- 9.5 kg, body fat = 17.3 +/- 4.2%, maximal O2 uptake = 46.9 +/- 5.5 l/min) were immersed in water ranging from 16.4 to 24.1 degrees C for up to 10 h. Core temperature (Tco) underwent an insignificant transient rise during the first hour of immersion, then declined steadily for several hours, although no subject's Tco reached 35 degrees C. Despite the continued decrease in Tco, shivering had reached a steady state of approximately 2 x resting metabolism. Heat debt peaked at 932 +/- 334 kJ after 2 h of immersion, indicating the attainment of heat balance, but unexpectedly proceeded to decline at approximately 48 kJ/h, indicating a recovery of mean body temperature. These observations were rationalized by introducing a third compartment of the body, comprising fat, connective tissue, muscle, and bone, between the core (viscera and vessels) and skin. Temperature change in this "mid region" can account for the incongruity between the body's heat debt and the changes in only the core and skin temperatures. The mid region temperature decreased by 3.7 +/- 1.1 degrees C at maximal heat debt and increased slowly thereafter. The reversal in heat debt might help explain why shivering drive failed to respond to a continued decrease in Tco, as shivering drive might be modulated by changes in body heat content.     

Mechanism of afterdrop after cold water immersion

It was hypothesized that if afterdrop is a purely conductive phenomenon, the afterdrop during rewarming should proceed initially at a rate equal to the rate of cooling. Eight male subjects were cooled on three occasions in 22 degrees C water and rewarmed once by each of three procedures: spontaneous shivering, inhalation of heated (45 degrees C) and humidified air, and immersion up to the neck in 40 degrees C water. Deep body temperature was recorded at three sites: esophagus, auditory canal, and rectum. During spontaneous and inhalation rewarming, there were no significant differences between the cooling (final 30 min) and afterdrop (initial 10 min) rates as calculated for each deep body temperature site, thus supporting the hypothesis. During rapid rewarming, the afterdrop rate was significantly greater than during the preceding cooling, suggesting a convective component contributing to the increased rate of fall. The rapid reversal of the afterdrop also indicates that a convective component contributes to the rewarming process as well.     

The effect of dynamic exercise on resting cold thermoregulatory responses measured during water immersion

The purpose of this study was to evaluate the effect of exercise on the subsequent post-exercise thresholds for vasoconstriction and shivering measured during water immersion. On 2 separate days, seven subjects (six males and one female) were immersed in water (37.5 degrees C) that was subsequently cooled at a constant rate of approximately 6.5 degrees C x h(-1) until the thresholds for vasoconstriction and shivering were clearly established. Water temperature was then increased to 37.5 degrees C. Subjects remained immersed for approximately 20 min, after which they exited the water, were towel-dried and sat in room air (22 degrees C) until both esophageal temperature and mean skin temperature (Tsk) returned to near-baseline values. Subjects then either performed 15 min of cycle ergometry (at 65% maximal oxygen consumption) followed by 30 min of recovery (Exercise), or remained seated with no exercise for 45 min (Control). Subjects were then cooled again. The core temperature thresholds for both vasoconstriction and shivering increased significantly by 0.2 degrees C Post-Exercise (P < 0.05). Because the Tsk at the onset of vasoconstriction and shivering was different during Pre- and Post-Exercise Cooling, we compensated mathematically for changes in skin temperatures using the established linear cutaneous contribution of skin to the control of vasoconstriction and shivering (20%). The calculated core temperature threshold (at a designated skin temperature of 32.0 degrees C) for vasoconstriction increased significantly from 37.1 (0.3) degrees C to 37.5 ( 0.3) degrees C post-exercise (P < 0.05). Likewise, the shivering threshold increased from 36.2 (0.3) degrees C to 36.5 (0.3) degrees C post-exercise (P < 0.05). In contrast to the post-exercise increase in cold thermal response thresholds, sequential measurements demonstrated a time-dependent similarity in the Pre- and Post-Control thresholds for vasoconstriction and shivering. These data indicate that exercise has a prolonged effect on the post-exercise thresholds for both cold thermoregulatory responses.     

Cardiac output variations in supine resting subjects during head-out cold water immersion

Five men, aged 31.2 years (SD 2.3), under semi-nude conditions and resting in a dorsal reclining position, were exposed to thermoneutral air for 30 min, followed immediately by a cold water (15°C) immersion for 60 min. Cardiac output was measured using a dualbeam Doppler flow meter. During immersion in cold water, cardiac frequency (f _c) showed an initial bradycardia. The lowest values were reached at about 10 min after immersion, 58.3 (SD 2.5) to 48.3 (SD 7.8) beats min^–1 (P < 0.05). By the 20th min of exposure,f _c had gradually risen to 70.0 beats min^–1 (SD 6.6,P < 0.05). This change could be due to the inhibition of the initial vagal reflex by increased catecholamine concentration. Stroke volume (V _s) was significantly increased (P < 0.05) during the whole cold immersion period. Cardiac output, increased from 3.57 (SD 0.50) to 6.26 (SD 1.33)1 min^–1 (P < 0.05) and its change with time was a function of bothV _s andf _c. On the other hand, systolic flow acceleration was unchanged during the period of immersion. The changes in the respiratory variables (ventilation, oxygen uptake, carbon dioxide output and respiratory exchange ratio) during immersion showed an initial hyperventilation followed, as immersion proceeded, by a slower metabolic increase due to shivering.     

Thermoregulation during cold water immersion is unimpaired by low muscle glycogen levels

This investigation studied the importance of muscle glycogen levels for body temperature regulation during cold stress. Physiological responses of eight euglycemic males were measured while they rested in cold (18 degrees C, stirred) water on two separate occasions. The trials followed a 3-day program of diet and exercise manipulation designed to produce either high (HMG) or low (LMG) preimmersion glycogen levels in the muscles of the legs, arms, and upper torso. Preimmersion vastus lateralis muscle glycogen concentrations were lower during the LMG trial (144 +/- 14 mmol glucose/kg dry tissue) than the HMG trial (543 +/- 53 mmol glucose/kg dry tissue). There were no significant differences between the two trials in shivering as reflected by aerobic metabolic rate or in the amount of body cooling as reflected by changes in rectal temperature during the immersions. Postimmersion muscle glycogen levels remained unchanged from preimmersion levels in both trials. Small but significant increases in plasma glucose and lactate concentration occurred during both immersions. Plasma glycerol increased during immersion in the LMG trial but not in the HMG trial. Plasma free fatty acid concentration increased during both immersion trials, but the change was apparent sooner in the LMG immersion. It was concluded that thermoregulatory responses of moderately lean and fatter individuals exposed to cold stress were not impaired by a substantial reduction in the muscle glycogen levels of several major skeletal muscle groups. Furthermore, the data suggest that, depending on the intensity of shivering, other metabolic substrates are available to enable muscle glycogen to be spared.     

Central venous pressure and plasma arginine vasopressin during water immersion in man

The influence of increased central venous pressure (CVP) on the plasma concentration of arginine vasopressin (pAVP) was examined in 7 healthy males subjected to water immersion (WI) up to the neck following overnight food- and fluid restriction. During WI the subject sat upright in a pool (water temperature = 35.0 degrees C) for 6 h. In control experiments the subject assumed the same position outside the pool wearing a water perfused garment (water temperature = 34.6 degrees C). CVP increased markedly during WI and after 20 min of immersion it attained a level which was significantly higher than the control value (10.9 +/- 1.5 (mean +/- SE) vs. 2.2 +/- 1.3 mm Hg, p less than 0.01). This increase was sustained throughout the 6 h WI period. Simultaneously, after 20 min pAVP during WI was significantly lower than control values (1.8 +/- 0.3 vs. 2.2 +/- 0.3 pg X ml-1, p less than 0.05) and sustained throughout WI. Systolic arterial pressure increased significantly by 7-10 mm Hg (p less than 0.05) after 2 h of WI, while diastolic arterial pressure was unchanged. Heart rate was decreased by 10 bpm throughout immersion. There was no change in plasma osmolality when comparing control with immersion. A pronounced osmotic diuresis, natriuresis and kaliuresis occurred during WI, counteracting an acute significant increase in plasma volume of 6.5 +/- 1.9% (P less than 0.01 within 20 min of immersion). We conclude that an increase in CVP due to WI is accompanied by suppressed pAVP.