Biomedical subjects
Publications and source records attributed to C B Wenger.
Exercise-related hyponatremia is an infrequent but potentially life-threatening accompaniment of prolonged exercise. This condition results from sodium losses in sweat, excessive water intake, or both. We review the risk factors for development of this condition and discuss evidence that there is a population at increased risk of hyponatremia during prolonged exercise.
PURPOSE: To evaluate long-term susceptibility to subsequent serious exertional heat illness (EHI) in military recruits who suffered exertional heat illness during basic training. METHODS: We identified Marine Corps members who completed at least 6 months of military service and suffered EHI treated as outpatients (N = 872) or inpatients (N = 50) during basic training in 1979-1991 at the Parris Island Marine Corps Recruit Depot, SC (EHI cases). We compared them to 1391 similar members (noncases) who did not experience EHI during basic training. These subjects were followed from 6 months after accession into the military through the subsequent 4 yr. Follow-up was through military personnel records to determine retention and military hospital databases to determine subsequent hospitalizations during military service. RESULTS: Military retention rates were slightly lower for those who suffered EHI during basic training, compared with those who did not (24% vs 30% at 4 yr, respectively). Outpatient EHI cases also had about 40% higher subsequent hospitalization rates in military hospitals than noncases during their continued military service, although these differences declined over time and diagnoses showed little relationship to EHI. EHI cases had higher rates of subsequent hospitalization for EHI, but the number was too small (five hospitalizations) to provide stable comparisons. CONCLUSION: Hospitalization for EHI is uncommon during subsequent military service after an initial episode during basic training, and occurrence of EHI during basic training has only a small impact on subsequent military retention and hospitalization.
A matched population-based case-control study was conducted on exertional heat illness (EHI) in male Marine Corps recruits in basic training at Parris Island, SC. Physical fitness and anthropometric measurements were obtained for 391 of 528 cases of EHI identified in this population during 1988-1992, and 1467 of 1725 controls matched to cases by initial training platoon. The risk for developing EHI increased with increase in body mass index (BMI = weight.height-2) as measured on arrival and with increase in time to complete a 1.5-mile run conducted during the first week. Recruits at highest risk for developing exertional heat illness had a BMI of 22 or more kg.m-2 and a 1.5-mile run-time for 12 of more minutes. These recruits had an eightfold higher risk for developing exertional heat illness during basic training when compared with those with BMI less than 22 kg.m-2 and 1.5-mile run-time under 10 min (P < 10(-6). Only one-fifth (18%) of male recruits met these criteria for high risk, but they accounted for nearly half (47%) of the exertional heat illness cases occurring during the 12-wk basic training course.
BACKGROUND: Exertional heat illness (EHI) is a recurring problem in military training resulting in loss of manpower and training effectiveness. A scientific approach to this problem requires quantitative analysis of factors related to its occurrence. METHODS: Review of clinic and hospital records identified all cases of EHI occurring among 217,000 Marine Corps recruits (90% male, 80% age 18-20 yr) entering 12-week basic training at Parris Island, SC during 1982-1991. RESULTS: There were 1454 cases, 89% males and 11% females; 11% of male and no female cases were hospitalized. The majority (88%) of cases occurred during May-September, with a peak rate of 2% of recruits in summer. Most of the cases occurred during the cooler early morning hours when recruits performed strenuous exercise. During 0700-0900 hours the rate of heat casualties increased substantially as the Wet Bulb Globe Temperature Index (WBGT) increased, beginning at levels as low as 65 degrees F. EHI rates increased 26- and 39-fold at WBGT 75- < 80 degrees F (over baseline rates at < 65 degrees F) for immediate and prior day exposures, respectively. Exposure to WBGT of 80 + degrees F was infrequent (25%) among the early morning cases at the time of illness, while it was common (87%) on the day prior to illness, suggesting a lasting effect of heat exposure. CONCLUSIONS: Risk for EHI in military training increases markedly as WBGT levels rise above 65 degrees F; cases occur primarily with strenuous exercise (e.g., running); and heat stress exposure on prior days may be important.
Five men underwent eight heat stress tests (HSTs) at 35 degrees C, each consisting of four 25-min treadmill walks (35% Vo2max), separated by 5-min rests, in four conditions: 1) 20% relative humidity (rh), subjects euhydrated and drinking ad libitum; 2) 20% rh, euhydrated; 3) 75% rh, euhydrated; and 4) 20% rh, hypohydrated 3% of body weight. In Conditions 2-4 subjects drank during the walks to maintain their pre-HST weight. In each condition we tested subjects once after 30 mg pyridostigmine bromide (PB) by mouth and once after placebo. PB lowered heart rate a mean of 3 beats/min overall, most with hypohydration. PB did not significantly affect rectal temperature (Tre), but reduced the rise in Tre during hypohydrated exercise. In Condition 2, chest skin temperature decreased more during exercise with PB. PB had no significant effect on other skin temperatures, sweating, hematocrit, hemoglobin, total plasma protein, osmolality, ad libitum drinking, rate of O2 uptake, or subject ratings of temperature, discomfort, or exertion. PB thus had little effect on physiological responses to moderate exercise-heat stress.
The side effects of chronic pyridostigmine bromide administration were studied in seven male soldiers performing moderate-intensity exercise in a desert environment. A 2-week, double-blind, placebo-controlled crossover design was employed in which pyridostigmine was administered for 7 consecutive days (30 mg orally, t.i.d.). Four hours each day were spent in the heat (42 degrees C, 20% relative humidity); 2 hours rest followed by 2 hours moderate exercise (40% maximal aerobic power). Each day, subjects completed four symptom questionnaires and received three focused physical examinations. Symptoms reported did not differ between treatment groups except for fewer headaches during pyridostigmine treatment. Soldiers were unable to distinguish the effects of pyridostigmine from placebo. Pyridostigmine was associated with lower resting diastolic blood pressure (approximately 4 mmHg, p less than 0.05), smaller pupil diameter (approximately 0.5 mm, p less than 0.01), decreased handgrip strength (approximately 3%, p less than 0.05), and higher final rectal temperature (approximately 0.1 degree C, p less than 0.01). Effects of this magnitude are not likely to appreciably limit performance. We conclude that chronic pyridostigmine administration does not negatively impact on soldiers' ability to perform physical work over repeated days in a desert environment.
We studied the effects of autologous erythrocyte infusion on blood volume and thermoregulation during exercise in the heat. By use of a double-blind design, nine unacclimated male subjects were infused with either 600 ml of a NaCl-glucose-phosphate solution containing a approximately 50% hematocrit (n = 6, reinfusion) or 600 ml of this solution only (n = 3, saline). A heat stress test (HST) was attempted approximately 2-wk pre- and 48-h postinfusion during the late spring months. After 30 min of rest in a 20 degrees C antechamber, the HST consisted of a 120-min exposure (2 repeats of 15 min rest and 45 min treadmill walking) in a hot (35 degrees C, 45% rh) environment while euhydrated. Erythrocyte volume (RCV, 51Cr) and plasma volume (PV, 125I) were measured 24 h before each HST, and maximal O2 uptake (VO2max) was measured 24 h after each HST. Generally, no significant effects were found for the saline group. For the reinfusion group, RCV (11%, P less than 0.01) and VO2max (11%, P less than 0.05) increased after infusion, and the following observations were made: 1) the increased RCV was associated with a reduction in PV to maintain the same blood volume as during the preinfusion measurements; 2) polycythemia reduced total circulating protein but did not alter F-cell ratio, plasma osmolality, plasma protein content, or plasma lactate at rest or during exercise-heat stress; 3) polycythemia did not change the volume of fluid entering the intravascular space from rest to exercise-heat stress; and 4) polycythemia tended to reduce the rate of heat storage during exercise-heat stress.
We evaluated the effectiveness of an air-cooled vest in reducing thermal strain of subjects exercising in the heat (49 degrees C dry bulb (db), 20 degrees C dew point (dp] in chemical protective clothing. Four male subjects attempted 300-min heat exposures at two metabolic rates (175 and 315 W) with six cooling combinations--control (no vest) and five different db and dp combinations. Air supplied to the vest at 15 scfm ranged from 20-27 degrees C db, 7-18 degrees C dp; theoretical cooling capacities were 498-687 W. Without the vest, endurance times were 118 min (175 W) and 73 min (315 W). Endurance times with the vest were 300 min (175 W) and 242-300 min (315 W). The five cooling combinations were similarly effective in reducing thermal strain and extending endurance time, although there was a trend for the vest to be more effective when supplied with air at the lower dry bulb temperature. At 175 W, subjects maintained a constant body temperature; at 315 W, the vest's ability to extend endurance is limited to about 5 hours.
Colloid osmotic pressure (COP) and pH were measured on the true plasma of human blood from five subjects tonometered with different concentrations of carbon dioxide. Measurements were also made on their separated plasma. COP (mmHg) of true plasma obtained from tonometered whole blood varied in proportion to the bicarbonate concentration (mEq/l): COP = 0.056 [HCO3-] + 23.3. In separated plasma, as CO2 concentration increased, COP decreased as pH decreased: COP = 1.99 (pH) + 11.0. When the change in COP due to the change in pH was subtracted from the observed change of COP due to CO2 exposure of whole blood, the difference was the change of COP due to the shift of fluid between plasma and red cells: COP adjusted for pH = 0.131 [HCO3-] + 21.5. The COP values of tonometered whole blood and separated plasma are taken to be equal at a pH of 7.40 (at the mixed venous point). The change in COP, adjusted for pH, for a given change in pCO2 is in keeping with the amount of fluid shift calculated from the measured changes in hematocrit and plasma protein concentration. An error in a previous paper (Kakiuchi et al., J. appl. Physiol. 44, 474-478, 1978) had led to an overestimation of the COP change from the exposure of whole blood to CO2 in vitro.
To determine the role of neurotransmitter in the response of forearm blood flow (ABF) to local (forearm) skin temperature (Tsk) we measured ABF of six subjects at Tsk from 25 to 40 degrees C before (control) and after brachial plexus block (BPB). Control experiments were conducted in an ambient temperature of 27-29 degrees C, adjusted to minimize the subject's overall thermal sensation. Tsk was regulated by blowing a controlled-temperature airstream through a plastic bag enclosing the arm. We first lowered Tsk to 25 degrees C and after 20 min began to measure ABF with Whitney strain gauges. We then raised Tsk by 2.5 degrees C steps to 40 degrees C and measured ABF every 30 s for at least 10 min at each level of Tsk. Mean ABF rose from 1.1 ml X 100 ml-1 X min-1 at Tsk of 25 degrees C to 2.1 ml X 100 ml-1 X min-1 at 32.5 degrees C to 13.7 ml X 100 ml-1 X min-1 at 40 degrees C in control experiments and from 2.8 to 4.4 to 14.8 ml X 100 ml-1 X min-1 after BPB. The effect of Tsk on ABF was highly significant (P less than 0.0001) but the effect of BPB was not (P approximately equal to 0.2). At thermoneutrality, the effect of Tsk on ABF is largely independent of neural activity, since this effect is unaffected by nerve block.
In this symposium, a diversity of perspectives was focused on how blood flow to the skin is controlled. Thus, control of the cutaneous circulation by reflexes aimed at body temperature regulation, blood pressure regulation, and the reflexes attending muscular exercise was discussed in detail, as were the similarities and differences between control of cutaneous arterioles and arteriovenous anastomoses. A mechanistic treatment of interaction between adrenergic control of cutaneous blood vessels and their temperature brought physical factors and pharmacological approaches to the consideration of reflex control. Finally, the more slowly developing changes in the control of the skin circulation that accompany circadian rhythms, changes in blood volume or its distribution, physical training, and acclimatization were discussed. Because the cutaneous circulation has potentially large vascular conductance, blood flow, and blood volume, control of the resistance and compliance vessels within the skin has an importance well beyond that of tissue nutrition. Indeed, overall hemodynamics are dependent on how much blood flow and how much blood volume are distributed to skin. Consequently, reflex factors, physical factors, and their interaction all have roles of importance with respect to exchange of heat with environment as well as maintenance of blood pressure, cardiac output, and blood flow to other tissues.
We measured forearm blood flow (ABF) bilaterally on six subjects during 15-min periods of leg exercise and the first 10 min of recovery. One forearm (control) was kept at about 33 degrees C skin temperature in all experiments. In experiments at ambient temperature (Ta) of 15 degrees C, the other arm (experimental) was kept at about 26, 33, and 40 degrees C, respectively, during three successive cycles of exercise and recovery. ABF in the 26 degrees C forearm was linearly related to and averaged 42% of control. The relation of ABF in the 40 degrees C forearm to control ABF showed a bend at control ABF of 4-5 ml X 100 ml-1 X min-1. Below the bend, experimental ABF average 213% of control. Above the bend, experimental ABF averaged 5.09 ml X 100 ml-1 X min-1 above control. In four subjects, after heating the experimental forearm to 40 degrees C, we measured ABF for 25-30 min at rest in Ta of both 15 and 25 degrees C. At 25 degrees C Ta, ABF in the heated forearms rose gradually, but control ABF showed little change. At 15 degrees C Ta, the effect on ABF of local heating to 40 degrees C was much reduced, apparently due to reflex vasoconstrictor signals.
To characterize the changes in the control of the heat loss responses associated with the circadian variation in body temperature, we studied five men during 20 min of exercise in 25 degrees C on 6 separate days. Experiments were conducted at six times, equally spaced over the 24-h day. Esophageal temperature (Tes) and chest sweat rate (msw) were measured continuously, and forearm blood flow (FBF) was measured one to two times per minute. The thresholds for sweating and forearm vasodilation were significantly higher at 1600 and 2000 than at 2400 and 0400, averaging 0.57 and 0.65 degrees C higher, respectively, at 1600 than at 0400. Resting Tes and the Tes thresholds for cutaneous vasodilation and sweating during exercise all showed a similar circadian rhythm. The level at which core temperature is regulated therefore varies over the 24-h day with the zenith occurring around 1600 and the nadir at 0400. However, whereas the slope of the msw-to-Tes relation did not change over the 24-h day, the slope of the FBF-to-Tes relation tended to increase between 0400 and 2400, implying that the circadian rhythm may be more complex than just a shift in the central reference temperature.
To investigate the interaction of thermal reflexes and baroreflexes in the control of the peripheral veins, we studied in supine humans the effects of lower body negative pressure (LBNP) and neck suction (NS) on forearm veins at ambient temperatures (Ta) of 18, 28, and 37 degrees C. Forearm venous volume (FVV)-venous pressure (FVP) relations (forearm venous capacitance) on six subjects showed an increase from 18 through 28 to 37 degrees C (P less than 0.001). Heart rate increased (P less than 0.001) and forearm venous capacitance decreased (P less than 0.001) in proportion to the level of LBNP applied from 20 to 50 Torr at all Ta. At 50 Torr LBNP, FVV at 30 cmH2O, FVP decreased from control values of 2.5, 3.8, and 4.4 to 1.6, 2.7, and 3.4 ml/100 ml at 18, 28, and 37 degrees C, respectively. We also studied venomotor responses using the occluded limb technique. Although LBNP caused venoconstriction, NS applied either alone or during LBNP produced no change in venomotor tone. Therefore we concluded that carotid baroreceptors play little role in reflex venomotor adjustments. Since changes in mean arterial and pulse pressures during LBNP did not account for the observed venomotor responses, we concluded that low-pressure baroreceptors initiate significant venoconstrictor reflexes over a wide range of Ta.
To study the effect of hyperosmolality on thermoregulatory responses, five men [average maximal O2 consumption (VO2 max) = 48 ml X kg-1 X min-1] cycled at 65-75% VO2max for up to 30 min in a 30 degrees C, 40% relative humidity environment under three conditions. First, control tests (C) were performed where preexercise plasma volume (PV) and osmolality (Osm) averaged 3,800 ml and 282 mosmol X kg-1, respectively. Second, exercise tests (D) were performed following dehydration induced by fluid restriction and mild exercise (30% VO2max) in hot (40 degrees C) ambient conditions. Each subject then rested in cool surroundings 1 h before performing the exercise test. Preexercise PV and Osm averaged 3,606 ml and 293 mosmol X kg-1, respectively. Third, exercise tests (I) were performed following dehydration, but during the 1-h rest interval, 3% saline was infused so that PV was restored to 3,826 ml and Osm averaged 294 mosmol X kg-1 prior to exercise. During D, esophageal temperatures (Tes) were significantly higher than C, an avg 0.56 degrees C after 20 min exercise due to a 0.22 degrees C increase in Tes threshold for vasodilation, a 39% reduction in slope of the forearm blood flow (BF)-Tes relationship, a 32% average reduction in maximal exercise BF, and a 0.22 degrees C increase in Tes sweating threshold. During I, responses were similar to D, except the BF-Tes slope and the maximum BF were not significantly different from C. Thus hyperosmolality modifies thermoregulation by elevating thresholds for both vasodilation and sweating even without decreases in PV.
In Figure 13 we have tried to summarize the interactions of thermal and nonthermal control of effector responses, the effects these responses have on the body during exercise, and the ways the changing state of the body feeds back on the central control systems. These systems were depicted in Figure 3 and are included in condensed form in Figure 13. Exercise affects thermoregulatory responses not only by increasing heat production, but also through a number of other mechanisms. For example, the thermoregulatory responses tend to reduce central venous pressure, and sweating without fluid replacement will increase plasma osmolality. The secondary effects of these changes on the control of the thermoregulatory responses may themselves have an important effect on the rise in Tc during prolonged exercise or exercise in the heat. In concluding, it is appropriate to briefly answer the questions raised in the introduction. In our view, the concept of shifting the set point is not different from the concept of resetting the "thermostat," and the temperature regulatory system is governed by only one set point, which does not change during exercise. Tsk does not change the set point as we have defined it. Rather it combines with thermal information from the core and other deep body thermo-detectors to produce a thermoregulatory command signal Tws distributed to all effector responses. To demonstrate a set point shift, one must show that the Tws thresholds for initiating all heat-dissipating responses shift in the same direction. Although this does not occur with exercise, it does occur with time of day, heat acclimation, endurance training, and fever. A hyperosmolar state also can raise the threshold for sweating and vasodilation uniformly, and therefore may also raise the set point. However, a change in posture, for example, which alters the threshold for vasodilation but not for sweating, does not alter the set point. We believe that a shift in threshold for a given effector may be produced by either a central or a peripheral mechanism. For example, an ion-osmotic influence on the sweating: Tc threshold may be at the level of the central nervous system or the sweat gland itself. However, a set point shift must be a central event, since it influences all effector responses uniformly. Is the set point governed by the ratio of sodium to calcium ions in the posterior hypothalamus? This is unlikely. Shifts in ion concentration can influence effector responses, but they do not appear to shift all effectors uniformly.
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Five healthy men exercised at 65-70% of maximum O2 uptake (VO2 max) for 30 min in an ambient temperature of 30 degrees C. Duplicate experiments were conducted at three levels of plasma volume:control, hypovolemia, in which blood volume (BV) was reduced an average of 490 ml (9.7%) with diuretics, and hypervolemia, in which BV was increased an average of 440 ml (7.8%) by infusing an isotonic solution containing 5% human serum albumin. Marked venoconstriction occurred during exercise in all conditions and persisted despite large increases in deep body temperature. The degree of venoconstriction was similar during control and hypervolemic conditions, but was potentiated during hypovolemia. The observed venoconstriction appeared to consist of two components: an early one related to autonomic adjustments at the onset of exercise, and a later one possibly related to progressive decreases in cardiac filling. Heart rate, cardiac stroke volume (SV), and cardiac output during exercise were significantly affected by changes in BV. During hypovolemia the average differences from control values were 10 beats X min-1, -14 ml, and -2.2 l X min-1, respectively; during hypervolemia the differences from control were -7 X min-1, 10 ml, and 1.0 l X min-1, respectively. The pattern of SV over the course of exercise indicates that pooling of blood in veins may be quantitatively more important than plasma water loss in reducing cardiac filling pressure in the heat.