Cardiovascular origins of heatstroke pathophysiology: an anesthetized rat model.

Opinion is divided on issues concerning a cardiovascular origin of heatstroke pathophysiology as well as those concerning the mechanism of circulatory failure in heat. Such controversies seem to arise because of insufficient data covering the prodromal period of heatstroke. A reappraisal of the nature and sequence of early circulatory responses to heat stress was, consequently, undertaken by subjecting male albino rats to an environmental temperature of 45 degrees C at 15% relative humidity until overt circulatory failure occurred. Although the initial circulatory responses were normal for mild exertion, an inapparent circulatory crisis developed, probably a result of the abolishment of compensatory splanchnic vasoconstriction. The impending threat of functional hypovolemia was, temporarily at least, obscured by cardiac compensation and the extent of cardiovascular commitments may, therefore, have been underestimated. This also suggests that cardiovascular adjustments during the stress of heat may prove to be an essential feature of heatstroke pathophysiology.

Epileptic-type convulsions and magnesium deficiency.

Immediately following 4 h of continuous exercise at +/- 45% Vo2max in heat, a 23-year-old, well-trained man displayed epileptic-type convulsions. One week preceeding this incident, he completed an identical work test successfully under room temperature conditions. An assessment of his physiological and biochemical results indicated only one abnormality: during exercise in heat, an abnormally low serum magnesium concentration prevailed for most of the test. Treatment with phenobarb and magnesium chloride enteric tablets ("Slow Mag", 2 x 535 mg/d) reversed the biochemical abnormality. After checking his resting serum magnesium, the subject subsequently heat acclimatized and repeated similar treadmill tests as before without any ill effects.

Heat acclimatization by a method utilizing microclimate cooling.

A new approach to heat acclimatization has been shown to be feasible during laboratory experimentation. Wearing microclimate suits containing dry ice as the coolant, three groups of men were subjected to a moderate work rate in three different environments for 4 h/d for 8 d. Physiological responses on a subsequent heat tolerance test indicate that the group subjected to an environment of 32.0 degrees C W. B. and 33.5 degrees C D.B. were fully heat acclimatized. The 33/35 degrees C group were also well-acclimatized but developed dangerously high body temperatures during the first 2 d. Only partial acclimatization was achieved by the 31/33 degrees C group. The reason why the men acquire heat acclimatization while wearing the microclimate suits in a hot environment is probably that microclimate cooling does not prevent body temperature from rising--it only prevents it from rising excessively. It should be remembered that only one-third of the body is cooled while the rest shows the normal sweating response.

Effects of plasma ascorbic acid levels on heat acclimatization in man.

Thirteen male volunteers were heat acclimatized for 4 h/day for 10 consecutive days. Three to four hours before each heat exposure, four of the subjects received an oral dose of 250 ascorbic acid, five received 500 mg ascorbic acid, and the remaining four a placebo. Rectal temperature, heart rate, and sweat rate were measured hourly during exposure. Venous blood samples were collected before each administration of drug or placebo. On days 1, 2, 3, 5, 8, and 10, blood samples were also collected just prior to heat exposure and after two and four hours of exposure. In the subjects receiving ascorbic acid, total circulating plasma ascorbic acid increased over the first three or four days to a plateau level some fourfold higher than in the subjects receiving the placebo. The plateau level was the same in the subjects receiving 250 mg and 500 mg ascorbic acid. The increased ascorbic acid concentration was shown to be associated with a reduction in total sweat output, independent of rectal temperature, and a reduction in rectal temperature, independent of total sweat output. The results indicate that ascorbic acid may be effective in reducing heat strain in unacclimatized individuals.

Effect of ascorbic acid on rate of heat acclimatization.

There is some indication in the literature that ascorbic acid (vitamin C) may reduce the physiological responses to heat stress. Consequently, the effect of ascorbic acid ingestion on heat-strain indicators has been studied on a group of 60 mining recruits undergoing climatic room acclimatization. Of the 60 men, 19 received a daily dose of 250 mg ascorbic acid; 21 a daily dose of 500 mg ascorbic acid; and 20 received a placebo daily. Measurements of rectal temperature, heart rate, and hourly sweat rate were made on all subjects during the 4 h of heat exposure per day for 10 days. The wet bulb temperature was 32.2 degrees C, the dry bulb 33.9 degrees C, the air movement 0.4 m/s, and the work rate 35 W. The results indicate that the rate and degree of acclimatization, as assessed by 4th-h rectal temperature, is enhanced by ascorbic acid supplementation and that no differences in response could be shown between daily dosages of 250 and 500 mg of vitamin C.

Acclimatization in a hot, humid environment: energy exchange, body temperature, and sweating.

Four trained young men, worked for 4 h/day at 43-50% of their maximum aerobic capacity for 3 days at 25 degrees C db, 18 degrees C wb and then for 10 consecutive days at 45 degrees C db, 32 degrees C wb. Their thermal status was assessed using direct calorimetry. As a group, the men showed classical acclimization responses, but there were marked individual differences. The calorimetric analysis revealed that reductions in strain were associated with minor changes in heat balance confined to the first and last hours of exposure. Events occurring within the first 4 days appeared to have little effect on body temperatures. Significant decreases in body temperature took place only when sweat and evaporation rate increased. A 10% increase in evaporation rate was accompanied by a 30% increase in sweat rate and a 200% increase in unevaporated sweat; thus, there is a wasteful overproduction of sweat. By the 10th day skin temperature was confined to the level necessary to evaporate sufficient sweat to achieve thermal balance with a fully wet body surface. The efficiency of heat transport within the body did not change with acclimatization.

Orthostatic responses in Caucasians and Bantu.

Nine Caucasian and 13 Bantu young men, all untrained and unacclimated to heat, were tilted head-up for 20 min before and after 4 h of exercise performed at a load of 35 W at room temperature of 23 degrees C and in heat (33.9 degrees C DB, 32.2 degrees C WB). In heat, all Bantu but only four Caucasians completed the 4 h of exposure. The change in systolic blood pressure from recumbency to orthostasis was negligible in the Bantu and adverse in the Caucasians, during pre-exercise tilting at 23 degrees C. Similar differences were found during tilting after exercise at 23 degrees C. Post-exercise orthostatic heart rate did not differ between the two groups despite higher exercise heart rats of the Bantu. Seven subjects in each group fainted during heart-orthostatism, and the difference in systolic blood pressure between recumbency and orthostasis in heat was substantially more adverse in the Caucasians. High relationships were found between exercise heart rate, orthostatic heart rate, and fainting episodes. The results suggested that Bantu make better orthostatic adjestments than Caucasians.

Orthostatism and heat acclimation.

Three groups of subjects (6 subj in each group) underwent the following precedures: group A was given a 20-min head-up tilt at 21 degrees C followed by 4 h of exercise at 33.9 degrees C DB, 32.2 degrees C WB, and a repetition of tilting after exercise in heat; group B underwent the same procedure at 21 degrees C; group C was tilted at 21 degrees C, rested in heat for 4 h and was retilted in heat. The above procedures were repeated for 8 days, and on the last day groups B and C underwent the same treatment as group A. Group A showed the usual decreases in heart rate and rectal temperature and an increase in sweat rate on acclimation. This corresponded to marked improvements in heat-orthostatism. While five subjects in group A fainted during post-exposure tilting on the first exposure, none fainted on the last day. Resting in heat (group C) did not cause any acclimation to work in heat. This corresponded to poor heat-orthostatism after the work-heat procedure when five subjects fainted. Mild training at 21 degrees C (group B) resulted in minor improvements to work in heat as evident by some improvements in heart rate responses after the 1st and 2nd h of exposure. This corresponded to better heat-orthostatism and fewer men fainting than in group C. The results indicated that heat-orthostatism improves on acclimation to the same extent as exercise heart rate and rectal temperature.