384 J. Physiol. (1964), 171, pp. 384-396With 3 text-figuresPrinted in Great Britain

THE EFFECT OF EXERCISE ON TEMPERATURE REGULATION

BY PAMELA A. BRADBURY, R. H. FOX, R. GOLDSMITH ANDI. F. G. HAMPTON

From the Division of Human Physiology, NVational Institute for MedicalResearch, Hampstead, London, N. W. 3

(Received 10 September 1963)

The mechanisms controlling sweat production in man have been inten-sively studied in recent years. Benzinger (1959, 1962), using a gradient-layer calorimeter, found that the rate of sweating was entirely dependenton the degree of elevation of the deep body or core temperature, which hemeasured at the tympanic membrane, provided that mean skin tempera-ture was above about 330 C. The relation between the core temperatureand sweat rate was the same, whether body temperature was raised byexposing the subject at rest to a hot climate or raised by the metabolicheat of physical exercise. Nielsen (1938), on the other hand, found thatduring exercise the rise in body temperature was dependent on the rateof metabolism, and not, within certain limits, upon the environmentalconditions; he concluded in effect that exercise produced a resetting of thecentral nervous system thermostat, and this conclusion was supported byvon Euler & Soderberg (1958). There is thus an apparent contradictionbetween these two findings; one leads to the conclusion that there is adirect relation between body temperature and the thermoregulatoryresponse, not affected by exercise, whereas the other implies a modificationof this response by exercise.The present study is an attempt to examine these two opposing hypo-

theses by measuring the sweat rates of subjects at different levels of energyexpenditure but with the same elevated level of body temperature.

METHODS

Subjects. Twenty fit young soldiers, average age 205 years (range 18-27 yr) volunteeredas subjects for the experiment. None had been exposed to a hot environment for at least9 months preceding the experiment. Their average height was 177*7 (range 187-170) cmand average weight was 73-91 (range 82.40-64 06) kg. One subject fell ill and was with-drawn from the experiment.

Design of experiment. The experiment was designed to compare the sweat losses of groupsof subjects at four different levels of energy expenditure while their body temperatureswere maintained at 38.5 C. A secondary aim was to determine whether the performanceof physical exercise during the controlled hyperthermia routine would alter the degree of

TEMPERATURE REGULATION AND EXERCISE 385heat acclimatization induced by a series of exposures. Figure 1 illustrates the plan of theexperiment. At the beginning and again at the end of the series of controlled hyperthermiasessions all the subjects took part in three 2 hr standard tests to assess the changes inacclimatization status. During the period of controlled hyperthermia the twenty subjectswere divided into five equal groups; Table 1 shows the treatment that each group received.Three groups, III, IV and V, were acclimatized by sessions of controlled hyperthermia:the other two groups acted as controls; Group I received no treatment while Group IIexercised in cool conditions.

Experimental routines

Standard tests. The standard tests, of 2 hr duration, consisted of alternating half-hourperiods of work and rest in rigidly controlled environmental conditions; details of the testroutine have been described previously (Fox, Goldsmith, Kidd & Lewis, 1963). The threestandard tests differed only in the environmental conditions and these are given in Table 2.Physiological variables were measured at the beginning and at the end of each test.

A, coolStandard B, hot dr /

tet C, hot wet

Controlled hyperthermia

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Fig. 1. The timetable of the experiment. The three standard tests are shown a&qtriangles. The diagonally shaded squares represent sessions of controlled hyper-thermia during which all subjects rested; the horizontally shaded squares thoseduring which subjects were allotted to their particular level of energy expenditure.

Controlled hyperthermia sessions. The experiments began at 0900 hr with the subjectsseated and resting for i hr. At the end of the rest period they entered a room in which theair was hot and saturated and where there was a considerable air movement (Table 2).They remained there until their body temperature rose to 38.50 C; this took an averageof 10-9 min. The subjects were then dressed in vapour-barrier suits which completelyenveloped the body except for the face. They were weighed and then either rested or workedfor 54 min before being weighed again. Body temperatures were controlled as close to38.50 C as possible by ventilation of the suits. The method was described in detail byFox et al. (1963); the only important alteration in the technique was the measurement ofaural temperature (Benzinger, 1959), in place of sublingual.

Physiological measurementsThe physiological variables measured were body temperature, sweat loss and heart rate.Body temperature. Sublingual oral temperatures in the standard tests and aural tempera-

tures during the sessions of controlled hyperthermia were measured by means of thermistorscoupled through Wheatstone bridges to meters accurate to + 0.050 C. The aural thermistorwas embedded in a small glass bead attached to fine wires. It was gently introduced into

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TEMPERATURE REGULATION AND EXERCISE 387the external auditory canal to lie close to the ear-drum membrane, but not actually touchingit. The wires were taped to the skin near the ear; a cotton-wool plug was inserted into theexternal auditory meatus and further insulation was provided by means of a thick padwhich covered the whole ear. This technique for measuring body temperature proved mostconvenient. The one important modification of the technique proposed by Benzinger (1959)was in having the temperature sensing end organ close to, instead of touching, the ear-drum membrane. Even light contact of the thermistor with the membrane produceddiscomfort. However, no difference in temperature could be detected when the thermistorwas in contact with the membrane or moved just away from it, provided the externalauditory meatus was well insulated from the environment. The deep body temperature ofall subjects was measured throughout two sessions (days 14 and 15) with radio pills (Fox,Goldsmith & Wolff, 1962).Skin temperature8 were measured with fine copper-constantan thermocouples. For the

standard tests the thermocouple was mounted across the open end of a V-shaped applicator.Measurements were made by recording the output from this thermocouple while it waslightly held to the skin site; the mean of four consecutive recordings at 3 sec intervals wasused. The mean skin temperature for each subject was obtained by averaging the valuesfrom six sites (forehead, insertion of deltoid, 3 cm above the nipple, 3 cm above the lowerangle of the scapula, anterior and medial surfaces of the thigh at the junction of the upperthird with the lower two thirds). For the measurements during controlled hyperthermiathe thermocouples were fixed in position on the skin at the same six sites by elastic strapswith wide-mesh nylon net over the regions of the thermocouple junctions. Skin tempera-tures of the subjects of Group III were measured in the sessions on days 7, 8 and 10 andagain on days 17, 19 and 22, and of Group V on days 9, 11, 14, 15, 18 and 21. The meanskin temperature for each session was computed by averaging readings recorded at 15 minintervals.Sweat lo8s. The total evaporative water loss was determined from weight change

(± 5-0 g). Allowances were made for weight changes due to fluid drunk and urine passed,but not for metabolism. This measurement will be referred to hereafter as the sweat loss.

Heart rate. Electrocardiograms were recorded for i min at the beginning and end of the2 hr standard tests and at the beginning and end of each hyperthermia session. From thesepulse rates were counted.

Effectivene88 of body temperature controlIt proved to be more difficult to maintain a constant elevated body temperature during

exercise than at rest (Table 3). The deviations from the target level were very marked atthe highest level of energy expenditure (Group V) and the mean temperature at this levelwas significantly higher (P < 0.01) than at the other two levels of work or at rest. Controlof aural temperature, in all three groups, improved as the experiment progressed. Meanaural temperatures tended to be lower at the end of the experiment and there was asignificant negative correlation between the experimental day and the mean controltemperature (r = - 0-214 P < 0.05); there was also a marked reduction in the deviationsfrom the target level. This improvement in temperature control with time is partly explainedby the increasing experience of the temperature controllers and also, especially at the highestwork rate, by the increase in sweat rates. The mean air flows used to ventilate the subjects'suits at the four levels of energy expenditure were: at rest = 30 I./min; stepping 15 cm =57 1./min; stepping 30 cm = 113 I./min and stepping 45 cm = 134 L./min.Deep body temperature, as measured by the radio pill, was usually lower than aural

temperature at the beginning of the session of controlled hyperthermia but rapidly roseabove it. The mean differences between aural and deep body temperature during the hourof controlled hyperthermia were 0.350 C + 0 16 for subjects at rest and 0.460 C + 022 forsubjects stepping 30 cm.

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Statistical analysisIn order to distinguish the effects of the different levels of energy expenditure on sweat

loss from the progressive effects of repeated exposure and also a possible influence of thedeviations from the control temperature, they had to be separated from one another. Fromthe data a model allowing for a quadratic effect of time and a linear effect of the deviationsfrom the control temperature was postulated. The equation was

8-s = a(d-d)+b(d2-d2)+c(t-t),where, for each day, s = sweat loss; d = day of exposure; t = mean control aural tempera-ture; s,d,t = the means of these values for the whole period; and a,b,c = constants. Thevalues of the constants a, b and c were estimated by the method of least squares. It wasfound that c was non-significant, so the simplified equation

s-s = a'(d-d) +b'(d2-d2)

was adopted and the values for a' and b' were estimated. From this equation a correctionfor the increase in sweat loss due to repeated exposures was computed for each subject foreach day. These values were then used to adjust the actual sweat losses on each day.Finally, the estimated sweat rates of the same subjects at different levels of energy expendi-ture were compared.

RESULTS

Standard testsThe changes in the four variables between the first and last sets of the

three standard tests are shown in Fig. 2. Although the subjects had beenrandomly assigned to the treatment groups, there were important differ-ences between the physiological responses of the groups in the first trio ofstandard tests. The most striking difference was in the mean oral tempera-tures of Groups III and IV at the end of the tests, suggesting that GroupIV began the experiment more acclimatized than Group III. This makesit difficult to draw conclusions on the acclimatization effects of the differenttreatments, since the initial levels could explain most of the differencesbetween the groups in the changes from the first to the last series of stand-ard tests. However, there seems little evidence for any important differ-ences as a result of the contrasting acclimatization procedures.

There were no significant differences in the changes between the twocontrol groups (I and II). Both groups showed small improvements insome of the variables. The measurement of oral temperature in StandardTest A proved unsatisfactory, owing to excessive local cooling due tomouth breathing. However, even in these cool conditions the effects ofacclimatization were clearly demonstrated in the other variables measured.

Controlled hyperthermiaSweat loss. There was a progressive increase of sweat loss throughout

the period of acclimatization, with a falling off in the rate of increasetowards the end (Fig. 3a). There was no statistical difference between the

389

390 PAMELA A. BRADBURY AND OTHERSrates of increase of the resting compared with the exercising groups. Itappeared therefore that the different regimes to which the three groupswere subjected had no effect on the speed of the acquisition of acclimatiza-tion to heat.

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An examination of the mean sweat losses of the group of subjects testedat four different levels of energy expenditure, illustrated in Fig. 3b,showed that sweat rate was increased by increasing the level of energyexpenditure.The deviations from the target control aural temperature, though

significant, were small and had only minor effects on sweat loss (9.2 + 4-9

TEMPERATURE REGULATION AND EXERCISE

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Fig. 3. The increase in sweat loss during the period of acclimatization; (a) showingthe results for Group 3 ---, and 4 - -; and (b) showing the effects of thedifferent levels of energy expenditure for Group 5. x = sessions while resting,0 = stepping 15 cm, C = stepping 30 cm, and * = stepping 45 cm.

g/m2/041° C). The equation for the increase in sweat loss was found to be

s- = 47 (d-d)-1-32 (d2-d2).

The estimates for the mean sweat loss, after the effect ofrepeated exposureshad been eliminated, in the three groups at the four different levels ofenergy expenditure are shown in Table 4. The significance of the differ-ences of sweat loss of the same subjects at different energy expenditure

391

392PAMELA A. BRADBURY AND OTHERSlevels are also shown. This analysis shows that sweat loss was significantlyaffected by the level of energy expenditure, sweat loss being higher at eachlevel of work than it was at rest.

Pulse rate. There were no significant changes in the mean pulse ratesof the three groups during controlled hyperthermia comparing the begin-ning and end of the 14 days. The mean pulse rate in the resting group(III) rose from 54-5 to 56-5 beats/30 sec, while in the working groups (IVand V) it fell from 81-7 to 80-4 beats/30 sec.Skin temperature. The mean skin temperature did not change signific-

antly between the beginning and the end of the period of acclimatization.The mean values for the beginning and end of the period respectivelywere: Group III, 37-65 and 37.790 C, Group V stepping 15 cm, 37*14 and37 09° C and stepping 45 cm, 36-18 and 36 33° C.No subject had a mean skin temperature below 34° C at any time. The

temperature at individual sites did occasionally fall below this level,especially when large volumes of air were being blown through the suits.

DISCUSSION

One aim of these experiments was to attempt to confirm the conclusionthat exercise does not play an essential part in the induction of acclimatiza-tion to heat (Fox et al. 1963). This aim was partly frustrated by the largedifferences between the groups at the first set of standard tests; however,it can be concluded that exercise during the period of acclimatization hadno effect on the rate at which acclimatization proceeded. These differencesillustrate the variations in the degree of acclimatization that may bepresent in an apparently homogeneous population and underlines thedifficulty of interpreting results obtained from small groups of subjects.Fortunately these differences did not affect the main purpose of the studywhich was concerned with one aspect of the control of thermoregulationand was dependent on comparison within the groups.

Benzinger (1962) has postulated that in man the anterior hypothalamiccentre is a terminal sensory organ for temperature reception which actsas a human thermostat by directly controlling sweating and the vasomotorregulation of cutaneous blood flow. He found that the centre is notspecifically affected by exercise and is uninfluenced by warmth receptorsin the skin but increasingly inhibited by stimulation of the skin coldreceptors as the mean skin temperature falls below 330 C. His maindeparture from the previously held concepts of thermoregulation (Picker-ing, 1958) lies in the much greater importance ascribed to the role of theanterior hypothalamic centre compared with the peripheral mechanisms.

There are two situations in which an alteration of the set point of thethermoregulatory centre has been postulated: one is in fever and the other

392

TEMPERATURE REGULATION AND EXERCISEduring muscular exercise. In a sustained fever regulation of body tem-perature by peripheral vasodilatation and sweating appears to be normalexcept that it is occurring at the higher body temperature (Dubois, 1948;Macpherson, 1959). The evidence for an apparently similar elevation of theset point during muscular exercise came from the work of Nielsen (1938).He showed that the rise in body temperature as a result of exercise wasdetermined by the degree of activity and was uninfluenced by the externalenvironment over a wide range of conditions. These observations havebeen repeatedly confirmed (Asmussen & Nielsen, 1947; Robinson, 1949;Eichna, Park, Nelson, Horvath & Palmes, 1950; Wyndham, Bouwer,Devine & Paterson, 1952; Wyndham, Strydom, Morrison, du Toit &Kraan, 1954; Lind, 1963).The results of the present experiment do not favour the hypothesis of

an elevation of the set point specifically as a result of muscular exercise.If the set point were raised by muscular exercise and the effect was pro-portional to the intensity of the exercise a progressive decrease in sweatloss would have been expected as the work rate was increased in thisexperiment in which body temperature was always elevated to 38.50 C.

In this study sweat loss increased with energy expenditure; this couldbe explained either as an artifact or as evidence that exercise stimulatessweating by a mechanism other than a rise in body temperature. Thepossibility that it is an artifact arises from a number of factors which itwas not possible to control. First, sweat loss was computed withoutcorrections for moisture lost in the breath or metabolic weight loss; bothof these would have increased during exercise. Secondly, it has beenshown that sweating is reduced by skin wetting (Buettner & Holmes,1959; Hertig, Riedesel & Belding, 1961; Collins & Weiner, 1962); in thepresent experiments the subjects were in a relatively drier climate at thehigher levels of energy expenditure because more air had to be blownthrough the suits to maintain their temperatures at 38-5° C. Finally,there was probably a greater stimulus to the sweating mechanism in theworking subjects as a result of their slightly higher mean control tempera-ture augmented by the steeper temperature gradient between core andear which was revealed by the radio pill measurements. On the other hand,the lower skin temperature in the working subjects would have tended toreduce sweat loss. Of these factors only the moisture loss in the breathand the possible effect of reduced skin wetting on sweating seem capableof explaining a substantial part of the observed increase. The moistureloss in the breath might have accounted for up to one third of the observedincrease. Partial drying of the skin may have occurred towards the endof the hour's exposure, especially at the highest work rate, but if this hadbeen an important factor the increase in sweat loss with work rate should

26 Physiol. 171

393

34 PAMELA A. BRADBURY AND OTHERShave been greater at the beginning compared with the end of the 12 daysof heat treatment, because the total sweat losses of the subjects were in-creasing over this period. It therefore seems unlikely that the whole ofthe effect can be explained as an artifact. The alternative explanation thatexercise affects the thermoregulatory mechanism is in agreement with theconclusions of Minard (1963) and Beaumont & Bullard (1963), but iscontrary to those of Benzinger (1962).

This effect of exercise on the thermoregulatory mechanism cannotaccount for the observation that normally during work body temperatureis controlled at an elevated level, the rise depending on the rate of workand being unaffected by the environment over a wide range of conditions(Nielsen, 1938). The elevation of body temperature above normal is inpart explained by the proportional nature of the central controllingmechanism. Thus, as the need for heat elimination increases, so thedeviation from the set point also has to increase. The degree of temperatureelevation is probably also partly explained as follows: the temperaturegradient from the core to the skin surface is determined by the rate ofmetabolic heat production and the rate of blood flow. With a rise inmetabolic heat production the gradient becomes steeper so that skintemperature tends to fall below 330 C. This cooling of the skin will producea partial local suppression of vasodilatation and sweating (Barcroft &Edholm, 1946; Fox, Goldsmith, Hampton & Lewis, 1964) and may alsocause a central depression of heat dissipation through stimulation of thecutaneous cold receptors (Benzinger, 1962). Body temperature would thenrise until equilibrium is re-established by a balance between the opposingactions of, on the one hand, the direct stimulation of the heat-dissipatingcentre by temperature, and on the other, the partial suppression of theperipheral heat dissipating response by skin cooling. This could alsoexplain the apparent absence or only a minimal effect from the environ-ment (Lind, 1963). In both Nielsen's (1938) and Lind's (1963) experimentsthe upper limit of the environmental conditions above which the constantrelation between the rise in deep body temperature and the level ofexercise no longer holds coincides with a rise of skin temperature above330 C. If this explanation is correct it has the unexpected implicationthat when man is working hard in a warm environment his temperatureregulation is the resultant of the opposing actions of the heat conservingand heat dissipating thermoregulatory mechanisms.

SUMMARY

1. The aims of the experiment were to test the effects on sweat loss ofdifferent levels of energy expenditure during controlled hyperthermia at

394

TEMPERATURE REGULATION AND EXERCISE

38.50 C and also to investigate the effect of the different routines on thedevelopment of heat acclimatization.

2. Twenty subjects were divided into five equal groups. Three groupswere acclimatized to heat by twelve daily sessions of 1 hr of controlledhyperthermia while they were either resting or working at one of threedifferent levels of energy expenditure. The other two groups acted ascontrols.

3. All the subjects were tested before and again after the period ofacclimatization in a series of three standard tests to measure the changesin their levels of acclimatization.

4. There were marked differences between the physiological responsesof the groups in the first set of standard tests. This made it difficult toevaluate the effects of working compared with resting on acclimatization,but no obvious difference was observed.

5. The results obtained during the sessions of controlled hyperthermiashowed that sweat losses during work were significantly higher than atrest (P < 001 to < 0-001).

6. The most likely explanation of these observations is that exercisedirectly stimulates sweating.

7. It is suggested that the rise in deep body temperature normallyobserved during exercise is due partly to the proportional nature of thecontrol mechanism and partly to the fall in skin temperature which locallyinhibits the heat dissipating responses.

We wish to thank the officers and men of the 2nd Battalion of the Grenadier Guards whotook part in these experiments.

REFERENCES

ASMUSSEN, E. & NIELSEN, M. (1947). The regulation of body temperature during workperformed with the arms and with the legs. Acta physiol. scand. 14, 373-382.

BARCROFT, H. & EDHOLM, 0. G. (1946). Temperature and blood flow in the human forearm.J. Physiol. 104, 366-376.

BEAUMONT, W. van & BULLARD, R. W. (1963). Sweating, its rapid response to muscularwork. Science, 141, 643-646.

BENZINGER, T. H. (1959). On physical heat regulation and the sense of temperature inman. Proc. nat. Acad. Sci., Wash., 45, 645-659.

BENZINGER, T. H. (1962). The thermostatic regulation of human heat production and heatloss. Proc. XXII int. Congr. Physiol. 415-438.

BUETTNER, K. J. K. & HOLMES, F. F. (1959). Diffusion of water vapour through humanskin in hot environment and with application of atropine. J. appl. Physiol. 14, 276-278.

COLLINS, K. J. & WEINER, J. S. (1962). Observations on arm-bag suppression of sweatingand its relationship to thermal sweat gland fatigue. J. Physiol. 161, 538-556.

DUBOIS, E. F. (1948). Fever and the Regulation of Body Temperature. Springfield, Illinois:Charles C. Thomas.

EICHNA, L. W., PARK, C. R., NELSON, N., HORVATH, S. M. & PALMEs, D. E. (1950). Thermalregulation during acclimatization in a hot, dry (desert type) environment. Amer. J.Physiol. 163, 585-597.

VON EULER, C. & SODERBERG, U. (1958). Coordinated changes in temperature thresholdsfor thermoregulatory reflexes. Acta physiol. scand. 42, 112-129.

395

396 PAMELA A. BRADBURY AND OTHERSFox, R. H., GOLDSMITE, R., HAMPTON, I. F. G. & LEWIs, H. E. (1964). The nature of the

increase in sweating capacity produced by heat acclimatisation. J. Physiol. 171, 368-376.Fox, R. H., GOLDSMITH, R., KIDD, D. J. & LEWIS, H. E. (1963). Acclimatization to heat

in man by controlled elevation of body temperature. J. Physiol. 166, 530-547.Fox, R. H., GOLDSMITH, R. & WOLFF, H. S. (1962). The use of a radio pill to measure deepbody temperature. J. Physiol. 160, 22-23 P.

HERTIG, B. A., RIEDESEL, M. L. & BELDING, H. S. (1961). Sweating in hot baths. J. appl.Physiol. 16, 647-651.

LIND, A. R. (1963). A physiological criterion for setting thermal environmental limits foreveryday work. J. appl. Physiol. 18, 51-56.

LUNDGREN, N. P. V. (1948). A type of cardiovascular step test. Proc. IX Int. Congr. ind.Med. 273-277.

MACPHERSON, R. K. (1959). The effect of fever on temperature regulation in man. Clin.Sci. 18, 281-287.

MINARD, D. (1963). Sweat rate during work and rest at elevated internal temperature.Fed. Proc. 22, 177.

NIELSEN, M. (1938). Die Regulation der Korpertemperatur bei Muskelarbeit. Skan. Arch.Physiol. 79, 193-230.

PICKERING, G. (1958). Regulation of body temperature in health and disease. Lancet, i,1-9.

ROBINSON, S. (1949). Physiological adjustment to heat. In Newburg, L. H. Physiologyof Heat Regulation and the Science of Clothing. Philadelphia: W. B. Saunders.

WYNDHAM, C. H., BOuWER, W. V. DE M., DEVINE, M. G. & PATERSON, H. E. (1952).Physiological responses of African labourers at various saturated air temperatures, windvelocities and rates of energy expenditure. J. appl. Phy8iol. 5, 290-298.

WYNDHAM, C. H., STRYDOM, N. B., MORRISON, J. F., DU Torr, F. D. & KRAAN, J. G. (1954).Responses of unacclimatized men under stress of heat and work. J. appl. Physiol. 6,681-686.