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Department of Clinical Pathophysiology, School of Health Sciences, University of Occupational and Environmental Health, 807-8555 Kitakyushu, Japan
Submitted 24 January 2003 ; accepted in final form 1 May 2003
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ABSTRACT |
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 TOP ABSTRACT METHODSRESULTSDISCUSSIONDISCLOSURESACKNOWLEDGMENTSREFERENCES |
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orthostatic tolerance; skin blood flow; power spectral analysis; blood pressure; exercise training
Two countermeasures at least are proposed to improve the baroreflex control of HR and to prevent orthostatic hypotension under hyperthermic conditions. One potential countermeasure is a reduction of external heat per se, including skin cooling via a water-perfused suit. Yamazaki and Sone (32) showed that whole body skin cooling using a water-perfused suit increases the spontaneous baroreflex response of HR and arterial blood pressure during supine rest and HUT compared with normothermic and whole body heating conditions. Wilson et al. (29) revealed recently that skin-surface cooling prevents a fall in cerebral blood velocity and arterial blood pressure during HUT in heat-stressed humans and results in the improvement of tilt tolerance. Thus cooling of the heated body rapidly increases the tolerance to orthostatic stress, although a special device is needed for the cooling. Another countermeasure is to make a physiological adaptation to heat stress. It has been reported that a heat acclimation program using exercise in a hot environment improves orthostatic tolerance in the heat (22). The improved orthostatic tolerance is related partly to a decrease of core temperature during heating as a result of potentiation of the sweating function. However, it remains unknown whether the increase of orthostatic tolerance in a hot environment after heat acclimation occurs with an adaptive change of cardiac baroreflex function.
In the present study, therefore, to test the hypothesis that exercise-heat acclimation improves the arterial baroreflex control of HR and increases orthostatic tolerance in heated humans, we examined the spontaneous baroreflex response of HR and thermoregulatory responses, including cutaneous vasomotor and sudomotor responses, during whole body heating before and after a 6-day exercise-heat acclimation program.
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METHODS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONDISCLOSURESACKNOWLEDGMENTSREFERENCES |
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Ten healthy adults (2 women and 8 men) participated in this study. Their average age was 22 ± 1 (SE) yr, average weight was 65.8 ± 4.3 kg, and average height was 170 ± 3 cm. All subjects were healthy nonsmokers with no history of cardiovascular disease. They were physically untrained and had not regularly performed a sports activity. The average peak oxygen uptake as evaluated from an incremental exercise test on a cycle ergometer (model 818E, Monark, Stockholm, Sweden) was 40.2 ± 2.7 ml · min-1 · kg-1 (women, 28.1 ± 0.4 ml · min-1 · kg-1; men, 43.3 ± 2.3 ml · min-1 · kg-1) before exercise-heat acclimation. The menstrual cycle in female subjects was evaluated from the recording of basal body temperature, and the experiments were conducted for 8 consecutive days in the follicular phase. In consideration of the effect of natural acclimatization, all experiments were conducted in winter from December to March. Written, informed consent was obtained after a thorough explanation of the present study, including its purpose and risks. The experiments were approved by the Ethics Committee of Medical Care and Research of the University of Occupational and Environmental Health.
Test Protocol
On test days before and after the exercise-heat acclimation program (days 1 and 8), each subject reported to the laboratory at 0900. In a climatic chamber (28°C ambient temperature, 50% humidity), the subject wore a tube-lined water-perfused suit that covered the body except for the head and the arms and was instrumented for the measurement of esophageal temperature (Tes) with a thermocouple. The subject rested supine on a tilt table and was equipped with skin thermocouples, skin electrodes, a cuff and a sensor for arterial tonometry, laser-Doppler flow probes, sweat capsules, and a thermocouple for monitoring of the respiratory pattern.
Heating test. After thermal equilibrium for 50-60 min, a heating test was conducted. The test protocol consisted of a 5-min normothermia and a 45-min heating period in the supine position. By changing the water temperature of the suit, the mean skin temperature (Tsk) was maintained at 
35°C during normothermia and 38.5°C during heating.
HUT test. After the 45-min heating period, a 6-min HUT was conducted during heating. The angle of the tilt table was raised to 75° over 10 s. During the tilt, the arms rested at heart level on shelves fixed to the table. The subjects were instructed not to voluntarily constrict their leg muscles during the tilt. The HUT test was terminated when one of the signs of presyncope was observed such as nausea, grayout, dizziness or a progressive reduction in systolic blood pressure (SBP) to below 75 mmHg. The recovery from the HUT was monitored for 3 min in the supine position.
Exercise-Heat Acclimation Program
The subjects were exposed to exercise-heat for 6 consecutive days (days 2-7) starting on the day after the preacclimation test. The exercise-heat protocol was four bouts of 20-min exercise at 50% peak oxygen uptake separated by 10-min rest periods in a hot environment (36°C, 50% relative humidity). The HR was monitored during the acclimation exposure.
Measurement and Analysis in Pre- and Postacclimation Tests
Tes was measured with a polyethylene-sealed thermocouple swallowed to the level of the heart. Tsk was measured by using copper-constantan thermocouples on the chest, upper back, lower back, abdomen, thigh, and calf, and mean Tsk was calculated (27).
Blood pressure was measured continuously by arterial tonometry (model JENTOW-7700, Colin, Komaki, Japan) by using the right radial artery. Mean arterial pressure (MAP) was one-third of the pulse pressure plus the diastolic blood pressure. HR was determined from the ECG. Laser-Doppler flow was monitored continuously with laser-Doppler flowmeters (model ALF21, Advance, Tokyo, Japan), and the glass-fiber sensor probes were placed at the flexor aspect of the left forearm and dorsal aspect of the left hand. Cutaneous vascular conductance (CVC) was calculated from the ratio of laser-Doppler flow to MAP. The changes in CVC were expressed as a percent change from the value during the pre-heating condition. The ECG, blood pressure, and respiratory waveforms were recorded on a data recorder (model PC208AX, Sony, Tokyo, Japan).
The local sweating rates (SR) for the chest and the left forearm were measured by the ventilated capsule method. Dry air was supplied to the sweat capsules (5.7-cm2 area) at the rate of 2.0 l/min. The humidity of the air flowing out of the capsules was measured with capacitance hygrometers (model HMP 133Y, Vaisala, Helsinki, Finland). The measured variables were recorded by a data logger (model DE1200 Universal, NEC Sanei, Tokyo, Japan) every 5 s. Data were averaged every 5 min during the heating test and for each last minute during the tilting and recovery periods.
Tes thresholds for initiation of sweating and cutaneous vasodilation were calculated by determining the point at which SR and CVC increased abruptly from the values in normothermic control. For the analyses of the responsiveness of HR, SR, and CVC to rising Tes, regression equations were calculated from measurements after 15 min of heating when the mean Tsk reached 38.5°C. The slopes (i.e., regression coefficient) of the linear relationships were compared between the pre- and postacclimation tests.
Power spectral density analysis. The power spectral density of the R-R interval was calculated by a fast Fourier transformation every 5 min during the heating test (VITAL RHYTHM 98III, NEC Medical Systems, Tokyo, Japan). The ECG waveform was sampled at 1,000 Hz, and R-R intervals were detected. The time series of the beat-to-beat R-R interval for 256 s was interpolated at 2 Hz by the Lagrange interpolation method. All analyses were performed between 0.02 and 0.5 Hz (total frequency band). The frequency range between 0.05 and 0.15 Hz was defined as the low-frequency band, and the range between 0.15 and 0.5 Hz was defined as the high-frequency band. The power in the low- and high-frequency bands was normalized by dividing by the power in the total frequency band. The high-frequency power was used as an index of cardiac parasympathetic activity (25).
Arterial baroreflex analysis. The sensitivity of arterial baroreflex control of HR was calculated every 5 min during the heating test and for the last 1 min during the tilting and recovery periods (2, 10, 17, 23, 32). This method permits repeatedly the calculation of the baroreceptor-heart rate reflex sensitivity within the operating range of the baroreceptors without the use of pharmacological agents or mechanical devices. The blood pressure and ECG waveforms were sampled at 1,000 Hz, and spontaneously occurring sequences of three or more consecutive heartbeats were detected during which both SBP and the R-R interval are simultaneously increased or decreased. When baseline HR is changed by a perturbation, the interpretation of cardiac baroreflex response is influenced by whether the dependent variable is expressed as the R-R interval or HR, because the relationship between the R-R interval and HR is a hyperbolic function (3, 16). In the present study, cardiac baroreflex control was analyzed by using both the HR and R-R interval as the dependent variables, because whole body heating or heat acclimation will induce a change of baseline HR. The beat-to-beat HR was calculated from the subsequent R-R interval in which SBP was measured. Only sequences where successive pressure pulses differed by at least 1.0 mmHg were selected. From each of these sequences, linear regressions were calculated for the relationship between SBP and HR (or R-R interval). Only sequences with a correlation coefficient of >0.85 were included. The slope (i.e., regression coefficient) of the linear relationship between SBP and HR (or R-R interval) was used for the sensitivity of cardiac baroreflex control. The slopes were averaged between the increasing and decreasing blood pressure, because no significant difference was observed between the slopes. The number of baroreflex slopes per minute and the percentage of the number of heartbeats used for analysis of the slope to the number of total heartbeats for each analyzed period were calculated.
Statistics
Data are expressed as means ± SE. Change of HR during exercise throughout the acclimation program was analyzed by using a one-way ANOVA for repeated measures. Effects of heating and exercise-heat acclimation were evaluated by using a two-way ANOVA for repeated measures. When significant F-ratios were obtained, least significant differences were calculated for comparisons between means. Effects of heat acclimation on the tilting time, the preheating values of each variable, the Tes thresholds, and the slopes of linear relationships in the responses of HR, SR, and CVC to Tes were determined by using Student's paired t-tests. Regression analysis was performed with the least squares methods. P < 0.05 was considered significant.
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RESULTS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONDISCLOSURESACKNOWLEDGMENTSREFERENCES |
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The HR during exercise decreased rapidly until the fourth day of the program and then decreased slowly until the sixth day. The result that the HR on the sixth day decreased by 22.1 ± 2.7 beats/min (P < 0.05) from the value on the first day indicates physiological adaptation to exercise in the hot environment. HUT induced presyncope in seven subjects in the preacclimation test and in six subjects in the postacclimation test. The average tilting time did not differ significantly between the pre- (241 ± 33 s) and postacclimation (283 ± 24 s) tests (Fig. 2).
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Figure 3 shows the changes of Tes, HR, and MAP in the pre- and postaclimation tests. The exercise-heat acclimation program significantly decreased Tes and HR in normothermia (P < 0.05, paired t-test) and did not decrease them during heating (P = 0.28 and P = 0.18, 2-way ANOVA), whereas it did not alter the magnitude of increases of Tes and HR during heating. HR increased linearly with rising Tes before and after heat acclimation (Figs.3 and 4). The slope of the HR-Tes relationship was similar statistically between the pre- (38.8 ± 4.1 beats · min-1 · °C-1) and the postacclimation (32.8 ± 5.0 beats · min-1 · °C-1) tests (P = 0.46, paired t-test). MAP was not changed significantly by whole body heating and heat acclimation.
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Whole body heating decreased (P < 0.05) the high-frequency power of R-R interval variability but did not change the low-frequency power in the pre- and postacclimation tests (Fig. 5). The exercise-heat acclimation program increased (P < 0.05) the high-frequency power in the preheating condition, whereas it did not change significantly that during the heating condition. In normothermic and heating conditions, the low-frequency power was not altered by heat acclimation.
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Cardiac baroreflex data are summarized in Fig. 6. When HR was used as the dependent variable of cardiac baroreflex response, the baroreflex slope was not changed significantly by whole body heating and heat acclimation (Fig. 6). HUT significantly decreased the baroreflex slope from the normothermic supine level. When R-R interval was used as the dependent variable of cardiac baroreflex response, whole body heating significantly decreased the baroreflex slopes in the pre- and postacclimation tests. Heat acclimation significantly increased the baroreflex slope in the preheating condition (18.2 ± 2.4 ms/mmHg in the preacclimation test, 22.7 ± 2.8 ms/mmHg in the postacclimation test; P < 0.05), but it did not alter those values during heating in the supine position (9.3 ± 0.8 and 11.1 ± 0.9 ms/mmHg during the 40-45 min of heating in the pre- and postacclimation tests, respectively) and the tilting position (2.4 ± 0.2 and 4.2 ± 1.0 ms/mmHg in the pre- and postacclimation tests, respectively). The decreases of baroreflex slope by HUT were similar between the pre- (6.9 ± 0.8 ms/mmHg) and postacclimation (6.9 ± 1.4 ms/mmHg) tests. Heating significantly increased the number of baroreflex sequences in the supine position and during HUT. Also, heating significantly increased the percentage of the number of heartbeats analyzed for the baroreflex slope to the number of total heartbeats in the supine position. The number of baroreflex sequences and the amount of baroreflex data of heartbeats did not differ between the pre- and postacclimation tests.
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Figure 7 depicts the cutaneous vascular and sweating responses to rising Tes at a mean Tsk of 38-39°C during whole body heating. After heat acclimation, the Tes thresholds for cutaneous vasodilation in the forearm and dorsal hand and for initiation of sweating in the forearm and chest were decreased (P < 0.05) compared with those before heat acclimation (Table 1). Heat acclimation did not significantly change the slopes of the relationships between CVC and Tes and between SR and Tes in the nonglabrous skin (Table 1).
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DISCUSSION |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONDISCLOSURESACKNOWLEDGMENTSREFERENCES |
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Shvartz et al. (22) reported that the number of subjects who fainted during tilting in a high-temperature environment gradually decreased during an 8-day exercise-heat acclimation program. In the report, they also revealed an increase of SR and a decrease of core temperature during the heat acclimation program (22). In the present study, however, heat acclimation did not increase significantly tilt tolerance when Tes was increased similarly by using a water-perfused suit in pre- and postacclimation tests, although it tended to increase slightly tilt tolerance (the prolongation of average tilting time by 43 ± 33 s). In the report by Shvartz et al. (22), core temperature was lower by 0.9°C during the tilt test in the eigth day of the program (i.e., the postacclimation tilt test) than that in the first day of the program (i.e., the preacclimation tilt test), which is in contrast to the present study in which no significant difference in Tes was observed immediately before tilting. Thus it is thought that the primary reason for the unchanged tilt tolerance after heat acclimation in the present study is the manipulatively maintained high body temperature during the pre- and postacclimation tests.
It is well documented that heat acclimation decreases HR during heat exposure in humans (6, 22, 26) and experimental animals (9). The pattern of change of HR during the exercise-heat acclimation program in the present study (Fig. 1) was in accordance with the prior finding that the majority of adaptive change of HR in the acclimation process occurs within 5 days, when subjects were exposed for consecutive days in a hot environment (1, 6, 22, 26). Horowitz and Meiri (9) have reported that in rats the heat acclimation-induced bradycardia is attained primarily by increased parasympathetic activity for up to 14 days of heat acclimation. The increased high-frequency power of R-R interval variability in the preheating condition after the 6-day heat acclimation program suggests that an increased vagal activity in the heart occurs during normothermia in the early days of the exercise-heat acclimation process. The short-term heat acclimation significantly decreased Tes in addition to HR in the preheating condition. The slope of the HR-Tes relationship did not differ significantly between pre- and postacclimation tests, and the HR at a given Tes in the preacclimation test was similar with that in the postacclimation test (Fig. 4). These findings suggest the decreased HR after heat acclimation is mediated primarily through the vagal pathway with the decrease in core temperature without a change of autonomic control of HR at a given core temperature in humans.
In healthy human subjects and normal experimental animals, the arterial baroreflex response of HR during heat stress has been reported to be greater (23), not different (3, 5, 8, 30-32), and attenuated (4, 33) compared with that during normothermia. It is likely that the inconsistency of results is partly due to the methodology used for the evaluation of the baroreflex response. For example, Yamazaki et al. (31) and Crandall (3) have reported that acute hyperthermia does not alter the carotid-cardiac baroreflex sensitivity evaluated from the maximal slope of the relationship between HR and carotid distending pressure, whereas it attenuates the tachycardiac response to rapid hypotensive stimulation due to a rise of operating point relative to the responding range in the baroreflex response curve. Our laboratory recently showed, by using the Valsalva maneuver, that heat stress decreases the baroreflex response of HR during a transient falling period of blood pressure, whereas it does not change the baroreflex response during a transient rising period of blood pressure (33). Crandall et al. (4) showed by using transfer function analysis, that whole body heating reduced the gain of baroreflex control of HR changes within a high-frequency range (0.2-0.3 Hz) without affecting the gain in a low-frequency range (0.03-0.15 Hz) and speculated that reduced vagal baroreflex regulation of HR may contribute to reduced orthostatic tolerance during heat stress. In contrast, the spontaneous baroreflex response of HR analyzed in the present study contains the baroreflex responses of HR to SBP changes in both the low- and high-frequency bands and remained unchanged during whole body heating. However, when R-R interval was used as the dependent variable for cardiac baroreflex, the baroreflex slope was reduced 50% by whole body heating. These findings suggest that heat stress decreases the responsiveness of cardiac vagal outflow to baroreceptor stimulation because spontaneous changes of R-R interval are proportional to changes in cardiac vagal activity in anesthetized dogs (11), whereas it does not alter the baroreflex response of "HR" that is meaningful as a factor controlling cardiac output (= HR x stroke volume).
The present study is the first report on the influence of exercise-heat acclimation on cardiac baroreflex control. The result derived from the present study shows that short-term heat acclimation does not change significantly the arterial baroreflex control of HR within the spontaneous changes of blood pressure in normothermia and mild hyperthermia. However, when R-R interval was used as the dependent variable for cardiac baroreflex, the baroreflex slope in normothermia was increased by heat acclimation. This finding suggests that exercise-heat acclimation augments the responsiveness of cardiac vagal activity to baroreceptor stimulation with decreasing baseline HR in normothermia.
Consistent with previous studies (15, 18, 20, 24), the threshold temperatures for vasodilation and sweating in nonglabrous skin were reduced after heat acclimation. Roberts et al. (18) examined the effects of exercise-heat acclimation for 10 days on the relations of forearm blood flow and chest SR to Tes, and they reported that the Tes thresholds for cutaneous vasodilation and sweating were lowered by heat acclimation without significant change in the slope of the relations. It has been postulated that the lowered Tes threshold for sweating after heat acclimation was mainly caused by a central mechanism (15). However, it has been observed during exercise in hot environments that exercise-heat acclimation increases the slope of the relation of forearm vascular conductance or upper arm SR to Tes (20, 24). The reason for the inconsistency of results may be the different methods used in the acclimation (i.e., ambient temperature, intensity and duration of exercise) and heating test (i.e., at rest or during exercise). We cannot eliminate any effects of local Tsk at the measuring points of SR and skin blood flow on the slopes (14, 28), because the local temperature was not controlled strictly. It is likely that the reduction of the threshold temperature for skin vasodilation and sweating with heat acclimation is linked to the decrease of the preheating level of core temperature (Fig. 3). It is speculated that heat acclimation modifies the system controlling heat dissipation response in nonglabrous skin as body temperature is centrally regulated at a lower temperature in the hypothalamus.
In conclusion, short-term heat acclimation increases the vasodilation and sweating responses in nonglabrous skin at a given core temperature with decreasing threshold temperature for the heat dissipation response but does not alter the tilt tolerance and the spontaneous baroreflex response of HR while a high body temperature is maintained during heat stress.
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DISCLOSURES |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONDISCLOSURESACKNOWLEDGMENTSREFERENCES |
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ACKNOWLEDGMENTS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONDISCLOSURESACKNOWLEDGMENTSREFERENCES |
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FOOTNOTES |
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The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
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, Individual data; 
, averaged data.
P < 0.05 compared with the preacclimation test.
