INTRODUCTION

TOP ABSTRACT INTRODUCTION METHODS RESULTS DISCUSSION REFERENCES

HEART RATE (HR) increases linearly as a function of exercise intensity in a thermoneutral environment and is closely related to the percentage of maximal O₂ uptake (%O_2 max) elicited (2, 19). Heat stress increases HR at rest and at submaximal exercise intensities (12, 13, 20-22, 30) as a result of a direct local effect of blood temperature on the sinoatrial node and altered autonomic nervous system activity (8, 10). However, most studies have reported that O₂ uptake (O₂) during submaximal exercise is not altered much in the heat (21) and that O_2 max is unchanged (20, 22, 25, 30) or reduced only slightly (6, 14, 18, 21, 24-28). These findings indicate that HR is dissociated from %O_2 max in the heat. However, whether the increase in HR during submaximal exercise is related to reduced O_2 max and, therefore, increased %O_2 max utilized in the heat is uncertain, because no studies have measured HR during submaximal exercise and O_2 max after sustained exercise at high ambient temperatures (T_a).

Two studies (17, 18) have reported a marked (16-25%) reduction in O_2 max in the heat. These reductions were found after mild exercise in the heat that elevated core temperature (T_c) (17, 18). If O_2 max is reduced during sustained exercise in the heat and O₂ during submaximal exercise is unchanged, then the O₂ at submaximal exercise intensities would represent a higher %O_2 max, and the HR-%O_2 max relation would be dissociated less than if O_2 max is assumed to be unchanged in the heat. The association between HR and %O_2 max is important, because HR is widely used to prescribe exercise intensity on the basis of its relation to %O_2 max.

Therefore, the aim of this study was to determine whether the elevation in HR resulting from submaximal exercise in the heat is related to increased percentage of peak O₂ uptake (%O_2 peak) utilized caused by reduced O_2 peak measured after exercise at the same T_a. We hypothesized that O_2 peak would be reduced and %O_2 peak utilized would be increased if they were measured after a period of submaximal exercise in high T_a that elevated T_c (preheating), as shown by Pirnay et al. (18), and that these changes would be associated with the elevation in HR.

	METHODS

TOP ABSTRACT INTRODUCTION METHODS RESULTS DISCUSSION REFERENCES

Subjects. Twenty-two healthy, endurance-trained male (n = 11, age = 23.1 ± 1.4 yr, height = 178.2 ± 1.3 cm, mass = 70.1 ± 2.6 kg, O_2 max = 64.7 ± 1.6 ml · kg¹ · min¹) and female (n = 11, age = 23.8 ± 1.2 yr, height = 164.8 ± 1.7 cm, mass = 56.0 ± 1.5 kg, O_2 max = 53.9 ± 2.3 ml · kg¹ · min¹) runners and triathletes served as subjects. The men and women had run 72.4 ± 12.8 and 59.5 ± 10.7 km/wk, respectively, for 6 wk and were accustomed to exercising in a hot environment. We used trained runners accustomed to the heat as subjects so that they would be able to perform the strenuous exercise needed to measure O_2 peak in the heat without adverse consequences. Participation was voluntary, and subjects were paid on completion of the study. The study was approved by the University's Institutional Review Board, and written consent was obtained before testing.

Experimental design. A repeated-measures experimental design in which subjects served as their own control was used. HR was measured at the end of 20 min of treadmill walking at a light intensity followed immediately by measurement of  O_2 peak at four T_a in all subjects. The relation of change in HR (HR) to change in O_2 peak (O_2 peak) and %O_2 peak (%O_2 peak) elicited during submaximal exercise with increasing heat stress was determined.

Treatments. The study was conducted in an environmental chamber at 50% relative humidity under the following four conditions in which T_a and pretest T_c were varied: 1) 25°C with a 20-min walking warm-up at ~33% of control O_2 max, 2) 35°C with a 20-min walking warm-up at ~33% of control O_2 max, 3) 40°C with a 20-min walking warm-up at ~33% of control O_2 max, and 4) 45°C with a 20-min walking warm-up at ~33% of control O_2 max. Holding relative humidity constant meant that ambient vapor pressure increased from 35 Torr at 25°C to 55 Torr at 45°C. A control O_2 max test (in 25°C, 50% relative humidity) was conducted before the treatments, which then were carried out in a random order. The conditions were designed to elevate T_c, skin temperature (T_sk), and circulatory strain to different degrees using active preheating before the O_2 peak test. In addition, they were designed to reflect the effects of high T_a on cardiovascular function during a modest bout of walking someone might perform for exercise. All subjects were tested at the same time of the day to minimize the effects of circadian rhythm on HR, and 2 days passed between testing of the same subject.

Test protocol. Subjects reported to the laboratory after a 3-h fast but well hydrated. They were instructed not to consume alcohol or drugs 48 h before testing, not to consume caffeine 12 h before testing, and to drink water and other noncaffeinated beverages liberally. On the morning of the test, subjects completed a 24-h history questionnaire designed to determine adherence to pretest instructions. Then skinfold thickness measures were taken for estimation of body fat (only done in the control test), and subjects measured their nude body weight. Next, subjects inserted rectal and esophageal thermistors for measurement of T_c, thermistors for measurement of T_sk were attached, and a strap containing the electrodes and transmitter for an HR monitor was placed around the chest. While being prepped, the subjects ingested water at room temperature to compensate for the estimated sweat loss that would occur during the 20-min walk. The amount of water ingested was estimated from pilot studies of weight loss of male and female runners who performed the protocol before the study.

Test procedures. To elicit O_2 max, subjects ran on the treadmill to exhaustion at a constant speed, with the grade increasing 2% every 2 min. A speed was chosen to exhaust subjects in 6-15 min of exercise. In the control test, after completion of the graded test, all subjects rested for 20 min and then ran to exhaustion at a grade 2% higher than the grade at the end of the graded test. The same protocol was used under all thermal conditions, except the follow-up run to exhaustion was not performed during the trials preceded by a 20-min walk because of concern for possible heat injury. Verbal encouragement was used on all tests to urge subjects to give maximal effort.

1

1

1

1

Statistical analysis. Statistical analyses were done with SPSS 10 for Windows (SPSS, Chicago, IL). Values are means ± SE. A one-way repeated-measures ANOVA was used to determine the significance of differences among the measures at different T_a for the metabolic, cardiorespiratory, mean T_sk, and RPE measures. A one-way repeated-measures analysis of covariance, with the resting T_c held constant, was used to determine the significance of differences among the measures under the different environmental conditions for the T_c measures. Simple contrasts (paired-samples t-tests) were used to determine differences between conditions. Simple linear regression and correlation were used to examine relations between measures. A two-tailed -level of 0.05 was used for all significance tests. The significance level was adjusted by using the modified Bonferroni adjustment for the family of contrasts performed.

	RESULTS

TOP ABSTRACT INTRODUCTION METHODS RESULTS DISCUSSION REFERENCES

Data on maximal metabolic, circulatory, temperature, performance, and perceptual measures from the graded exercise test are contained in Table 1. O_2 peak measured after 20 min of walking was significantly lower in the heat (Table 1) than in the neutral environment by 4% at 35°C, 9% at 40°C, and 17% at 45°C. Performance time (exercise time during the graded maximal test) was also reduced in the heat. The reduction in O_2 peak was not due to lack of effort in the heat, because indicators of maximal effort suggested that a maximal effort was given under all conditions. Mean maximal HR was within 5 beats/min in all conditions, respiratory exchange ratio was always 1.1, and, RPE was ~19 in all conditions. Dehydration also was an unlikely contributor to the reductions in O_2 peak, because weight loss was <0.7% of body weight. The reduction in O_2 peak from control was related to a progressive increase in T_es (r = 0.57, P < 0.05) and mean T_sk (r = 0.77, P < 0.05) as T_a increased.

The metabolic, circulatory, and temperature data at the end of 20 min of submaximal exercise are presented in Table 2. O₂ was significantly lower by 2-4% in the heat (35, 40, and 45°C) than in the thermoneutral environment (25°C), but the differences in O₂ among conditions with increased T_a were not significant. Mean T_sk increased with increasing environmental temperature. T_es and T_re, on the other hand, did not change much until 45°C (although T_es was higher in 40°C than in 25°C), during which they were higher than in the other conditions (Table 2). HR increased progressively in a curvilinear fashion with increasing T_a (Fig. 1). For the four conditions, HR increased progressively between minutes 5 and 20 by an average of 7, 8, 16, and 30 beats/min, respectively, reflecting the combined effects of cardiovascular drift and heat stress. O₂ as a percentage of the control-test O_2 max (%O_2 max) was slightly lower in the heat (Fig. 1), reflecting the reduced submaximal O₂. However, when O₂ was expressed as %O_2 peak measured after 20 min of submaximal exercise in each of the thermal conditions, %O_2 peak during submaximal exercise increased in a curvilinear fashion with increasing T_a (Fig. 1). The mean discrepancy between %O_2 peak and %O_2 max ranged from 1.4% at 35°C to 6.7% at 45°C. A comparison of the scatter diagrams of the relation of HR at the end of submaximal exercise to %O_2 peak and %O_2 max is presented in Fig. 2. The comparison illustrates the tendency for HR at high T_a to be associated with higher %O_2 peak than %O_2 max.

View larger version (16K): [in this window] [in a new window]   Fig. 1.   Changes in heart rate and percentage of control maximal O2 uptake (%O2 max) with increasing environmental temperature. %O2 peak, percentage of measured peak O2 uptake. bpm, Beats/min.

View larger version (13K): [in this window] [in a new window]   Fig. 2.   Scatter diagram of relation of heart rate at the end of 20 min of submaximal exercise to %O2 peak (A) and %O2 max (B).

HR calculated at the end of the submaximal exercise in the heat from the HR in the thermoneutral condition (25°C, HR = HR_heat  HR_25°C) correlated significantly with the reduction in O_2 peak measured immediately after the 20 min of submaximal exercise in the heat (r = 0.79; Fig. 3). This correlation is inflated, however, because data from the different conditions are combined. The increase in HR across conditions would reflect changes linked to changes in %O_2 peak as well as changes unrelated to changes in %O_2 peak. For example, HR from control was significantly related to increases in T_es (r = 0.68) and mean T_sk (r = 0.82), even after controlling for %O_2 peak (partial r = 0.36 and 0.71, P < 0.05). The correlations between HR and %O_2 peak within a thermal condition were lower (r = 0.32-0.42) and not statistically significant, in part because of the restricted range of values within any condition. The slopes from the regression equations describing the relation of HR to the decrease in O_2 peak were less within the conditions and roughly parallel: 0.55-0.61 (mean 0.58) beats · min¹ · %¹. Thus, on average, each 1% decrease in O_2 peak was associated with an increase in HR of ~0.6 beats/min.

View larger version (19K): [in this window] [in a new window]   Fig. 3.   Relation of elevations in heart rate during submaximal exercise above heart rate in 25°C to reductions in O2 peak in the heat. Solid lines, individual regression lines within a temperature condition; dashed line, common regression line. Heart rate, change in heart rate in the heat from 25°C; O2 peak decrease, reduction in O2 peak in the heat expressed as a percentage of control O2 max. For 35°C, y = 0.59x + 2.48 (r = 0.32); for 40°C, y = 0.61x + 8.47 (r = 0.32); for 45°C, y = 0.55x + 20.92 (r = 0.42); for the common regression line, y = 1.46x + 1.84 (r = 0.79).

	DISCUSSION

TOP ABSTRACT INTRODUCTION METHODS RESULTS DISCUSSION REFERENCES

We found that, during sustained, low-intensity exercise in the heat, increased HR is related, in part, to increased %O_2 peak utilized, which is caused by reduced O_2 peak measured immediately after 20 min of low-intensity exercise at the same T_a. As T_a was progressively increased from 25 to 45°C, the mean HR during submaximal exercise and the mean %O_2 peak utilized increased in an identical fashion. However, because the HR-O_2 peak relation was not described by a single common regression line across conditions, other factors also contributed to the rise in HR during submaximal exercise as T_a increased. Nevertheless, these results support our hypothesis that, during sustained, low-intensity exercise in the heat, increased HR is related, in part, to reduced O_2 peak measured in the heat and indicate that the dissociation of HR from %O_2 peak during exercise in the heat is less than if O_2 max is assumed to be unchanged.

The responses of O₂, mean T_sk, T_re, T_es, and HR during submaximal exercise with increasing T_a were similar to those reported previously. O₂ during submaximal exercise has been reported to be unchanged or slightly lower or higher (21). The small decrease of ~50 ml/min we observed during the hot conditions was of little practical consequence but resulted in increases in %O_2 peak that were slightly less than they would have been if O₂ was unchanged. Mean T_sk increased progressively and reflected T_a as expected. T_re and T_es changed little during the 20 min of submaximal exercise at 35 and 40°C but increased by ~0.5°C at 45°C. This pattern of findings is similar to that reported by Lind (15), with T_c remaining constant at a level proportional to the metabolic rate across a wide range of thermal conditions but increasing above some critical level when heat stress becomes uncompensable.

HR at the end of 20 min of treadmill walking increased exponentially with increasing heat stress. As T_a increased from 25 to 45°C and ambient vapor pressure increased from 35 to 55 Torr (50% relative humidity), HR increased a total of 30 beats/min. This response is consistent with other studies. Many studies have shown that HR is higher at rest (11) and at submaximal exercise intensities (12, 20-22, 30) in the heat than in a thermoneutral environment. The elevated HR in the heat is due to vagal withdrawal, increased sympathetic nervous system activity, and, when T_c increases, a direct local effect of increased core (blood) temperature on the sinoatrial node (8, 10, 11). Circulatory control by the autonomic nervous system during exercise in the heat reflects inputs to the brain from a variety of sources, including mechanoreceptors and metaboreceptors in active skeletal muscle, providing information concerning relative exercise intensity, other brain centers, including those receiving and integrating information on T_c and T_sk, and circulatory changes mediated by the baroreflexes (16). During submaximal exercise at a given intensity, the rise in HR is independent of a change in O₂; there is a parallel shift to the left of the regression of HR on O₂ as T_a is increased above thermoneutral (~25°C), with the increase in HR at a given exercise intensity averaging ~1 beat · min¹ · °C¹ change in T_a between 25 and 45°C (12, 20, 30). Increases in ambient vapor pressure at a given T_a further increase HR during exercise (13). Furthermore, Lind (15) showed that when heat stress becomes uncompensable, HR during submaximal exercise increases disproportionately with increasing levels of heat stress. In our study, heat stress was clearly uncompensable at 45°C, as evidenced by the substantially increased T_es and T_re at the end of 20 min of walking.

Whether O_2 max is reduced as a result of heat stress has been debated. Some studies report no change (20, 22, 25, 30), whereas others have reported small or modest reductions on the order of 150-350 ml/min or 3-8% (6, 14, 18, 21, 24-28). Two studies (17, 18) have found marked reductions (16-25% or 750-985 ml/min) in O_2 max during heat stress, when T_c was elevated before the O_2 max test. The results of the present study support both findings. With moderate levels of heat stress (T_a = 35 and 40°C) and active preheating that resulted in moderate increases in T_c and mean T_sk, small reductions were found in O_2 max. However, with greater heat stress (45°C) and active preheating that resulted in higher levels of T_c and mean T_sk, large reductions were observed in O_2 max, probably due to a very high level of circulatory strain (19). During brief periods of maximal exercise in the heat, O_2 max is typically not markedly reduced, because the skin may vasoconstrict at high intensities as O_2 max is approached, protecting muscle blood flow and elevating maximal stroke volume and cardiac output to the same levels observed under thermoneutral conditions (19). Furthermore, the rightward shift of the skin blood flow-internal temperature relation that occurs with exercise (10) may not occur during brief periods of maximal exercise, because T_c may not reach (or reach only late in the exercise) the reset level of this relation. Under conditions in which T_c and T_sk are increased by sustained exercise (active preheating) before the measurement of O_2 max in the heat, skin vasodilation occurs (rightward shift of the skin blood flow-internal temperature relation), relative skin vasoconstriction may be less, and O_2 max is reduced roughly in proportion to the rise in T_c and mean T_sk (17, 18), as in the present study. It may be that, under conditions of high level of cardiovascular strain associated with high T_sk and T_c, extensive skin vasodilation resulting in reduced central blood volume and stroke volume cannot be reversed, as suggested many years ago by Williams et al. (30).

HR increases fairly linearly with increased exercise intensity in a thermoneutral environment (2, 19). The relation of HR to %O_2 max is stronger than to O₂, probably because the stimuli that increase autonomic nervous system activity and T_c (5), the primary factors that affect HR during exercise, are most closely linked to %O_2 max (19, 23).

Several studies have reported increased HR during submaximal exercise in the heat with no change or a reduction in O₂ during submaximal exercise and no reduction in O_2 max, indicating dissociation in the relation of HR to %O_2 max (20, 22, 30). We found that O_2 peak measured immediately after 20 min of submaximal exercise in high T_a was reduced, and, as a result, the calculated %O_2 peak utilized during walking was increased compared with a thermoneutral environment if %O_2 peak was calculated using O_2 peak measured immediately after submaximal exercise, but not if %O_2 max was calculated using the control O_2 max. The effect of reduced O_2 peak on the %O_2 peak utilized compared with the effect if %O_2 max was assumed to be unchanged in the heat was on average very small, however, at 35 and 40°C (1.5-3.1 points) and modest at 45°C (6.7 points). The higher %O_2 peak at high T_a means that the dissociation of HR from %O_2 peak is less than if it is assumed that O_2 max is not reduced in the heat.

Only a portion of the increase in HR during submaximal exercise in the heat above that observed in 25°C was related to the decrease in O_2 peak measured immediately after the exercise in the same T_a. The remainder of the increase was related to factors not associated with altered O_2 peak. Thus there was still substantial dissociation of HR from %O_2 peak, and the relation of %O_2 peak to HR across the different thermal conditions in this study was quite different from the normal relation based on data at different metabolic intensities under thermoneutral conditions (7) (Fig. 4). The linear regression equation describing the relation of %O_2 peak (y) to HR during the 20-min walk expressed as percentage of maximum HR (x) is as follows: y = 0.33x + 14.75. The equation of the same relation based on %O_2 max is as follows: y = 0.05x + 29.21. Franklin (7) described the same relation under thermoneutral conditions but with varying exercise intensity as y = 1.31x  43.5. The difference in the slopes in these equations indicates that the %O_2 peak corresponding to a one-beat HR is much less in the heat. Alternatively, with progressive increases in T_a, HR increases more with a given increase in %O_2 peak than in a thermoneutral environment. These data indicate that a majority of the increased HR during exercise in the heat is related to factors other than those linked to %O_2 peak and reinforce the conclusion by others (12) that the normal HR-%O_2 max relation under thermoneutral conditions on which predictions of O_2 max and exercise prescriptions are based is not applicable during exercise in the heat.

View larger version (17K): [in this window] [in a new window]   Fig. 4.   Relation of %O2 peak (y = 0.33x + 14.75) and %O2 max (y = 0.05x + 29.21) to heart rate as percentage of maximum at the end of 20 min of submaximal exercise in the heat. Franklin (7), regression equation published by Franklin (7) (y = 1.31x  43.5).

Our findings have practical implications for exercise prescription in the heat. The general advice regarding exercise in the heat has been to stay within the target HR zone, because HR is sensitive to heat stress and provides an index of the overall physiological strain (9). Because HR at submaximal intensities is elevated in the heat, exercise intensity must be reduced to maintain the same HR as in a thermoneutral environment. Reduction of the exercise intensity lowers the O₂ elicited. If O_2 max is assumed to be unchanged in the heat, then the calculated %O_2 max utilized also is lower during exercise at the same HR in the heat than in a thermoneutral environment. The findings of our study do not change this conclusion but indicate that, during sustained low-intensity exercise at high T_a, the reduction in the %O_2 peak utilized when exercising at the same HR as in a thermoneutral environment would not be as great as previously assumed, because O_2 peak is substantially reduced under these conditions, and, therefore, the %O_2 peak is higher than if no change in O_2 max is assumed.

Because relative exercise intensity (%O_2 max) is thought to be an important component of the training stimulus for increasing O_2 max (29), similar percent improvements in O_2 max might be expected after training at a given %O_2 max in the heat and in a thermoneutral environment, despite the lower absolute O₂ elicited. However, the increase in O_2 max with training in warm (35°C) compared with cold (20°C) water at the same absolute O₂, but different (~25 beats/min) HR, was the same (31, 32), suggesting that the lower absolute O₂ elicited at the same %O_2 max in the heat provides less of a stimulus for increasing O_2 max with training. Unfortunately, O_2 max was only assessed in air in a thermoneutral environment; O_2 max in the warm water may have been reduced. Additional studies are needed to determine whether the absolute or relative metabolic intensity is a more important stimulus for increasing O_2 max in a hot climate in which O_2 max is reduced.

We conclude that elevation in HR during submaximal exercise in the heat is related, in part, to increased %O_2 peak utilized, which is caused by reduced O_2 peak measured during exercise in the heat. At high T_a, the dissociation of HR from %O_2 peak measured after sustained submaximal exercise is less than if O_2 max is assumed to be unchanged during exercise in the heat.