We tested the hypothesis that elevation in heart rate (HR) during submaximal exercise in the heat is related, in part, to increased percentage of maximal O2 uptake (%V˙o 2 max) utilized due to reduced maximal O2 uptake (V˙o 2 max) measured after exercise under the same thermal conditions. Peak O2 uptake (V˙o 2 peak), O2 uptake, and HR during submaximal exercise were measured in 22 male and female runners under four environmental conditions designed to manipulate HR during submaximal exercise and V˙o 2 peak. The conditions involved walking for 20 min at ∼33% of controlV˙o 2 max in 25, 35, 40, and 45°C followed immediately by measurement ofV˙o 2 peak in the same thermal environment. V˙o 2 peak decreased progressively (3.77 ± 0.19, 3.61 ± 0.18, 3.44 ± 0.17, and 3.13 ± 0.16 l/min) and HR at the end of the submaximal exercise increased progressively (107 ± 2, 112 ± 2, 120 ± 2, and 137 ± 2 beats/min) with increasing ambient temperature (Ta). HR and %V˙o 2 peak increased in an identical fashion with increasing Ta. We conclude that elevation in HR during submaximal exercise in the heat is related, in part, to the increase in %V˙o 2 peak utilized, which is caused by reduced V˙o 2 peak measured during exercise in the heat. At high Ta, the dissociation of HR from %V˙o 2 peak measured after sustained submaximal exercise is less than ifV˙o 2 max is assumed to be unchanged during exercise in the heat.
- maximal oxygen uptake
- core temperature
- heat stress
- treadmill exercise
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 (%V˙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 (V˙o 2) during submaximal exercise is not altered much in the heat (21) and thatV˙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 %V˙o 2 max in the heat. However, whether the increase in HR during submaximal exercise is related to reducedV˙o 2 max and, therefore, increased %V˙o 2 max utilized in the heat is uncertain, because no studies have measured HR during submaximal exercise and V˙o 2 max after sustained exercise at high ambient temperatures (Ta).
Two studies (17, 18) have reported a marked (16–25%) reduction inV˙o 2 max in the heat. These reductions were found after mild exercise in the heat that elevated core temperature (Tc) (17, 18). IfV˙o 2 max is reduced during sustained exercise in the heat and V˙o 2 during submaximal exercise is unchanged, then theV˙o 2 at submaximal exercise intensities would represent a higher %V˙o 2 max, and the HR-%V˙o 2 max relation would be dissociated less than if V˙o 2 max is assumed to be unchanged in the heat. The association between HR and %V˙o 2 max is important, because HR is widely used to prescribe exercise intensity on the basis of its relation to %V˙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 (%V˙o 2 peak) utilized caused by reducedV˙o 2 peak measured after exercise at the same Ta. We hypothesized thatV˙o 2 peak would be reduced and %V˙o 2 peak utilized would be increased if they were measured after a period of submaximal exercise in high Ta that elevated Tc (preheating), as shown by Pirnay et al. (18), and that these changes would be associated with the elevation in HR.
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,V˙o 2 max = 64.7 ± 1.6 ml · kg−1 · min−1) and female (n = 11, age = 23.8 ± 1.2 yr, height = 164.8 ± 1.7 cm, mass = 56.0 ± 1.5 kg,V˙o 2 max = 53.9 ± 2.3 ml · kg−1 · min−1) 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 measureV˙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.
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 V˙o 2 peak at four Ta in all subjects. The relation of change in HR (ΔHR) to change in V˙o 2 peak(ΔV˙o 2 peak) and %V˙o 2 peak(Δ%V˙o 2 peak) elicited during submaximal exercise with increasing heat stress was determined.
The study was conducted in an environmental chamber at 50% relative humidity under the following four conditions in which Taand pretest Tc were varied: 1) 25°C with a 20-min walking warm-up at ∼33% of controlV˙o 2 max, 2) 35°C with a 20-min walking warm-up at ∼33% of controlV˙o 2 max, 3) 40°C with a 20-min walking warm-up at ∼33% of controlV˙o 2 max, and 4) 45°C with a 20-min walking warm-up at ∼33% of controlV˙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 controlV˙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 Tc, skin temperature (Tsk), and circulatory strain to different degrees using active preheating before theV˙o 2 peak test. In addition, they were designed to reflect the effects of high Ta 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.
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 Tc, thermistors for measurement of Tsk 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.
The subjects then completed a 20-min walk at ∼33% of controlV˙o 2 max followed by a graded running test to exhaustion. During the exercise,V˙o 2 and other metabolic variables of interest, HR, rectal temperature (Tre), esophageal temperature (Tes), and Tsk, were measured. Metabolic, cardiorespiratory, and temperature measures were recorded every 5 min during the 20-min walk and every 2 min during the graded running test. A metabolic cart (Vmax 29, Sensormedics) was used to measure the metabolic variables over a sampling period of 30 s.V˙o 2 averaged over the final 2 min of the walk and over two consecutive 30-s periods of the graded test were used in the data analysis. Then subjects dried off and measured their nude body weight to determine the amount of weight loss (dehydration).
To elicit V˙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.
Attainment of V˙o 2 max in the control condition was determined by using a modification of the plateauing criterion of Taylor et al. (28). The criterion for determining a plateau was an increase inV˙o 2(ml · kg−1 · min−1) between the last two stages of <50% of the expected increase on the basis of the American College of Sports Medicine metabolic equation (1). The criterion varied depending on treadmill speed and ranged from 1.3 (5.5 miles/h) to 2.2 ml · kg−1 · min−1(9 miles/h). With use of this criterion, all subjects demonstrated a plateau in V˙o 2: 11 during the continuous graded test and 11 during the subsequent run.
Because we hypothesized that a plateau inV˙o 2 might not be demonstrated in the heat if performance was limited by hyperthermia and because follow-up tests were not possible, V˙o 2 peakwas assumed to be obtained for the four tests that followed the 20-min walk if V˙o 2 was equal to theV˙o 2 max in the control condition (within the margin of the plateau criterion, criterion 1) or if HR was within 5 beats/min of that during the control condition (criterion 2). If neither criterion was met, the test was repeated on another day (5 cases) during which one of the above criteria was satisfied. The number of subjects who achievedcriterion 1 (or both criteria) at Ta of 25, 35, 40, and 45°C were 18, 9, 2, and 0, respectively, with the remaining subjects satisfying criterion 2.
Tre was measured with a thermistor (model 4491E, Yellow Springs Instruments) inserted 12 cm beyond the anal sphincter. Tes was measured by using a thermistor (model 4491E, Yellow Springs Instruments) inserted through the nasal cavity and into the esophagus a distance equal to one-fourth of the standing height. Mean Tsk was calculated according to the formula of Burton (4) from measurements of Tsk with thermistors (model 409B, Yellow Springs Instruments) on the forearm, beneath the scapula, and on the thigh. All thermistors were connected to a telethermometer (model 44TD or 4600, Yellow Springs Instruments). The accuracy of all thermistors was verified using water baths of various temperatures before use.
HR was measured using a Polar Vantage XL HR monitor (model 145900). Rating of perceived exertion (RPE) was measured using Borg's 15-point category scale (3). Finally, body weight was measured to the nearest 0.02 kg with an electronic scale (model FW-150KA1, A & D).
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 Ta for the metabolic, cardiorespiratory, mean Tsk, and RPE measures. A one-way repeated-measures analysis of covariance, with the resting Tc held constant, was used to determine the significance of differences among the measures under the different environmental conditions for the Tc 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 α-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.
Data on maximal metabolic, circulatory, temperature, performance, and perceptual measures from the graded exercise test are contained in Table 1.V˙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 inV˙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 inV˙o 2 peak, because weight loss was <0.7% of body weight. The reduction inV˙o 2 peak from control was related to a progressive increase in Tes (r = −0.57,P < 0.05) and mean Tsk (r= −0.77, P < 0.05) as Ta increased.
The metabolic, circulatory, and temperature data at the end of 20 min of submaximal exercise are presented in Table2. V˙o 2 was significantly lower by 2–4% in the heat (35, 40, and 45°C) than in the thermoneutral environment (25°C), but the differences inV˙o 2 among conditions with increased Ta were not significant. Mean Tsk increased with increasing environmental temperature. Tes and Tre, on the other hand, did not change much until 45°C (although Tes 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 Ta (Fig. 1). For the four conditions, HR increased progressively between minutes 5 and20 by an average of 7, 8, 16, and 30 beats/min, respectively, reflecting the combined effects of cardiovascular drift and heat stress. V˙o 2 as a percentage of the control-test V˙o 2 max(%V˙o 2 max) was slightly lower in the heat (Fig. 1), reflecting the reduced submaximalV˙o 2. However, whenV˙o 2 was expressed as %V˙o 2 peak measured after 20 min of submaximal exercise in each of the thermal conditions, %V˙o 2 peak during submaximal exercise increased in a curvilinear fashion with increasing Ta (Fig.1). The mean discrepancy between %V˙o 2 peak and %V˙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 %V˙o 2 peak and %V˙o 2 max is presented in Fig.2. The comparison illustrates the tendency for HR at high Ta to be associated with higher %V˙o 2 peak than %V˙o 2 max.
ΔHR calculated at the end of the submaximal exercise in the heat from the HR in the thermoneutral condition (25°C, ΔHR = HRheat − HR25°C) correlated significantly with the reduction inV˙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 %V˙o 2 peak as well as changes unrelated to changes in %V˙o 2 peak. For example, ΔHR from control was significantly related to increases in Tes (r = 0.68) and mean Tsk(r = 0.82), even after controlling for Δ%V˙o 2 peak (partial r= 0.36 and 0.71, P < 0.05). The correlations between ΔHR and Δ%V˙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 ΔHR to the decrease inV˙o 2 peak were less within the conditions and roughly parallel: 0.55–0.61 (mean 0.58) beats · min−1 · %−1. Thus, on average, each 1% decrease inV˙o 2 peak was associated with an increase in HR of ∼0.6 beats/min.
We found that, during sustained, low-intensity exercise in the heat, increased HR is related, in part, to increased %V˙o 2 peak utilized, which is caused by reduced V˙o 2 peak measured immediately after 20 min of low-intensity exercise at the same Ta. As Ta was progressively increased from 25 to 45°C, the mean HR during submaximal exercise and the mean %V˙o 2 peak utilized increased in an identical fashion. However, because the ΔHR-ΔV˙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 Ta increased. Nevertheless, these results support our hypothesis that, during sustained, low-intensity exercise in the heat, increased HR is related, in part, to reducedV˙o 2 peak measured in the heat and indicate that the dissociation of HR from %V˙o 2 peak during exercise in the heat is less than if V˙o 2 max is assumed to be unchanged.
The responses of V˙o 2, mean Tsk, Tre, Tes, and HR during submaximal exercise with increasing Ta were similar to those reported previously. V˙o 2 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 %V˙o 2 peak that were slightly less than they would have been ifV˙o 2 was unchanged. Mean Tskincreased progressively and reflected Ta as expected. Tre and Tes 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 Tc 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 Ta 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 Tcincreases, 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 Tc and Tsk, and circulatory changes mediated by the baroreflexes (16). During submaximal exercise at a given intensity, the rise in HR is independent of a change inV˙o 2; there is a parallel shift to the left of the regression of HR on V˙o 2 as Ta is increased above thermoneutral (∼25°C), with the increase in HR at a given exercise intensity averaging ∼1 beat · min−1 · °C−1change in Ta between 25 and 45°C (12, 20,30). Increases in ambient vapor pressure at a given Ta 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 Tes and Tre at the end of 20 min of walking.
Whether V˙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 V˙o 2 max during heat stress, when Tc was elevated before theV˙o 2 max test. The results of the present study support both findings. With moderate levels of heat stress (Ta = 35 and 40°C) and active preheating that resulted in moderate increases in Tc and mean Tsk, small reductions were found inV˙o 2 max. However, with greater heat stress (45°C) and active preheating that resulted in higher levels of Tc and mean Tsk, large reductions were observed in V˙o 2 max, probably due to a very high level of circulatory strain (19). During brief periods of maximal exercise in the heat, V˙o 2 max is typically not markedly reduced, because the skin may vasoconstrict at high intensities as V˙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 Tc may not reach (or reach only late in the exercise) the reset level of this relation. Under conditions in which Tc and Tsk are increased by sustained exercise (active preheating) before the measurement ofV˙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, andV˙o 2 max is reduced roughly in proportion to the rise in Tc and mean Tsk (17,18), as in the present study. It may be that, under conditions of high level of cardiovascular strain associated with high Tsk and Tc, 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 %V˙o 2 max is stronger than toV˙o 2, probably because the stimuli that increase autonomic nervous system activity and Tc(5), the primary factors that affect HR during exercise, are most closely linked to %V˙o 2 max(19, 23).
Several studies have reported increased HR during submaximal exercise in the heat with no change or a reduction inV˙o 2 during submaximal exercise and no reduction in V˙o 2 max, indicating dissociation in the relation of HR to %V˙o 2 max (20, 22, 30). We found that V˙o 2 peak measured immediately after 20 min of submaximal exercise in high Ta was reduced, and, as a result, the calculated %V˙o 2 peak utilized during walking was increased compared with a thermoneutral environment if %V˙o 2 peak was calculated usingV˙o 2 peak measured immediately after submaximal exercise, but not if %V˙o 2 max was calculated using the control V˙o 2 max. The effect of reducedV˙o 2 peak on the %V˙o 2 peak utilized compared with the effect if %V˙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 %V˙o 2 peak at high Ta means that the dissociation of HR from %V˙o 2 peak is less than if it is assumed that V˙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 inV˙o 2 peak measured immediately after the exercise in the same Ta. The remainder of the increase was related to factors not associated with alteredV˙o 2 peak. Thus there was still substantial dissociation of HR from %V˙o 2 peak, and the relation of %V˙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 %V˙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 %V˙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 Δ%V˙o 2 peak corresponding to a one-beat ΔHR is much less in the heat. Alternatively, with progressive increases in Ta, HR increases more with a given increase in %V˙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 %V˙o 2 peak and reinforce the conclusion by others (12) that the normal HR-%V˙o 2 max relation under thermoneutral conditions on which predictions ofV˙o 2 max and exercise prescriptions are based is not applicable during exercise in the heat.
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 V˙o 2 elicited. IfV˙o 2 max is assumed to be unchanged in the heat, then the calculated %V˙o 2 maxutilized 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 Ta, the reduction in the %V˙o 2 peak utilized when exercising at the same HR as in a thermoneutral environment would not be as great as previously assumed, because V˙o 2 peak is substantially reduced under these conditions, and, therefore, the %V˙o 2 peak is higher than if no change in V˙o 2 max is assumed.
Because relative exercise intensity (%V˙o 2 max) is thought to be an important component of the training stimulus for increasingV˙o 2 max (29), similar percent improvements in V˙o 2 max might be expected after training at a given %V˙o 2 max in the heat and in a thermoneutral environment, despite the lower absoluteV˙o 2 elicited. However, the increase inV˙o 2 max with training in warm (35°C) compared with cold (20°C) water at the same absoluteV˙o 2, but different (∼25 beats/min) HR, was the same (31, 32), suggesting that the lower absoluteV˙o 2 elicited at the same %V˙o 2 max in the heat provides less of a stimulus for increasing V˙o 2 max with training. Unfortunately, V˙o 2 max was only assessed in air in a thermoneutral environment;V˙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 V˙o 2 max in a hot climate in which V˙o 2 max is reduced.
We conclude that elevation in HR during submaximal exercise in the heat is related, in part, to increased %V˙o 2 peak utilized, which is caused by reduced V˙o 2 peak measured during exercise in the heat. At high Ta, the dissociation of HR from %V˙o 2 peak measured after sustained submaximal exercise is less than ifV˙o 2 max is assumed to be unchanged during exercise in the heat.
We thank the subjects for their enthusiasm and willingness to participate in the study. We also thank Monika Strychova, Justin Shepard, Tom Rogozinski, and Derek Hales for invaluable help with the data collection.
Address for reprint requests and other correspondence: S.Á. Arngrı́msson, Div. of Sport and Physical Education, Iceland University of Education, Lindarbraut 4, 840 Laugarvatn, Iceland (E-mail:).
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.
First published September 27, 2002;10.1152/japplphysiol.00508.2002
- Copyright © 2003 the American Physiological Society