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J Appl Physiol 100: 414-420, 2006. First published October 20, 2005; doi:10.1152/japplphysiol.00541.2005
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Relationship between ventilatory response and body temperature during prolonged submaximal exercise

Keiji Hayashi,1 Yasushi Honda,1 Takeshi Ogawa,1 Narihiko Kondo,2 and Takeshi Nishiyasu1

1Institute of Health and Sports Science, University of Tsukuba, Tsukuba City; and 2Faculty of Human Development, Kobe University, Kobe, Japan

Submitted 9 May 2005 ; accepted in final form 19 September 2005


   ABSTRACT
TOP
 ABSTRACT
METHODS
 RESULTS
 DISCUSSION
 GRANTS
 ACKNOWLEDGMENTS
 REFERENCES
 
We examined whether an increase in skin temperature or the rate of increase in core body temperature influences the relationship between minute ventilation (VE) and core temperature during prolonged exercise in the heat. Thirteen subjects exercised for 60 min on a cycle ergometer at 50% of peak oxygen uptake while wearing a suit perfused with water at 10°C (T10), 35°C (T35), or 45°C (T45). During the exercise, esophageal temperature (Tes), skin temperature, heart rate (HR), VE, tidal volume, respiratory frequency (f), respiratory gases, blood pressure (BP), and blood lactate were all measured. We found that oxygen uptake, carbon dioxide output, BP, and blood lactate did not differ among the sessions. Tes, HR, VE, and f remained nearly constant from minute 10 onward in the T10 session, but all of these parameters progressively increased in the T35 and T45 sessions, and significantly higher levels were seen in the T45 than the T35 session. For all but two subjects in the T35 and T45 sessions, plotting VE as a function of Tes revealed no threshold for hyperventilation; instead, increases in VE were linearly related to Tes, and there were no significant differences in the slopes or intercepts between the T35 and T45 sessions. Thus, during prolonged submaximal exercise in the heat, VE increases with core temperature, and the influences of skin temperature and the rate of increase in Tes on the relationship between VE and Tes are apparently small.

core temperature; skin temperature; ventilation; respiration

IT IS THOUGHT THAT DURING exercise, ventilation is stimulated by several factors, including output from central command, input from active muscles, and input from central and peripheral chemoreceptors, among others (2, 9, 21, 35, 45). It also has been reported that increases in body temperature stimulate ventilation both during exercise (9, 10, 14, 17, 31, 39) and when at rest (3, 4, 6, 13, 16, 24, 38, 40, 42). In that regard, our laboratory previously showed that cooling the lower body after exercise in the heat decreases both core temperature and skin temperature (Tsk), which in turn reduces minute ventilation (VE) during subsequent exercise in the heat (17). However, it is unclear from that study whether it was the reduction of Tsk or core temperature that mediated the reduction in VE. Nybo and Nielsen (31) suggested that an increase in core temperature is the best predictor of increased VE during exercise in the heat, but VE is reportedly also sensitive to changes in Tsk (4, 5, 22, 27). Thus it is unclear whether an increase in Tsk also contributes to the increase in VE seen during prolonged submaximal exercise.

It also has been suggested that the rate of the increase in body temperature may influence ventilation during exercise and at rest (4, 24, 40, 46). When Bazett (4), Landis et al. (24), and Saxton (40) manipulated bath water temperature or air temperature and/or humidity to increase core body temperature at various rates, they found that VE was greater when core temperature was increased faster. Moreover, White and Cabanac (46) reported that, during incremental exercise, ventilation was greater at any given core temperature when the rate of increase was faster and that the core temperature threshold for hyperventilation was lowered under the same conditions. However, those investigators changed the rate of increase in core temperature by changing the rate of increase in workload. In addition, they expressed ventilatory responses in terms of the inspired ventilatory equivalents for O2 and CO2 (i.e., VI/VO2 and VI/VCO2, respectively; where VI is inspired ventilation; VO2 is oxygen uptake, and VCO2 is carbon dioxide output) and the core temperature threshold for hyperventilation as the core temperature at which VI/VO2 and VI/VCO2 began to increase. But as these parameters are also known to be, respectively, the anaerobic threshold and the starting point of respiratory compensation (45), their approach does not exclude the effects of the increasing workload on ventilatory responses, so the effect of the rate of increase in body temperature during exercise at a constant workload remains to be determined.

Some researchers have suggested that there is a core temperature threshold for hyperventilation, irrespective of whether the subject is exercising or at rest (6, 34, 40, 46). For instance, Saxton (40) reported that resting VE is augmented when core temperature increases 1.5°C from basal body temperature, and Cabanac and White (6) reported that the core temperature threshold for hyperventilation is 38.5°C (Tes). Petersen and Vejby-Christensen (34) were the first to suggest that there might be a core temperature threshold for hyperventilation during exercise and that it is ~38°C (rectal temperature). In addition, White and Cabanac (46) reported that, during incremental exercise, hyperventilation was induced when core temperature reached 37.5–37.9°C (Tes); again, however, it difficult to distinguish the temperature threshold from the anaerobic threshold using their data. It thus remains unclear whether a body temperature threshold for hyperventilation can be seen during submaximal exercise.

With all of that as background, our aim in this study was to examine whether Tsk or the rate of increase in core temperature affects the relationship between VE and core temperature during prolonged exercise and whether a core temperature threshold for hyperventilation can be seen during the exercise.


   METHODS
TOP
 ABSTRACT
 METHODS
RESULTS
 DISCUSSION
 GRANTS
 ACKNOWLEDGMENTS
 REFERENCES
 
Subjects.   Thirteen healthy male subjects [mean age = 24.5 ± 0.7 (SE) yr; height = 171.6 ± 1.4 cm; weight = 68.0 ± 2.0 kg; peak VO2 (VO2 peak) = 48.1 ± 2.0 ml·kg–1·min–1] participated in the study, which was approved by the Human Subjects Committee of the University of Tsukuba. All participants provided written, informed consent. Before any data were collected, the subjects were allowed to practice the cycle exercise they would be asked to perform during the experiments until they were accustomed to its style.

VO2 peak test.   VO2 peak was determined during an incremental cycling exercise to volitional fatigue. The exercise was performed on a cycle ergometer (model 818E, Monark) that had been customized for semirecumbent cycling. Exercise was started at 60 W, after which the load was increased at a rate of 15 W/min throughout the entire exercise period. Subjects pedaled at 60 rpm, and volitional fatigue was defined as an inability to pedal at more than 50 rpm. The expired gas was analyzed using an electric gas flowmeter (model RM300i, Minato Medical Science, Osaka, Japan) and a mass spectrometer (model Arco-1000, Arco System, Kashiwa, Japan); the former was calibrated with the aid of an appurtenant calibration instrument that can blow in a fixed volume (2 liters), and the latter was calibrated using gases of known concentration. VE, VO2, and VCO2 were calculated at 60-s intervals. VO2 peak was taken as the highest value of VO2 achieved by a given subject, as some subjects did not achieve a plateau. The VO2 peak test was carried out in an environmental chamber maintained at 25°C and 50% relative humidity. The room was force ventilated at a rate of 3,000–4,000 l/min to prevent any increase in the CO2 concentration of the room air.

Experimental design.   Subjects were asked to abstain from strenuous exercise, alcohol, and caffeine for 24 h before performing the exercise protocols. They were asked to drink 10 ml water/kg body weight the night before the experiment and then again on the morning of the experiment. Each subject came to laboratory after consuming only a light breakfast, and then he rested for 30 min sitting in a chair. During this time, a thermocouple was inserted via the nasal passage to measure Tes. This thermocouple was inserted to a distance equivalent to one-fourth of the subject's height. The subject then voided urine, was weighed, and moved to the environmental chamber, where he sat in a chair behind the ergometer to rest for 30 min. During this time, a heart rate (HR) monitor, thermocouples for measuring Tsk, and a cuff and electrodes for measuring arterial blood pressure (BP) were attached. Then the subject put on a water-perfused suit that covered the entire body with the exception of the face, hands, and feet. A plastic garment was then put on over the suit to suppress evaporation. In addition, each subject wore a cotton glove on the left hand. The right hand was left uncovered so that capillary blood could be collected for measurement of blood lactate concentration ([lactate]). Before starting the experiment, the suit was perfused with water at 34–35°C.

The subjects performed the cycle exercise at 50% of VO2 peak. At the onset of exercise, the water temperature was changed to 10°C (T10), 35°C (T35), or 45°C (T45), and the exercise was continued for 60 min or volitional exhaustion. Each subject completed three experiments separated by at least 5 days in random order. They tried to consume similar diets for 24 h before the three experiments. No fluid was provided during any experiment.

Measurements.   During the experiments, Tes and Tsk data were collected via copper constantan thermocouples, which were sampled every 1 s via a data logger system (model WE7000, Yokogawa, Tokyo, Japan) and averaged over 1-min periods. Measurements of Tsk were made at six sites (chest, upper back, lower back, abdomen, thigh, and calf) and used to calculate mean Tsk (Tsk) (43). HR was recorded every 5 s using a Vantage NV heart rate monitor (Polar) and averaged over 1-min periods. BP in the right brachial artery was measured in triplicate every 5 min using an automated sphygmomanometer (model STBP-780, Nippon Colin, Komaki, Japan). Mean arterial BP (MAP) was taken as the diastolic pressure plus one-third of the pulse pressure. The expired gas was measured using the same analyzers used in the VO2 peak test (see above). Capillary blood from the fingertip was collected for measuring [lactate] just before exercise, every 15 min during exercise, and just before the end of exercise. [Lactate] was measured with a lactate analyzer (model YSI 1500, Yellow Springs Instruments, Yellow Springs, OH) calibrated using a calibration kit provided by the manufacturer. Ratings of perceived exertion (RPE) were assessed every 5 min using Borg's scale.

Data analysis.   To evaluate the effects of Tsk and the rate of increase in core temperature on the relationship between ventilation and Tes, VE, tidal volume (VT), and respiratory frequency (f) were plotted as functions of Tes, after which the slopes and intercepts of the linear regression lines were compared. To exclude the fast component of VE kinetics, only data collected after the 5th min of exercise were analyzed.

All values are reported as means ± SE. Two-way ANOVA was used to analyze the data. After the main effects had been identified, a post hoc least significant difference test was carried out. In the T45 session, most subjects could not complete 60 min of exercise; consequently, data for minutes 50–60 were not analyzed in that session (n ≤ 5). Because Tes was nearly constant after minute 10 during the T10 experiment, paired t-tests were used to compare the T35 and T45 sessions with respect to the rates of increase in Tes and the slopes and intercepts of their linear regression lines calculated after VE, VT, and f were plotted as functions of Tes. Values of P < 0.05 were considered significant.


   RESULTS
TOP
 ABSTRACT
 METHODS
 RESULTS
DISCUSSION
 GRANTS
 ACKNOWLEDGMENTS
 REFERENCES
 
Before the trials, Tsk and Tes did not differ among the T10, T35, and T45 sessions [Tsk = 35.0 ± 0.2, 35.1 ± 0.2, and 35.1 ± 0.2°C, respectively; Tes = 36.7 ± 0.1, 36.7 ± 0.1, and 36.7 ± 0.1°C, respectively (not significant)]. Tsk declined during exercise in the T10 session, whereas it increased in the other two sessions: at the end of the exercise, Tsk in the T10, T35, and T45 sessions were 32.3 ± 0.5, 37.7 ± 0.1, and 39.1 ± 0.2°C, respectively. At the times indicated in Fig. 1, A and B, moreover, both Tsk and Tes were significantly higher in the T35 session than in the T10 session, and they were significantly higher in the T45 session than in both the T35 and T10 sessions.


Figure 1
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  		Fig. 1. Time-dependent changes in mean skin temperature (A), esophageal temperature (B), heart rate (C), and mean arterial blood pressure (MAP; D) during exercise in the 45° water (T45), 35° water (T35), and 10° water (T10) sessions. Most of the 13 subjects could not complete the T45 protocol; the numbers adjacent to the symbols in A indicate the number of subjects still exercising at the corresponding time and apply to B–D. aP < 0.05 T35 vs. T45 at all points within the bracket. bP < 0.05 T35 vs. T10. cP < 0.05 T45 vs. T10.

 
With respect to the hemodynamic parameters, HR was maintained within a range of 118–124 beats/min during exercise in the T10 session, but it increased steadily during exercise in the T35 and T45 sessions (Fig. 1C). MAP was stable throughout the exercise protocol and did not significantly differ among sessions (Fig. 1D).

Figure 2 shows the time-dependent changes in VE, VT, f, and end-tidal partial pressure of CO2 (PETCO2) during exercise. In the T10 session, VE remained nearly constant at 43–45 l/min throughout the exercise, but it increased steadily to significantly higher levels in the T35 and T45 sessions. In addition, the magnitude of the increase in the T45 session was significantly greater than in the T35 session at the times indicated in Fig. 2A. Although no statistically significant difference in VT was observed among the sessions (Fig. 2B), f increased significantly during exercise in the T35 and T45 sessions, and again the largest increases occurred in the T45 session (Fig. 2C). PETCO2 declined correspondingly during exercise in the T35 and T45 sessions, with significantly larger declines occurring in the T45 session than in either the T10 or T35 session (Fig. 2D). No statistically significant differences were observed in VO2 and VCO2 among the three sessions, and the respiratory exchange ratio was always <1.


Figure 2
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  		Fig. 2. Time-dependent changes in minute ventilation (A), tidal volume (B), respiratory frequency (C), and end-tidal PCO2 (PETCO2; D) during exercise in the T45, T35, and T10 sessions. aP < 0.05 T35 vs. T45 at all points within the brackets. bP < 0.05 T35 vs. T10. cP < 0.05 T45 vs. T10.

 
RPE continuously increased during exercise in all sessions (Fig. 3A). The highest values were observed in the T45 session, which were significantly higher than those in the T35 session, which were in turn significantly higher than those in the T10 session. Levels of [lactate] were <2 mmol/l during exercise in all sessions, but they significantly differed between T10 and T35 at minute 60 (P < 0.05) (Fig. 3B).


Figure 3
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  		Fig. 3. Time-dependent changes in rating of perceived exertion (RPE; A) and blood lactate concentration ([lactate]; B) during exercise in the T45, T35, and T10 sessions. aP < 0.05 T35 vs. T45 at all points within the brackets. bP < 0.05 T35 vs. T10. cP < 0.05 T45 vs. T10.

 
To assess the effects of Tsk and the rate of increase in core temperature on the relationship between ventilation and Tes, we plotted VE, VT, and f as functions of Tes using the data obtained after the first 5 min of exercise in the T35 and T45 sessions (Fig. 4, Table 1). Core temperature threshold for hyperventilation was determined using two linear regression lines calculated by the method of least squares and representing the smallest sum of two residual sums of squares. The threshold was determined as the intersecting point of these two regression lines. Using this regression analysis, we found that two subjects showed a clear threshold for hyperventilation, but the other one showed ventilatory responses that increased linearly with Tes. For these 11 subjects, the two regression lines were almost parallel and intersected outside the range of measured Tes (e.g., some intersected at a temperature that was less than baseline Tes, whereas others intersected at a temperature that was higher than the Tes when subjects stopped exercising). We therefore presumed that ventilatory responses increased or decreased linearly with Tes. Furthermore, we found there to be no significant differences in the slopes or intercepts between the T35 and T45 sessions. As mentioned above, during exercise, Tsk was significantly higher in the T45 session (Tsk = 36–39°C) than in the T35 session (Tsk = 35–38°C); accordingly, the rate of increase in Tes seen in the T45 session (3.61 ± 0.19°C/h) was about twice that seen in the T35 session (1.92 ± 0.12°C/h) (P < 0.05). That we observed no statistically significant difference in the ventilatory responses (VE, VT, and f) to changes in Tes between the T35 and T45 sessions indicates that their relationships were not affected by Tsk or the rate of increase in core temperature during prolonged exercise at a constant workload with Tsk at 35–39°C and the rate of increase in Tes at 1.9–3.6°C/h. When plotting VE as a function of Tsk, the close correlation between VE and Tsk was similar to that between VE and Tes (the slopes were 6.6 ± 2.6 l·min–1·°C–1 in the T35 and 5.3 ± 1.2 l·min–1· °C–1 in the T45 session, and the intercepts were –199.2 ± 97.2 l/min in the T35 and –152.1 ± 45.2 l/min in the T45 session), and there was no significant differences in the slope or intercept between the T35 and T45 sessions.


Figure 4
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  		Fig. 4. Esophageal temperature-dependent changes in minute ventilation (A), tidal volume (B), and respiratory frequency (C) during exercise in the T35 and T45 sessions.

 

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  		Table 1. Slopes and intercepts of regression lines calculated after plotting the indicated ventilatory parameter against Tes and the values at Tes = 37°C

 

   DISCUSSION
TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
GRANTS
 ACKNOWLEDGMENTS
 REFERENCES
 
The major findings of the present study are the following: 1) that when core temperature is steady during submaximal dynamic exercise with body surface cooling, HR and VE are also steady; 2) that VE increases with body surface warming and that the change in VE is linearly related to the increase in body temperature; 3) that the increase in VE is secondary to an increase in f; 4) that the increase in Tsk and the rate of increase in core temperature during exercise do not influence the relationship between the increase in VE and the increase in Tes with Tsk at 35–39°C and the rate of increase in Tes at 1.9–3.6°C/h; and 5) that a core temperature threshold for hyperventilation is not seen during prolonged exercise at 50% VO2 peak.

After the first 10 min of exercise, Tes, Tsk, HR, VE, and f remained steady with body surface cooling in the T10 session, but these parameters progressively increased with exercise time when the body surface was warmed in the T35 and T45 sessions (Figs. 1 and 2). This suggests that the increases in HR and VE seen with body surface warming during exercise at 50% VO2 peak are associated with an increase in core body temperature, which is consistent with earlier studies (15, 31, 47). Moreover, because in the present study Tsk and the rate of increase in core body temperature differed significantly in the T35 and T45 sessions, comparison of the responses in those groups should further our understanding of the effects of those parameters on ventilation during exercise in the heat.

It was previously reported that, in subjects at rest, an acute increase (4) or decrease (5, 22, 27) in Tsk would augment VE without affecting core temperature. This suggests that these ventilatory responses are driven by reflexes initiated by thermoreceptors in the skin and mediated at the midbrain level (22). The discrepancy between those earlier findings and our present ones may be related to the degree of thermal stimulation of the skin. Those investigators changed Tsk by >10°C within 1 min (5, 22, 27), after which VE obtained with and without this aggressive cooling were compared. In the present study, however, we compared the ventilatory responses under conditions in which the difference in Tsk during the exercise in the T35 and T45 sessions was only ~2°C, and Tsk changed comparatively slowly (Tsk increased 0.2°C/min in the T35 session and 0.4 °C/min in the T45 session). In addition, Bazett (4) and Landis et al. (24) observed that VE is increased with the rate of increase in body temperature. Saxton (40) observed a similar tendency, but he did not detect a significant effect of rate because of the small number of subjects in that study (n = 4). To our knowledge, only White and Cabanac (46) have investigated the effect of the rate of increase in body temperature on ventilatory responses during exercise. They suggested that a higher rate of increase in body temperature augments ventilation during incremental exercise. The discrepancy between their results and ours in the present study may be related to the difference in the magnitudes of the rates of increase in body temperature: the rate of change in their study (between 3.80 ± 0.43 and 6.28 ± 0.43°C/h) was about twice that in ours (between 1.92 ± 0.12 and 3.61 ± 0.19°C/h). A second possible reason for the discrepancy relates to the fact that they changed the rate of increase in body temperature by changing the rate of increase in workload. Consequently, the augmented increase in VE could reflect the increase in workload and not the increase in core temperature.

It is thought that during exercise VE is modulated by a variety of factors, including output from central command, input from central or peripheral chemoreceptors, and input from muscle mechanoreceptors and metaboreceptors via group III and IV muscle afferents, among others (2, 9, 21, 35, 45). Notably, these factors also are reportedly influenced by changes in body temperature. For example, hyperthermia increases levels of anaerobic metabolites (11, 12, 15), which in turn stimulate signaling by central or peripheral chemoreceptors or muscle metaboreceptors to increase VE (9, 13, 21, 31, 45). However, we detected no significant difference in [lactate], except between the T10 and T35 sessions at minute 60; indeed, [lactate] was maintained at <2 mmol/l during exercise in all sessions (Fig. 3C). Moreover, there were no significant differences in VO2 and VCO2 among the sessions; they remained virtually constant throughout the exercise in all sessions. Thus the hyperventilation observed in the T35 and T45 sessions does not appear to have been caused by metabolic factors.

So what then did cause the observed increase in VE? One possibility is augmented signaling from central command (2, 9, 31, 45). Taking RPE as an index of central command signaling, our findings indicate that output from central command increases in proportion to the increase in Tes (Figs. 1B and 3A), which is consistent with findings made in earlier studies (15, 29, 31). For instance, increased signaling from central command is induced by central fatigue, which is relevant to hyperthermia (29, 32). A second possibility is that the increase in VE reflects augmented input from chemoreceptors. In that case, hyperthermia-induced reductions in blood pH (36, 37), increases in chemosensitivity (8, 28, 33), and/or increases in plasma norepinephrine derived from increased sympathetic nerve activity (7, 20, 41) lead to increases in peripheral chemoreceptor activity (9, 18). A third possibility is that the activity of group III and IV muscle afferents, induced by an increase in muscle temperature (19, 23), and increased activity of the ventral respiratory group, induced by an increase in brain temperature (44), lead to an increase in VE. However, although all of these processes can potentially contribute to hyperthermia-induced increases in VE, the extent to which they were involved in the increase seen in the present study remains to be determined.

Martin et al. (25) examined the effect of core temperature on ventilation in an effort to understand the mechanism underlying VE drift during prolonged exercise. They compared VE under two conditions [increased core temperature (rectal) elicited either by exercise or immersion in 39°C water] and reported that increases in core temperature elicited by exercise augmented VE, whereas increases elicited by passive heating did not. They concluded, therefore, that increased core temperature did not itself mediate VE drift. Nevertheless, several other studies, including this one, found that exercise-induced increases in VE are prevented if there is no rise in core temperature (10, 31), which makes it difficult to conclude that body core temperature does not play a role in VE drift.

The present study showed that VE increased at 5–6 l·min–1·1°C–1 increase in Tes (Fig. 4, Table 1), that the increase in VE was induced by an increase in f, and that f increased at ~7 breaths·min–1·1°C–1 increase in Tes during exercise at a constant workload (50% VO2 peak). These findings are consistent with earlier ones; however, those studies did not show the degree to which f increases as body temperature increased (25, 26, 34). Ours is thus the first study to show that f increases linearly with increases in body core temperature. On the other hand, Barltrop (3), Gaudio and Abramson (13), and Senay and Christensen (42) increased the body temperature of resting subjects 1–2°C from normothermia and reported that VE increased 1–2 l·min–1·1°C–1 increase in oral or rectal temperature, whereas Cabanac and White (6) reported that ventilation abruptly increased when Tes increased to >38.5°C. Moreover, all of those studies showed that in resting subjects increases in VE are induced by increases in VT (4, 6, 13, 40). This suggests that when body temperature increases at rest VE is augmented by an increase in VT but that during exercise it is augmented by an increase in f. The mechanisms underlying the different pathways leading to the increases in VE at rest and during exercise have not yet been investigated.

Limitations.

When plotting VE as a function of Tsk in the T35 and T45 sessions, it should be borne in mind that Tsk also has a linear relationship with VE. Our regression analysis showed that VE increased at 5–6 l·min–1·1°C–1 with increases in Tsk, but because in each session Tes and Tsk increased simultaneously, we could not isolate the respective effects. Furthermore, the rate of increase in VE with increasing Tsk (5–6 l·min–1·°C–1) was too large; the difference in Tsk between the T45 and T10 sessions 40 min into the exercise was ~7°C, but the difference in VE was <12 l/min. We therefore suggest that this increase in VE was induced mainly by the increase in Tes and that the influence of Tsk was small. In addition, Tsk in the T45 sessions (39.1 ± 0.2°C) was significantly higher than that in the T35 sessions (37.7 ± 0.1°C), but the difference was small. To investigate more clearly the independent effect of Tsk on VE, it would be better to change Tsk substantially without changing core temperature, for example by using fan cooling to induce a plateau in Tes in the cold and in the heat (10 and 35°C) (1, 31) or cooling abruptly to decrease Tsk without changing core temperature during exercise. These experiments are clearly needed in the future.

When we plotted VE as a function of Tes, a core temperature threshold for hyperventilation was detected in only 2 of our 13 subjects. We suggest that there are two possible reasons why we generally did not observe a core temperature threshold. We only analyzed data obtained after 5 or more min of exercise; consequently, it would be impossible to identify a core temperature threshold if it appeared before minute 5 (i.e., if the threshold were lower than 36.8–36.9°C in Tes). In addition, even if there were a threshold between the Tes values at minutes 5 (Tes = 36.8–36.9°C) and 10 (Tes = 37.2–37.3°C), it would have been undetectable because of the small amount of the data collected at that point. As just mentioned, however, we did detect apparent core temperature thresholds for hyperventilation in two subjects; moreover, we observed a great deal of individual variability in the slopes and intercepts of the calculated linear regression lines when VE, VT, and f were plotted against Tes. The functional significance of this variability among individuals remains to be determined.

In summary, we examined ventilatory responses to increases in body temperature to determine the extent to which Tsk and/or the rate of increase in core temperature contributes to the increase in VE seen during dynamic submaximal exercise and to determine whether there is a core temperature threshold for hyperventilation during exercise, as there is at rest. We found that both HR and VE are significantly affected by core temperature and that the increase in VE during dynamic exercise reflects an increase in f. Our findings further indicate that VE increases linearly with increases in core temperature, that a core temperature threshold for hyperventilation was not seen during prolonged exercise at 50% VO2 peak, and that Tsk or the rate of increase in core temperature does not affect the relationship between VE and Tes with Tsk at 35–39°C and the rate of increase in Tes at 1.9–3.6°C/h.


   GRANTS
TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 GRANTS
ACKNOWLEDGMENTS
 REFERENCES
 
This study was supported by grants from the Center of Excellence projects and the Ministry of Education, Science, and Culture, Japan.


   ACKNOWLEDGMENTS
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 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
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 ACKNOWLEDGMENTS
REFERENCES
 
We sincerely thank the volunteer subjects. We also greatly appreciate the help of Dr. William Goldman (English editing and critical comments).


   FOOTNOTES
 

Address for reprint requests and other correspondence: T. Nishiyasu, Institute of Health and Sports Science, Univ. of Tsukuba, Tsukuba City, Ibaraki 305-8574, Japan (e-mail: nisiyasu{at}taiiku.tsukuba.ac.jp)

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.


   REFERENCES
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 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 GRANTS
 ACKNOWLEDGMENTS
 REFERENCES
 

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