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J Appl Physiol 91: 1520-1528, 2001;
8750-7587/01 $5.00
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Vol. 91, Issue 4, 1520-1528, October 2001

Thermoregulatory and aerobic changes after endurance training in a hypobaric hypoxic and warm environment

Yoshiaki Takeno, Yoshi-Ichiro Kamijo, and Hiroshi Nose

Department of Sports Medicine, Research Center on Aging and Adaptation, Shinshu University School of Medicine, Matsumoto 390-8621, Japan


    ABSTRACT
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

Plasma volume (PV) expansion by endurance training and/or heat acclimatization is known to increase aerobic and thermoregulatory capacities in humans. Also, higher erythrocyte volume (EV) fractions in blood are known to improve these capacities. We tested the hypothesis that training in a hypobaric hypoxic and warm environment would increase peak aerobic power (VO2 peak) and forearm skin vascular conductance (FVC) response to increased esophageal temperature (Tes) more than training in either environment alone, by increasing both PV and EV. Twenty men were divided into four training regimens (n = 5 each): low-altitude cool (610-m altitude, 20°C ambient temperature, 50% relative humidity), high-altitude cool (2,000 m, 20°C), low-altitude warm (610 m, 30°C), and high-altitude warm (HW; 2,000 m, 30°C). They exercised on a cycle ergometer at 60% VO2 peak for 1 h/day for 10 days in a climate chamber. After training, PV increased in all trials, but EV increased in only high-altitude trials (both P < 0.05). VO2 peak increased in all trials (P < 0.05) but without any significant differences among trials. FVC response to increased Tes was measured during exercise at 60% of the pretraining VO2 peak at 610 m and 30°C. After the training, Tes threshold for increasing FVC decreased in warm trials (P < 0.05) but not in cool trials and was significantly lower in HW than in cool trials (P < 0.05). The slope of FVC increase/Tes increase increased in all trials (P < 0.05) except for high-altitude cool (P > 0.4) and was significantly higher in HW than in cool trials (P < 0.05). Thus, against our hypothesis, the VO2 peak for HW did not increase more than in other trials. Moreover, slope of FVC increase/Tes increase in HW increased most, despite the similar increase in blood volume, suggesting that factors other than blood volume were involved in the highest FVC response in HW.

endurance training; altitude; skin blood flow; aerobic power; blood volume; humans


    INTRODUCTION
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

HYPERVOLEMIA INDUCED BY ENDURANCE exercise training and/or heat acclimatization has been suggested to increase aerobic and thermoregulatory capacities (15). This theory appears to be supported mainly by studies investigating the effects of acute plasma volume (PV) expansion on the functions (23). There are several studies showing that acute PV expansion increased maximal aerobic capacity by increasing cardiac stroke volume (5, 11, 23). In addition, skin blood flow (SkBF) during submaximal exercise in a hot environment was reportedly increased by intravenous infusion of saline (19) or albumin solution (7). Because similar increases in SkBF were observed after water immersion (18), posture change from the upright to supine position (1), and negative-pressure breathing (17), the increased SkBF by PV expansion might be caused by stretch of baroreceptors due to increased venous return to the heart.

In contrast to these findings, there have been few studies showing the merits of PV expansion by endurance training or heat acclimatization in thermoregulation, although there are some in maximal aerobic capacity (3, 14). Convertino et al. (3) studied the relative role of exercise training and heat exposure in PV expansion and suggested that not only exercise training but also heat exposure increased PV in an additive way. Costill et al. (4) measured the body fluid and electrolyte balance during recovery from thermal dehydration and suggested that PV expansion was induced by increased extracellular fluid volume, attained by enhanced renal water and Na retention mechanisms during this period. Although both studies suggested the involvement of heat exposure in PV expansion, neither examined the effects on thermoregulation. Although Roberts et al. (21) reported that the sensitivity in cutaneous vasodilation in response to increased esophageal temperature (Tes) was more enhanced after endurance training in a hot environment than in a cool environment, they did not measure PV. Thus heat acclimatization is known to be a major factor in expanding PV, although it is not clear whether the expansion really contributes to the enhanced sensitivity of cutaneous vasodilation, as deduced by the findings from acute PV expansion (7, 19). The first purpose of this study was to clarify this issue.

The second aim of the present study was to assess the effects of altitude training on temperature regulation. Sawka et al. (24) examined the effects of increased fractions of erythrocyte volume (EV) in blood on thermoregulation during exercise in a hot environment. They reported that the increased fraction of EV improved thermoregulation during exercise by reducing Tes thresholds for sweating and increasing sweating sensitivity in response to increased Tes. As for the mechanism, they postulated that the increased arterial oxygen content, induced by EV expansion, might allow systemic oxygen transport requirements for a given level of submaximal exercise to be achieved with lower muscle blood flow, which might enable redistribution of blood flow to the skin. From these findings, we hypothesized that endurance training at a high altitude would expand EV (22) and increase O2 conductance in muscles (27), thus reducing blood flow to muscle and enabling redistribution of blood flow to the skin. Furthermore, because PV was reported to increase after heat acclimatization (3, 14), endurance training in a hypobaric hypoxic and warm environment would cause total blood volume (BV) expansion by increasing both EV and PV more than in either environment alone, leading to higher maximal aerobic power and SkBF through not only increased cardiac stroke volume (14, 29) but also baroreflex-induced vasodilation in the skin (17) and muscles (12).

To accomplish these aims, the maximal aerobic capacity and sensitivity of cutaneous vasodilation were measured before and after endurance training in four different environments: low-altitude cool (LC; 610 m, 20°C), low-altitude warm (LW; 610 m, 30°C), high-altitude cool (HC; 2,000 m, 20°C), and high-altitude warm (HW; 2,000 m, 30°C). The findings were analyzed in relation to EV and PV.


    METHODS
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

This study was approved by the Review Board on Human Experiments, Shinshu University School of Medicine. Subjects gave their written, informed consent before participating in the study. The blood properties and physical characteristics of young male subjects [age 23 ± 4 (SD) yr] before each training program are shown in Table 1. The experiments were conducted between May and June and between September and February 1999, to ensure that the subjects were not heat acclimated before training.

                              
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  		Table 1.   Body weight, HRmax, VO2 peak, and blood properties before and after 10-day training

Training Programs

Twenty male subjects were divided into four trials according to the environmental conditions for training: 1) LC [atmospheric pressure (Patm), 710 mmHg (610 m); ambient temperature (Ta), 20°C; relative humidity (RH), 50%; n = 5]; 2) HC [Patm, 595 mmHg (2,000 m); Ta, 20°C; RH, 50%; n = 5]; 3) LW (Patm, 710 mmHg; Ta, 30°C; RH, 50%; n = 5); and 4) HW (Patm, 595 mmHg; Ta, 30°C; RH, 50%; n = 5). The environmental conditions were adjusted within the range of ±1 mmHg for Patm, ±0.1°C for Ta, and ±1% for RH in an artificial climate chamber. The low altitude of 610 m was adopted because our laboratory is located at that altitude. The exercise training was performed without fan cooling.

Subjects performed cycle ergometer training at 60% of peak aerobic power (VO2 peak) for 1 h each day. Training was composed of two 30-min bouts of exercise separated by 10-min rest for 10 days and lasted for 5 days/wk for 2 wk, in an artificial climate chamber. Because VO2 peak increased with training, the exercise intensity was readjusted 5 min after the start of exercise each day so that subjects exercised at a heart rate (HR) of ~140 beats/min, which was assumed to be equivalent to 60% of VO2 peak each day. The reason for adopting the HR at 5 min as the target HR to be readjusted was that the HR depended on the relative exercise intensity before body temperature started to increase. After 5 min of exercise, HR gradually increased in parallel with the increase in Tes, despite the constant exercise intensity. Total sweat loss (SL) was estimated from body weight loss after exercise and is expressed in milliliters per kilogram body weight.

Protocols and Measurements

PV, VO2 peak, and forearm skin vascular conductance (FVC) response to increased Tes were measured before and after the training, according to that order, on separate days. The pretraining measurements were accomplished at least 2 days before the start of training, and the posttraining measurements at least 5 days after the cessation of training in the order of PV, FVC response, and VO2 peak. The measurements of PV and FVC response were completed within at least 2 days after the training to avoid de-acclimatization to heat.

PV. On the day of PV measurement, subjects reported to the laboratory at 7:00 AM normally hydrated but without having taken any food for 10 h before the measurement. PV was determined by using the Evans blue dye dilution method (9) for each subject in the sitting position after 30 min of rest at 28°C Ta and 50% RH. The BV was calculated from the PV, and hematocrit (Hct) was corrected for trapped plasma (0.96) and the F-cell ratio (0.91) (10). EV was calculated as EV = BV - PV. The aliquots of blood were also used to determine blood chemicals, as described in detail in Blood Properties.

VO2 peak. VO2 peak was determined with graded exercise by using a cycle ergometer in the upright position (Table 1). Clad in shorts and shoes, subjects entered an environmental chamber adjusted to 710-mmHg Patm, 25°C Ta, and 50% RH. After the electrocardiogram electrodes were applied, subjects pedaled at 60 cycles/min at an initial intensity of 60 W. The intensity was increased by 60 W every 3 min <180 W, above that intensity by 30 W every 2 min <240 W, and then by 15 W every 2 min until subjects did not keep the rhythm due to exhaustion. The oxygen consumption rate was calculated from measurements of ventilation volume and expired fractions of O2 and CO2 (Aeromonitor AE260, Minato, Tokyo, Japan) every 15 s. In the high-altitude (H) trials, VO2 peak at 595 mmHg and Ta at 25°C were also measured to determine the exercise intensity for training at 2,000 m. VO2 peak in the semirecumbent position was also measured with graded exercise to determine exercise intensity for the FVC response test.

FVC response test. Subjects reported to the laboratory at 8:00 AM normally hydrated but without breakfast. Clad in shorts and shoes, subjects emptied their bladders; entered the chamber controlled at 710-mmHg Patm, 30°C Ta, and 50% RH; then sat in the contour chair of the cycle ergometer in a semirecumbent position and rested for 60 min while all measurement devices were applied. After the baseline measurements were taken at rest for 10 min, subjects exercised in the semirecumbent position at 60% of pretraining VO2 peak for 30-40 min without fan cooling. Forearm SkBF (FBF), HR, systolic (SAP) and diastolic (DAP) arterial pressures, Tes, and skin temperature (Tskin) were measured at rest and during exercise, as described in detail below.

HR was recorded every 1 min from the trace of an electrocardiogram (Life Scope 8, Nihon Kohden, Tokyo, Japan). SAP and DAP were automatically measured every 1 min from the right upper arm at the heart level, by inflation of the cuff with a sonometric pickup of Korotroff's sound (STBT-780, Colin, Komaki, Japan). Mean arterial pressure (MAP) was calculated as (SAP + 2 DAP)/3.

Tes was monitored every 5 s with a copper constantan placed in a polyethylene tubing (PE-90). The tip of the tube was advanced at a distance of one-fourth of the subject's standing height from the external nares. Subjects were instructed to avoid swallowing saliva during measurement. Tskin was also measured every 5 s with thermocouples attached to three skin sites: right forearm, chest, and left thigh. The Tes and Tskin measurements were averaged every 1 min. Mean Tskin (<A><AC>T</AC><AC>&cjs1171;</AC></A>skin) was calculated according to the equation reported by Roberts et al. (21).

FBF was measured every 1 min by venous occlusion plethysmography by using a Whitney mercury-in-Silastic strain gauge placed around the left forearm (28). The venous occlusion cuff was inflated to 60 mmHg, while the hand was eliminated from the circulation with a wrist cuff inflated to 300 mmHg. FVC was determined by dividing FBF with MAP.

Analyses for the Tes vs. FVC Relationship

As shown in Fig. 1, the Tes vs. FVC relationship was fitted with three regression equations in mean values by using a standard Y minimized regression analysis. The first one was determined by eye from the first sharp increase in Tes before the increase in FVC: 2-10 min in the LC trial, 2-7 min in the HC trial, 2-7 min in the LW trial, and 2-6 min in the HW trial after the start of exercise. Then the second component was determined from the rapid increase in FVC: 10-15 min in the LC trial, 7-12 min in the HC trial, 7-17 min in the LW trial, and 6-12 min in the HW trial. The third component was determined from the measurements after the second component. The Tes threshold for increasing FVC and the second slope of increase (Delta ) in FVC (Delta FVC) at a given Delta Tes (Delta FVC/Delta Tes) were determined in each subject for statistical analyses, and the findings are summarized in Table 2. The threshold and slope were determined by three separate investigators who were familiar with the method, and the three values measured by them were averaged. In addition, the change in the Tes vs. FVC relationship after training was analyzed by subtracting the pretraining FVC from the posttraining FVC at every 0.1°C increment of Tes during exercise in each subject. The missing FVC values at a given Tes were estimated from neighboring points by interpolation (Fig. 2).


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  		Fig. 1.   Relationship between forearm skin vascular conductance (FVC) and esophageal temperature (Tes) during FVC response test before (open circle ) and after () 10-day training. The regression equations of the 2nd component in the low-altitude warm (LW; 610 m, 30°C) trial are y = 28.5x - 1,061 (r = 0.985, P < 0.01) before training and y = 36.4x - 1,350 (r = 0.974, P < 0.01) after training, with a 28% increase in the slope (P < 0.05). Similarly, the equations in the high-altitude warm (HW; 2,000 m, 30°C) trial are y = 25.5x - 944 (r = 0.992, P < 0.01) and y = 36.0x - 1,327 (r = 0.963, P < 0.01) before and after training, respectively, with a 41% increase in the slope (P < 0.05). There were no significant differences in the slopes of the 2nd component in the other trials. The means ± SE for 5 subjects are presented for each trial. LC, low-altitude cool trial (610 m, 20°C); HC, high-altitude cool trial (2,000 m, 20°C).


                              
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  		Table 2.   Tes threshold for increasing FVC, Delta FVC/Delta Tes, and SL during FVC response test before and after 10-day training



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  		Fig. 2.   Change in FVC response at a given level of Tes after training. Values are derived from those in Fig. 1 and are presented as the means ± SE for 5 subjects as differences in the FVC values before and after training. Significant differences from the values before training: dagger  P < 0.05 and dagger dagger P < 0.01. Significant differences from the values in the LC trial: * P < 0.05 and ** P < 0.01.

Blood Properties

The blood to determine PV was also used to measure the Hb concentration (in g/dl; cyanomethohemoglobin method) and Hct (in percent; microcentrifuge method). After the remaining blood was centrifuged, the aliquots of plasma were used to determine the plasma protein concentration (in g/dl; refractometry) and plasma osmolality (Posmol; in mosmol/kgH2O; freezing point depression method; one-ten osmometer; Fiske).

Statistics

One-way ANOVA for repeated measures was used to test the difference in exercise intensity and SL during the 10-day training in each trial. Significant differences at various times were determined with Fisher's least significance difference test (Fig. 3A1, B1, C1, and D1). This ANOVA was also used to test the differences in the variables of body weight, VO2 peak, and blood properties (Table 1); and Tes threshold for increasing FVC, Delta FVC/Delta Tes, and SL (Table 2) before and after training in each trial. One-way ANOVA was used to test the differences among the trials in the changes of these variables after training (Tables 1 and 2). This ANOVA was also used to test the differences in the integrated values of HR, Delta HR, exercise intensity, and SL for the 10-day training among the trials (Fig. 3A2, B2, C2, and D2). Two-way ANOVA for repeated measures was used to test the differences in HR, MAP, Tes, and <A><AC>T</AC><AC>&cjs1171;</AC></A>skin during exercise for the FVC response test before and after training, with significant differences at various times determined with Fisher's least significant difference test (Table 3). All values in each trial are reported as means ± SE of five subjects. The null hypothesis was rejected at the level of P < 0.05. Because there were only five subjects per trial, which limited the statistical power (1 - beta ) in the comparison of variables among the trials, we confirmed that the effect size was >0.40 for the F test in ANOVA, classified as large effect size by Cohen (2), where statistical power is 0.25 in Tables 1 and 2 (4 trials, n = 20) and 1.00 in Fig. 2 (4 trials, n = 200). Both values were shown in the comparison of mean values among the trials to demonstrate the power of statistical analyses.


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  		Fig. 3.   A1: heart rate (HR) at the first 5 min of exercise during each day's training for 10 days. A2: HR at the first 5 min was integrated for 10 days to compare total relative exercise intensity among the trials. B1: increase in HR (Delta HR) along with the 60-min exercise as the difference between 5- and 60-min values. B2: Delta HR values for each day were integrated for 10 days to compare total relative heat stress among the trials. C1: absolute exercise intensity during each day's training. C2: exercise intensity integrated for the 10-day training. D1: sweat loss (SL) during each day's training. D2: SL integrated for the 10-day training. Values are presented as the means ± SE for 5 subjects. B1, C1, and D1: shaded and solid symbols indicate significant increases from the values on the 1st day of training at the levels of P < 0.05 and P < 0.01, respectively. Significant differences between the cool and warm trials, * P < 0.05 and ** P < 0.01. NS, nonsignificantly different from the values in the LC trial.


                              
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  		Table 3.   Change in HR, MAP, Tes, and &Tmacr;skin during FVC response test before and after 10-day training


    RESULTS
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

HR, Exercise Intensity, and SL Changes During Each Day's Exercise Training for 10 Days

Figure 3A1 shows HR at the first 5 min of exercise during each day's training for 10 days. Exercise intensity was readjusted after the first 5 min of exercise before Tes increased so that subjects trained themselves at the same relative intensity, ~60% VO2 peak, each day during the training period. As shown in Fig. 3A1, the HR during the first 5 min was maintained at 135-140 beats/min. The HR integrated for the 10-day training period was ~1,400 (beats · min-1 · 10 days-1) without any significant differences among the trials, as shown in Fig. 3A2 (P > 0.67), suggesting that the relative exercise intensity was similar during the 10-day training among the trials.

Although subjects exercised at a constant exercise intensity, their HR increased with increased body temperature, which is known as "cardiovascular drift" (6). Figure 3B1 shows the Delta HR from 5 to 60 min of exercise, during each day's exercise training, for 10 days. The Delta HR in the cool (C) trials was only ~15 beats/min and was maintained at this level until the end of training. In contrast, the Delta HR values for the warm (W) trials were ~25 beats/min on the first day of training, which were significantly higher than those in the C trials. However, the Delta HR for the LW trial rapidly decreased on the 7th day of training and remained at the reduced level thereafter, with significant differences from the value on the 1st day of training. However, the Delta HR for the HW trial was maintained at the level of the 1st day throughout the 10-day training. Significant differences between the LW and HW trials were observed after 7 days (P < 0.01). As shown in Fig. 3B2, the integrated Delta HR was highest in the HW trial, with significant differences between the LC and LW trials (P < 0.05) and between the HC and HW trials (P < 0.01), suggesting that cardiovascular drift during exercise, an index of heat loading, was significantly higher in the W trials than in the C trials.

Figure 3C1 shows the exercise intensity during each day of the training period. The intensity in all trials increased gradually with training, and a significant increase occurred on the 2nd day in the LC trial, on the 4th day in the HC and LW trials, and on the 5th day in the HW trial. However, as shown in Fig. 3C2, the exercise intensity, integrated for the 10-day training period, was 1,400-1,600 (W/10 days) without any significant differences among the trials (P > 0.35), suggesting that integrated exercise intensity for 10-day training was similar among the trials.

Figure 3D1 shows total SL after 1-h exercise each day of the training period. The SL in all trials increased gradually along with the training, and significant increases occurred on the 2nd day in the HC trial, on the 4th day in the LW trial, on the 5th day in the HW trial, and on the 6th day in the LC trial. As shown in Fig. 3D2, the SL integrated for the 10-day training period was 203 ± 21 ml/kg in the LW trial, which was significantly higher than the 140 ± 8 ml/kg in the LC trial (P < 0.01). Moreover, the integrated SL in the HW trial was 176 ± 15 ml/kg, which was significantly higher than the 121 ± 11 ml/kg in the HC trial (P < 0.05). However, there were no significant differences in SL between the H and low-altitude (L) trials.

Physical Characteristics, BV, and Blood Properties

As shown in Table 1, there were no significant changes in body weight after training in any trial. VO2 peak in all trials increased significantly by 7-11% (P < 0.05) but without significant differences among the trials. BV and PV in all trials increased significantly (P < 0.05) after training but without significant differences among the trials (P > 0.49). EV in the H trials, however, increased significantly but not in the L trials. Hb concentration in the L trials decreased significantly but not in the H trials, with significantly less decreases in the H trials than in the L trials, where the statistical power was 0.58 and the effects size was 0.66. Hct did not change significantly after training in any trial, but the reduction after training for the H trials was significantly lower than that for the L trials (P < 0.05), where the statistical power was 0.50 and the effects size was 0.60. There were no significant differences in plasma protein concentration and Posmol before and after training in any trial.

FVC Response Test

Table 3 shows the HR, MAP, Tes, and <A><AC>T</AC><AC>&cjs1171;</AC></A>skin responses during the FVC response test. Although the measurements were performed every 1 min, only the values at rest and at 5, 10, and 30 min of exercise are presented to avoid a complex table, after three-point moving average was performed in each variable. Statistical analyses were performed on all values obtained every 1 min. HR and Tes at rest and during exercise were reduced significantly after training in all trials, and MAP during exercise in all trials except the LC trial was significantly reduced. There were no significant differences in <A><AC>T</AC><AC>&cjs1171;</AC></A>skin response to exercise among the trials and also before and after training in any trials except the LW trial, in which significant reductions in <A><AC>T</AC><AC>&cjs1171;</AC></A>skin were observed at rest and during exercise after training.

Figure 1 illustrates FVC as a function of Tes during the FVC response test, and the Tes threshold for increasing FVC, Delta FVC/Delta Tes of the second component, and SL in each subject are summarized in Table 2 for statistical analyses. The Tes threshold was significantly decreased in the LW (P < 0.05) and HW (P < 0.01) trials after training. The magnitude of the Tes threshold in the HW trial was significantly higher than in the LC trial (P < 0.05), where the statistical power was 0.52 with an effect size of 0.62. The second slope of Delta FVC/Delta Tes increased significantly in the LC, LW, and HW trials (P < 0.05), whereas in the HC trial it remained unchanged. The magnitude of the increase in the slope for the HW trial was significantly higher than in the LC trial (P < 0.05), where the statistical power was 0.65 with an effect size of 0.71. The SL decreased significantly in the HW trial (P < 0.05), whereas that in the HC trial tended to increase after training but without any significant difference among the trials.

Figure 2 shows the change in FVC response to increased Tes after training. In the LC trial, the FVC response was significantly enhanced above 37.4°C Tes after training (P < 0.05), whereas that in the HC trial tended to be reduced, and significant differences were observed above 37.4°C Tes relative to that in the LC trial (P < 0.01). The FVC response in the LW trial was significantly improved above 37.2°C Tes (P < 0.05) but was not significantly different from that in the LC trial. In contrast, the FVC response in the HW trial was significantly improved compared with that in the LW trial, and significant increases relative to that in the LW trial were observed over the range of Tes, except for 37.7 and 37.9°C (P < 0.01). The statistical power and effective size for the comparison among the trials were 1.00 and 0.49, respectively.


    DISCUSSION
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

The present study was conducted to test the hypothesis that training in a hypobaric hypoxic and warm environment would increase VO2 peak and sensitivity of cutaneous vasodilation in hyperthermia more than training in either environment alone, by increasing both PV and EV. However, the increases in VO2 peak and BV were similar among the trials, although EV increased significantly higher in the H trials, whereas it remained unchanged in the L trials. In addition, the FVC response to increased Tes tended to be enhanced more in the W trials than in the C trials, despite the similar increase in BV, with the highest magnitude in the HW trial and the lowest in the HC trial. These findings suggest that factors other than BV, related to atmospheric temperature and Patm for endurance training, were involved in the varied FVC response.

In the present study, the number of subjects per trial would be too small for sufficient statistical analyses in the comparison of variables among the trials. However, this number of subjects was maximal for us to accomplish the study within a limited period of 1 yr to avoid any seasonal effects on the results. As mentioned above, we rejected the null hypothesis at P < 0.05 after confirming that the level of the effect size was >0.40, which was recognized as a large level in the F test of ANOVA (2).

Another concern in the design of the present study was the examination of the aerobic capacity and FVC response to increased Tes up to 5 days after the cessation of training, during which period responses would be returning toward pretraining levels. However, PV measurement and the FVC response test were performed within 2 days after the training, followed by the VO2 peak measurement. Moreover, as shown in Table 3, HR at 5 min after the start of exercise for the FVC response test was reduced by ~5 beats/min at the same intensity of 60% pretraining VO2 peak, a 5-8% reduction in relative exercise intensity, almost equal to the relative increase in VO2 peak. Thus posttraining VO2 peak was likely to remain unchanged after the posttraining FVC response test.

As shown in Table 1, VO2 peak increased by 300 ml/min (5%), and BV increased by 200-250 ml (4-5%) in every trial. Coyle et al. (5) reported that VO2 peak increased by 200 ml/min (4%) after acute expansion of 200 ml of PV. Hopper et al. (11) reported that, in untrained adult men, stroke volume during submaximal exercise increased by 11% in response to acute expansion of 400 ml of PV. Also, 200 ml of acute EV expansion were reported to increase maximal aerobic power by 200-500 ml/min (23). Thus, in the present study, the increase in VO2 peak at a given increase in BV was almost identical to that obtained from acute expansion of PV or EV (5, 11, 23), suggesting that the increase in VO2 peak was at least partially caused by the increase in BV in the present study.

As shown in Fig. 1 and Table 2, the Tes threshold for increasing FVC was lowered significantly in the LW trial but not in the LC trial. The second slope of Delta FVC/Delta Tes was significantly increased in both trials, but the magnitude of the increase was fourfold higher in the LW trial than in the LC trial. Moreover, as shown in Fig. 2, the enhanced FVC response in the LW trial occurred at lower Tes than in the LC trial. These findings were obtained despite the similar increase in BV, suggesting that factors other than BV were involved in the higher increase in FVC response in the LW trial.

Roberts et al. (21) examined the effects of endurance training or heat acclimatization on FBF response to increased Tes and reported that the Tes threshold for cutaneous vasodilation decreased significantly more by exercise training in a hot environment than in a cool environment, although the changes in the slope of Delta FBF/Delta Tes were small and inconsistent. As for the mechanism, Nadel et al. (16) suggested that the lowered Tes threshold for sweating after heat acclimatization was mainly caused by central mechanisms, such as a reduction in the central nervous system point of zero sweating drive, whereas the increased sensitivity of sweating at a given Delta Tes was mainly caused by peripheral mechanisms, such as an increased sensitivity to the central sweating drive at the glandular level. Recently, Shido et al. (26) reported in humans that heat exposure at a fixed time of day shortened the sweating latency and decreased the rectal temperature threshold for sweating at the same time of day when exposed to heat, whereas it remained unchanged at other times of the day. Because BV and Posmol remained unchanged throughout their study, they suggested that central modification of thermoregulation would lower the threshold after heat exposure. Thus not only peripheral, but also central, mechanisms might be involved in a more enhanced FVC response for the LW trial. Experimentally, integrated Delta HR (Fig. 3B1) and SL (Fig. 3D1) during training were significantly greater in the LW trial than in the LC trial, suggesting more heat loading during training in the LW trial.

The FVC response in the HC trial remained unchanged, despite the significant increases in EV and PV (Figs. 1 and 2, Table 2). Sawka et al. (24) reported that an ~200-ml increase in EV by acute infusion of erythrocyte attenuated the Delta Tes during exercise in a hot environment. Recently, they reported that a 200-ml increase in EV reduced the Tes threshold for sweating and enhanced the sensitivity of sweating at a given Delta Tes (25). They postulated that polycythemia would enable a greater fraction of cardiac output to perfuse the skin and enhance sweating because oxygen transport requirements for a given level of submaximal exercise would be achieved with lower muscle blood flow. To examine that hypothesis, Patterson et al. (20) recently studied the effects of acute infusion of 400 ml of whole blood, of which Hct was 60%, on temperature regulation during exercise. However, they found that the SkBF response was attenuated by increased EV, whereas sweating was enhanced. They suggested that the lower core temperature due to enhanced sweating reduced the SkBF response. In the HC trial, EV was significantly increased by 92 ml, and SL in the FVC response test increased in four of five subjects but with no statistical significance in mean values. Thus the present findings appear to agree with those of Patterson et al. (20), suggesting that the increased EV did not increase the FVC response in the HC trial.

In contrast, the exposure to a hypobaric hypoxic and hot environment in the HW trial appeared to increase the FVC response by a greater extent than in the LW trial (Fig. 2 and Table 2). This finding may be explained by more heat loading in the HW trial than in the LW trial after 7 days of training. As shown in Fig. 3B1, cardiovascular drift estimated from Delta HR in the LW trial decreased after 7 days of training, which may have been caused by enhanced heat dissipation due to increased evaporative heat loss and/or heat conductance (8). However, Delta HR in the HW trial remained unchanged until the end of training. Because cardiovascular drift is known to reflect increased Tes (6), the higher Delta HR in the HW trial after 7 days of training suggested that the Tes during exercise training remained higher in the HW trial than in the LW trial until the end of the 10-day training. The higher Tes loading in the HW trial might have increased the FVC response more in the LW trial by modifications of central and peripheral thermoregulatory mechanisms, as described above (16, 26).

The precise reason for the higher Delta HR (or Tes) in the HW trial compared with the LW trial after 7 days of training is unclear. However, Kolka et al. (13) studied the body temperature regulation during exercise on a cycle ergometer at 60% of altitude-specific VO2 peak in an artificial chamber, where the altitudes were simulated sea level, 2,596 m, and 4,575 m and where Ta was controlled at 30°C and 30% RH, equivalent to the environment of the W trials in the present study. They reported that the sensitivities of the increases in FBF and the sweat rate at a given Delta Tes were both reduced with increasing altitude. Thus the higher heat loading and higher Tes in the HW trial compared with the LW trial may have been caused by the reduced heat dissipation function at 2,000 m, which may overcome the effect of the increased FVC response in the HW trial measured at 610 m (Fig. 1).

Another possible explanation for the most enhanced FVC response in the HW trial was due to the significant increase in EV of 130 ml for the HW trial. Sawka et al. (25) reported that the sensitivity of the sweating response to increased Tes at a given increase in EV was more enhanced in heat-acclimatized subjects than in those unacclimatized. If it is true also in the case of the FVC response, the increased EV would have enhanced the sensitivity synergistically with heat acclimatization in the HW trial. Thus heat acclimatization in a hypobaric hypoxic environment increased the sensitivity of Delta FVC/Delta Tes more than in a normobaric and normoxic environment, which might be related to the increased EV in addition to heat exposure.

In summary, the VO2 peak in all trials increased similarly with a concomitant increase in BV but without any significant differences among the trials against our hypotheses. Moreover, the FVC response to hyperthermia varied among the trials, regardless of BV, increasing more after training in a warm environment than in a cool environment at a given altitude. However, the magnitude of the increase in FVC response was more enhanced after heat acclimatization at a high altitude than at sea level. Thus the FVC response after endurance training was affected by other factors than BV, such as by Patm as well as temperature for training.


    ACKNOWLEDGEMENTS

We thank the volunteer subjects for participating in this study.


    FOOTNOTES

This study was supported in part by grants from the Uehara Memorial Foundation; the Descente and Ishimoto Memorial Foundation for the Promotion of Sports Science; and the Ministry of Education, Science, Sports and Culture of Japan. For this study, Y. Takeno was a recipient of the Recognition Award for Meritorious Research at Experimental Biology 2000 from the American Physiological Society, Environmental and Exercise Physiology Section.

Address for reprint requests and other correspondence: H. Nose, Dept. of Sports Medicine, Shinshu Univ. School of Medicine, 3-1-1 Asahi Matsumoto 390-8621, Japan (E-mail: nosehir{at}sch.md.shinshu-u.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.

Received 28 November 2000; accepted in final form 25 May 2001.


    REFERENCES
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

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J APPL PHYSIOL 91(4):1520-1528
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