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Departments of 1Sports Medical Sciences and 2Anesthesiology and Resuscitation, Shinshu University Graduate School of Medicine, Matsumoto, Japan
Submitted 30 July 2004 ; accepted in final form 8 March 2005
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ABSTRACT |
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 TOP ABSTRACT METHODSRESULTSDISCUSSIONGRANTSREFERENCES |
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O2 peak) for 1 h/day for 10 days at 30°C. Before and after ET, thermoregulatory responses were measured during 20-min exercise at pretraining 70% O2 peak in the same environment as during ET under isoosmotic or hyperosmotic conditions. Hyperosmolality by 
10 mosmol/kgH2O was attained by acute hypertonic saline infusion. After ET, O2 peak and blood volume (BV) both increased by 4% (P < 0.05), followed by a decrease in THFVC (P < 0.05) but not by that in THSR. Although there was no significant decrease in Posmol at the thresholds after ET, the sensitivity of increase in THFVC at a given increase in Posmol [
THFVC/Posmol,°C·(mosmol/kgH2O)–1], determined by hypertonic infusion, was reduced to 0.021 ± 0.005 from 0.039 ± 0.004 before ET (P < 0.05). The individual reductions in THFVC/Posmol after ET were highly correlated with their increases in BV around THFVC (r = –0.89, P < 0.005). In contrast, there was no alteration in the sensitivity of the hyperosmotic suppression of sweating after ET. Thus the downward shift of THFVC after ET was partially explained by the blunted sensitivity to hyperosmolality, which occurred in proportion to the increase in BV. esophageal temperature threshold; plasma volume
Posmol is known to increase with relative exercise intensity due to free plasma water loss into the contracting muscles (19, 24). Takamata et al. (26) suggested that increased Posmol with exercise intensity caused an upward shift of THFVC during light and moderate exercise. More recently, Mitono et al. (14) suggested that reduced Posmol by hypotonic saline infusion decreased THFVC during moderately intense exercise. Thus the downward shifts of THFVC and THSR after exercise training or heat acclimatization would be caused by an attenuated increase in Posmol at a given intensity of exercise due to increased maximal aerobic power. Alternatively, the downward shift of the thresholds would be caused by the attenuated sensitivity of the hyperosmotic suppression of cutaneous vasodilation or sweating. Indeed, Takamata et al. (27) suggested in passively heated subjects that the upward shift of the thresholds by acute hyperosmolality was attenuated in subjects excreting diluted sweat who were assumed to have acclimatized to heat (1).
The purpose of this study was to test our hypotheses that decreased THFVC and THSR after 10-day endurance training would be caused by either an attenuated increase in Posmol at a given intensity of exercise or the blunted sensitivity of hyperosmotic suppression.
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METHODS |
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This study was approved by the Review Board on Human Experiments, Shinshu University School of Medicine. Nine healthy male volunteers gave written informed consent before participating in this study. Their age was 20.3 ± 0.3 yr (range 19–22 yr), height 172 ± 2 cm (range 164–182 cm), weight 62.1 ± 1.9 kg (range 54.4–70.9 kg), peak oxygen consumption rate (O2 peak) 3.58 ± 0.08 l/min (range 3.32–3.98 l/min), and maximal heart rate (HRmax) 192 ± 2 beats/min (range 187–204 beats/min). Four of nine subjects underwent 10-day endurance training (ET) between February and May and the remainder between June and September. Because the pretraining baselines of their physical characteristics, blood properties, and thermoregulatory responses were not significantly different between the groups (P > 0.05), they were pooled for the analyses.
Protocols
Before ET, O2 peak was first determined, and 2 days later, the blood volume (BV) measurement and the thermoregulatory response test were performed under isoosmotic conditions (IC) on the same day, and 2 days later, the thermoregulatory response test was repeated under hyperosmotic condition (HC) attained by prior infusion of hypertonic saline as described below. Within 24 h after the termination of ET, the BV measurement and the thermoregulatory response test were performed in IC on the same day, and, 24 h later, the thermoregulatory response test was repeated in HC. O2 peak after ET was determined within 24–48 h after the test. All measurements except for O2 peak were performed at the same time in the morning to avoid any effect of circadian variations.
On the day of the experiment in IC, subjects reported to the laboratory at 7:30 AM, normally hydrated but having fasted for 10 h before the experiment. They had been told to refrain from any beverages containing caffeine or alcohol and salty foods the day before the experiment. After sitting for 60 min at 28°C ambient temperature (Ta) and 50% relative humidity (RH), BV was determined as described below. After the BV measurement, they put on shorts and shoes, emptied their bladders, and entered the artificial climate chamber at 30°C Ta and 50% RH for the thermoregulatory response test.
On the day of the experiment in HC, subjects reported to the laboratory at 6:45 AM under the same condition as in IC. After subjects sat for at least 20 min in the same environment as in IC, a control blood sample was taken, and they then took 20 mg of furosemide and rested in a sitting position for 2 h with permission to urinate. The total urine volume during this period was 1,800 ml. After the treatment, they entered the artificial climate chamber for the thermoregulatory response test, sat on the contoured seat of the cycle ergometer, and then received an infusion of 3% saline for 90 min at 0.1 ml·min–1·kg body wt–1. As a result, Posmol increased by 10 mosmol/kgH2O while the plasma volume (PV) remained at the same level as in IC, which was assumed to increase by 500 ml if not pretreated with furosemide.
Thermoregulatory Response Test
While subjects rested in a semirecumbent position for at least 30 min in IC and HC, all measurement devices were applied. After the baseline measurements were taken for 10 min, subjects exercised at 70% of pretraining O2 peak at 60 cycles/min for 20 min without fan cooling. The heart rate (HR), systolic (SAP) and diastolic arterial pressures (DAP), Tes, skin temperature, forearm skin blood flow (FBF), and chest sweat rate (SR) were measured every minute during exercise, and the details are described as below. Blood samples were taken at rest and every 5 min during exercise.
Ten-Day ET Regimen
Subjects exercised on a cycle ergometer in an upright position at 60% of O2 peak at 30°C Ta and 50% RH for 60 min/day for 10 days. The 60-min exercise consisted of two sets of 30-min exercise separated by 10-min rest with ad libitum water intake amounting to 1,000 ml. As O2 peak increased with ET, the exercise intensity was readjusted at 5 min after the start of exercise each day so that subjects exercised at a target HR equivalent to 60% of O2 peak, determined from the relationship between oxygen consumption rate (O2) and HR at the O2 peak measurement. 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 the body temperature started to increase.
Measurements
O2 peak.
O2 peak was measured with graded exercise using a cycle ergometer in an upright position at 25°C Ta and 50% RH. After 3-min baseline measurements at rest, subjects started pedaling at 60 cycles/min without loading. The exercise intensity was increased by 60 W every 3 min until 180 W and, above this intensity, by 30 W every 2 min until 240 W and then by 15 W every 2 min until subjects were not able to maintain the rhythm due to exhaustion. O2 was determined every 15 s from the oxygen and carbon dioxide fractions in the expired gas and the ventilatory volume (Aeromonitor AE260, Minato, Tokyo, Japan). O2 peak was determined after averaging three maximal values at the end of the exercise. HR was recorded every minute from an electrocardiogram trace (Life Scope 8, Nihon Kohden, Tokyo, Japan). HRmax was adopted at O2 peak. O2 peak in a semi-recumbent position was also determined before ET for the thermoregulatory response test throughout the experiment.
BV. On the day of the thermoregulatory response test in IC before and after ET, PV was determined by the Evans blue dye dilution method (10). After 60-min sitting as mentioned above, a control blood sample was taken, the dye was injected at 0.2 mg/kg body wt, and blood samples were taken at 10 and 20 min after the injection. The background absorbance due to turbidity was corrected using a regression equation for the relationship between 620 and 740 nm (6, 20), and the absorbance of a 10-min plasma sample was used to calculate PV. BV was calculated from PV and Hct, which was corrected for trapped plasma (0.96) and F-cell ratio (0.91) (11). The BV values in IC before and after ET were used as the values before diuretic administration for the thermoregulatory response test in HC before and after ET, respectively. After hypertonic saline infusion in HC before and after ET, we confirmed that Hct and the hemoglobin concentration ([Hb]) at rest returned to the values in IC. The change in BV during the thermoregulatory response test in IC and HC was determined from changes in Hct and [Hb] (10).
HR, blood pressures, and body temperature. HR was recorded every minute. SAP and DAP were measured every minute from the right upper arm at the heart level by inflating the cuff with a sonometric pickup of Korotkoff's sound (STPB-780, Colin, Komaki, Japan). Mean arterial pressure (MAP) was calculated as DAP + (SAP – DAP)/3. Tes was measured with a thermocouple in a polyethylene tube (PE-90), with the tip of the tube located at a distance of one-fourth of the subject's standing height from the external nares. Skin temperature was measured at the forearm (Tfa), chest (Tch), and thigh (Tth) with thermocouples. Mean skin temperature (Tskin) was determined as Tskin = 0.25·Tfa + 0.43·Tch + 0.32·Tth (21).
SR and FBF. SR was determined by the relative humidity and temperature of the air (THP-B3T, Shinei, Tokyo, Japan) flowing out of a 12.56-cm2 chest capsule at a rate of 1.5 l/min. FBF was measured by venous occlusion plethysmography with a mercury-in-Silastic tube strain gauge placed around the upper left forearm positioned above the heart level. The hand was eliminated from the circulation with a wrist cuff inflated to 280 mmHg, and venous return from the forearm was occluded with an upper arm cuff inflated to 60 mmHg (30). Forearm skin vascular conductance (FVC) was determined by FBF/MAP (in ml·min–1·100 ml–1·100 mmHg–1, expressed here as units). Tes, Tskin, and SR were recorded every 5 s and were represented every 30 s on average. FBF was measured twice every minute and was represented every minute on average.
Blood chemicals. Two of five milliliters of a sampled blood aliquot was used to determine Hct (microcentrifuge) and [Hb] (cyanomethemoglobin), and the remaining 3-ml aliquot of blood was centrifuged, and the plasma was placed in a chilled tube and stored at –85°C until assayed. The plasma was used to determine the plasma protein concentration by refractometry, Posmol by freezing-point depression (One-ten Osmometer, Fiske, MA), plasma sodium concentration ([Na+]p) by flame photometry (480 Flame Photometer, Corning, Medfield, MA), and plasma lactate concentration ([Lac–]p) by enzyme electrode (YSI 2300 Stat Plus, YSI, OH). These plasma electrolyte concentrations are expressed in millimoles per kilogram H2O after correction for plasma protein.
Data Analyses
Relationships between Tes and FVC or SR.
Figure 1 shows the Tes vs. FVC or SR relationships during the thermoregulatory response test. The Tes vs. FVC relationship in each subject was fitted with three regression equations using standard Y minimized regression analysis as described by Takeno et al. (28). The first was determined visually from the first sharp increase in Tes before the rapid increase in FVC, the second was determined from the rapid increase in FVC, and the third was determined from measurements after the second component. The THFVC from the cross point of the first and second regression lines and the slope of increase () in FVC (FVC) at a given Tes (FVC/Tes) were determined in each subject for statistical analyses, and the results are summarized in Table 1. The THFVC and FVC/Tes were determined by three separate investigators familiar with the method, and the three values were averaged. THSR and SR/Tes were also determined by the same method. These determinations were performed with the experimental designs blinded to the investigators.
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THFVC/Posmol) and THSR (THSR/Posmol) at a given increase in Posmol was determined from the differences in the thresholds and Posmol between IC and HC. For the determination, we used Posmol at 5 min of exercise or after averaging the values at 5 and 10 min of exercise, because THFVC and/or THSR were observed around those times. The time at the threshold was determined by interpolating the thresholds to the trace of Tes as a function of time during the thermoregulatory response test (Table 1). Statistics
The effects of ET on thermoregulatory responses were tested by one-way ANOVA for repeated measures in Fig. 2. The effects of ET or hyperosmolality on thermoregulatory responses were tested by two-way ANOVA for repeated measures in Table 1. Three-way ANOVA for repeated measures was used to test the effects of ET or hyperosmolality on cardiovascular and thermal responses at 1-min intervals in Table 2, and blood properties at 5-min intervals in Table 3. Subsequent post hoc tests to determine significant differences in the various pairwise comparisons were performed using Fisher's least significant difference test. The null hypothesis was rejected when P < 0.05. Results during the thermoregulatory response test were represented only at rest and at 5, 10, and 20 min of exercise to avoid complicating Tables 2 and 3. Regression analysis was performed using the least Y square method. Values are represented as means ± SE for nine subjects.
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RESULTS |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONGRANTSREFERENCES |
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O2 peak increased by 0.14 ± 0.03 l/min (P < 0.01), but with no significant changes in body weight and HRmax.
Table 2 shows HR, MAP, Tes, and Tskin during the thermoregulatory response test in IC and HC before and after ET. In IC, HR at rest remained unchanged after ET but decreased by 10 beats/min during exercise (P < 0.05), whereas MAP at rest decreased by 3 mmHg after ET (P < 0.05) and the decrease was sustained during exercise. In HC, regardless of before and after ET, HR increased and MAP decreased at rest compared with in IC. In IC, Tes at rest decreased by 0.16°C after ET (P < 0.05) and the decrease was sustained during exercise. In HC, before and after ET, Tes at rest increased by 0.20°C compared within IC (P < 0.05) and the increase was sustained during exercise.
Table 3 shows BV, Posmol, [Na+]p, and [Lac–]p during the thermoregulatory response test in IC and HC before and after ET. In IC, after ET, BV at rest increased by 207 ± 54 ml (P < 0.05) and the increase was sustained during exercise. There were no significant differences in BV between IC and HC at rest and during exercise, suggesting that the presumed increase in BV by hypertonic saline was completely cancelled by pretreatment with furosemide. In HC, before and after ET, Posmol and [Na+]p at rest increased by 10 mosmol/kgH2O and 5 mmol/kgH2O, respectively, compared within IC (P < 0.05), and the differences were sustained during exercise. In IC, after ET, [Lac–]p decreased at 10 and 20 min of exercise compared with before ET (P < 0.05).
Figure 1 shows FVC and SR responses to increased Tes during the thermoregulatory response test in IC and HC before and after ET. The results are summarized in Table 1. After ET, the upward shift of THFVC in HC was significantly lower than before ET (P < 0.05). FVC/Tes tended to increase after ET but with no significant differences. On the other hand, the upward shift of THSR in HC was not altered after ET (P > 0.55). SR/Tes was not changed after ET or in HC regardless of before and after ET.
Figure 2 shows THFVC/Posmol and THSR/Posmol before and after ET. THFVC/Posmol was 0.021 ± 0.005°C·(mosmol/kgH2O)–1 after ET, significantly lower than 0.039 ± 0.004°C·(mosmol/kgH2O)–1 before ET (P < 0.05). On the other hand, THSR/Posmol was 0.047 ± 0.007°C·(mosmol/kgH2O)–1 after ET, not different from 0.056 ± 0.011°C·(mosmol/kgH2O)–1 before ET (P > 0.50). To calculate Posmol before and after ET, the values of Posmol at 5 min of exercise in IC and HC were adopted, because THFVC and THSR were observed around 6 and 5 min of exercise, respectively, as in Table 1. In addition, we confirmed the results after averaging the values of Posmol at 5 and 10 min of exercise; THFVC/Posmol was 0.022 ± 0.006°C·(mosmol/kgH2O)–1 after ET, significantly lower than 0.039 ± 0.005°C·(mosmol/kgH2O)–1 before ET (P < 0.05), whereas THSR/Posmol was 0.044 ± 0.004°C·(mosmol/kgH2O)–1 after ET, not different from 0.055 ± 0.009°C·(mosmol/kgH2O)–1 before ET (P > 0.30).
As in Figure 3, the decrease in THFVC/Posmol after ET [(THFVC/Posmol)] was negatively correlated with the increase in BV (BV) in nine subjects (r = –0.89, P < 0.005). BV at 5 min of exercise was adopted, because THFVC was observed around that time. We also found a significant correlation between (THFVC/Posmol) and BV (r = –0.73, P < 0.05) after averaging the values of Posmol and BV at 5 and 10 min of exercise.
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DISCUSSION |
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TOPABSTRACTMETHODSRESULTSDISCUSSIONGRANTSREFERENCES |
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It has been reported that THFVC increased with increased Posmol by hypertonic saline infusion during exercise (8) or passive heating (25). Although the effects of acute hyperosmolality on thermoregulation have been reported, few studies have applied this concept to examine the mechanisms for downward shift of the threshold after exercise training or heat acclimatization, which has been discussed only from the viewpoint of increased sensitivity of thermosensitive neurons in the hypothalamus (16). In this study, THFVC/Posmol was reduced after ET, and the reduction for individuals was highly correlated with the increased BV around THFVC (Fig. 3).
To our knowledge, the blunted hyperosmotic suppression of thermoregulation after exercise training or heat acclimatization was first reported by Takamata et al. (27). They studied the sensitivity of the hyperosmotic suppression of sweating and cutaneous vasodilation in passively heated subjects and found that the upward shift of the thresholds at a given increase in Posmol by acute hyperosmolality was attenuated in subjects excreting diluted sweat who were assumed to have acclimatized to heat. As they suggested, if sensitivity is not attenuated in the subjects, the further increase in Posmol due to diluted sweat would enhance the hyperosmotic suppression of thermoregulation, although it is advantageous to maintain BV by mobilizing fluid from intracellular fluid space (18).
However, against these observations, there have been several studies suggesting that arginine vasopressin release to altered Posmol, as an index of the sensitivity of osmoreceptors, is enhanced after ET. Claybaugh et al. (2) measured urine excretion and arginine vasopressin responses to a given amount of water intake in fit and unfit subjects and suggested that both responses were attenuated in fit subjects compared with those in unfit subjects. Moreover, Freund et al. (9) suggested that plasma arginine vasopressin response to graded exercise was not different between fit and unfit subjects, although the increase in Posmol during exercise was significantly reduced in fit subjects. These results suggest that the blunted osmotic suppression of cutaneous vasodilation after ET was not caused by reduced sensitivity of osmosensitive structures in the circumventricular organs (12) but by other mechanisms. Experimentally, Takamata et al. (27) reported that arginine vasopressin response to acute hyperosmolality remained unchanged in the subjects who excreted diluted sweat, suggesting that the attenuated hyperosmotic suppression was limited to thermoregulation.
The high correlation between the reduction in THFVC/Posmol and the increase in BV (Fig. 3) suggests that blunted osmotic suppression occurred in proportion to the increase in BV. Several mechanisms for hypervolemia after exercise training or heat acclimatization have been suggested: increased activity in the renin-angiotensin-aldosterone system (3), increased plasma albumin synthesis (17), or blunted sensitivity of volume receptors (2). On the other hand, it was also reported that voluntary water intake (22) and/or thirst sensation (29) in dehydration were attenuated after head-out water immersion, suggesting that the stretch of intrathoracic baroreceptors due to increased BV suppresses the dipsogenic stimulation by hyperosmolality. Thus the cause and effect relationship between the reduced THFVC/Posmol and the increased BV remains unknown.
In this study, THSR/Posmol did not decrease after ET, different from THFVC/Posmol (Fig. 2). These results did not agree with the results reported by Takamata et al. (27) that the hyperosmotic suppression of sweating was also attenuated in subjects assumed to have acclimatized to heat. However, their results were obtained by comparing interindividual variations of sodium concentration in sweat and thermoregulatory responses, whereas ours were obtained from the changes in thermoregulatory responses before and after 10-day ET, so that other unknown factors caused by heat acclimatization over a longer period might be involved in the previous study (27). Moreover, the differences in protocol of the thermoregulatory response test should be considered in passively heated subjects for the previous study (27) and in exercising subjects for this study.
There have been a few studies suggesting that the efferent path to cutaneous vessels was different from that to sweat glands. It has been reported that the upward shift of THSR by acute hypovolemia was much less than that of THFVC (7, 15) and the stimulation of arterial baroreflexes by phenylephrine or sodium nitroprusside did not alter the sudomotor activity in resting subjects (31), suggesting that the sudomotor system is less sensitive to changed BV or baroreflexes. In addition, Kellogg et al. (13) demonstrated that THFVC increased during exercise compared with during passive heating, but THSR did not. Moreover, Crandall et al. (4) reported in hyperthermic subjects that cutaneous vasodilation was suppressed by isometric handgrip exercise, whereas SR was inversely enhanced. In this study, THFVC/Posmol decreased after ET, whereas THSR/Posmol did not. Moreover, THFVC significantly decreased after ET, whereas THSR did not (Table 1). Thus THFVC is more influenced by reduced BV, exercise, and 10-day ET than THSR.
Against our hypothesis, the relative exercise intensity was reduced by only 5% after ET. As a result, there were no significant differences in the increases in Posmol, [Na+]p, and [Lac–]p around THFVC or THSR during the thermoregulatory response test before and after ET (Table 3). These results suggest that the downward shift of THFVC after ET in this study was not caused by either the attenuated increase in Posmol or the stimulation by lactic acid of chemoreceptors in the contracting muscles (5).
Summarizing these results, the decreased sensitivity of the hyperosmotic suppression of cutaneous vasodilation might be involved in the reduction of the Tes threshold for this response after 10-day ET. Thus the adaptation of body fluid regulatory system might play an important role in thermoregulatory adaptation after this period of ET.
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FOOTNOTES |
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The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
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