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J Appl Physiol 103: 1221-1226, 2007. First published July 26, 2007; doi:10.1152/japplphysiol.00153.2007
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Relationship between resting ventilatory chemosensitivity and maximal oxygen uptake in moderate hypobaric hypoxia

Takeshi Ogawa,1 Keiji Hayashi,1 Masashi Ichinose,1 and Takeshi Nishiyasu1

1Institute of Health and Sports Science, University of Tsukuba, Tsukuba City, Japan

Submitted 6 February 2007 ; accepted in final form 20 July 2007


   ABSTRACT
TOP
 ABSTRACT
METHODS
 RESULTS
 DISCUSSION
 GRANTS
 ACKNOWLEDGMENTS
 REFERENCES
 
This study tested the hypothesis that the extent of the decrement in VO2max and the respiratory response seen during maximal exercise in moderate hypobaric hypoxia (H; simulated 2,500 m) is affected by the hypoxia ventilatory and hypercapnia ventilatory responses (HVR and HCVR, respectively). Twenty men (5 untrained subjects, 7 long distance runners, 8 middle distance runners) performed incremental exhaustive running tests in H and normobaric normoxia (N) condition. During the running test, VO2, pulmonary ventilation (VE) and arterial oxyhemoglobin saturation (SaO2) were measured, and in two ventilatory response tests performed during N, a rebreathing method was used to evaluate HVR and HCVR. Mean HVR and HCVR were 0.36 ± 0.04 and 2.11 ± 0.2 l·min–1·mmHg–1, respectively. HVR correlated significantly with the percent decrements in VO2max (%dVO2max), SaO2 [%dSaO2 = (N–H)·N–1·100], and VE/VO2 seen during H condition. By contrast, HCVR did not correlate with any of the variables tested. The increment in maximal VE between H and N significantly correlated with %dVO2max. Our findings suggest that O2 chemosensitivity plays a significant role in determining the level of exercise hyperventilation during moderate hypoxia; thus, a higher O2 chemosensitivity was associated with a smaller drop in VO2max and SaO2 under those conditions.

ventilation; hypoxia ventilatory response; moderate altitude

IT IS KNOWN that VO2max is reduced at altitude with a reduction in amount of inspired oxygen pressure (13, 15, 26). The effect of hypoxia (2,400~3,000 m) on VO2max (12, 13, 22) is more pronounced in subjects with higher VO2max (12, 13), as these individuals show a lower hemoglobin O2 saturation (SaO2) when exercising under hypoxic conditions (13, 22). One of the mechanisms that could account for the reduction in SaO2 seen during maximal exercise under hypoxic conditions is a reduction in the peak exercise ventilation (VEmax). In fact, it is known that VEmax contributes to both VO2max and SaO2 during maximal exercise (6, 8). Increasing pulmonary ventilation increases alveolar oxygen pressure and alveolar gas exchange, leading to increased SaO2. For that reason, it is likely that the magnitude of the decline in VEmax that occurs with increasing altitude, compared with sea level, is reflected by the magnitude of the decrements in VO2max and SaO2 (6).

Increased minute ventilation (VE) at rest, aimed at maintaining arterial oxygenation at an appropriate level (27), is one of the adaptations underlying acute acclimatization to an increase in altitude. Moreover, arterial hypoxic or hypercapnic ventilatory chemosensitivity can be evaluated based on the magnitude of the increase in VE when chemoreceptors are stimulated by inhalation of hypoxic (hypoxia ventilatory response; HVR) or hypercapnic gases (hypercapnia ventilatory response; HCVR). Functionally, one would expect individuals with a higher HVR to be more able to adapt to hypoxia than those with a lower HVR, who would be more likely to develop altitude sickness (16, 18, 24, 25). HVR thus could be an indicator of the ability to climb to extreme altitudes. Interestingly, trained athletes often have lower HVRs and HCVRs than untrained subjects (3, 20). As far as we know, however, there has never been a systematic examination of the relationship between chemosensitivity (HVR and/or HCVR) and VO2max or exercise performance at moderate altitude (around 2,500 m), which is often used as a training strategy by athletes.

Benoit et al. (1) reported that HVR correlates with SaO2 and VE during exhaustive exercise under hypoxic conditions (simulated 5,400 m above sea level). Thus HVR or HCVR is likely to be related to both the ventilatory responses seen during exercise under hypoxic conditions and to the magnitude of the decrement in VO2max seen at moderate altitude. The purpose of this study was to assess the influence of ventilatory chemosensitivity on the magnitude of the decrement in VO2max seen under conditions of moderate hypobaric hypoxia (H; 2,500 m above sea level, which is often used for altitude training). It was hypothesized that the extent of the decrement in VO2max related to HVR and HCVR, which are, in turn, associated with VE and SaO2 during exhaustive exercise. To test this idea, we studied 20 subjects (2 groups of trained athletes and a group of untrained healthy men) as they performed an incremental exhaustive running test in a hypobaric chamber under normobaric and hypobaric conditions.


   METHODS
TOP
 ABSTRACT
 METHODS
RESULTS
 DISCUSSION
 GRANTS
 ACKNOWLEDGMENTS
 REFERENCES
 
Twenty men participated in this study. All were lowlanders and had not been exposed to altitude above 1,000 m within the 6 mo prior the study. Five were untrained graduate physical education students (UN), and the others were athletes on the track and field team; seven of those were long distance runners (LD) and eight were middle distance runners (MD). With this population, there was a fairly large range of VO2max at sea level (44.8–79.9 ml·kg–1·min–1). The subjects were divided into a higher HVR group (HH; n = 10) or a lower HVR group (LH; n = 10) based on HVRs [HH > mean value of HVR in all subjects (0.36 l·min–1·%–1) > LH] to compare the influence of HVR on VO2max in the H condition. All of the subjects provided written informed consent to participate this study, and the study was approved by the Human Subjects Committee of the University of Tsukuba.

After familiarization with the experimental procedures, the subjects performed a treadmill running test in an environmental chamber (Shimazu; Kyoto, Japan) at the University of Tsukuba under normobaric N and H conditions in random order. In the H condition, the subject performed at an air pressure of 560 Torr (equivalent to an altitude of 2,500 m above sea level). The temperature in the environmental chamber was set at 20.0°C, and the room was force ventilated to avoid CO2 accumulation.

Maximal exercise test.   Following a warm-up outside the laboratory, an incremental test to exhaustion was carried out on the treadmill. The treadmill inclination was set at 0°, and the initial running speed was set at 160 or 140 m/min. The treadmill speed was then increased every 2 min so that 280 or 260 m/min was reached within 15 min, after which the running speed was increased 10 m/min each 1 min until exhaustion.

Respiratory variables were determined in two ways. The expired gas was collected into Douglas bags, which were opened for 1 min at each running speed. The O2 and CO2 fractions (FO2 and FCO2) were monitored using a mass-spectrometer (ARCO1000; ARCO; Chiba, Japan) and VE (BTPS) was measured using a dry gas meter (DC-5A; Shinagawa; Tokyo, Japan). VO2, VCO2, and the ventilatory equivalent for VO2 (VE/VO2) were then determined. In addition, an automatic open-circuit respirometer (RM-300i; MINATO medical Science; Osaka, Japan) and mass-spectrometer (ARCO1000; ARCO; Chiba, Japan) was used to obtain online breath-by-breath data, which were averaged every 5 s. In hypobaric hypoxic exercise measurements, although rare, there can be a problem in synchronizing of ventilation with gas concentration for calculating the VO2 when respiratory frequency is very high. This is because of the larger time constant of gas concentration measurement (pump capacity of mass spectrometer is weakened mechanically in the hypobaric condition). Thus we used the Douglas bag method to calculate VO2max and online data only to monitor the subject's condition and to confirm that maximal values were obtained during the test immediately, i.e., all subjects accomplished the following criteria for VO2max: 1) VO2 reached plateau state, despite increases in running speed; 2) the respiratory quotient was over 1.1; and 3) a maximal heart rate that was 90% of the age prediction (220 – age) was reached.

Fingertip blood samples were analyzed using a lactate analyzer (YSI 1500 SPORT; Yellow Spring Industry, Yellow Spring, OH) to measure blood lactate (BLa) levels and determine the peak BLa concentration. Blood samples were taken at rest and 2.5, 5, and 7.5 min after exhaustion had occurred. SaO2 was measured by pulse oximetry from the second finger (N-200; Nellcor, Hayward, CA), and heart rate (HR) was measured using a HR monitor (Vantage NV; POLAR, Kemple, Finland).

HVR test.   HVR was measured using a rebreathing method. On the day before the test, the subjects refrained from doing heavy exercise or drinking alcoholic or caffeine-containing drinks. On the test day, the subjects entered the environmental chamber and rested on a comfortable chair for 20 min. Then a mask connected to a closed one-way circuit with a 10-liter rubber bag (room air) was placed on the subject. The subject then watched a documentary video program so as not to be aware of the hypoxia during the test. For the first 4 min with the stopcock open ("the one-way rebreathing circuit"), the subjects breathed room air to measure control ventilation values. Then the stopcock was closed and rebreathing began. Because the subjects rebreathed their expiratory gas, their inspiratory oxygen pressure decreased gradually. During the rebreathing period, expiratory gas was passed through a CO2 absorber (WAKO LIME-A; Wako Pure Chemical Industries; Osaka, Japan), so that end-tidal CO2 was maintained at control levels throughout the test, which was terminated when SaO2 had declined to 72–75%. VE, FO2, and FCO2 were monitored breath-by-breath using a respirometer (RM300i; MINATO Medical Science; Osaka, Japan) and a mass spectrometer (ARCO1000; ARCO, Chiba, Japan). SaO2 was monitored by pulse oximetry (N-500; Nellcor, Hayward, CA) from the forehead. The subjects performed the HVR test twice, with a recovery period of at least 20 min in between. HVR was calculated as the slope of the liner regression line relating SaO2 and VE.

HCVR test.   On a different day, HCVR was measured using a rebreathing method that was essentially as described above (21). The subjects wore a mask that was connected to a closed one-way circuit with 10-liter rubber bag containing the test gas (7% CO2, 93% O2). Control ventilation was measured during the first 4 min of the test, after which the rebreathing started. Rebreathing was terminated when the inspired CO2 fraction reached 9.2%. VE and gas concentrations were monitored breath-by-breath, and this test was performed twice with a 20-min recovery period in between tests. HCVR was calculated as the slope of the regression line relating end-tidal CO2 and VE.

Statistical analysis.   Data were expressed as means ± SE. Double factor repeated ANOVA was carried out to assess the difference between subject characteristics and conditions (N vs. H). Least significant difference test was performed to determine interaction between main effects. Pearson product moment correlations were determined between variables. Values of P < 0.05 were considered significant.


   RESULTS
TOP
 ABSTRACT
 METHODS
 RESULTS
DISCUSSION
 GRANTS
 ACKNOWLEDGMENTS
 REFERENCES
 
VO2max test.   The subject profiles and the results of the incremental exercise tests are summarized in Tables 1 and 2, respectively. VO2max was significantly higher in the athletes (LD and MD) than in the untrained subjects (UN; Table 1), and the mean VO2max for all the subjects was significantly lower in the H than the N condition (Table 2). The mean percent decrement in VO2max between the N and H condition (%dVO2max) for all subjects was 16.7 ± 1.2%, and %dVO2max was significantly correlated with VO2max in the N condition (r = 0.68; P < 0.01). VEmax was significantly higher in the H than the N condition (Table 2), and the percent difference in VEmax between H and N (%dVEmax) correlated significantly with %dVO2max (Fig. 1). SaO2 at exhaustion was significantly lower in the H than the N condition, and the percent difference in SaO2 between the H and N condition (%dSaO2) also correlated significantly with %dVO2max (Fig. 1). Peak HR (HRmax) was significantly lower in the H than the N condition, but there was no difference in the respective postexercise peak BLa values (Table 2).


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  		Table 1. Subjects profile

 

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  		Table 2. Results of VO2max test

 

Figure 1
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  		Fig. 1. Relationships between percent decrements in maximum oxygen consumption (%dVO2max) in the hypobaric hypoxic (H) condition and cardiorespiratory responses during exhaustive running. %dVO2max correlated significantly with both percent decrements in arterial oxygen saturation (%dSaO2; A) and peak exercise ventilation (%dVEmax; B). bullet, Untrained subjects; {blacktriangleup}, long-distance runners; {blacklozenge}, middle-distance runners.

 
HVR and HCVR.   Slopes of the HVR and HCVR relations are shown in Tables 1 and 3. Table 3 shows the mean values of HVRs and HCVRs in the first and second trials, respectively. There is no significant difference between the first and second trials. The mean values for the two tests were 0.36 ± 0.04 l·min–1·%–1 and 2.11 ± 0.21 l·min–1·mmHg–1 (HVR and HCVR, respectively), which are consistent with those reported by Harms and Stager (7) in physically active men (0.16~0.61 l·min–1·%–1 in HVR, 1.78~2.73 l·min–1·mmHg–1 in HCVR). Neither the HVRs nor the HCVRs obtained for the three groups significantly differed (Table 1), but although HVR correlated significantly with VO2max in the N condition (Fig. 2), HCVR did not.


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  		Table 3. Reproducibility of the rest ventilatory chemosensitivity test

 

Figure 2
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  		Fig. 2. Relationship between hypoxia ventilatory response (HVR) and VO2max in the normoxia (N) condition (A) or %dVO2max in the H condition (B). HVR correlated significantly with both VO2max and %dVO2max. bullet, Untrained subjects; {blacktriangleup}, long-distance runners; {blacklozenge}, middle-distance runners.

 
We divided the subjects into two groups based on HVR. The cardiorespiratory responses and chemosensitivity of two groups are shown at Table 4. VO2max in the H condition and in the N condition were not different between the higher HVRs group (HH) and the lower HVRs group (LH). However, the percentage decrement in VO2max is larger in LH than HH. In HH group, VEmax was significantly increased in the H condition compared with the N condition, but not in LH. SaO2 was decreased to a greater extent in LH compared with HH.


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  		Table 4. Cardiorespiratory response in maximal running in hypobaric hypoxic condition

 
The relationships between HVR and the respiratory variables measured during the maximal exercise test are summarized in Figs. 2 and 3. %dVO2max correlated significantly with HVR (Fig. 2), as did both SaO2 and %dSaO2 in the H condition (Fig. 3). HVR also was significantly related to VE/VO2 in both the H (Fig. 3) and N conditions (r = 0.47; P < 0.05). No relationship was observed between HCVR and any of the respiratory variables in either condition during maximal exercise.


Figure 3
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  		Fig. 3. Relationships between HVR and variables of cardiorespiratory responses during exhaustive running. HVR correlated significantly with VE/VO2 (A), %dSaO2 (B), and SaO2 in the H condition (C). bullet, Untrained subjects; {blacktriangleup}, long-distance runners; {blacklozenge}, middle-distance runners.

 

   DISCUSSION
TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
GRANTS
 ACKNOWLEDGMENTS
 REFERENCES
 
The major findings of the present study were the following. 1) The HVR was negatively correlated with the effect of simulated 2,500 m altitude on the percent decrement in VO2max (%dVO2max), the percent decrement in SaO2 (%dSaO2), and VE/VO2, whereas the HCVR had no relationship with any of the measured variables. 2) %dVO2max correlated with the percent difference in VEmax between the N and H conditions (%VEmax). 3) The subjects with lower HVR (LH) expressed the greater decrement in VO2max, smaller increase in VEmax, and larger decrease SaO2 in the H condition compared with the subjects with higher HVR (HH). Taken together, these findings suggest that at moderate altitude, ventilatory chemosensitivity to hypoxia could to some extent determine the ventilatory response to exercise and VO2max, given the impact that VE has on alveolar and arterial PO2 and SaO2.

HVR and HCVR are known to be affected by the subjects' condition (i.e., exercise, arterial PCO2, arterial PO2, caffeine, etc.). Thus, to obtain reproducible values, the rebreathing test was performed in the morning and the subjects had refrained from doing heavy exercise or drinking alcoholic or caffeine-containing drinks on the day before. The mean values of first and second trials were not significantly different (Table 3) and the mean values for two tests (0.36 ± 0.04 l·min–1·%–1 and 2.11 ± 0.21 l·min–1·mmHg–1; HVR and HCVR, respectively) were similar to those reported by Harms and Stager (7) in physically active men (0.16~0.61 l·min–1·%–1 in HVR, 1.78~2.73 l·min–1·mmHg–1 in HCVR). Thus we believe that our HVR and HCVR measurements are reliable. Furthermore, the significant negative correlation between HVR and VO2max seen in the present study is consistent with those of earlier findings (3).

We observed a significant negative correlation between HVR and %dVO2max, suggesting that the chemosensitivity to hypoxia at rest may explain some of the individual differences in %dVO2max in the H condition. In addition, the magnitude of %dVO2max also was associated with VO2max in the N condition, which also is consistent with previous studies (12, 13). We also observed that HVR is related to VE/VO2 and SaO2 during maximal exercise in the H condition in both endurance athletes and active but untrained subjects. Moreover, the subjects with the lowest HVRs tended to show the largest %dSaO2 during maximal exercise (Fig. 3). These suggest that during maximal exercise at moderate altitude, the ventilatory chemosensitivity drive could affect the extent of hyperventilation and oxyhemoglobin desaturation.

Previous studies reported that during maximal exercise under hypoxic conditions (9.2~14%O2), SaO2 (6, 13), and VE (5, 15) were linked to the magnitude of the decrement in VO2max. We observed that in the H condition %dVEmax was related to the %dSaO2, which was in turn related to the %dVO2max. This is consistent with the idea that a larger increase in VEmax could have attenuated the hypoxia-induced oxyhemoglobin desaturation at moderate altitude (1, 7).

Harms and Stager (7) reported that subjects with low chemosensitivity (HVR and HCVR) showed hypoventilation and a low SaO2 during intensive exercise under normoxic conditions, whereas Benoit et al. (1) reported that HVR correlated with VE/VCO2 and SaO2 during maximal exercise under severely hypoxic conditions (9.2% O2). Thus resting ventilatory chemosensitivity to hypoxia may be related to the exercise ventilatory responses under both normoxic and severely hypoxic conditions. By contrast, Gavin et al. (6) found no relationship between HVR and VEmax in hypoxia. This discrepancy may be explained by differences in the population analyzed. Whereas all of the subjects studied by Gavin et al. (6) were trained athletes, those studied by ours included both trained athletes and untrained subjects. It is also noteworthy that in Gavin et al. (6) the coefficient of variation of VO2max was 5.81 in high HVR subjects and 7.95 in low HVR subjects, whereas it was 12.33 in Benoit et al. (1) and 13.10 in ours. These larger coefficients of variation could underlie the higher correlations between the variables studied.

We observed that in LH subjects, the extent of increase in VEmax in the H condition was smaller and that the extent of decrease in SaO2 and in VO2max in the H condition was greater compared with HH subjects. These suggest that at moderate altitude, subjects with lower ventilatory chemosensitivity to hypoxia would reach a lower SaO2 and larger decrease in VO2max due to the lower degree of hyperventilation. Thus the subjects with lower HVR would not induce significant the hyperventilation to maintain the gas exchange for SaO2 during exercise in a hypoxic condition compared with the subjects with higher HVR. Inadequate hyperventilation, therefore, could reduce the oxygen supply to active muscles during maximal running in moderate altitude.

Since most of the subjects achieved higher VEmax in the H condition, arterial PCO2 could have been slightly lower in the H condition than the N condition. Thus it is possible that lower HCVR could be facilitated an increase in VE during hypoxic stimulation. However, contrary to HVR, HCVR had no correlation to the ventilatory response maximal exercise in the H condition, suggesting that CO2 chemosensitivity does not affect ventilatory during exercise in moderate altitude.

Endurance athletes reportedly can reach the mechanical limitation of lung function during strenuous exercise in normoxia (5, 10, 17). Consequently, subjects showing a lesser degree of hyperventilation in the H condition likely could have been unable to increase VEmax due to a mechanical limitation on flow that was independent of HVR. We did not measure flow-volume parameters, however. Further investigation will be needed to determine the degree to which mechanical flow resistance affects the ventilation in the H condition.

In addition, hypoxemia could act on the central nervous system (CNS) to limit central command (motor drive; Refs. 4, 11). In his review of the central nervous limitations on exercise performance, Kayzer (11) suggested that during continuous exhaustive exercise, a reduction in motor unit recruitment occurs during hypoxia and that this would lead to a reduction in performance with no sign of muscle metabolic fatigue. It is thus possible that the level of VEmax seen in the H condition reflected a premature end of the exercise caused by a direct or indirect effect of low PaO2 on the CNS. That said, this possibility seems unlikely in our case, as our subjects performed to exhaustion in both the N and H conditions (with the help of vigorous verbal encouragement), and BLa values after exhaustion were similar under both conditions. This means that in both the N and H conditions our subjects were forced to generate a high degree of motor drive (central command) when exhausted. Moreover, earlier reports have shown that individuals can perform maximal exercise during more severe acute hypoxia (PaO2 as low as 31 mmHg) with a lower VE/VO2 (4) than we used in the present investigation.

Desaturation could also have been caused by a diffusional limitation during hypoxia. It has been hypothesized that such a diffusional limitation is accentuated by the higher cardiac output due to a reduction in the transit time of the blood in some alveolar capillaries (9). However, we detected no relationship between the reduction in HRmax with hypoxia and the change in SaO2, which suggests that other factors, apart from cardiac output, also play a role. The reduction in HRmax seen in the H condition is consistent with earlier observations made by others [Benoit et al. (2), 3,800 m; Calbet et al. (4), 10.5% O2; Martin et al. (14), 13% O2] and our laboratory (19).

We measured HVR and HCVR at rest condition and found the relationship between HVR and ventilatory response during maximal exercise in the H condition. Since previous studies suggested that HVR is enhanced during exercise (14, 23, 27), a role of chemosensitivity for ventilatory response during exercise may be more important than that at rest. Further study is needed to clarify the importance of chemosensitivity in ventilatory responses and VO2max in the H condition by evaluating HVR during exercise.

Practical implications.   One limitation of training at altitude is that athletes cannot maintain the same absolute intensity as when training at sea level. Most likely, those athletes who lose a higher fraction of their VO2max will have more difficulty maintaining training intensity at altitude. The present study shows that assessing the HVR may be a useful means of identifying athletes who will likely show an inadequate hyperventilation and greater desaturation during intensive exercise at moderate altitude, and consequently, a greater reduction of VO2max.

In summary, we evaluated the relationships between the ventilatory chemosensitivity to O2 and CO2 (HVR and HCVR) and VO2max under conditions of hypobaric hypoxia. The subjects with lower HVR expressed the greater decrement in VO2max, smaller increase in VEmax, and larger decrease SaO2 in the H condition compared with the subjects with higher HVR. Our findings suggest that whereas O2 chemosensitivity plays an important role in the ventilatory response during exercise at moderate altitude, CO2 chemosensitivity appears to have no definite role.


   GRANTS
TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 GRANTS
ACKNOWLEDGMENTS
 REFERENCES
 
This study was supported by grants from University of Tsukuba Research Projects, COE projects, and the Ministry of Education, Science, and Culture, Japan.


   ACKNOWLEDGMENTS
TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 GRANTS
 ACKNOWLEDGMENTS
REFERENCES
 
We are grateful to the University of Tsukuba track and field distance team for participation in this study.


   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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