Japanese Journal of Physiology, 50, 449–455, 2000
Respiratory Compensation Point during Incremental Exercise as Related to Hypoxic Ventilatory Chemosensitivity and Lactate Increase in Man
Nariko TAKANO
Physiology Laboratory, Department of School Health, Faculty of Education, Kanazawa University, Kanazawa, 920–1192 Japan
Abstract: The pulmonary ventilationÐO up- sures were normalized for body surface area. In 2 take (VE-VO2) relationship during incremental ex- the males, the individual difference in RCP was ercise has two inflection points: one at a lower inversely correlated with those of HVR and VO , termed the ventilatory threshold (VT); and ⌬slope (pϽ0.05), and in the females, similar ten- 2 another at a higher VO2, the respiratory compen- dencies persisted, while the correlation did not sation point (RCP). The individuality of RCP was reach statistically significant levels (0.05ϽpϽ studied in relation to those of the chemosensitivi- 0.1). There was no significant correlation be- ties of the central and peripheral chemorecep- tween RCP and HCVR in either sex. A multiple tors, which were assessed by resting estimates linear regression analysis showed that 40 to 50% of hypercapnic ventilatory response (HCVR) and of the variance of RCP was accounted for by hypoxic ventilatory response (HVR), respectively, those of HVR and ⌬slope, both of which were re- and the rate of lactic acid increase during exer- lated linearly and additively to RCP, this relation cise, which was estimated as a slope difference being manifested in the males but not in the fe- (⌬slope) between a lower slope of VCO -VO re- males without consideration of the menstrual 2 2 lationship (VCO2: CO2 output) obtained at work cycle. These results suggest that the individuality rates below VT and a higher slope at work rates of RCP depends partly on the chemosensitivity between VT and RCP. Twenty-two male and six- of the carotid bodies and the rate of lactic acid in- teen female subjects underwent a 1 min incre- crease during incremental exercise. [Japanese mental exercise test until exhaustion, in which Journal of Physiology, 50, 449Ð455, 2000] VT, RCP and ⌬slope were determined. All mea-
Key words: heavy exercise, respiratory compensation point, exercise hyperpnea, carotid body, lactic acidosis.
During incremental exercise in normal humans, pul- steeper increase in VE against VO2 occurs. The VO2 monary ventilation (VE) linearly increases with in- point of the onset of this VE augmentation is termed creasing O2 uptake (VO2), but the increment of VE the respiratory compensation point (RCP), above against VO2 becomes steeper at two VO2 points [1]. which the VE augmentation (hyperventilation) induces The first inflection point, occurring at a lower VO2, is a fall in arterial PCO2, with resulting constraint of fur- termed the ventilatory threshold (VT) [2], above ther falls of arterial pH due to severer lactic acidosis which various kinds of ventilatory stimuli such as a [7]. Peripheral chemoreceptors have been implicated fall in arterial pH due to lactic acidosis, hyperkalemia as the site at which the ventilatory stimuli act because and augumentation of arterial PCO2 oscillation are of the absence of compensatory hyperventilation and newly induced [3–6]. With further increases in the subsequent fall in PCO2 during heavy exercise in ventilatory stimuli as exercise becomes heavier, a carotid body–resected patients [8, 9].
Received on April 24, 2000; accepted on July 13, 2000 Correspondence should be addressed to: Nariko Takano, Physiology Laboratory, Department of School Health, Faculty of Education, Kanazawa University, Kanazawa, 920–1192 Japan. Tel: ϩ81–76–264–5568, Fax: ϩ81–76–234–4117, E-mail: [email protected]
Japanese Journal of Physiology Vol. 50, No. 4, 2000 449 N. TAKANO We hypothesized that, in individuals with greater tics are shown in Table 1. Body surface area was cal- carotid body chemosensitivities, compensatory hyper- culated from the height and weight measurements ventilation would begin at lower work rates at which using calculation formulas for Japanese men and smaller changes in the concentration of ventilatory women [19]. The subjects were all healthy non-smok- stimuli to the carotid bodies would be associated. The ers, of which 15 subjects were training as short and present study was undertaken to test this hypothesis. middle-distance runners, 4 subjects as long-distance In addition, involvement of central chemosensitivity runners in after-class activities, and 18 subjects were in the individual variance of RCP was also investi- taking part in recreational sports. Because of the vary- gated. Peripheral chemosensitivity was assessed by ing sports training status, physical fitness levels that hypoxic ventilatory responsiveness (HVR) and central were evaluated as maximum O2 uptake differed chemosensitivity by hypercapnic ventilatory respon- greatly among the subjects (Table 1). No special con- siveness (HCVR), both at rest. Since it has been re- sideration for menstrual cycle was given for the fe- ported that HVR [10–12] and HCVR [13] increase male subjects, to whom the phases of the menstrual with increasing exercise intensity, and that the exer- cycle on the day of the study were not inquired. cise estimates of HVR depend on the resting estimates Measurements. During the tests, the subjects of HVR [11, 12, 14], the individual differences in ex- breathed through a respiratory mask (dead space, ercise estimates of chemosensitivities at varying work 200 ml) to which a hot-wire flowmeter was fixed in rates were assumed to be predicted from those in the order to measure respiratory flow. Respiratory gas was resting estimates. continuously sampled (200 ml/min) from a nostril and Cooper et al. [15] divided the CO2 output–O2 up- introduced into a CO2-O2 gas analyzer (MG-360, Mi- take (VCO2-VO2) relationship up to RCP during incre- nato Medical Co., Japan), with which the CO2 and O2 mental exercise into two linear components. The inter- concentrations were analyzed through infrared ab- section point of the two linear components per se has sorption and zirconium oxide reaction, respectively. been described as V-slope AT (AT: anaerobic thresh- Signals from the flowmeter and gas analyzer were fed old, expressed in terms of VO2 level) and a more reli- into a signal processor (RM-200, Respiromonitor, Mi- able, non-invasive estimate of AT [7]. It has been ar- nato Medical Co., Japan) and processed breath-by- gued that the lower linear component with a lower breath to obtain pulmonary ventilation (VE), O2 up- slope (S1) in the VCO2-VO2 relationship reflects the take (VO2), CO2 output (VCO2), ventilatory equiva- aerobic metabolism (respiratory quotient) of the work- lents for O2 and CO2 (VE/VO2 and VE/VCO2, respec- ing muscles and the upper linear component with a tively) and end-tidal PO2 and PCO2. Heart rate (HR) higher slope (S2), aerobic metabolism plus “excess was monitored through an electrocardiogram. Arterial CO2” derived from bicarbonate buffering of lactic acid oxygen saturation (SO2) was measured using a finger taking place intramuscularly and extracellularly [16] if oximeter (Pulsox 8, Canon Co., Japan). the body CO2 stores are stable [15, 17]. Therefore, it Tests. Three tests were given to the subjects in would be assumed that the difference between S2 and the following order. Before the tests, the subjects un- S1 reflects an “approximate” rate of lactic acid in- derwent a training session in order to familiarize them crease occurring intramuscularly and extracellularly, with the equipment for the tests. although it does not reflect the “total” amount of lactic Transient hypoxic test for HVR assessment. This acid increase in the body fluids, a small portion of was based on the method of Shaw et al. [20]. A reser- which is buffered by the non-bicarbonate buffer sys- voir bag containing pure N2 was connected to the res- tem [18]. In the present study, the difference of S2 and piratory mask. After VE and HR reached a steady S1 (⌬slope) was also examined and used as an esti- state during air breathing, the inspired gas was mate of the rate of lactic acid increase at the work switched to N2 and three to eight breaths of N2 were rates below RCP. The aim of this was to explore the imposed on the subjects, followed by air breathing. relationship between the rate of lactic acid increase Subsequent hypoxic transients with a different number and RCP during incremental exercise (i.e., whether of N2 breaths were resumed after end-tidal PO2, SO2 the greater the former is, the lower the latter is). and HR returned to air-breathing levels. If SO2 levels during N2 breathing approached 70%, the subject was METHODS switched back to room air. The highest VE (actually calculated as the mean value of the two highest con- Subjects. Twenty-two male students and sixteen secutive VE) and the lowest SO2 achieved during the female students volunteered for this study after giving period of N2 breathing were obtained for each hypoxic written, informed consent. Their physical characteris- transient. Then, using the data from all six hypoxic
450 Japanese Journal of Physiology Vol. 50, No. 4, 2000 RCP during Incremental Exercise
transients, a linear regression of the highest VE and using Pearson’s correlation coefficients. Comparisons the lowest SO2 was analyzed for each subject by the in the measurements between male and female sub- least-squares method. The slope of the regression line, jects were analyzed using Welch’s test for unpaired ⌬VE/–⌬SO2, was designated as hypoxic ventilatory re- samples. The level of pϽ0.05 was considered to be sponsiveness (HVR). significant. CO2 rebreathing test for HCVR assessment. This was based on the method of Read [21]. After VE and RESULTS HR reached a steady state during air breathing, the subjects rebreathed a 7% CO2–93% O2 gas contained Mean results of the measurements and the variability in a reservoir bag for 4 min, during which end-tidal among the subjects are shown in Table 1 for each sex. PCO2 and VE were measured. A regression line of the Since it has been reported that HVR and HCVR are end-tidal PCO2–VE relationship was calculated and the affected by body surface area [23], all variables stud- slope (⌬VE/⌬PCO2) was defined as hypercapnic venti- ied were corrected for body surface area. Correlation latory responsiveness (HCVR). analysis was performed to examine how the variability Incremental exercise test. After 2 min unloaded of RCP can be explained by those of HVR, HCVR cycling on a bicycle ergometer, the subjects exercised and ⌬slope. The analysis was made on each sex, be- at a 1 min incremental work load until exhaustion. The cause there were sex differences in RCP and HVR increment of the load was 25 W/min at the pedalling (Table 1) even after the correction for body size. rate of 70 rpm for the male subjects and 15 W/min at Higher HVR in females than in males has been ob- 50 rpm for the female subjects. During the test, VO2, served by some investigators, while the inverse rela- VCO2, VE/VO2, VE/VCO2, and end-tidal PCO2 were tion has also been reported by others (see Aitken et al. measured. [23]). Based on changes in VE/VO2, VE/VCO2 and end- Table 2 shows that RCP correlated significantly and tidal PCO2 with changing VO2 associated with the inversely with HVR and ⌬slope in the male subjects work rate, ventilatory threshold (VT) was identified as and similar tendencies persisted in the female sub- the VO2 point at which transition of VE/VO2 from jects, although the correlation with HVR and ⌬slope, falling to rising phases occurred before transition of Table 1. Mean results and variability of the measure- E CO V /V 2 from falling to rising phases, and that of ments. end-tidal PCO2 from increasing and then leveling off (i.e., isocapnic buffering) to decreasing occurred. The Male Female Measurement ϭ ϭ VO2 point at which the latter two transitions occurred (n 22) (n 16) was defined as respiratory compensation point (RCP) Age (year) 22Ϯ121Ϯ1 [7, 22]. Changes in end-tidal PCO2 during isocapnic (19–35) (19–33) buffering phase (corresponding to the VO2 range be- Weight (kg) 64Ϯ150Ϯ2 tween VT and RCP) were ascertained to be virtually (54–75) (41–62)** zero, in actual being 0.95Ϯ0.25 (meanϮSEM) Height (cm) 172Ϯ1 160Ϯ2 mmHg. Maximum O2 uptake (VO2 max) was deter- (160–180) (150–172)* 2 Ϯ Ϯ mined as the average value of breath-by-breath data of Body surface area (m ) 1.75 0.02 1.59 0.03 (1.55–1.89) (1.38–1.77)** VO2 during the last 1 min of the exercise test. The VCO -VO relationship was divided into two Ϫ1 Ϫ2 2 2 VO2 max (l min m ) 1.74Ϯ0.05 1.26Ϯ0.05 linear components, which had a lower slope (S1) and a (1.36–2.14) (1.00–1.83)** Ϫ1 Ϫ2 Ϯ Ϯ higher slope (S2), respectively. S1 was calculated using VT (l min m ) 0.70 0.04 0.56 0.03 the VCO -VO plots within the VO ranges from the (0.43–1.01) (0.40–0.78)** 2 2 2 Ϫ1 Ϫ2 Ϯ Ϯ start of loaded cycling to VT, and S , using those from RCP (l min m ) 1.35 0.05 1.05 0.05 2 (1.00–1.76) (0.63–1.48)** VT to RCP by the least-squares method. For the S1 HVR 0.18Ϯ0.02 0.26Ϯ0.02 calculation, the data immediately after the start of the (l minϪ1 mϪ2 (Ϫ%)Ϫ1) (0.06–0.29) (0.11–0.42)* loaded cycling in which the respiratory gas exchange HCVR 1.27Ϯ0.20 1.20Ϯ0.17 Ϫ1 Ϫ2 Ϫ1 ratio (VCO2/VO2) transiently fell were excluded. The (l min m mmHg ) (0.40–4.53) (0.61–3.22) ⌬ § Ϯ Ϯ difference between the two slopes (⌬slope) was used slope 0.33 0.02 0.31 0.02 (0.19–0.50) (0.20–0.43) as an estimate of the rate of lactic acid increase per VO2 increase at the work rates below RCP. Values are meansϮSEM and ranges in parentheses. § Rate Ϯ Ϫ1 Ϫ1 Statistics. The results are presented as means of excess CO2 output (l min ) per VO2 increase (l min ). SEM. Correlations between two variables were tested Gender difference at * pϽ0.05 and ** pϽ0.01.
Japanese Journal of Physiology Vol. 50, No. 4, 2000 451 N. TAKANO
Table 2. Correlation analysis between RCP and each of HVR, HCVR and ⌬slope.
Correlation coefficient Sex n HVR HCVR ⌬slope
Male 22 Ϫ0.423* 0.365 Ϫ0.617** Female 16 Ϫ0.461 0.060 Ϫ0.464 All 38 Ϫ0.566** 0.250 Ϫ0.423**
* pϽ0.05 and ** pϽ0.01.
Table 3. Multiple linear regression analysis between RCP and two independent variables of HVR and ⌬slope. Fig. 1. Relationship between HVR and RCP of individ- ϭ Partial correlation coefficient ual subjects. Closed circles indicate males (n 22), and 2 open circles, females (nϭ16). Sex nr HVR ⌬slope
Male 22 Ϫ0.533* Ϫ0.678** 0.510** Female 16 Ϫ0.395 Ϫ0.399 0.235 All 38 Ϫ0.590** Ϫ0.462** 0.435**
r 2: coefficient of determination of a multiple linear regres- sion model as described by RCPϭa[HVR]ϩb[⌬slope]ϩ constant. * pϽ0.05 and ** pϽ0.01.
Table 4. Correlation analysis between VúO2 max and each of RCP, HVR, HCVR and ⌬slope.
Correlation coefficient Sex n RCP HVR HCVR ⌬slope Fig. 2. Relationship between ⌬slope and RCP of indi- Ϫ Ϫ vidual subjects. For explanation, see Fig. 1. Male 22 0.815** 0.201 0.227 0.672** Female 16 0.708** Ϫ0.435 0.115 Ϫ0.328 All 38 0.785** Ϫ0.504** 0.163 Ϫ0.320* respectively, did not reach significant levels (0.05Ͻ pϽ0.1). Figures 1 and 2 illustrate the distributions of * pϽ0.05 and ** pϽ0.01. RCP-HVR relation and RCP-⌬slope relation, respec- tively, in both sexes. Combining the data of both variation. In the female subjects, however, the results sexes, significant correlation was seen in RCP-HVR of the partial correlation were not significant. Com- and RCP-⌬slope relations. On the other hand, there bining the results of both sexes, results were signifi- was no significant correlation between RCP and cant. The results of r2 (Table 3) indicated that 40 to HCVR for either sex or in the combination of both 50% of the variability of RCP could be explained by sexes (Table 2). a multiple linear regression model with HVR and To test whether the two variables (HVR and ⌬slope, although the results of the female subjects did ⌬slope) were linearly and additively related to the not reach significant levels (pϭ0.07). RCP variability (i.e., whether relationship among the three variables can be described as RCPϭa[HVR]ϩ DISCUSSION b[⌬slope]ϩconstant), a multiple linear regression analysis was applied. As shown in Table 3, in the The multiple linear regression analysis between the male subjects, the partial correlation for each the variance of RCP and those of HVR and ⌬slope HVR and ⌬slope was significant and the magnitudes demonstrated that the latter two variables were related of the correlation coefficient were similar in both independently and at similar rates to RCP variation in variables; the results indicating that HVR and ⌬slope the male subjects, while this relationship did not hold were related independently and at similar rates to RCP true for the female subjects. In the present study, the
452 Japanese Journal of Physiology Vol. 50, No. 4, 2000 RCP during Incremental Exercise individual difference in HVR during exercise was as- of the chemosensitivity of the carotid bodies on the sumed to be predicted by that in the resting estimate onset of hyperventilatory responses, detectable as VT of HVR [11, 12, 14]. A lower correlation between rest- and RCP, during incremental exercise. Hogan et al. ing and exercise estimates of HVR in women than in [30] reported that, as compared to VT during exercise men [12] might partly explain the lower partial corre- at 15-W increment every 3 min while breathing air, lation between RCP and HVR in our female subjects. there was a shift to higher levels of VT with reduced In addition, no special regard of the menstrual cycle chemosensitivity by breathing 60% O2, and there was was paid to the female subjects. The luteal phase of no change with an elevated chemosensitivity by 17% the menstrual cycle has been reported to produce O2. At such a slower rate of work incrementation, VT greater ventilatory response at rest and during exer- has been assumed to approximately equal RCP [5]. cise [24, 25], greater HVR [24–26] and a lower extent On the other hand, Henson et al. [31] failed to demon- of blood lactate increase during heavy exercise strate an inhibitory effect of dopamine, which is an in- [26, 27] compared to the follicular phase. Therefore, hibitory neuromodulator in the carotid bodies, on ven- in the luteal phase, a decrease in arterial pH associ- tilatory responses during 1-min incremental exercise ated with a given increase in blood lactate during (i.e., infused dopamine did not diminish the ventila- heavy exercise (i.e., at a given level of ⌬slope) might tory responses or delay the onset of compensatory hy- be smaller due to a greater fall in arterial PCO2 as a perventilation) in spite of having an inhibitory effect result of greater ventilatory response during exercise on the hypoxic ventilatory response assessed at rest. [26, 27] as compared with the follicular phase. This Henson et al. [31] therefore postulated that either the sequence might lead to a higher level of RCP in the carotid bodies respond differently to hypoxia than to luteal phase. However, previous studies have failed to acute metabolic acidosis and/or hyperkalemia that are find a dependency of RCP on the menstrual cycle [26] induced during heavy exercise, or the carotid bodies or on blood progesterone concentrations at similar are not the sole mediators of compensatory hyperven- levels of blood lactate increase during heavy exercise tilation during heavy exercise. [28]. At any rate, heterogeneity in the phases of men- Agreeing with Henson’s postulation [31], we sup- strual cycle in our female subjects might have caused pose that factors other than HVR and ⌬slope might be a lower partial correlation between RCP and ⌬slope. involved in the 50 to 60% RCP variance. They are Further studies are required as to whether relationship marked increases in Kϩ and catecholamine concentra- between RCP and each of HVR and ⌬slope depends tions, pH/PCO2 oscillation of the arterial blood and the on sex and menstrual cycle in woman. O2-labile component estimated by Dejours’ O2 test, With some reservations for woman, the present which likely result in increased activities of the study indicates that 40 to 50% of the RCP variance carotid bodies during exercise [3–6]. Increased plasma was describable in a multiple linear regression model concentrations of Kϩ [14, 32] and catecholamines [33] with HVR and ⌬slope (Table 3). This implies that, in have also been considered to contribute to increases the subjects with higher HVR, RCP indicating the in HVR during exercise. In the present study, the rest- onset of compensatory hyperventilation for metabolic ing estimate of HVR was used as an index of the acidosis during exercise could occur at lower levels of exercise estimate of HVR based on previous studies work rate even if the ⌬slope indicating an approxi- [11, 12, 14] showing that individuals with higher HVR mate rate of lactic acid increase during moderate to at rest tended to have higher HVR during exercise, al- heavy exercise was the same. It follows that in indi- though this tendency (correlation between both) was viduals with higher HVR, the fall in pH due to lactic lower for women, as mentioned above. acidosis at a given level of heavy work rate would be Besides the carotid chemoreceptor mediation, cen- restricted to a smaller extent because compensatory tral command mediation might be involved in RCP hyperventilation could start at lower levels of work determination, such that an augmented central com- rate as compared with individuals with lower HVR. mand signal possibly due to increased muscle fatigue Rausch et al. [29] have evidenced the importance of at heavy exercise might produce hyperventilation [34]. the carotid chemoreceptor sensitivity in constraining On the contrary, less involvement of the chemosensi- the fall of arterial pH by demonstrating a more rapid tivity of the central chemoreceptors was found in the restoration of arterial pH toward the normal level dur- present study (Table 2). ing heavy exercise while breathing 12% O2 and a Recently, Oshima et al. [22] reported a positive cor- slower restoration while breathing 80% O2 as com- relation between RCP and VO2 max, in which the sub- pared to restoration while breathing air. jects with higher VO2 max had higher levels of RCP. Other investigators have also studied the influence After Oshima et al. [22], a correlation analysis
Japanese Journal of Physiology Vol. 50, No. 4, 2000 453 N. TAKANO between VO2 max and each of RCP, HVR, HCVR and 3. McLoughlin P, Popham P, Linton RAF, Bruce RCH, and ⌬slope was performed on the subjects of the present Band M: Exercise-induced changes in plasma potas- study. The results are shown in Table 4, indicating that sium and the ventilatory threshold in man. J Physiol (Lond) 479: 139–147, 1994 RCP correlated positively with VO2 max in both sexes, 4. Nye PCG: Identification of peripheral chemoreceptor while HVR and ⌬slope tended to correlate weakly and stimuli. Med Sci Sports Exerc 26: 311–318, 1994 inversely with VO2 max. The inverse correlation be- 5. Ward SA: Peripheral and central chemoreceptor con- trol of ventilation during exercise in humans. Can J tween VO2 max and ⌬slope might be associated with a training effect of diminishing lactate increase during Appl Physiol 19: 305–333, 1994 6. Whipp BJ: Peripheral chemoreceptor control of exer- heavy exercise [35]. On the other hand, regarding the cise hyperpnea in humans. Med Sci Sports Exerc 26: correlation between HVR and VO2 max, the previous 337–347, 1994 studies are controversial: some studies have shown an 7. Beaver WL, Wasserman K, and Whipp BJ: A new inverse correlation [36, 37], but others no correlation method for detecting anaerobic threshold by gas ex- [11, 38, 39]. change. J Appl Physiol 60: 2020–2027, 1986 8. Wasserman K, Whipp BJ, Koyal SN, and Cleary MG: Thus, the positive correlation between VO and 2 max Effect of carotid body resection on ventilatory and RCP found by Oshima et al. [22] and us appears to be acid-base control during exercise. J Appl Physiol 39: accounted for partly by reduction in the chemosensi- 354–358, 1975 tivity of the carotid bodies and/or lactic acidosis with 9. Honda Y, Myojo S, Hasegawa S, Hasegawa T, and Severinghaus W: Decreased exercise hyperpnea in increasing VO2 max. These alterations would make it possible to perform higher intensities of exercise with- patients with bilateral carotid chemoreceptor resection. J Appl Physiol 46: 908–912, 1979 out excessive hyperventilation in response to meta- 10. Weil JV, Byrne-Quinn E, Sodal IE, Kline JS, McCullough bolic acidosis, and hence, intense breathlessness dur- RE, and Filley GF: Augmentation of chemosensitivity ing heavy exercise [40]. during mild exercise in normal man. J Appl Physiol 33: In conclusion, the present study demonstrated that 813–819, 1972 the individual difference in the onset of compensatory 11. Martin BJ, Weil JV, Sparks KE, McCullough RE, and hyperventilation for lactic acidosis during incremental Grover RF: Exercise ventilation correlates positively with ventilatory chemoresponsiveness. J Appl Physiol exercise, detectable as RCP, was dependent partly on 45: 557–564, 1978 the hypoxic ventilatory chemosensitivity of the carotid 12. Regensteiner JG, Pickett CK, McCullough RE, Weil JV, bodies and the rate of lactic acid increase during exer- and Moore G: Possible gender differences in the effect cise. That is, earlier onsets of compensatory hyper- of exercise on hypoxic ventilatory response. Respira- ventilation could be seen in individuals with higher tion 53: 158–165, 1988 13. Poon CS and Greene JG: Control of exercise hyperp- chemosensitivities of the carotid bodies, even at the nea during hypercapnia in humans. J Appl Physiol 59: same rate of lactic acid increase during exercise, and 792–797, 1985 in individuals with greater rates of lactic acid in- 14. Igarashi T, Nishimura M, Akiyama Y, Yamamoto M, crease, even with the same chemosensitivity of the Miyamoto K, and Kawakami Y: Effect of aminophylline ϩ carotid bodies. This relation was manifested in the on plasma [K ] and hypoxic ventilatory response male subjects but not in the female subjects, where during mild exercise in men. J Appl Physiol 77: 1763–1768, 1994 consideration of the menstrual cycle was not given. 15. Cooper CB, Beaver WL, Cooper DM, and Wasserman Based on the present results, the higher RCP seen in K: Factors affecting the components of the alveolar the subjects with higher VO2 max was ascribed partly to CO2 output–O2 uptake relationship during incremental lower levels of HVR and/or lactic acid increase during exercise in man. Exp Physiol 77: 51–64, 1992 heavy exercise. 16. Wasserman K: Coupling of external to cellular respira- tion during exercise: the wisdom of the body revisited. Am J Physiol 266: E519–E539, 1994 This work was supported partly by a Grant-in-Aid for Scien- 17. Ward SA, Whipp BJ, Koyal S, and Wasserman K: Influ-
tific Research (No. 08670078) from the Ministry of Educa- ence of body CO2 stores on ventilatory dynamics dur- tion, Science, Sports and Culture of Japan. ing exercise. J Appl Physiol 55: 742–749, 1983 18. Beaver WL, Wasserman K, and Whipp BJ: Bicarbonate buffering of lactic acid generated during exercise. J REFERENCES Appl Physiol 60: 472–478, 1986 1. Whipp BJ, Davis JA, Torres F, and Wasserman K: A test 19. Kurazumi Y, Horikoshi T, Tsuchikawa T, and Matsubara to determine parameters of aerobic function during ex- N: The body surface area of Japanese. Jpn J Biomete- ercise. J Appl Physiol 50: 217–221, 1981 orol 31: 5–29, 1994 (in Japanese) 2. Brooks GA: Anaerobic threshold: review of the concept 20. Shaw RA, Schonfeld SA, and Whitcomb ME: Progres- and directions for future research. Med Sci Sports sive and transient hypoxic ventilatory drive test in Exerc 17: 22–34, 1985 healthy subjects. Am Rev Respir Dis 126: 37–40, 1982
454 Japanese Journal of Physiology Vol. 50, No. 4, 2000 RCP during Incremental Exercise
21. Read DJC: A clinical method for assessing the ventila- dopamine on ventilatory response to incremental exer- tory response to carbon dioxide. Aust Ann Med 16: cise in man. Respir Physiol 89: 209–224, 1992 20–32, 1967 32. Qayyum MS, Barlow CW, O’Connor DF, Paterson DJ, 22. Oshima Y, Miyamoto T, Tanaka S, Wadazumi T, Kuri- and Robbins PA: Effect of raised potassium on ventila- hara N, and Fujimoto S: Relationship between isocap- tion in euoxia, hypoxia and hyperoxia at rest and dur- nic buffering and maximal aerobic capacity in athletes. ing light exercise in man. J Physiol (Lond) 476: 365– Eur J Appl Physiol 76: 409–414, 1997 372, 1994 23. Aitken ML, Franklin JL, Pierson DJ, and Schoene RB: 33. Conway MA, and Petersen ES: Effects of -adrenergic Influence of body size and gender on control of ventila- blockage on the ventilatory responses to hypoxic and tion. J Appl Physiol 60: 1894–1899, 1986 hyperoxic exercise in man. J Physiol (Lond) 393: 24. Schoene RB, Robertson HT, Pierson DJ, and Peterson 43–55, 1987 AP: Respiratory drives and exercise in menstrual cy- 34. Kaufman MP and Forster HV: Reflexes controlling cir- cles of athletic and nonathletic women. J Appl Physiol culatory, ventilatory and airway responses to exercise. 50: 1300–1305, 1981 In: Handbook of Physiology, Section 12, Exercise: Reg- 25. Takano N: Changes of ventilation and ventilatory re- ulation and Integration of Multiple Systems, ed. Rowell sponse to hypoxia during the menstrual cycle. Pflügers LB and Shepherd JT, Am Physiol Soc, New York, pp Arch 402: 312–316, 1984 382–447, 1996 26. Dombovy ML, Bonekat HW, Williams TJ, and Staats 35. Stallknecht B, Vissing J, and Galbo H: Lactate produc- BA: Exercise performance and ventilatory response tion and clearance in exercise. Effects of training. A in the menstrual cycle. Med Sci Sports Exerc 19: mini-review. Scand J Med Sci Sports 8: 127–131, 1998 111–117, 1987 36. Byrne-Quinn E, Weil JV, Sodal IE, Filley GF, and Grover 27. Jurkowski JEH, Jones NL, Toews CJ, and Sutton JR: RF: Ventilatory control in the athlete. J Appl Physiol 30:
Effects of menstrual cycle on blood lactate, O2 delivery, 91–98, 1971 and performance during exercise. J Appl Physiol 51: 37. Scoggin CH, Doekel RD, Kryger MH, Zwillich CW, and 1493–1499, 1981 Weil JV: Familial aspects of decreased hypoxic drive in 28. Bonekat HW, Dombovy ML, and Staats BA: Proges- endurance athletes. J Appl Physiol 44: 464–468, 1978 terone-induced changes in exercise performance and 38. Godfrey S, Edwards RHT, Copland GM, and Gross PL: ventilatory response. Med Sci Sports Exerc 19: Chemosensitivity in normal subjects, athletes, and pa- 118–123, 1987 tients with chronic airway obstruction. J Appl Physiol 29. Rausch SM, Whipp BJ, Wasserman K, and Huszczuk 30: 193–199, 1971 A: Role of the carotid bodies in the respiratory com- 39. Mahler DA, Morits ED, and Loke J: Ventilatory re- pensation for the metabolic acidosis of exercise in hu- sponses at rest and during exercise in marathon run- mans. J Physiol (Lond) 444: 567–578, 1991 ners. J Appl Physiol 52: 388–392, 1982 30. Hogan MC, Cox RO, and Welch HG: Lactate accumu- 40. Takano N, Inaishi S, and Zhang Y: Individual differ- lation during incremental exercise with varied inspired ences in breathlessness during exercise, as related to oxygen fractions. J Appl Physiol 55: 1134–1140, 1983 ventilatory chemosensitivities in humans. J Physiol 31. Henson LC, Ward DS, and Whipp BJ: Effect of (Lond) 499: 843–848, 1997
Japanese Journal of Physiology Vol. 50, No. 4, 2000 455