The decrement in our subjects' V˙O2max from 760 Torr during HH of 566 Torr can be estimated from the data presented in Table 4. For variables measured at sea level, prediction of the decrement in V˙O2max at 566 Torr can be estimated by the following equation: Equation 
For estimation of the absolute V˙O2max of our male and female subjects for a given HH of 682, 632, or 566 Torr, the following equations using sea level data can be used: Equation [2-4]
Gender differences. Pertinent data grouped by gender are presented in Table 1 and 5. These results are presented owing to the significant inclusion of gender in the multiple regression model. On average, males were taller, heavier, more lean, and of higher cardiorespiratory endurance (V˙O2max, L·min−1) than the female subjects (Table 1). There was no gender main effect difference in V˙O2max when expressed as mL·kg−1 LBM·min−1 (P = 0.1934) (Table 5). V˙O2max (mL·kg−1 LBM·min−1) significantly decreased with increasing HH (P < 0.0001) and occurred with a significant gender-altitude interaction (P = 0.0026). However, no gender difference was evident at any altitude. V˙O2max (mL·kg−1 LBM·min−1) significantly decreased from 760 at 682 Torr (P = 0.0001) for males and from 760 at 632 Torr (P = 0.0048) for females.
Data of the change in V˙O2max (L·min−1) with increasing HH revealed significant main effects for gender (P < 0.0001) and HH (P < 0.0001) and a significant gender-HH interaction (P = 0.0001) (Table 5). Males had a significantly larger V˙O2max at all HH conditions than did the females (P < 0.003). V˙O2max significantly decreased from SL in males at 682 Torr (P = 0.0028) and for females at 632 Torr (P = 0.0001).
Results for V˙E at V˙O2max (V˙Emax) revealed significant main effects for gender (P < 0.0001) and HH (P = 0.0029) and a nonsignificant gender-HH interaction (P = 0.0995) (Table 5). Males had significantly larger V˙Emax for each HH condition than females; however, both males and females had similar increases in maximal ventilation with increasing HH. Results for the ventilatory equivalent for oxygen (V˙E/V˙O2) at V˙O2max (V˙E/V˙O2max) revealed no gender difference (P = 0.5025), a significant HH main effect (P < 0.0001), and a nonsignificant gender-HH interaction (P = 0.151) (Table 5). Males had a larger V˙E/V˙O2max than females, and both males and females increased V˙E/V˙O2 similarly with increasing HH.
Results for maximal heart rate revealed a nonsignificant main effect for gender (P = 0.857), a significant main effect for HH (P = 0.008), and a nonsignificant gender-HH interaction (P = 0.1261) (Table 5). Maximal heart rate decreased from SL for both genders at 632 Torr (P = 0.0061).
Results for SaO2 revealed no gender difference (P = 0.4227), a significant main effect for HH (P < 0.0001), and a nonsignificant interaction (P = 0.57) (Table 5). For both males and females, SaO2 at V˙O2max decreased significantly from sea level by 682 Torr (P < 0.0001).
The results confirmed each of our hypotheses. We demonstrated that the males and females of this study had a detectable reduction in V˙O2max at 682 Torr. Linear extrapolation of mean data indicated that the decrement in V˙O2max commenced at 705 Torr. However, the high between subjects variability for the decrement in V˙O2max during HH and the findings from multiple regression indicated that it is inappropriate to characterize this relationship by a single curve. A large portion (89%) of the between subjects variability in the decrement in V˙O2max could be explained using multiple (N = 5) variables. In addition to sea level V˙O2max, the ΔV˙O2max during HH is further increased in individuals who have a low SL-LT, greater reduction in ΔSaO2max, large LBM, and are male. Conversely, the multiple determinants of the V˙O2max decrement indicate that individuals with a large V˙O2max, but who have a large SL-LT, have a small LBM, and do not exhibit a large hypoxemia, will not decrease their V˙O2max during HH to the extent anticipated based on SL-V˙O2max alone.
Discussion of these findings will be structured by the type of variable and by the type of statistics performed.
Univariate findings. Our study investigated changes in V˙O2max from sea level during three low to moderate HH conditions. Using mean data, the decrement in V˙O2max with decreasing barometric pressure was significant at 682 Torr and decreased linearly thereafter to 566 Torr. In comparison, only two other studies have evaluated changes in V˙O2max that included more than three hypoxic conditions within pressures ranging from 760 to 440 Torr (1,43). Andersen et al. (1) quantified a curvilinear decrement in V˙O2max in seven male subjects from sea level (753 Torr) to each of 559, 477, 440, 422, and 404 Torr. The occurrence of statistical significance for the decreases in V˙O2max at each altitude were not reported. Conversely, Squires and Buskirk (45) reported a linear decrease in V˙O2max during barometric pressure conditions between approximately 680 and 580 Torr, with significance occurring at 656 Torr (1219 m).
The concept of a critical altitude for inducing a reduction in V˙O2max may be inappropriate. For example, Gore et al. (15) documented a reduction in V˙O2max in elite trained endurance athletes during acute HH equivalent to an increased altitude of 580 m (695 Torr). The findings of Gore et al. (14,15) and similar findings of a greater V˙O2max decrement during hypoxia in more endurance-trained individuals (26,27,31,43,50) have led to the interpretation that more fit individuals will experience greater decrements in V˙O2max during hypoxia. Our data indicate that such an interpretation is not true for all individuals, even when of different endurance training status and cardiorespiratory endurance fitness. For example, data of V˙O2max at each HH condition are presented in Fig. 4 for a subset of the male and female subjects used in the study. The two most endurance-trained male subjects of this study had relatively minor reductions in V˙O2max. A larger but less endurance-trained subject had a more dramatic decrement in V˙O2max. This larger decrement was also associated with a relatively large decrease in SaO2. The same trends were evident for the female subjects (Fig. 4). Clearly, the decrement in V˙O2max during hypoxia is caused and related to multiple factors, and no one variable can be stated as the principle determinant of the decrement in all individuals.
Multiple regression findings. Because of the multiple variables associated with the decrement in V˙O2max during hypoxia, we performed step-wise multiple regression analyses to explain the decrement in V˙O2max using several independent variables (Table 3 and 4). The results showed that SL-V˙O2max explained the greatest variability in the decrement in V˙O2max, with further significant contributions provided by SL-LT, ΔSaO2max, LBM, and gender. The combination of these variables explained approximately 89% of the variance (r2) in the decrement in V˙O2max. Although our subject number was large relative to other studies on this topic, it remains small for application of multiple regression analyses. Because of our sample size, it is likely that the multiple correlations we report are inflated, as is typical for multiple regression using a subject to independent variable number ratio lower than 10:1 (24,34). Nevertheless, based on the originality of our methodology and findings, our data contribute significantly to the current knowledge on the decrement in V˙O2max during hypoxia.
Our results clearly indicate that the concept of an average decrement in V˙O2max with increasing HH is inappropriate. Cardiorespiratory and muscular endurance (SL-V˙O2max and SL-LT), ΔSaO2max, LBM, gender, and perhaps other variables all combine to determine the absolute decrement and therefore need to be considered when estimating the influence of hypoxia on a person's V˙O2max.
The fact that gender significantly contributed to the explanation of total variance in V˙O2max is important. There is a component of the oxygen transport and utilization cascade that is different between genders and unrelated to the remaining independent variables we measured. This is a meaningful finding, for as indicated in the data of Tables 1 and 5, the females of the study were on average less fit (V˙O2max, L·min−1), of smaller LBM, yet of similar relative fitness (V˙O2max-mL·kg−1 LBM·min−1), hematology, and ΔSaO2max to the male subjects.
It is now well accepted that tissue oxygen diffusion limitation is an important component of oxygen transfer to contracting skeletal muscle and has an independent role in decreasing V˙O2max during hypoxia (37,39,49). Wagner (49) has theorized that as hypoxia becomes more extreme, the importance of peripheral oxygen diffusion to V˙O2max increases. This fact may be revealed in how the slope (coefficient) for SL-V˙O2max for each HH condition (see eq. 2-4) decreased with increasing HH. However, less is known of the extent of individual differences in peripheral oxygen diffusion during normoxia or hypoxia and what peripheral factors are associated with these between-subject differences. Nevertheless, Shephard et al. (42) revealed that increases in the muscle mass exercised are associated with more severe reductions in V˙O2max during hypoxia, thus indicating the potential for the size of the active muscle mass to influence peripheral oxygen diffusion. In addition, Wagner (48) has estimated peripheral oxygen diffusion and identified larger values for trained than untrained individuals.
We propose that the unique gender, LT and LBM contributions to the decline in V˙O2max with increasing HH may be related to the role of peripheral oxygen diffusion in the measurement of V˙O2max, especially during HH. Both male and female subjects with a larger LBM and sea level V˙O2max experienced the greatest absolute decrements in V˙O2max with increasing HH. This finding is consistent with the muscle atrophy associated with chronic exposure to severe hypoxia (16,17). Presumably, the adaptation of muscle atrophy during chronic hypoxia decreases muscle fiber dimensions and decreases the distance for peripheral oxygen diffusion, hence increasing the transfer of oxygen from blood to within skeletal muscle fibers.
The unique importance of SL-LT is revealed by the altered correlation direction of V˙O2max decrement and SL-LT between the univariate and multiple regression analyses. The univariate correlation between V˙O2max decrement and SL-LT was 0.517. However, the partial correlation after SL-V˙O2max was entered in to the multiple regression model changed to −0.4567. This can be interpreted to indicate that the univariate correlation between SL-LT and a greater V˙O2max decrement during HH was predominantly owing to colinearity caused by a high correlation between SL-LT and SL-V˙O2max (Table 3). When the variability in SL-LT owing to SL-V˙O2max was removed, individuals with a high SL-LT actually had a smaller decrement in V˙O2max during HH. Thus, the unique benefit of a high LT to exercise during HH may be to decrease the V˙O2max decrement. This alteration in interpretation of the LT to V˙O2max decrement findings would have been overlooked using simple univariate correlation, as in the results of Koistinen et al. (26).
The interpretation of the between subjects differences in SL-LT to reflect differences in peripheral skeletal muscle characteristics are supported by the results of Green et al. (18,19). Green et al. demonstrated that during 5-7 d of endurance training at 67% V˙O2max, alterations in muscle metabolism occurred before increases in muscle mitochondrial enzyme activities and V˙O2max (18). Furthermore, additional research of endurance training through 8 wk revealed decreases in muscle lactate accumulation and increased glycogen sparing during the first week (3-7 d) (19). No additional improvement in these measures occurred during the remaining 7 wk. Conversely, increases in V˙O2max were not maximized until 4 wk of training (19). The authors concluded that the majority of metabolic adaptations to endurance training occur independently of increases in the oxidative potential of the trained skeletal muscle and whole body V˙O2max. Clearly, there are yet to be clarified functions of peripheral metabolism that are independent of oxygen supply and utilization to contracting skeletal muscle.
Maximal Heart Rate
Previous research on the maximal heart rate (HRmax) response to exercise during acute hypoxia has been equivocal. Elliot and Atterbom (12) reported that HRmax did not decrease in men and women at V˙O2max from 1,576 m to 2,743 and 3,962 m. Similar results for different levels of hypoxia have also been reported (9,18,46). However, Koistinen et al. (26) reported a significant decrease in HRmax by 6 b·min−1 from sea level to 3000 m, and Andersen et al. (1) reported a significant decrease in HRmax by 10 b·min−1 between sea level and 5,000 m. Other researchers have also shown a decrease in HRmax during acute hypoxia (10,31,33,40), with larger decrements in HRmax during severe hypoxia as studied in Operation Everest II research (9,36,51).
Our reporting of a significant decrease in HRmax from 760 to 632 Torr, even though such a decrease was of a mean difference of approximately 2 b·min−1, indicates that HRmax is affected by hypoxia at even low altitudes above sea level. Nevertheless, the physiological implications of such a small difference may be negligible.
We report an exponential decrease in SaO2max with increasing HH. An exponential decrease in resting SaO2 during increasing HH was reported by Schoene et al. (41) and Ferretti et al. (13). Conversely, Squires and Buskirk (45) reported a linear decrease in SaO2max in 12 men during HH equivalent to 712, 680, 656, 632, and 575 Torr. SaO2 ranged from 90.7 to 79.1% for 712 and 575 Torr conditions, respectively. The hypoxemia at 575 Torr from Squires and Buskirk (45) was more extreme than our average of approximately 85% for both males and females at 566 Torr (Fig. 2). The most logical explanations for these discrepancies are based on the moderate altitude acclimatization of the subjects used in our study, the moderate hypoxic exposures, and the lower likelihood for exercise-induced hypoxemia in many of the subjects we studied. As previously stated, our subjects were of varied fitness and resided between 1,640 and 2,460 m, which would have induced a chronic hyperventilation, a raised alveolar PO2, and a higher SaO2 at rest and during exercise. As Schoene et al. (41) and Ferretti et al. (13) studied more extreme ranges of hypoxia (to PB = 240 and 430 Torr, respectively), there would have been a greater hemoglobin desaturation and a greater likelihood for results to mirror the oxyhemoglobin dissociation curve. As our results compare favorably with those of Ferretti et al. (13) and Schoene et al. (41), it seems that the decrement in SaO2 during mild to moderate hypoxia closely mirrors reductions based on the sigmoidal oxyhemoglobin dissociation curve. However, it is likely that reductions will be larger for more endurance-trained subjects owing to a greater exercise-induced hypoxemia (14,15,45).
Our research is based on correlation analyses, and the associations between variables cannot be interpreted as cause and effect. However, the multiple regression approach to explain the statistical variability in the decrement in V˙O2max during HH produced results that are both supported by experimental research and add to the findings of such research. Furthermore, multiple regression analyses are interpreted to extend simple correlation analyses toward cause-effect associations (32). Consequently, the results from multiple regression analyses provide direction for future experimental cause-effect research (24,34).
We documented gender-specific differences in the decrement in V˙O2max during increasing HH and that SL-V˙O2max, SL-LT, LBM, hemoglobin desaturation, and gender all significantly contribute to explain the ΔV˙O2max. An accurate estimation of the decrease in V˙O2max with increasing altitude cannot be made without accounting for the aforementioned variables. In addition, the association between V˙O2max decrement during hypoxia and SL-V˙O2max may decrease with increasing hypoxia, indicating that other factors may be more influential in influencing the decrement. Consequently, we propose that a lower LT and larger LBM are associated with a limitation in peripheral oxygen diffusion during exercise at V˙O2max, especially during HH. These findings indicate that for both men and women, for a given V˙O2max individuals who have a large LT, have less hypoxemia, and have a small LBM will retain more of their SL exercise potential during acute HH.
There are many important applied interpretations of our results. As it is clear that certain individuals demonstrate a superior retention of SL-V˙O2max during hypoxia, these individuals should perform better at altitude. Whether these individuals may also benefit more from altitude training is unknown. Based on our findings, coaches and athletes can better understand the tolerance to hypoxia and thereby improve selection of athletes who may be more likely to compete better at altitude.
Clearly, more research of peripheral oxygen diffusion and muscle fiber and capillary morphology need to be conducted to elucidate their influence on oxygen transport and utilization by skeletal muscle during HH. In addition, further research of more elite athletes needs to be conducted to develop similar prediction equations for V˙O2max and performance decrement during hypoxia. Finally, care should be taken in the interpretation of results from univariate analyses used to compare mean differences between two or more groups in physiological research. Our data reveal that what might seem as a group difference may in fact be the result of differences on other functional and anatomical measurements that influence the dependent variable.
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Validation of finger pulse oximetry. Use of the Poet oximeter during exercise had previously been validated to arterial blood SaO2 during exercise to V˙O2max on six highly trained competitive cyclists. Before the exercise test, 1% lidocaine was injected superficial to the distal radial artery, a 20-gauge catheter was placed percutaneously, and a three-way stopcock was attached to the catheter. Approximately 2 mL of dead space blood was sampled and discarded before each 3-mL specimen collection. Exercise was characterized by 45 min of steady state cycling, followed immediately by a 2-min stage duration incremental protocol to peak V˙O2. A blood specimen was collected at rest, after 30 and 45 min of exercise, and at peak V˙O2. Simultaneous recordings of hemoglobin saturation were recorded using finger pulse oximetry. The arterial blood samples were used for determination of PaO2, PaCO2, pH, and calculated hemoglobin saturation at a core temperature of 37°C by automated blood gas analysis (GEM Premier, Mallinckrodt Sensor Systems). Quality control calibrations of the blood gas analyzer were performed twice daily resulting in an accuracy in the measurement of PaO2, PaCO2, and pH of ± 1 mm Hg, ± 1 mm Hg, and ± 1%, respectively.
Data from six males performing steady state and incremental cycle ergometry exercise to peak V˙O2 was used to compare SaO2 measurements obtained from finger pulse oximetry to those calculated from measurement of blood partial pressures of oxygen sampled from the radial artery (N = 24 paired data points). Values for arterial blood SaO2 ranged from 98 to 89%, whereas those estimated by pulse oximetry ranged from 99 to 87%. Assessment of the accuracy of the Poet finger pulse oximeter during exercise was conducted by quantifying agreement as proposed by Bland and Altman (5). Differences between pulse oximetry and the calculated intra-arterial SaO2 from measurements of arterial PO2 were determined, and the mean ± SD of these differences was computed. These data were supported by correlation analysis, and reporting of the slope and y intercept of the line of best fit. SaO2 determined from arterial blood and pulse oximetry had close and acceptable agreement (Fig. 5) (r = 0.798, slope = 0.918, y intercept = 6.615%, mean ± SD of differences = −1.01 ± 1.84%) (5), indicating the validity of finger pulse oximetry during exercise to V˙O2max (32).
Keywords:© Williams & Wilkins 1998. All Rights Reserved.
ALTITUDE; OXYGEN TRANSPORT; OXYGEN DIFFUSION; HYPOXEMIA