The mean ˙VO2peak during the CRHI runs was significantly less(P < 0.05) than the mean ˙VO2max calculated as the average of the highest ˙VO2 values obtained from the five GXT, but not significantly different (P > 0.05) from ˙VO2max determined using the other two methods (Table 2). The mean peak blood lactate (6.43 ± 1.7 mmol·l-1) and RER(1.04 ± 0.05) from the CRHI runs were significantly less (P< 0.05) than the means of the peak values obtained from the five GXT (8.12± 1.9 mmol·l-1 and 1.07 ± 0.04). The mean peak HR(188.5 ± 7.9 bpm) from the CRHI runs was not significantly different from the mean of the peak values obtained from the five GXT (188.9 ± 4.8 bpm). These data indicate that in the highly trained individuals tested for this study, the total ˙VO2 during the CRHI runs increased to a point equal to or slightly less than, but not above, the ˙VO2max measured during a running GXT, regardless of the approach used to obtain the value representing the ˙VO2max plateau.
The objective of the present study was to determine whether the slow-component rise in ˙VO2 measured during a CRHI run to exhaustion leads to a total ˙VO2 that exceeds the˙VO2max measured during a running GXT. We found that˙VO2peak determined during CRHI runs did not exceed˙VO2max determined from multiple GXT. These results suggest that in highly trained runners, the slow-component rise in ˙VO2 during CRHI running does not alter ˙VO2max measured during running.
Several studies have compared ˙VO2max measured with a GXT and with a single bout of CRHI exercise. These studies found that˙VO2max either was not different(22,31) or was higher with the CRHI exercise(16). However, the duration of the CRHI exercise was less than 5 min, which may be insufficient to determine the impact of the slow-component rise. Further, the slow-component rise was not reported in these studies, and it is not known whether the rise was sufficient for a valid test of the hypothesis.
Several factors could explain why other studies have reported instances in which the slow-component rise in ˙VO2 during a CRHI bout of exercise lead to a total ˙VO2 that exceeded ˙VO2max(4,6,11,28,29). First, the approach used to determine ˙VO2max and the criteria used to verify that it was achieved were different. In all reported instances of this phenonmen we are aware of, ˙VO2max was determined as the highest˙VO2 on a single GXT. Rigorous plateauing criteria were not always applied. Thus, there is the distinct possibility that ˙VO2max was not achieved or that the single-test results reflected random variation that was not representative. We did observe that for a given individual, a˙VO2peak from a CRHI run could exceed ˙VO2max measured during a single GXT. However, when ˙VO2max was definitively established using a traditional criterion for the plateauing of˙VO2 as a function of work rate and when multiple tests were used to ensure a representative value, the mean ˙VO2peak from the CRHI runs was not systematically greater than ˙VO2max, regardless of the method used to establish ˙VO2max.
We chose to present three measures of ˙VO2max that used different approaches for calculating a representative value for the˙VO2 plateau. This minimized any bias toward a low or high˙VO2max that might be a function of the approach used to represent the plateau. The mean of the ˙VO2max values obtained from the five GXT resulted in the highest estimate of ˙VO2max. Using only the highest value from each test, however, could overestimate ˙VO2max by capitalizing on random error of measurement. The mean ˙VO2 of the two work rates with the highest average ˙VO2 provided the second highest estimate of ˙VO2max. This estimate represented values on the highest portion of the ˙VO2 plateau, but excluded values that by definition were on the plateau, but were slightly lower. The estimate based on the asymptote from the exponential curve fit produced the lowest estimate of ˙VO2max. This was because the asymptote was influenced by all of the points on the plateau, not just selected high points as for the other two estimates.
Random biological variability and measurement error could explain or contribute to instances in which the peak ˙VO2 during a CRHI bout of exercise exceeded the ˙VO2max measured on a GXT by a small amount. In the present study, the standard errors of measurement for˙VO2max and for the peak ˙VO2 during the CRHI runs were 0.089 and 0.091 l·min-1, respectively, or 2.1% of the means. These values are consistent with previous studies in which the standard error of measurement for ˙VO2max has varied from 2.1 to 6.5%(2,8,9,10,17,18,19,20,21,32). This variation reflects technical as well as biological error, with the later accounting for approximately 90% of the variation (17). The variability is less if stringent criteria for the attainment of˙VO2max are used (7,21).
Second, it is possible that the mode of exercise used for the tests could affect whether the slow-component rise in ˙VO2 leads to a total˙VO2 that exceeds ˙VO2max. In all studies that we are aware of in which this phenomenon has occurred, cycling was used as the mode of exercise (4,6,11,28,29). Because the peak ˙VO2 during a cycling GXT is typically lower than the ˙VO2max during an uphill treadmill running GXT(15), and therefore does not represent the highest possible ˙VO2, the slow-component rise in ˙VO2 may lead to a total ˙VO2 that exceeds the cycling ˙VO2peak but not the treadmill ˙VO2max. In other words, there may be“room” for ˙VO2peak to be increased in cycling, but not in running. This is possible because cardiac output is not maximal and total peripheral resistance is not reduced to a minimum during cycling(15). If, for example, the slow-component rise in˙VO2 is the result of progressive increase in fast-twitch muscle recruitment and increased metabolite accumulation (26), cycling ˙VO2peak could be increased as a result of reduced total peripheral resistance caused by greater vasodilation in the active muscles and augmentation of venous return and cardiac output. A study similar to the present one using cycling as the mode of exercise is needed to determine whether mode of exercise does, in fact, affect the results. We selected uphill running as the mode of exercise for this study, so that there would be no question that ˙VO2max had been measured. However, the results cannot be generalized to other modes of exercise in which the peak˙VO2 is less than the treadmill ˙VO2max.
A third difference between our study and others is that the subjects in the present study were highly trained, whereas those in most other studies investigating the slow-component rise in ˙VO2 were untrained. Although the slow-component rise in ˙VO2 occurs during exercise at intensities above the lactate threshold regardless of fitness level(14), the magnitude of the increase is less for endurance-trained individuals compared with untrained(34) and is decreased after endurance training at the same absolute work rate (6). Whether the slow-component rise is less in trained individuals at the same%˙VO2max is unknown. In the present study, the mean change in ˙VO2 between the 3rd minute and end of the CRHI run was substantial (0.7 ± 0.15 l·min-1) and similar to that observed in less well-trained subjects in many studies. Therefore, we do not believe the use of trained subjects biased the study toward the findings we obtained. The consistency with which the trained subjects terminated the CRHI run at or very near˙VO2max suggests the same phenomenon is likely to be observed in the untrained, assuming a definitive ˙VO2max defined by the plateauing of ˙VO2 as a function of work rate is determined as in the present study. The use of trained subjects may have been responsible, in part, for that fact that all subjects demonstrated a plateau in˙VO2 as a function of work rate during the GXT, since trained individuals more consistently achieve a plateau than untrained subjects(23).
For the CRHI bouts of exercise, treadmill speeds were chosen that would elicit exhaustion in 7-14 min. This duration permitted a high relative intensity, but provided sufficient time for the slow-component rise to develop. Whether the same results would have been obtained if different treadmill speeds and relative intensities had been used is unknown. Poole et al. (28) have emphasized that during sustained exercise at power outputs above the “critical power,” an intensity between the lactate threshold and ˙VO2max above which a steady state for˙VO2 is not established, ˙VO2 rises progressively to a point near ˙VO2max at fatigue. Thus, in theory, any intensity above the critical power should have been appropriate for this study, because˙VO2 should ultimately rise to ˙VO2max. We elected to use an intensity predicted by the ACSM equation (1) to elicit approximately 100% ˙VO2max (99 ± 5%) so that if a slow-component rise occurred, and ˙VO2 increased above that predicted based on the relation of ˙VO2 to work rate at intensities below lactate threshold, ˙VO2 should rise above ˙VO2max measured on the GXT. On the other hand, because ˙VO2max by definition represents the highest attainable ˙VO2, it is possible that if ˙VO2max was not altered by conditions associated with the CRHI runs, no slow component would occur. We felt that using an exercise intensity near ˙VO2max would provide the most direct test of the issue. The findings did not entirely conform to either of these theoretical predictions. A clear slow-component rise in ˙VO2 defined by the increase in ˙VO2 between the end of minute 3 and the termination of exercise occurred, but ˙VO2 increased toward the expected˙VO2 based on work rates during sub-maximal exercise rather than above it as might be expected (28,36,37). It appeared as if the fast-component response was reduced compared with that expected (3,4,24). Our data are consistent, however, with other studies of high-intensity exercise above the“critical power” during which ˙VO2 approaches and may equal ˙VO2max (28); the magnitude and time course of the slow-component rise were similar to those reported by others during very heavy exercise(2,4,29,34). One explanation for why˙VO2 did not rise above the expected ˙VO2 could be that the expected ˙VO2 was not accurately estimated. It is very possible that the distance runners used as subjects were more economical than predicted by the ACSM equation (1) and, therefore, the expected˙VO2 may have been lower than that estimated by the equation. If this is true, and the expected ˙VO2 was lower than˙VO2max, then the fast-component ˙VO2 would account for a greater portion of the response and the slow-component ˙VO2 would have risen above the expected ˙VO2. If the fast-component˙VO2 response was, in fact, reduced, a possibility suggested by Paterson and Whipp (24), it would be in conflict with studies on cycling (3,4,35) that have found the time constant for the fast-component response is constant across intensities during heavy exercise. Whether mode of exercise affects the fast- and slow-component responses is unknown. Regardless of the explanation for the apparently different fast-component response, it is clear that the slow-component response did not result in a total ˙VO2 that exceeded ˙VO2max.
The mechanism responsible for the slow-component rise in ˙VO2 is controversial and there is controversial and there is no definitive explanation. Increased fast-twitch muscle fiber recruitment, body temperature, catecholamines, ventilation, blood lactate and H+ ions, and other factors have been suggested as possible causes(6,13,26,27,29,34,35). A recent synthesis of evidence (26) concluded that changes in body temperature, catecholamines, ventilation, and lactate or H+ ions are unlikely to have important cause-and-effect relationships with the slow-component ˙VO2 rise. Increased recruitment of fast-twitch muscle fibers may be the most tenable hypothesis, although this remains to be established. Regardless of the mechanism, the data from the present study suggest that in highly trained individuals the slow-component rise in ˙VO2 does not lead to a total ˙VO2 that exceeds the ˙VO2max as traditionally measured with an uphill running GXT. This implies that under these conditions, the factors responsible for the slow-component rise in ˙VO2 during CRHI running do not alter˙VO2max.
The results of this study have implications for the measurement of˙VO2max. The finding that the slow-component rise in˙VO2 during CRHI running did not lead to a total ˙VO2 that exceeded ˙VO2max measured with running GXT in which the work rate was progressively increased at 3-min intervals means that the traditional approach of measuring ˙VO2max using a GXT is acceptable. Higher values are not obtained with a test protocol involving a sustained CRHI run in which the slow-component rise in ˙VO2 is allowed to develop. Whether this is the case for other modes of exercise in which the peak˙VO2 is below the treadmill ˙VO2max remains to be established.
The results of this study also provide new insight concerning the limits of the slow-component rise in ˙VO2. Whatever the physiological perturbation is that causes the excess ˙VO2 during heavy submaximal running, its effect does not extend to maximal running and apparently does not alter maximal cardiac output and peripheral oxygen extraction at maximal exercise.
We conclude that in highly trained individuals, the slow-component rise in˙VO2 during CRHI running does not exceed the ˙VO2max measured during a running GXT. This means that factors responsible for the slow-component rise in ˙VO2 during prolonged high-intensity exercise do not alter ˙VO2max. Additional research is needed to determine whether these findings generalize to other modes of exercise in which the ˙VO2peak is less than the treadmill running˙VO2max.
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