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1Department of Physiology, St. George's Hospital Medical School, London, United Kingdom; and 2Canadian Centre for Activity and Ageing, School of Kinesiology, and Department of Physiology and Pharmacology, The University of Western Ontario, London, Ontario, Canada
Submitted 31 July 2005 ; accepted in final form 4 November 2005
| ABSTRACT |
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O2) response to ramp incremental (RI) exercise does not consistently demonstrate plateau-like behavior at the limit of tolerance, and hence the requirements for a maximum
O2 commonly are not met, despite apparent maximum effort. We sought to determine whether an appended step exercise (SE) test at a work rate greater than that achieved in a preceding ramp test would establish the plateau criterion. Seven healthy male adults performed RI cycle ergometry (20 W/min) to the limit of tolerance, followed by 5-min recovery (20 W) and then an SE test at 105% (RISE-105) of the final work rate (WRpeak) achieved during RI. Five of these subjects also performed an RI test followed by SE at 95% WRpeak (RISE-95).
O2 was measured breath by breath using a turbine and mass spectrometer. The average of the final 15 s of RI or SE was used to establish respective
O2 peaks. When
O2 peak was approached, a constant
O2 value (e.g., a plateau) was not discernable during any RI or SE component of the tests. Although the WRpeak [mean (SD)] was higher during the SE portion [359 W (SD 31)] than during the RI portion [341 W (SD 29)] of the RISE-105, the peak
O2 was not different [SE, 4.30 l/min (SD 0.51); RI, 4.33 l/min (SD 0.52); P = 0.49; n = 7]. Similarly, in the RISE-95 test, WRpeak was 310 W (SD 31) for the SE portion and 326 W (SD 32) for the RI portion, yet the peak
O2 values were not different [SE, 4.12 l/min (SD 0.53); RI, 4.11 l/min (SD 0.48); P = 0.78; n = 5]. The lack of notable difference between the
O2 peaks established at different WRpeak values in our RISE protocols provides the plateau criterion for verification of maximum
O2 in a single test session, even when the data response profiles do not themselves evidence a plateau. square-wave exercise; maximal aerobic power; O2 uptake kinetics
O2), Hill and Lupton (11) observed that "the rate of oxygen intake per minute due to exercise... increases as the speed increases, reaching a maximum... for speeds beyond about 260 metres per min ... . However much the speed be increased beyond this limit, no further increase in oxygen intake can occur ... ." With the data from this and a subsequent study (10), Hill and colleagues presented the concept and the criterion for establishing maximal
O2 (
O2 max). The criterion of no further increase in
O2 with increasing work rates (WRs) has subsequently been applied to test protocols, such as discrete steps (where square waves of a range of WRs are performed, each separated by a period of rest; e.g., Refs. 1, 8, 11, 19, 23) and incremental step (where WR is progressively incremented as a series of step changes, typically lasting for 24 min each; see Ref. 17 for discussion) and incremental ramp [where the power requirement increments as a "smooth" function with time (8, 27)] protocols. Ramp exercise tests performed to the subject's limit of tolerance have become a widely used strategy of choice, as they allow the estimation of a subject's lactate threshold, peak
O2, and the steady-state gain of the
O2-WR response (i.e., 
O2/
WR), and they even provide information regarding the kinetics of the
O2 response (6, 8, 27). However, despite an apparent maximum effort by the subject, a plateau in
O2 is not a common feature of the response. As reviewed by Bassett and Howley (2), "even under carefully controlled laboratory conditions a variable percentage (30% to 95%) of subjects will exhibit a plateau in
O2 at the end of a graded exercise test." Thus there is uncertainty as to whether the final
O2 at the end of the test represents the subject's true "maximal"
O2 or only a "peak"
O2 for this test.
Recently, Day et al. (7) examined the frequency of a
O2 plateau during ramp incremental (RI) cycle ergometer exercise, and whether there was any relationship between this peak
O2 and the peak
O2 measured during a separate single or a series of maximal constant-WR step exercise (SE) tests of increasing WR, each performed on a separate day. In that study, while a
O2 plateau was not seen consistently during the RI test, the peak
O2 achieved did not differ from that measured during the individual SE tests, demonstrating, in each individual, that the peak
O2 did not change over a range of different WRs. This is consistent with the peak
O2 attained during a maximal-effort RI test being representative of the subject's actual
O2 max, despite no evidence of a
O2 plateau (8). However, while this peak value is highly likely to be equal to the
O2 max, one cannot "know" that it is so without confirming evidence.
The purpose of this study, therefore, was to determine whether a constant-load SE test performed subsequent to a maximal RI test (but as part of a single-session protocol) would provide the necessary criterion for establishing
O2 max, even when the data from the individual components of the test do not themselves manifest a plateau. We tested the following hypotheses: 1) that the peak
O2 during an RI test would not be different from that achieved during a subsequent SE test performed at a WR 5% greater than the peak WR (WRpeak) from the RI test, thereby providing the potential to satisfy the "
O2 max" criterion, and 2) that the peak
O2 during SE even performed at a WR 5% lower than the WRpeak from an RI test would also not be different from that achieved during the RI test.
| METHODS |
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Exercise protocol.
Subjects reported to the air-conditioned laboratory at approximately the same time each day. Exercise was performed on a computer-controlled, electromagnetically braked cycle ergometer (Excalibur Sport, Lode, Groningen, The Netherlands). Subjects performed an RI exercise test (WR increased at 1 W/3 s, giving a ramp slope of 20 W/min) from a baseline of 20 W to the limit of tolerance (WRpeak); this was defined as the subject being unable to maintain a pedal cadence of at least 50 rpm, despite strong verbal encouragement from the investigators (i.e., this was the "fatigue" criterion used for each component of the exercise protocol). At the point of fatigue, the WR was lowered back to the 20-W baseline level for a 5-min recovery phase, after which the WR was increased instantaneously as a step function (SE) to a level corresponding to 105% of the previously established WRpeak (i.e., RISE-105) until they again reached the limit of tolerance. The WR was then reduced back to the 20-W baseline for 6 min, after which the test was ended. On a separate occasion, five of these subjects performed an additional protocol that was identical to the RISE-105 protocol, except that the post-ramp SE component corresponded to 95% WRpeak (i.e., RISE-95). For those subjects performing both the RISE-105 and RISE-95 protocols, the testing days were separated by at least 5 days. Thus, for a given subject, the peak
O2 achieved during each of the RI exercise tests could be compared with the peak
O2 achieved during the subsequent SE tests.
Materials and methods. Inspiratory and expiratory gas flow and volumes were measured throughout each of the exercise tests by means of a low-dead space (90 ml), low-resistance (<1.5 cmH2O at 3 l/s) turbine transducer (VMM, Interface Associates, Laguna Niguel, CA); the volume turbine was calibrated before each test by using a syringe of known volume (3.0 liters) over a range of flows. Respired gas was sampled continuously from the mouthpiece (1 ml/s) by a mass spectrometer (QP9000, Morgan Medical, Gillingham, Kent, UK) and analyzed for fractional concentrations of O2, CO2, and N2. The mass spectrometer was calibrated before, and verified at the end of, each test by using precision-analyzed gas mixtures. The time delay between the volume and gas concentration signals was measured by passing a bolus of gas through the system using a solenoid valve (4), thereby allowing the volume and gas concentration signals to be appropriately phase aligned (14). Following analog-to-digital conversion, the electrical signals from these devices were sampled every 20 ms and processed on-line by digital computer for breath-by-breath computation and display of pulmonary gas-exchange variables. The calibration and validation procedures have been described previously (3). Heart rate (HR) was measured from the R-R interval of the electrocardiogram (Q-5000, Quinton Instruments) by using a six-lead electrode placement and digitized to the computer for beat-to-beat HR determination.
Analysis.
Breath-by-breath data for each individual trial were edited to remove occasional errant breaths resulting from, for example, swallows, coughs, or sighs, and which were not considered part of the underlying physiological response, as previously described (5). Editing was performed on
O2 data using the criterion of breaths lying outside 4 SDs of the local mean (15, 22).
Deviations from linearity of the
O2-time relationship during the RI tests were assessed, as described previously (7). Linear regression of the
O2-time data was performed by using standard least squares fitting procedures (Origin, Microcal) through the linear portion of the
O2 response, i.e., after excluding the initial 4 min (to exclude the influence of
O2 kinetics on the early response) and the final 3 min (to exclude the influence of a possible
O2 "plateau" at the end of the test) of
O2 data. This linear fit was then extrapolated to the end of the ramp test, and the presence of, or a tendency toward, a
O2 plateau was determined by the difference between the actual
O2 response at the point of fatigue and the extrapolated linear fit. The difference between the actual
O2 data and the model linear fit (i.e., "residuals") was plotted to better visualize any deviation from linearity, and any difference was quantified by averaging the residuals for the final 15 s of the RI test. The peak
O2 reached during each of the RI and SE tests was calculated as the average
O2 for the individual breaths taken during the final 15 s of each of the exercise tests. [This time window represents the balance between 1) the short averaging duration required by the rapid
O2 response during the SE test, and 2) inclusion of sufficient data to yield an appropriately accurate average determined by the magnitude of the breath-to-breath fluctuations.]
Statistics.
Because not all subjects completed all exercise tests, two separate statistical analyses were applied. The peak
O2 for each of the components of the RISE-105 (n = 7) protocol (i.e., RI followed by SE to 105% of the RI WR) was analyzed by using a one-way ANOVA for repeated measures. Comparison of the peak
O2 for each of the components of the RISE-105 and RISE-95 protocols (n = 5) was made by using a two-way ANOVA for repeated measures. A significant F-ratio was further analyzed by using Students-Newman-Keuls post hoc analysis. Statistical significance was accepted at P < 0.05. All values are reported as the mean (SD).
| RESULTS |
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O2 response for any of the subjects during the RI tests, although there was a "tendency" toward a plateau in 2 of 12 (i.e., 17%) RI tests, in the sense that a deceleration in the rate of increase of the
O2 response was seen such that the actual peak
O2 was less than the extrapolated value by >0.10 l/min. Of the remaining RI tests, an accelerated
O2 response was seen in 4 of 12 (i.e., 33%) tests, with no discernible nonlinearity in the remaining 6 tests (i.e., 50%). The residuals between the actual
O2 data at the point of fatigue and the extrapolated linear fit of the
O2-time relationship on the RI tests did not differ from "zero," averaging only 63 ml/min (SD 209) (RISE-105; n = 7 subjects), 52 ml/min (SD 254) (RISE-105; n = 5 subjects), and 3 ml/min (SD 200) (RISE-95; n = 5 subjects).
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O2 profile during the RISE-105 and RISE-95 protocols for a representative subject is presented in Fig. 1. The group mean peak
O2 for the RI component of the RISE-105 protocol was 4.33 l/min (SD 0.52). Despite the WR for the SE component of the RISE-105 protocol being 5% greater than the WRpeak for the RI component [SE, 359 W (SD 31); RI, 341 W (SD 29)], the peak
O2 was similar between the two components [SE, 4.30 l/min (SD 0.51); RI, 4.33 l/min (SD 0.52)] (Table 1; Fig. 2). The SE duration in the RISE-105 test was 88.3 s (SD 15.4), on average, but the peak
O2 difference between the SE and RI components was only 31 ml/min (SD 112), i.e., <1% of the peak
O2 for the RI component. For all seven subjects, the peak
O2 values for the two components of the RISE-105 protocol were highly correlated (r = 0.98), with a slope (0.96) and intercept (0.14 l/min) for the relationship that was not significantly different from that of the line of identity. At the limit of tolerance, respiratory exchange ratio (RER) was significantly lower during SE than RI [SE, 1.01 (SD 0.07); RI, 1.14 (SD 0.04); P < 0.05], but HR was not statistically different [SE, 180 beats/min (SD 8); RI, 184 beats/min (SD 9)].
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O2 values for the four components were not significantly different [RISE-105: RI, 4.15 l/min (SD 0.50); SE, 4.09 l/min (SD 0.45); RISE-95: RI, 4.11 l/min (SD 0.48); SE, 4.12 l/min (SD 0.53)] (Table 1), despite differences in WRs (Table 1; see Fig. 4, A and B). Also, the repeated RI peak
O2 values were highly correlated (r = 0.96), with the slope (0.913) and intercept (0.317 l/min) for the relationship being not different from that of the line of identity (Fig. 3). The average duration of the SE components of the tests was 89.0 s (SD 18.5) for RISE-105 and 130.4 s (SD 20.2) for RISE-95. The difference in peak
O2 between the SE and RI components for the two protocols was 60 ml/min (SD 121) (RISE-105) and 11 ml/min (SD 73) (RISE-95); i.e.,
1% of the peak
O2 from the respective RI component. In each case, the relationship between the peak
O2 for the RI and SE components was highly correlated (RISE-105, r = 0.98; RISE-95, r = 0.99), with slopes and intercepts not significantly different from those of the lines of identity (Fig. 4). RER at the limit of tolerance was significantly higher during RI compared with SE [RISE-105: RI, 1.16 (SD 0.03); SE, 1.00 (SD 0.08); RISE-95: RI, 1.15 (SD 0.05); SE, 1.04 (SD 0.05)] (Table 1), but HR was not significantly different between the two conditions (Table 1).
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O2 profiles during the RISE-105 and RISE-95 protocols for a representative subject are overlaid on a common time scale in Fig. 5A. It is clear that, for this subject, a
O2 plateau is not evident during the RI components of the RISE-105 and RISE-95 protocols, and that the peak
O2 during the SE components are not different from each other and are not different from the peak
O2 of the RI components of both the RISE-105 and RISE-95 protocols. This is summarized for all subjects in Fig. 5B. When the peak
O2 for each of the components of the RISE-105 (n = 7 and 5) and RISE-95 (n = 5) are plotted against WR at the limit of tolerance, it is clear that peak
O2 is similar across all components, despite a large range in WRpeak values; i.e., in either test, a
O2 plateau was established.
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| DISCUSSION |
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O2 response to RI exercise does not consistently demonstrate plateau-like behavior at the subject's limit of tolerance (as reviewed in Refs. 2, 12, 28, and illustrated in Fig. 1). A plateau in the
O2 response is also not consistently apparent at the limit of tolerance during SE, especially for bouts of short tolerable duration. Thus the requirement for determining a
O2 max (i.e., no increase in
O2, despite a further increase in WR) is not consistently met, despite apparent maximum effort. It should be noted, however, that, in the classical
O2 max reports of Mitchell et al. (19) and Taylor et al. (23), there is no stated or implicit requirement for the data response to "plateau" during a particular SE test, only that at another discrete time the highest value achieved is not, or is only minimally, higher, despite a higher "requirement" as reflected by the higher WR.
To establish (or not) the existence of a
O2 max using the established criterion, in this study we describe a test incorporating both RI and SE tests, where 1) the WR is greater in SE than RI (i.e., SE is 105% of the WRpeak achieved during the RI protocol), and 2) the WR is greater in RI than SE (i.e., SE is 95% of the WRpeak achieved during the RI protocol). We demonstrated the following. 1) A
O2 plateau was not seen at the limit of tolerance in any of the data responses during the 12 RI tests, and a tendency toward a plateau (i.e., a decelerated rate of increase of the
O2 response) was seen in only two tests. 2) The peak
O2 achieved during the SE component of the RISE-105 protocol was not significantly different from the peak
O2 achieved during the RI component, despite the WR being 5% higher than the WRpeak of the RI component; that is, while there was no discernible plateau in the actual data profile, a plot of the highest values achieved as a function of WR did yield the plateau requirement for a
O2 max in every case. 3) The same result was seen again in the RISE-95 protocol, where the peak
O2 achieved in the RI and SE components were not different, despite the WR in SE being 5% lower than the WRpeak in RI. 4) The constancy of the peak
O2 when combining the
O2 response from the RI and SE components of the RISE-105 (and RISE-95) protocol further satisfies the criterion necessary for a
O2 max on the basis of a plateau in
O2; in other words, the
O2 plateau is manifest in the plot of
O2 with increasing WR (Fig. 5B), even though, from a single RI exercise test, the
O2 response profile does not itself plateau (Fig. 5A).
Attempts to establish a plateau in the
O2 response during continuous incremental protocols have yielded widely varying results; a
O2 plateau is typically attained in <50% of subjects (7, 8, 12, 25). For tests using increments of 3 min or so, of course, the final increment must be maintained for a sufficient duration for the dynamic phase of the
O2 transient to be complete, or else a plateau-like result would be inevitable in the plot of the response. However, in any of the instances in which there is not a discernible plateau in
O2, one cannot know with certainty whether the peak
O2 achieved at the point of fatigue reflects the subject's true
O2 max. Recently, Day et al. (7) described the
O2-WR responses for 71 subjects performing RI exercise tests. They reported that, near the limit of tolerance for these subjects, a plateau-like
O2 response (or deceleration of the
O2 response) was seen in only 12 of 71 subjects (i.e., 17%), while in 19 subjects (i.e., 27%) there was actually an accelerated rise in
O2, and in 40 subjects (i.e., 56%) there was a continued linear increase up to the limit of tolerance (7). During the 12 RI tests performed in the present study, 17% (2 of 12 tests) demonstrated a deceleration in the
O2 response at the limit of tolerance, 33% demonstrated an accelerated
O2 response, and 50% demonstrated a linear
O2 response, quite consistent with the findings of Day et al. (7).
To confirm whether the peak
O2 from a single RI exercise test (which does not exhibit a plateau in the
O2 response) reflects a true
O2 max, we modified the protocol for RI testing by appending, as part of the same protocol, a constant-load SE test, whereby (following a 5-min period of 20 W cycling) the WR was increased instantaneously to 105% of the WRpeak achieved by the subject during the RI component. The subjects were required to again exercise to their limit of tolerance. In this study, despite an increase in WR (average, 18 W; range, 1419 W) for the SE component of the RISE-105 protocol, the peak
O2 was not different from that of the RI component (approximately 30 ml/min), whereas a
O2 that was greater by at least 207 ml/min (range, 156226 ml/min) would be expected based on the measured
O2 gain (
11.7 ml·min1·W1; range, 11.212.4 ml·min1·W1) for these subjects.
It should be noted, however, that, during an RI exercise test, the linear phase of the
O2 response necessarily lags behind the steady-state
O2 response by the effective time constant (or mean response time), such that the
O2 for any WR will be less than the steady-state value for that WR (28). Therefore, in the present study, the peak
O2 measured at the limit of tolerance likely corresponds not to the WRpeak measured at that instant, but to a lower WR occurring earlier in the RI test; i.e., its "steady-state" equivalent (26). The choice of the ramp slope for the initial phase of the protocol should, therefore, be made with caution: too great a slope would lead to the potential for inappropriately high muscular force demand for the subsequent SE test, which, by its nature, is a challenging one. Target ramp durations of 1012 min are likely to be adequate.
Tests where peak
O2 was repeatedly established during a single experiment have been described previously. However, protocols using identical consecutive ramp protocols (e.g., Refs. 13, 18) typically result in the same end-exercise WR and, therefore, do not establish the constancy of peak
O2 with increasing WR. A protocol incorporating both RI and SE components as used in the present study has been previously described for leg cycle ergometry and treadmill running (16). Similar to the present study, these authors suggested a protocol consisting of a "progressive phase" and a subsequent "verification phase" (separated by 515 min of resting recovery to allow HR to return to
100 beats/min). In this case, however, experiments to test the validity of this concept were not made.
In the present study, five subjects completed both RISE-105 and RISE-95 protocols. Despite the SE components of both tests being very short (e.g.,
90130 s), the subjects were still able to rapidly attain peak
O2 values that corroborated the maximum. This is presumably possible via a combination of influences from the short recovery duration between RI and SE components, the
O2 slow component (7), and/or "speeding" effects of prior exercise (9). During the RISE-95 test (where the WR for the SE component was set at 5% below the WRpeak achieved in the RI component), however, it is important that the subpeak WR chosen for the SE phase not be "too low," as it is only during WRs above the subject's "critical power" where
O2 has a trajectory toward
O2 max (20, 21). Due to the short duration of the SE portion of the RISE-105, the RISE-95 test may be seen as preferable, because the SE phase is conveniently short but still long enough to ensure that
O2 attains the maximum. Alternatively, it may be beneficial to undertake longer recovery durations between the RI and SE portions of the RISE-105 test (e.g., Ref. 16), which is also likely to increase the SE duration. In either case, the present data suggest that these considerations may represent refinements of the RISE protocol rather than necessities.
In agreement with the results of Day et al. (7), the peak
O2 during both the RI and SE components of the RISE-95 protocol were not different, despite the WR being
16 W lower during the SE component. However, whereas Day et al. established that a true
O2 max (i.e.,
O2 plateau) was achieved in their six subjects, this could only be confirmed after separate experiments, with each undertaken on a separate day. In the present study, we extend these findings to show that, in those subjects completing both the RISE-95 and RISE-105 protocols, the peak
O2 was not different between any of the RI or SE components (see Figs. 4 and 5B). The inclusion of a WR greater than that achieved during RI (e.g., RISE-105) allows the "no increase in
O2 with an increase in WR" criterion to be established. Interestingly, this is also the case with the RISE-95 protocol, but here the RI WR acts as the greater of the two and allows the same criterion to be established. A lower WR in the SE compared with RI component of the RISE-95 protocol might be perceived as preferable in conditions where higher WRs might not be recommended and subject or patient safety is a concern. Taken together, these data show that, when the peak
O2 values for each of the RI and SE components of two RISE protocols are plotted as a function of WR, a plateau in
O2 is clearly evident (Fig. 5B).
In this test, it is unlikely that the two different forcing functions (i.e., RI and SE) could result in identical but submaximal
O2 values. The RISE protocol, therefore, has the potential to confirm
O2 max (i.e., the special condition of the peak
O2) within a single test assuming maximal subject effort on both components. In addition, it provides the beneficial information of the standard RI protocol, e.g., estimated lactate threshold, the steady-state
O2 gain or "efficiency" (
O2/
WR), respiratory compensation point, and other related respiratory measures, including the mean response time for
O2 kinetics. Establishing a
O2 that cannot be increased within a single test, despite the subject's utmost effort, eliminates the necessity to look to other respiratory, metabolic, and cardiovascular variables [i.e., RER, blood lactate concentration, and HR (8), all poor validating indexes, in this regard] to corroborate a "maximum effort." For example, in the present study, the average RER was
1.15; however, about one-half of the subjects were shown to have attained a
O2 max without reaching this value (the caution required in interpreting this variable is exemplified in the RER values from the SE tests, which, due to the kinetics of carbon dioxide output relative to
O2, as well as being subsequent to a large hyperventilation, were consistently below the 1.15 "landmark," despite the
O2 being established as a maximum). Blood lactate was not measured here, but peak HR was within the very broad bounds of the predicted maximum, despite being <100% of predicted in most cases.
It has been suggested that subjects who show a tendency to manifest a plateau in the
O2 response at, or near, the limit of tolerance somehow manifest a more "effortful" test than those who do not (e.g., Ref. 24). While this issue cannot be resolved by these experiments, the precise molecular mechanism(s) of fatigue in such tests remains to be elucidated. If we assume that the induction of the limit of tolerance is related to the perceptual consequences of some cluster of (presumably intramuscular) fatigue metabolites reaching an intolerable level, then this could occur in a particular subject, whether or not the
O2 has plateaued. However, the increased anaerobic contribution during the period in which plateauing is manifest would, of course, accelerate the achievement of this intolerable (presumably limiting) level, but the similarity of the maximally achieved value in such disparate test formats argues against any appreciable "lack of effort" in those subjects who did not evidence a "plateau" during the incremental test.
Thus these data imply that, during RI testing, when subjects give a "maximal" effort, the peak
O2 achieved during the RI test is likely to be the same as the subject's
O2 max, even if a plateau is not evident. However, confirmation that a "maximal"
O2 was reached can only be made with an appropriate further test, in this case by incorporating an SE (or constant load) exercise test at a WR slightly above (present study) or even slightly below (present study; Ref. 7) the WRpeak achieved during the RI component of the test. In both instances, the plateau in
O2 is confirmed when plotting peak
O2 from each of the RI and SE components as a function of WR, even if the individual
O2 data themselves do not plateau, thereby establishing the major criterion for a "maximum"
O2.
| GRANTS |
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| ACKNOWLEDGMENTS |
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Present address of H. B. Rossiter and B. J. Whipp: Institute of Membrane and Systems Biology, Centre of Sport and Exercise Sciences, Faculty of Biological Sciences, Univ. of Leeds, Leeds LS2 9JT, UK.
| FOOTNOTES |
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The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
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J. F. de Groot, T. Takken, S. de Graaff, R. H.J.M. Gooskens, P. J.M. Helders, and L. Vanhees Treadmill Testing of Children Who Have Spina Bifida and Are Ambulatory: Does Peak Oxygen Uptake Reflect Maximum Oxygen Uptake? Physical Therapy, July 1, 2009; 89(7): 679 - 687. [Abstract] [Full Text] [PDF] |
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T D Noakes How did A V Hill understand the VO2max and the "plateau phenomenon"? Still no clarity? Br. J. Sports Med., July 1, 2008; 42(7): 574 - 580. [Abstract] [Full Text] [PDF] |
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N. J. A. Berger, I. T. Campbell, D. P. Wilkerson, and A. M. Jones Influence of acute plasma volume expansion on VO2 kinetics, VO2peak, and performance during high-intensity cycle exercise J Appl Physiol, September 1, 2006; 101(3): 707 - 714. [Abstract] [Full Text] [PDF] |
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