Journal of Applied Physiology Ad Instruments
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

J Appl Physiol 95: 2014-2022, 2003. First published July 25, 2003; doi:10.1152/japplphysiol.00590.2002
8750-7587/03 $5.00
This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF) Free
Right arrow All Versions of this Article:
95/5/2014    most recent
00590.2002v1
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (23)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Scheuermann, B. W.
Right arrow Articles by Barstow, T. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Scheuermann, B. W.
Right arrow Articles by Barstow, T. J.

O2 uptake kinetics during exercise at peak O2 uptake

Barry W. Scheuermann1 and Thomas J. Barstow2

1Department of Health, Exercise and Sport Sciences, Texas Tech University, Lubbock, Texas 79409; and 2Department of Kinesiology, Kansas State University, Manhattan, Kansas 66506

Submitted 2 July 2002 ; accepted in final form 21 July 2003


   ABSTRACT
TOP
 ABSTRACT
METHODS
 RESULTS
 DISCUSSION
 DISCLOSURES
 ACKNOWLEDGMENTS
 REFERENCES
 
Compared with moderate- and heavy-intensity exercise, the adjustment of O2 uptake (O2) to exercise intensities that elicit peak O2 has received relatively little attention. This study examined the O2 response of 21 young, healthy subjects (25 ± 6 yr; mean ± SD) during cycle ergometer exercise to step transitions in work rate (WR) corresponding to 90, 100, and 110% of the peak WR achieved during a preliminary ramp protocol (15-30 W/min). Gas exchange was measured breath by breath and interpolated to 1-s values. O2 kinetics were determined by use of a two- or three-component exponential model to isolate the time constant ({tau}2) as representative of O2 kinetics and the amplitude (Amp) of the primary fast component independent of the appearance of any O2 slow component. No difference in O2 kinetics was observed between WRs ({tau}90 = 24.7 ± 9.0; {tau}100 = 22.8 ± 6.7; {tau}110 = 21.5 ± 9.2 s, where subscripts denote percent of peak WR; P > 0.05); nor in a subgroup of eight subjects was {tau}2 different from the value for moderate-intensity (<lactate threshold) exercise ({tau}2 = 25 ± 12 s, P > 0.05). As expected, the Amp increased with increasing WRs (Amp90 = 2,089 ± 548; Amp100 = 2,165 ± 517; Amp110 = 2,225 ± 559 ml/min; Amp90 vs. Amp110, P < 0.05). However, the gain (G) of the O2 response ({Delta}O2/{Delta}WR) decreased with increasing WRs (G90 = 8.5 ± 0.6; G100 = 7.9 ± 0.6; G110 = 7.3 ± 0.6 ml·min-1·W-1; P < 0.05). The Amp of the primary component approximated 85, 88, and 89% of peak O2 during 90, 100, and 110% WR transitions, respectively. The results of the present study demonstrate that, compared with moderate- and heavy-intensity exercise, the gain of the O2 response (as {Delta}O2/{Delta}WR) is reduced for exercise transitions in the severe-intensity domain, but the approach to this gain is well described by a common time constant that is invariant across work intensities. The lower {Delta}O2/{Delta}WR may be due to an insufficient adjustment of the cardiovascular and/or pulmonary systems that determine O2 delivery to the exercising muscles or due to recruitment of motor units with lower oxidative capacity, after the onset of exercise in the severe-intensity domain.

maximal exercise; citrate synthase; fitness; efficiency; muscle fiber type

THE OBSERVATION THAT MUSCLE and pulmonary O2 uptake (O2) increase approximately exponentially to a new steady state after an abrupt increase in exercise of moderate intensity [i.e., below the lactate threshold (LT)] has long been appreciated. However, the mechanism that limits the rate at which O2 approaches the new steady state during moderate-intensity exercise continues to be debated (40). Several investigators suggest that O2 kinetics are fundamentally determined by the inertia of intramuscular metabolic processes. For example, a number of studies (2, 30, 35) have shown similar kinetics for the rate of phosphocreatine breakdown and the increase in O2 at the onset of moderate-intensity exercise, consistent with the view that O2 kinetics are determined by the rate of rise of mitochondrial oxidative phosphorylation. Additionally, increasing O2 delivery to the exercising muscle by breathing hyperoxic gas mixtures (10, 18, 27) or increasing muscle perfusion (12-14) does not speed O2 kinetics, at least during moderate-intensity upright exercise. However, other studies have shown that under conditions in which O2 delivery to the exercising muscles is compromised, either by altering blood flow (17, 20, 28) or reducing arterial O2 content (10, 18, 32), O2 kinetics become slowed, suggesting that O2 delivery can modify O2 kinetics.

During exercise above the LT, an additional increase in O2 of delayed onset occurs that projects to a value above the O2 requirement predicted from the O2-work rate relationship for exercise below the LT (3, 6, 43). Similar to the arguments made for moderate-intensity exercise, longer kinetics for the primary rise in O2 during exercise above LT compared with below LT has been used as evidence for an O2-delivery limitation (34), whereas studies reporting similar O2 kinetics during exercise below and above the LT have been used to argue for an intramuscular metabolic limitation (6). Despite the equivocal findings for the time constant of the primary fast rise in O2 (i.e., phase II kinetics), studies have established that during heavy constant-work rate exercise, the overall O2 cost increases (3, 16, 36) so that the {Delta}O2/{Delta}WR is appreciably greater during heavy-intensity exercise (i.e., >12 ml·min-1·W-1) compared with exercise below the LT (i.e., ~10 ml·min-1·W-1). It has been suggested that the within-subject {Delta}O2/{Delta}WR for the primary rise in O2 is invariant across exercise intensities up to 100% of peak O2 (O2 peak) (3). However, this postulation has not be systematically examined at exercise intensities approaching O2 peak.

Most investigations examining O2 kinetics after the onset of heavy-intensity exercise have, for the most part, utilized a work rate that approximates 30-50% of the difference in the metabolic rate between the LT and O2 peak. Comparatively little research has examined O2 kinetics during the on-transient to a step increase in work rate that projects to a O2 near or above peak aerobic capacity. Hughson and colleagues (19) reported a progressive slowing of the time constant for the on-transient as exercise intensities approached ~125% O2 peak, which they interpreted as an O2-delivery limitation to O2 kinetics. However, Bangsbo et al. (1), on the basis of direct measurements of the arterial-venous O2 difference and muscle blood flow during exercise at 120% O2 peak, concluded that the limitation in muscle O2 uptake after the onset of severe exercise was not associated with insufficient O2 delivery but, rather, was due to an inability of the muscle to extract O2. It should be noted that Bangsbo et al. examined the exercise response during single-leg knee extension exercise, and therefore the demand on the cardiovascular system would not be equivalent to the maximal response required by the protocol of Hughson et al. Furthermore, a recent study by Krustrup et al. (24) has demonstrated that, during repeated bouts of intense knee extension exercise, O2 extraction reaches an upper limit, but muscle O2 and muscle blood flow are higher during the subsequent bouts of exercise, consistent with an O2-delivery limitation at the onset of the initial exercise bout.

Although these studies (1, 19, 24) considered the time course with which O2 adjusted, none of the studies systematically examined the {Delta}O2/{Delta}WR relationship during exercise at or near exercise intensities associated with O2 peak. Recent evidence suggests that factors such as fitness, muscle fiber type, and/or exercise intensity (3-5) may influence the gain (as {Delta}O2/{Delta}WR) of the primary fast component of the O2 response after the onset of heavy exercise. Understanding the integrative strategy that the cardiovascular system adopts to meet the metabolic demands during exercise in the severe-intensity domain (i.e., eliciting O2 peak) would significantly contribute to our understanding of muscle energetics and limitations to exercise tolerance in this exercise domain. Thus the purpose of the present study was to examine O2 kinetics (as both the time constant and the initial gain) during the on-transient of severe exercise designed to elicit O2 peak and to compare the results with the O2 response during moderate (<LT) and heavy (halfway between the LT and O2 peak) exercise.


   METHODS
TOP
 ABSTRACT
 METHODS
RESULTS
 DISCUSSION
 DISCLOSURES
 ACKNOWLEDGMENTS
 REFERENCES
 
Subjects. Twenty-one subjects (15 men, 6 women; age 25 ± 6 yr; height 177 ± 8 cm; body mass 76.9 ± 15.6 kg) participated in this study. The experimental protocol was approved by the Institutional Review Board for Research Involving Human Subjects at Kansas State University. Each subject provided written, informed consent after the exercise protocol and all foreseeable risks and benefits associated with participation in the study had been explained.

Materials and protocol. Each subject reported to the Human Exercise Physiology Laboratory at Kansas State University on 4 separate days. All exercise testing was completed within a 2- to 3-wk period. Subjects were requested to abstain from heavy exercise for at least 24 h before each exercise test. Each subject was asked to consume a light meal before arriving at the laboratory. All exercise tests were performed at approximately the same time of day for each subject.

All exercise testing was performed on an electronically braked cycle ergometer (Corival 400, Lode, The Netherlands). The seat and handlebar positions on the cycle ergometer were adjusted for each subject before the first exercise test and replicated on subsequent testing days. Preliminary exercise testing of each subject was performed to familiarize the subjects with the exercise protocol, for the determination of the estimated LT, and for the determination of O2 peak and peak work rate. The exercise test consisted of 4 min of unloaded cycling followed by a progressive increase in exercise intensity whereby the work rate was increased as a ramp function (15-30 W/min) to volitional fatigue. For all exercise tests, subjects were asked to maintain a pedal frequency of 70 rpm. The highest O2 averaged over a 10-s interval was taken as O2 peak. The peak work rate (WRpeak) was taken as the highest 1-s value achieved immediately before fatigue. The LT was estimated by visual inspection from gas exchange indexes by using the V-slope method, ventilatory equivalents, and end-tidal gas tensions according to established approaches (7, 41).

On each of three subsequent visits to the laboratory, each subject performed a constant-work-rate test corresponding to either 90, 100, or 110% of the WRpeak achieved during the initial ramp exercise test. Each trial consisted of 4 min of unloaded cycling followed by a step increase in work rate that continued to exhaustion. The subjects were verbally encouraged to maintain a pedal frequency of 70 rpm throughout the exercise duration. The order of the tests was randomized with no less than 48 h allowed between test days.

Although the primary purpose of the present study was to examine the O2 response to exercise intensities that elicit the O2 peak, additional comparisons were made within a subgroup of eight subjects who agreed to perform additional constant-work-rate tests at both moderate and heavy exercise intensities. From the results of the initial ramp test, a work rate was determined that would elicit a O2 corresponding to 80% LT and approximately halfway between the LT and O2 peak, i.e., {Delta}50% = LT + [(O2 peak - LT)0.50]. On 3 separate days, each subject performed two transitions from a baseline of loadless cycling to the moderate work rate (80% LT). Each transition was 6 min in duration and was separated by 6 min of loadless cycling. One repetition at the heavy work rate ({Delta}50%), 8 min in duration, was performed each day. This arrangement of tests resulted in six on-transitions to 80% LT and three on-transitions to {Delta}50% exercise. At least 48 h were allowed for recovery between test days.

Pulmonary gas exchange (O2 and CO2 production) and minute expired ventilation were measured breath by breath throughout exercise by use of a metabolic measurement system (Medgraphics Cardio2, Medical Graphics, St. Paul, MN). The system was calibrated before each exercise test according to the manufacturer's instructions. The volume signal, obtained from measurements of flow using a Pitot flow sensor, was calibrated before each exercise test by manually pumping a 3-liter syringe through the sensor over a range of flows similar to that achieved during moderate through to maximal exercise. The O2 and CO2 analyzers were calibrated by using gases of known concentrations before each exercise test. Heart rate was determined from the electrocardiogram with the leads placed in a modified V5 configuration and stored in the breath-by-breath data file.

On a separate occasion, muscle samples were obtained from the vastus lateralis for the determination of citrate synthase (CS) activity and muscle fiber-type distribution. The muscle biopsy technique of Bergström (8) was used. The skin overlying the biopsy site of the right leg was initially prepared with the use of local anesthetic (2% lidocaine), after which a small incision was made. The first muscle sample was mounted in an embedding compound and frozen in isopentane that was cooled to its freezing point in liquid nitrogen. The second muscle sample was immediately frozen in liquid nitrogen. Muscle samples were stored at -80°C until later analysis. Serial cross sections (~8-10 µm) were cut in a cryostat that was maintained at -20°C. Myofibrillar adenosine triphosphatase activity was determined histochemically by preincubating the sections at a pH of 9.2. Muscle fibers were classified as either type I or type II according to lability to the alkaline preincubation. For each subject, between 180 and 800 fibers were analyzed. The fiber-type distribution was expressed as a percentage of the total number of fibers counted. CS activity, a measure of muscle oxidative capacity, was determined in duplicate by using standard techniques (38).

Data analysis. For the on-transient to severe exercise (i.e., 90, 100, and 110% WRpeak), the breath-by-breath data were linearly interpolated to 1-s values. For moderate (80% LT) and heavy ({Delta}50%) exercise, the breath-by-breath data for each step transition in work rate were linearly interpolated at 1-s intervals, time aligned to the onset of exercise, and ensemble averaged to provide a single on-transient for 80% LT and {Delta}50% exercise for each subject. The time course of O2 after the onset of exercise was described for each subject and exercise intensity by use of a model that provides an estimate of the baseline (BSL), amplitudes (A1, A2, and A3), time delays (TD2 and TD3), and time constants ({tau}1, {tau}2, and {tau}3) (37). Model parameters were determined by using least-squares nonlinear regression in which the convergence criteria were satisfied by minimizing the sum of squared errors. The first exponential term begins coincident with the onset of exercise (i.e., no time delay), whereas the exponential terms describing the primary fast component and the O2 slow component, if present, begin after independent time delays. For exercise below the LT, the parameter estimates for the on-transient were determined as a function of time (t) by using a two-component exponential model

(1)
For exercise above the LT, the parameter estimates for the on-transient were determined by using a three-component exponential model

(2)
The exponential term describing phase I kinetics (i.e., the cardiodynamic phase) after the onset of exercise was truncated at the onset of phase II (i.e., at TD2), and the relevant amplitude of phase I (A'1) was calculated according to the equation

(3)
Thus the first exponential term is descriptive up to the value of TD2. The physiologically relevant increase in O2, that is, the amplitude of phase I and phase II (A'2) was determined as the sum of A'1 and A2. In turn, A'2 was used to determine the gain ({Delta}O2/{Delta}WR, where {Delta}WR is change in work rate) of the primary fast component. In order for the primary fast component to be accurately described (both {tau}2 and A'2) by an exponential model, the duration of the primary rise in O2 before the onset of the O2 slow component must be sufficiently long (>=4 times {tau}2). This criterion was satisfied in 20 of the 21 subjects.

Statistical analysis. The O2 kinetic parameters were analyzed by using a one-way repeated-measures ANOVA design with exercise intensity (90, 100, and 110% WRpeak) as the main effect. In addition, the O2 kinetic parameters for the subgroup (n = 8) were analyzed by using a one-way repeated-measures ANOVA design for an exercise intensity effect (80% LT, {Delta}50%, 90%, 100%, and 110% WRpeak). A significant F ratio was further analyzed by using Student-Newman-Keuls post hoc analysis. Least-squares linear regression analysis was used to examine correlations between variables of interest. Statistical significance was accepted at the P < 0.05 level. All values are reported as group means ± SD.


   RESULTS
TOP
 ABSTRACT
 METHODS
 RESULTS
DISCUSSION
 DISCLOSURES
 ACKNOWLEDGMENTS
 REFERENCES
 
Peak exercise, muscle fiber-type distribution, and CS activity. Of the 21 subjects who participated in the study, the exercise response of 20 subjects (14 men, 6 women) was examined. For the one subject that was excluded, the exercise duration at the highest exercise intensity was too brief and, therefore, O2 kinetics at the onset of exercise could not be accurately described. The group mean O2 peak was 3,363 ± 791 ml/min (43.7 ± 9.0 ml·min-1·kg-1). O2 at the estimated LT was 1,754 ± 533 ml/min, which corresponded to 52 ± 7% O2 peak. The group mean % of type I muscle fibers was 36 ± 10% with a range of distribution of 26-68%. The underlying distribution of muscle fiber types was correlated (r = 0.47, P < 0.05) with fitness (expressed as O2 peak, ml·min-1·kg-1). The group mean CS activity was 13.8 ± 4.7 µmol·g wet wt-1/min with a range of values observed from 6.2 to 22.3 µmol·g wet wt-1·min-1. A significant correlation was observed between O2 peak and CS activity (r = 0.59, P < 0.05) (Fig. 1A).



View larger version (14K):
[in this window]
[in a new window]
  		Fig. 1. Relationships between peak O2 uptake (O2) and citrate synthase (CS) activity (vastus lateralis) (A), O2 kinetics (phase II time constant) and CS activity (B), and O2 kinetics and peak O2 (C) in 20 subjects. No difference was observed for O2 kinetics (i.e., {tau}2) for any of the work rates examined; therefore, the average value for each subject was used. Each relationship was significant.

 

O2 kinetics. As expected, the amplitude of the primary fast component (i.e., A'2) of O2 increased (P < 0.05) with increasing exercise intensity (Table 1). However, as the exercise intensity approached maximal aerobic capacity, the gain of the primary fast component (G = {Delta} O2/{Delta}WR) decreased so that {Delta}O2/{Delta}WR was lower (P < 0.05) during exercise at WR110 (G110, 7.3 ± 0.6 ml·min-1·W-1) than WR90 (G90, 8.5 ± 0.6 ml·min-1·W-1) (Table 1). The O2 response of an individual subject during the transitions to near-maximal exercise intensities is presented in Fig. 2. The amplitude of the primary fast component (plus the O2 cost of unloaded cycling) approximated 84.7 ± 4.5, 87.1 ± 5.3, and 88.9 ± 4.5% of O2 peak for exercise at WR90, WR100, and WR110, respectively. For the eight subjects who completed the additional exercise below (80% LT) and above ({Delta}50%) the LT, the gains were similar for moderate (80% LT, 9.8 ± 0.4 ml·min-1·W-1) and heavy ({Delta}50%, 9.6 ± 0.4 ml·min-1·W-1) exercise but progressively fell (P < 0.05) for exercise at WR90, WR100, and WR110 (Fig. 3A). No relationship was observed between muscle fiber-type distribution and either {Delta}O2/{Delta}WR (r = 0.13-0.27, P > 0.05) or A'2 (r = 0.20-0.34, P > 0.05) for any of the work rates examined.


View this table:
[in this window]
[in a new window]
  		Table 1. Parameter estimates for a step increase in work rate corresponding to 90, 100, and 110% of peak work rate achieved during the initial ramp exercise test

 


View larger version (19K):
[in this window]
[in a new window]
  		Fig. 2. Breath-by-breath O2 response of an individual subject during a step transition corresponding to 90% (dotted line), 100% (dark solid line), and 110% (thin dotted line) of the peak work rate (WR) achieved during a preliminary ramp exercise test. O2 response is presented both as the absolute response (A) and the gain (B) to indicate the progressive decrease in the {Delta}O2/{Delta}WR with increasing exercise intensity.

 


View larger version (13K):
[in this window]
[in a new window]
  		Fig. 3. Mean ± SD response for the gain (A) and the phase II O2 kinetics (B) in a subgroup of 8 subjects that completed moderate, heavy, and severe exercise. *Significant decrease (P < 0.05) in the gain (i.e., {Delta}O2 /{Delta}WR relationship) compared with moderate-intensity exercise [80% of the lactate threshold (LT)].

 

For each subject, the slope of the O2-work rate relationship (i.e., {Delta}O2/{Delta}WR) for exercise below the LT during the initial ramp exercise test was used to predict the initial primary rise in O2 for WR90, WR100, and WR110. Figure 4 shows the difference between this predicted value and the actual O2 achieved for each work rate. As can be seen, for each work rate, the difference between the predicted O2 and the actual O2 achieved increased as a function of fitness (O2 peak) (r = 0.53-0.72, P < 0.05). To test whether these relationships were due solely to the fitter subjects performing higher work rates (with an associated higher O2), we compared the difference between the gain for the <LT exercise with the initial gain for WR90, WR100, and WR110, in the eight subjects who also completed both <LT and >LT exercise bouts. For WR90 and for the average for all three work rates, there still was a significant relationship between the decline in gain and fitness as O2 peak (WR90: r = 0.86, P < 0.05; average response: r = 0.75, P = 0.05). For the other work rates, the relationships were positive but did not achieve significance (WR100: r = 0.57; WR110: r = 0.46; both P > 0.05; for n = 8, r must be 0.621 for P < 0.05). Thus, in general, the fitter the subject, the greater was the decline in the gain of the initial primary O2 response, irrespective of the absolute O2 demand.



View larger version (13K):
[in this window]
[in a new window]
  		Fig. 4. Relationship indicating the difference between the predicted O2 and the achieved O2 during phase II as a function of fitness as peak O2 during a step transition in exercise intensity corresponding to 90% (A), 100% (B), and 110% (C) of the peak work rate achieved during a preliminary ramp exercise test. The relationship was significant at each exercise intensity examined.

 

O2 kinetics, expressed as the time constant ({tau}2) for the primary fast component, were not different between exercise intensities that approached O2 peak (Table 1). Furthermore, in the subset of eight subjects, O2 kinetics ({tau}2) during exercise at 80% LT (24.7 ± 12.1 s) and {Delta}50% (24.7 ± 6.7 s) were similar to the values observed during the on-transition to exercise at WR90, WR100, and WR110 (Fig. 3B). Because no difference was observed for {tau}2 across the range of exercise intensities examined in the present study, the three values for {tau}2 obtained for each subject were averaged before the relationships with fitness (O2 peak) and CS activity were examined. As shown in Fig. 1, B and C, a negative correlation was observed between O2 kinetics (as {tau}2) and both CS activity (r = 0.59, P < 0.05) and O2 peak (r = 0.66, P < 0.05). No relationship was observed between muscle fiber-type distribution and O2 kinetics ({tau}2; r = 0.09-0.29, P > 0.05) for any of the near-maximal work rates examined.


   DISCUSSION
TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
DISCLOSURES
 ACKNOWLEDGMENTS
 REFERENCES
 
A general consensus on the appropriate description of the O2 response during the on-transient for work rates that project to a O2 above that of O2 peak has not been reached (42). In the present study, we chose to examine the primary fast component (i.e., phase II) during three separate step transitions in work rate approximating 90, 100, and 110% O2 peak in an effort to better characterize the rate at which O2 adjusts to exercise in the severe-intensity domain. The results of the present study are in agreement with recent reports (21a, 34a) demonstrating that the gain for the initial primary rise in O2 (as {Delta}O2/{Delta}WR) systematically decreases as the exercise intensity approaches the individual's maximal aerobic capacity. Furthermore, the decline in the gain compared with that for moderate (<LT) exercise was positively related to fitness as O2 peak. In addition, we found that phase II kinetics (as {tau}2) were not different between sub- and supramaximal work rates. Indeed, {tau}2 remained invariant across exercise intensities from moderate, below LT exercise (80% LT) to supramaximal work rates (WR110). In contrast to the results of previous studies at lower exercise intensities (4, 5), muscle fiber-type distribution was not associated with either the gain ({Delta}O2/{Delta}WR) or the kinetics ({tau}2) of the primary fast component for exercise in the severe-intensity domain. Thus O2 kinetics for heavy (>LT) and severe (near-maximal) exercise violate the rule of superposition (i.e., a constant gain as the forcing function, power output in this case, is increased) and thus cannot be characterized as a linear system for exercise intensities near O2 peak.

The experimental design of the present study was such that the work rates performed were 10% below and above the power output associated with O2 peak, which allowed for small differences in the O2 response for exercise transitions in the severe-exercise-intensity domain to be systematically examined. The difficulties associated with characterizing the O2 response to supramaximal work rates have been reviewed (42). The most important question is whether the early O2 response initially projects toward the predicted O2 on the basis of the gain ({Delta}O2/{Delta}WR) for <LT exercise and subsequently becomes limited only as O2 peak is approached, presumably by the cardiovascular system, or, alternatively, the kinetics of the cardiovascular system and specifically O2 delivery are limiting from the onset of exercise, independent of the O2 requirement. In the first instance, Whipp (42) conceptualized that O2 kinetics would appear to be speeded (relative to lower work rates) in this domain of exercise because O2 would rise at a faster absolute rate until O2 peak is reached. Using a similar three-exponential model to the one used here to characterize the O2 response, Hughson et al. (19) indeed found progressive speeding of the phase II kinetics as work intensity was increased from 57 to 96 to 125% of O2 peak. However, Hughson et al. argued that, because the cardiovascular system (and thus O2 delivery) is limited at exercise intensities eliciting O2 peak, O2 kinetics should be determined by using the predicted O2, which theoretically would reflect the reference for the metabolic error signal, rather than the observed asymptotic value for the primary rise in O2, which reflects an O2 transport limitation. In this case, O2 kinetics would be slowed throughout the range of response in this exercise domain because of the limitations of O2 transport. Consistent with this interpretation, Hughson et al. found that O2 kinetics became slowed (longer {tau}) with increasing work rates, when the asymptotic exponential value predicted from the moderate exercise {Delta}O2/{Delta}WR was used (but see Time course of the primary fast component). Although the present study does not resolve this issue directly, our results demonstrate that both the gain (i.e., {Delta}O2/{Delta}WR) and the kinetics of the O2 response must be examined to understand the metabolic adjustment to exercise in the severe-intensity domain.

Gain ({Delta}O2/{Delta}WR) of the primary fast component. In contrast to previous studies (4, 5), {Delta}O2/{Delta}WR was not associated with muscle fiber-type distribution for either near-maximal (n = 20) or submaximal (n = 8) exercise. These results are in contrast to previous studies that reported a positive correlation between {Delta}O2/{Delta}WR and the proportion of type I muscle fibers for both the primary fast component of constant work rate exercise (4) and the slope during ramp exercise (5). Although the reason for this discrepancy is not readily apparent, the lack of a positive association in the present study may be explained in part, by the relatively small range of fiber-type distributions found between subjects in this study (see RESULTS) compared with previous reports (4, 5). Alternatively, there is not a preferential recruitment of less efficient type II fibers (37) or, more likely, the difference in efficiency between type I and type II fibers in humans is within measurement error (9, 31).

Neither the amplitude (A'2) nor the gain ({Delta}O2/{Delta}WR) of the O2 response to the near-maximal work rates correlated with fitness. The lack of an association between fitness and {Delta}O2/{Delta}WR is in contrast with previous observations (4, 5, 29). However, the primary exercise intensities examined in the present study were higher than those of the previous studies, which were of moderate or heavy intensity (4, 5, 29). The apparent lack of an association between fitness and {Delta}O2/{Delta}WR in the present study may also be related, in part, to the inability of those individuals with the highest levels of fitness to achieve their predicted O2 (based on the {Delta}O2/{Delta}WR for <LT exercise; see Time course of the primary fast component).

Although the {Delta}O2/{Delta}WR relationship has been reported in several previous studies that have examined O2 kinetics, few studies (3, 6, 33) have systematically examined the {Delta}O2/{Delta}WR relationship across the exercise intensities examined in the present study. For the 20 subjects who completed the three highest exercise intensities, the group mean value for the gain in O2 was 7.3 and 8.5 ml·min-1·W-1 for WR110 and WR90, respectively, values that are significantly lower than expected for moderate to heavy-intensity exercise (3, 6, 34, 36, 37). Indeed, in the subgroup of eight subjects, {Delta}O2/{Delta}WR was significantly lower for near-maximal exercise than either moderate (80% LT) or heavy-intensity ({Delta}50%) exercise (Fig. 3). Previously, Barstow et al. (3) reported a tendency for the gain of the primary fast component to be lower at exercise intensities approaching O2 peak (see Figs. 5 and 8 of Ref. 3). Only four subjects completed the exercise protocol in that study, and, therefore, the observation could not be rigorously tested. Recent results (29) from our laboratory in a different group of subjects suggest that, compared with relatively sedentary subjects, fitter subjects tend to undershoot the predicted value for A'2 during heavy-intensity exercise, consistent with the results of the present study. In a similar study, Özyener et al. (33) found a trend for the gain of the primary response to fall from 11.5 to 11.0 to 10.7 to 10.0 ml·min-1·W-1 for moderate, heavy, very heavy, and severe exercise in six subjects, but only the gain for the severe bout (which required 110% O2 peak) was significantly different from the rest.

The mechanism(s) underlying the lower {Delta}O2/{Delta}WR for exercise transitions eliciting O2 peak cannot be elucidated from the results of this study. One possible interpretation of a lower {Delta}O2/{Delta}WR after the onset of near-maximal exercise is that the cardiovascular system and O2 delivery do not adjust sufficiently in the severe exercise domain (19). Consistent with this, Koga et al. (22) reported a lower {Delta}O2/{Delta}WR for the primary fast component during supine compared with upright heavy-intensity exercise, which they suggested reflected an O2 delivery limitation. In addition, MacDonald et al. (26) reported that enhanced muscle blood flow (and thus O2 delivery) achieved by performing a prior bout of heavy exercise resulted in a higher muscle O2 early in the exercise transition. This increased primary O2 response after warm-up with heavy exercise has been shown to be associated with a reduced contribution of anaerobiosis (11), consistent with this interpretation.

In apparent conflict with this interpretation, however, is the finding of a similar time constant for exercise below and above the LT observed in the present study, which argues against an O2 delivery limitation (see also Time course of primary fast component). It is unclear whether an O2 delivery limitation can result in a change in the {Delta}O2/{Delta}WR relationship independent of a change in {tau}2. Indeed, when O2 delivery is artificially compromised by {beta}-blockade (17, 21) or hypoxic hypoxia (10, 18, 25, 39), the effect is of a prolonged time constant but no change in the steady-state response (or gain), even for >LT exercise (10, 25).

An alternative interpretation for the reduced gain is that the {Delta}O2/{Delta}WR determined for <LT exercise is inappropriate for exercise intensities that approach maximal efforts. For example, as previously suggested by others (21a, 34a), it is possible that exercise at these perimaximal intensities, which would lead to fatigue within a few minutes, involves recruitment of type II motor units with reduced oxidative capacity. It might be envisioned that these fibers could accomplish the required contribution to the total power output but with a greater relative contribution of anaerobiosis and concomitant reduced relative contribution of oxidative phosphorylation (O2). In this case, the early quasi-steady state implied by A'2 could be in fact the target "steady-state" O2 for the recruited motor units at the onset of that exercise intensity. In this case, the initial O2 gain response would not represent the O2 requirement for total ATP resynthesis, as is assumed for the steady-state O2 of moderate- (<LT) intensity exercise. Support for this interpretation comes from the recent results from Krustrup et al. (23) who estimated that oxidative phosphorylation (O2) accounted for 80% of the ATP resynthesis during 90 s of exercise at 50% O2 peak, but only 59% of the total ATP resynthesis during exercise requiring 110% O2 peak. Further studies will be required to resolve the underlying mechanism(s) of the lower {Delta}O2/{Delta}WR in the severe exercise domain.

In the present study, it was observed that the individuals with the highest fitness as O2 peak demonstrated on average the greatest decline in gain of the initial O2 response during near-maximal exercise. The reason(s) for this greater discrepancy with increasing fitness is not readily apparent. If the difference between the predicted and actual O2 in the present study reflects an O2 delivery limitation, then our results suggest that the mismatch between O2 demand and muscle perfusion during the on-transient of the near-maximal exercise is greater in fit subjects (as O2 peak). Although it is only speculation, one potential mechanism that may contribute to a reduced O2 delivery would be a progressive arterial desaturation in the fitter subjects at the high work rates utilized in this study (15).

Time course of the primary fast component. In the present study, the kinetics (as {tau}2) of the primary rise in O2 were similar for exercise intensities ranging from 80% LT to 110% O2 peak. These findings are consistent with the previous results of Barstow and Molé (6) and those recently reported by Özyener et al. (33) for a similar range of exercise intensities. As noted above, one interpretation of the invariant time constant for work rates spanning below LT to perimaximal levels is that the primary rise in phase II O2, and by inference muscle O2 kinetics (35), are determined by the same physiological mechanism across this wide range of work intensities. Because O2 kinetics during <LT exercise are generally assumed to be determined by some as yet unidentified intracellular locus of limitation (often termed "metabolic inertia"), this interpretation implies that O2 kinetics in phase II of near-maximal exercise are also determined by the same (intracellular) locus of limitation and thus are independent of the kinetics of O2 delivery.

However, for large muscle exercise like cycling, O2 peak is thought to be limited by O2 delivery. It is currently unclear whether or when during the transition from light exercise to a near-maximal work rate O2 delivery becomes limiting to the muscle O2 response. As hypothesized by Whipp (42) and demonstrated by Hughson et al. (19), part of the dilemma in discerning potential O2 delivery limitation during the transition to near-maximal work rates from pulmonary O2 responses is the dependence of the estimated time constant on the amplitude used. When the actual O2 response itself is described by a three-exponential model as used here (19), or a two-exponential model for the phase II-III responses only (33), the primary (phase II) time constant has been found to remain invariant (present work, Ref. 33) or even speed (19), whereas the observed gain declines either significantly (present work, Ref. 19) or insignificantly (33). In contrast, when the amplitude is selected a priori on the basis of extrapolation of the {Delta}O2/{Delta}WR determined for <LT exercise (but see above), the resulting time constant is slowed relative to that seen during moderate exercise (19). Resolution of this uncertainty must await further study. We would note, however, that the three-exponential model provides an accurate description of the actual aerobic adjustment to severe exercise, relatively free of assumptions as to what the O2 response "should or should not" be doing.

We also found that {tau}2 was significantly inversely related both to fitness (as O2 peak) and to CS activity. The constancy of the phase II time constant across exercise intensities and the association between {tau}2 and both fitness and CS activity are consistent with the view that O2 kinetics are limited by intramuscular (biochemical) processes within the exercising muscles. However, this observation alone does not preclude the possibility that O2 delivery limits O2 kinetics under these conditions, even for exercise intensities near O2 peak.

Limitations. In the present study, each subject performed a single transition to three separate work rates in the severe-exercise-intensity domain. Our results, which are similar to those reported by others (33), demonstrated considerable variability in {tau}2 within an individual at these severe work rates. However, as already indicated, the group mean values for {tau}2 were invariant across work rates in the severe domain. In fact, the {tau}2 reported for each of the three exercise transitions in the severe-intensity domain was not different from {tau}2 observed for both moderate (80% LT) and heavy-intensity ({Delta}50%) exercise, which was determined by using six and three repetitions, respectively.

In summary, the primary results of the present study demonstrate that the amplitude of the O2 response of exercise in the severe-exercise-intensity domain is reduced compared with that predicted from the {Delta}O2/{Delta}WR relationship for <LT exercise, supporting the view that O2 kinetics do not exhibit characteristics of a dynamic linear system. The time constant for the primary fast phase was similar for exercise below and above the LT, as well as for near-maximal work rates. In addition, the present study demonstrated that the difference between the predicted O2, based on the <LT {Delta}O2/{Delta}WR relationship, and the actual O2 achieved during the phase II was greater with increasing levels of fitness. Although the reason(s) for this widening difference between the predicted and achieved O2 with increasing fitness is not readily apparent, it may reflect either an O2-delivery limitation or, perhaps, recruitment of motor units with a reduced oxidative capacity relative to those recruited at lower work rates. If true, this implies that the {Delta}O2/{Delta}WR relationship for <LT exercise may not be appropriate for exercise in the severe-intensity domain.


   DISCLOSURES
TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 DISCLOSURES
ACKNOWLEDGMENTS
 REFERENCES
 
B. W. Scheuermann was supported by a Medical Research Council of Canada Post Doctoral Fellowship. Funding for this project was provided in part by the National Heart, Lung, and Blood Institute Grant HL-46769 to T. J. Barstow.


   ACKNOWLEDGMENTS
TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 DISCLOSURES
 ACKNOWLEDGMENTS
REFERENCES
 
We thank the subjects who volunteered their time to participate in this study. The technical assistance of Brian Frazier and Kristin Meadows is greatly appreciated.

Present address of B. W. Scheuermann: Assistant Professor, Department of Kinesiology, The University of Toledo, 2801 Bancroft St., Toledo, OH 43606.


   FOOTNOTES
 

Address for reprint requests and other correspondence: B. W. Scheuermann, Dept. of Kinesiology, M.S. 201, The University of Toledo, Toledo, OH 43606 (E-mail: barry.scheuermann{at}utoledo.edu).

The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.


   REFERENCES
TOP
 ABSTRACT
 METHODS
 RESULTS
 DISCUSSION
 DISCLOSURES
 ACKNOWLEDGMENTS
 REFERENCES
 

  1. Bangsbo J, Krustrup P, Gonzalez-Alonso J, Boushel R, and Saltin B. Muscle oxygen kinetics at onset of intense dynamic exercise in humans. Am J Physiol Regul Integr Comp Physiol 279: R899-R906, 2000.[Abstract/Free Full Text]
  2. Barstow TJ, Buchthal SD, Zanconato S, and Cooper DM. Changes in potential controllers of human skeletal muscle respiration during incremental exercise. J Appl Physiol 77: 2169-2176, 1994.[Abstract/Free Full Text]
  3. Barstow TJ, Casaburi R, and Wasserman K. O2 uptake kinetics and the O2 deficit as related to exercise intensity and blood lactate. J Appl Physiol 75: 755-762, 1993.[Abstract/Free Full Text]
  4. Barstow TJ, Jones AM, Nguyen PH, and Casaburi R. Influence of muscle fiber type and pedal frequency on oxygen uptake kinetics of heavy exercise. J Appl Physiol 81: 1642-1650, 1996.[Abstract/Free Full Text]
  5. Barstow TJ, Jones AM, Nguyen PH, and Casaburi R. Influence of muscle fibre type and fitness on the oxygen uptake/work rate slope during incremental exercise. Exp Physiol 85: 109-116, 2000.[Abstract]
  6. Barstow TJ and Molé PA. Linear and nonlinear characteristics of oxygen uptake kinetics during heavy exercise. J Appl Physiol 71: 2099-2106, 1991.[Abstract/Free Full Text]
  7. Beaver WL, Wasserman K, and Whipp BJ. A new method for detecting anaerobic threshold by gas exchange. J Appl Physiol 60: 2020-2027, 1986.[Abstract/Free Full Text]
  8. Bergström J. Muscle electrolytes in man. Scand J Clin Lab Invest 14, Suppl 68: 1-110, 1962.[Web of Science][Medline]
  9. Bosco C, Montanari G, Ribacchi R, Giovenali P, Latteri F, Iachelli G, Faina M, Colli R, Dal Monte A, La Rosa M, Cortili G, and Saibene F. Relationship between the efficiency of muscular work during jumping and the energetics of running. Eur J Appl Physiol 56: 138-143, 1987.
  10. Engelen M, Porszasz J, Riley M, Wasserman K, Maehara K, and Barstow TJ. Effects of hypoxic hypoxia on O2 uptake and heart rate kinetics during heavy exercise. J Appl Physiol 81: 2500-2508, 1996.[Abstract/Free Full Text]
  11. Gerbino A, Ward SA, and Whipp BJ. Effects of prior exercise on pulmonary gas-exchange kinetics during high-intensity exercise in humans. J Appl Physiol 80: 99-107, 1996.[Abstract/Free Full Text]
  12. Grassi B, Gladden LB, Samaja M, Stary CM, and Hogan MC. Faster adjustment of O2 delivery does not affect O2 onkinetics in isolated in situ canine muscle. J Appl Physiol 85: 1394-1403, 1998.[Abstract/Free Full Text]
  13. Grassi B, Gladden LB, Stary CM, Wagner PD, and Hogan MC. Peripheral O2 diffusion does not affect O2 on-kinetics in isolated in situ canine muscle. J Appl Physiol 85: 1404-1412, 1998.[Abstract/Free Full Text]
  14. Grassi B, Hogan MC, Kelley KM, Aschenbach WG, Hamann JJ, Evans RK, Patillo RE, and Gladden LB. Role of convective O2 delivery in determining O2 on-kinetics in canine muscle contracting at peak O2. J Appl Physiol 89: 1293-1301, 2000.[Abstract/Free Full Text]
  15. Harms CA, McClaran SR, Nickele GA, Pegelow DF, Nelson WB, and Dempsey JA. Effect of exercise-induced arterial O2 desaturation on O2 max in women. Med Sci Sports Exerc 32: 1101-1108, 2000.[Web of Science][Medline]
  16. Henson LC, Poole DC, and Whipp BJ. Fitness as a determinant of oxygen uptake response to constant-load exercise. Eur J Appl Physiol 59: 21-28, 1989.
  17. Hughson RL. Alterations in the oxygen deficit-oxygen debt relationships with {beta}-adrenergic receptor blockade in man. J Physiol 349: 375-387, 1984.[Abstract/Free Full Text]
  18. Hughson RL and Kowalchuk JM. Kinetics of oxygen uptake for submaximal exercise in hyperoxia, normoxia, and hypoxia. Can J Appl Physiol 20: 198-210, 1995.[Web of Science][Medline]
  19. Hughson RL, O'Leary DD, Betik AC, and Hebestreit H. Kinetics of oxygen uptake at the onset of exercise near or above peak oxygen uptake. J Appl Physiol 88: 1812-1819, 2000.[Abstract/Free Full Text]
  20. Hughson RL, Shoemaker JK, Tschakovsky ME, and Kowalchuk JM. Dependence of muscle O2 on blood flow dynamics at the onset of forearm exercise. J Appl Physiol 81: 1619-1626, 1996.[Abstract/Free Full Text]
  21. Hughson RL and Smyth GA. Slower adaptation of O2 to steady state of submaximal exercise with {beta}-blockade. Eur J Appl Physiol 52: 107-110, 1983.
  22. Jones AM, Carter H, Pringle JSM, and Campbell IT. Effect of creatine supplementation on oxygen uptake kinetics during submaximal cycle exercise. J Appl Physiol 92: 2571-2577, 2002.[Abstract/Free Full Text]
  23. Koga S, Shiojiri T, Shibasaki M, Kondo N, Fukuba Y, and Barstow TJ. Kinetics of oxygen uptake during supine and upright heavy exercise. J Appl Physiol 87: 253-260, 1999.[Abstract/Free Full Text]
  24. Krustrup P, Ferguson RA, Kjær M, and Bangsbo J. ATP and heat production in human skeletal muscle during dynamic exercise: higher efficiency of anaerobic than aerobic ATP resynthesis. J Physiol 549: 255-269, 2003.[Abstract/Free Full Text]
  25. Krustrup P, González-Alonso J, Quistorff B, and Bangsbo J. Muscle heat production and anaerobic energy turnover during repeated intense dynamic exercise in humans. J Physiol 536: 947-956, 2001.[Abstract/Free Full Text]
  26. Linnarsson D, Karlsson J, Fagraeus L, and Saltin B. Muscle metabolites and oxygen deficit with exercise in hypoxia and hyperoxia. J Appl Physiol 36: 399-402, 1974.[Free Full Text]
  27. MacDonald MJ, Naylor HL, Tschakovsky ME, and Hughson RL. Peripheral circulatory factors limit rate of increase in muscle O2 uptake at onset of heavy exercise. J Appl Physiol 90: 83-89, 2001.[Abstract/Free Full Text]
  28. MacDonald MJ, Pedersen PK, and Hughson RL. Acceleration of O2 kinetics in heavy submaximal exercise by hyperoxia and prior high-intensity exercise. J Appl Physiol 83: 1318-1325, 1997.[Abstract/Free Full Text]
  29. MacDonald MJ, Shoemaker JK, Tschakovsky ME, and Hughson RL. Alveolar oxygen uptake and femoral artery blood flow dynamics in upright and supine leg exercise in humans. J Appl Physiol 85: 1622-1628, 1998.[Abstract/Free Full Text]
  30. Mallory LA, Scheuermann BW, Hoelting BD, Weiss ML, McAllister RM, and Barstow TJ. Influence of peak O2 and muscle fiber type on the efficiency of moderate exercise. Med Sci Sports Exerc 34: 1279-1287, 2002.[Medline]
  31. McCreary CR, Chilibeck PD, Marsh GD, Paterson DH, Cunningham DA, and Thompson RT. Kinetics of pulmonary oxygen uptake and muscle phosphates during moderate-intensity calf exercise. J Appl Physiol 81: 1331-1338, 1996.[Abstract/Free Full Text]
  32. Medbo JI. Type I and type II fibres work with the same mechanical efficiency during bicycling. In: Muscle and Motility: Proceedings of XIXth European Conference in Brussels, edited by Maréchal G and Carraro U. Andover, Hampshire, UK: Intercept, 1990, p. 303-308.
  33. Murphy PC, Cuervo LA, and Hughson RL. A study of cardiorespiratory dynamics with step and ramp exercise tests in normoxia and hypoxia. Cardiovasc Res 23: 825-832, 1989.[Web of Science][Medline]
  34. Özyener F, Rossiter HB, Ward SA, and Whipp BJ. Influence of exercise intensity on the on- and off-transient kinetics of pulmonary oxygen uptake in humans. J Physiol 533: 891-902, 2001.[Abstract/Free Full Text]
  35. Paterson DH and Whipp BJ. Asymmetries of oxygen uptake transients at the onset and offset of heavy exercise in humans. J Physiol 443: 575-586, 1991.[Abstract/Free Full Text]
  36. Pringle JSM, Doust JH, Carter H, Tolfrey K, Campbell IT, and Jones AM. Oxygen uptake kinetics during moderate, heavy and severe intensity `submaximal' exercise in humans: the influence of muscle fibre type and capillarisation. Eur J Appl Physiol 89: 289-300, 2003.[Web of Science][Medline]
  37. Rossiter HB, Ward SA, Doyle VL, Howe FA, Griffiths JR, and Whipp BJ. Inferences from pulmonary O2 uptake with respect to intramuscular [phosphocreatine] kinetics during moderate exercise in humans. J Physiol 518: 921-932, 1999.[Abstract/Free Full Text]
  38. Roston WL, Whipp BJ, Davis JA, Cunningham DA, Effros RM, and Wasserman K. Oxygen uptake kinetics and lactate concentration during exercise in humans. Am Rev Respir Dis 135: 1080-1084, 1987.[Web of Science][Medline]
  39. Scheuermann BW, Hoelting BD, Noble ML, and Barstow TJ. The slow component of O2 uptake is not accompanied by changes in muscle EMG during repeated bouts of heavy exercise. J Physiol 531: 245-256, 2001.[Abstract/Free Full Text]
  40. Siere PA. Citrate synthase. Methods Enzymol 13: 3-11, 1969.
  41. Springer C, Barstow TJ, Wasserman K, and Cooper DM. Oxygen uptake and heart rate responses during hypoxic exercise in children and adults. Med Sci Sports Exerc 23: 71-79, 1991.[Web of Science][Medline]
  42. Tschakovsky ME and Hughson RL. Interaction of factors determining oxygen uptake at the onset of exercise. J Appl Physiol 86: 1101-1113, 1999.[Abstract/Free Full Text]
  43. Wasserman K, Whipp BJ, Koyal SN, and Beaver WL. Anaerobic threshold and respiratory gas exchange during exercise. J Appl Physiol 35: 236-243, 1973.[Free Full Text]
  44. Whipp BJ. The slow component of O2 uptake kinetics during heavy exercise. Med Sci Sports Exerc 26: 1319-1326, 1994.[Web of Science][Medline]
  45. Whipp BJ and Wasserman K. Oxygen uptake kinetics for various intensities of constant-load work. J Appl Physiol 33: 351-356, 1972.[Free Full Text]



This article has been cited by other articles:


Home page
 J. Appl. Physiol.Home page
S. Koga, D. C. Poole, L. F. Ferreira, B. J. Whipp, N. Kondo, T. Saitoh, E. Ohmae, and T. J. Barstow
Spatial heterogeneity of quadriceps muscle deoxygenation kinetics during cycle exercise
J Appl Physiol, December 1, 2007; 103(6): 2049 - 2056.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
S. Koga, D. C. Poole, T. Shiojiri, N. Kondo, Y. Fukuba, A. Miura, and T. J. Barstow
Comparison of oxygen uptake kinetics during knee extension and cycle exercise
Am J Physiol Regulatory Integrative Comp Physiol, January 1, 2005; 288(1): R212 - R220.
[Abstract] [Full Text] [PDF]

Home page
 J. Physiol.Home page
D. P Wilkerson, I. T Campbell, and A. M Jones
Influence of nitric oxide synthase inhibition on pulmonary O2 uptake kinetics during supra-maximal exercise in humans
J. Physiol., December 1, 2004; 561(2): 623 - 635.
[Abstract] [Full Text] [PDF]

Home page
 J. Appl. Physiol.Home page
D. P. Wilkerson, K. Koppo, T. J. Barstow, and A. M. Jones
Effect of prior multiple-sprint exercise on pulmonary O2 uptake kinetics following the onset of perimaximal exercise
J Appl Physiol, October 1, 2004; 97(4): 1227 - 1236.
[Abstract] [Full Text] [PDF]

Home page
 J. Appl. Physiol.Home page
T. A. Bauer, E. P. Brass, M. Nehler, T. J. Barstow, and W. R. Hiatt
Pulmonary VO2 dynamics during treadmill and arm exercise in peripheral arterial disease
J Appl Physiol, August 1, 2004; 97(2): 627 - 634.
[Abstract] [Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF) Free
Right arrow All Versions of this Article:
95/5/2014    most recent
00590.2002v1
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (23)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Scheuermann, B. W.
Right arrow Articles by Barstow, T. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Scheuermann, B. W.
Right arrow Articles by Barstow, T. J.

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online
Copyright © 2003 by the American Physiological Society.