Effect of muscle mass on V˙o 2kinetics at the onset of work

J Appl Physiol 90: 461–468, 2001. Effect of muscle mass on V̇O2 kinetics at the onset of work SHUNSAKU KOGA,1 THOMAS J. BARSTOW,2 TOMOYUKI SHIOJIRI,3 TETSUO TAKAISHI,4 YOSHIYUKI FUKUBA,5 NARIHIKO KONDO,6 MANABU SHIBASAKI,6 AND DAVID C. POOLE2 1 Applied Physiology Laboratory, Kobe Design University, Kobe 651-2196; 3Yokohama City University, Yokohama 236-0027; 4Nagoya City University, Nagoya 467-8501; 5Hiroshima Women’s University, Hiroshima 734-8558; 6Kobe University, Kobe 657-0011, Japan; and 2Department of Kinesiology, Kansas State University, Manhattan, Kansas 66506-0302 Received 6 January 2000; accepted in final form 5 September 2000 pulmonary and muscle O2 uptakes (V̇O2) increase with a finite kinetic profile. There remains considerable debate as to whether the speed of these kinetics reflects sluggishness of O2 delivery to the muscle or, alternatively, some intramuscular limitation such as microvascular O2 delivery-to-O2 requirement mismatch or oxidative enzyme inertia (2, 8, 18, 26, 31, 38, 39). Experimental paradigms that are expected to impair muscle O2 de- livery, such as reduced arterial O2 content (CaO2), invariably slow pulmonary V̇O2 kinetics for both moderate and heavy work rates (WRs) [below ventilatory threshold (,VT) and above VT (.VT), respectively] (9, 12, 19, 24, 26, 38). In contrast, attempts to speed V̇O2 kinetics by augmenting CaO2 and/or O2 delivery in healthy subjects performing upright cycle ergometry have been successful only for the .VT domain (15, 27). In normal healthy subjects, if the speed of the pulmonary V̇O2 kinetics were indeed limited by the rapidity of the cardiovascular response and this response remained independent of muscle mass recruited, it would be expected that exercise with a smaller muscle mass [i.e., one-leg (1L) exercise vs. two-leg (2L) exercise] would result in faster V̇O2 kinetics. Thus, if this were the case, it may be hypothesized that decreasing the muscle mass recruited would shift the site of limitation of V̇O2 kinetics more toward the exercising muscle(s). Current thinking would suggest that the expected faster V̇O2 kinetics with a smaller muscle mass is more likely to be true for .VT than for ,VT exercise. This investigation tested the hypothesis that the V̇O2 kinetics would be speeded by reducing the muscle mass recruited for .VT exercise but not for ,VT exercise. The 1L vs. 2L cycling exercise paradigm utilized for this study permits evaluation of the effect of recruited muscle mass on V̇O2 kinetics in the absence of differences in fiber type and muscle recruitment profiles. In previous studies that used a conventional cycle ergometer for 1L exercise (11, 21, 35), the contracting muscles were required to sustain muscular tension throughout the entire cycle of the single limb movement, thereby creating different muscle recruitment strategies and likely altered physiological conditions within the muscle compared with that for 2L exercise. We developed a motorized 1L cycle ergometer that minimized the muscular contractions during the kneehip flexion (pedal-up) phase, which allowed the subjects to match more closely the muscle contraction pattern for 2L exercise. As confirmation, the present Address for reprint requests and other correspondence: S. Koga, Applied Physiology Laboratory, Kobe Design Univ., 8-1-1 Gakuennishi-machi, Nishi-ku, Kobe 651-2196, Japan (E-mail: s-koga @kobe-du.ac.jp). 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. Koga, Shunsaku, Thomas J. Barstow, Tomoyuki Shiojiri, Tetsuo Takaishi, Yoshiyuki Fukuba, Narihiko Kondo, Manabu Shibasaki, and David C. Poole. Effect of muscle mass on V̇O2 kinetics at the onset of work. J Appl Physiol 90: 461–468, 2001.—The dependence of O2 uptake (V̇O2) kinetics on the muscle mass recruited under conditions when fiber and muscle recruitment patterns are similar following the onset of exercise has not been determined. We developed a motorized cycle ergometer that facilitated oneleg (1L) cycling in which the electromyographic (EMG) profile of the active muscles was not discernibly altered from that during two-leg (2L) cycling. Six subjects performed 1L and 2L exercise transitions from unloaded cycling to moderate [,ventilatory threshold (VT)] and heavy (.VT) exercise. The 1L condition yielded kinetics that was unchanged from the 2L condition [the phase 2 time constants (t1, in s) for ,VT were as follows: 1L 5 16.868.4 (SD), 2L 5 18.4 6 8.1, P . 0.05; for .VT: 1L 5 26.8 6 12.0; 2L 5 27.8 6 16.1, P . 0.05]. The overall V̇O2 kinetics (mean response time) was not significantly different for the two exercise conditions. However, the gain of the fast component (the amplitude/work rate) during the 1L exercise was significantly higher than that for the 2L exercise for both moderate and heavy work rates. The slow-component responses evident for heavy exercise were temporally and quantitatively unaffected by the 1L condition. These data demonstrate that, when leg muscle recruitment patterns are unchanged as assessed by EMG analysis, on-transient V̇O2 kinetics for both moderate and heavy exercise are not dependent on the muscle mass recruited. exercise energetics; one-leg exercise; pulmonary gas exchange; muscle recruitment; control of muscle oxygen uptake AT THE ONSET OF MUSCULAR EXERCISE, http://www.jap.org 8750-7587/01 $5.00 Copyright © 2001 the American Physiological Society Downloaded from journals.physiology.org/journal/jappl (054.081.105.228) on December 7, 2022. 461 ˙ O KINETICS AND MUSCLE MASS V 2 462 study found that the electromyographic (EMG) profile for motorized 1L cycle ergometry differed markedly from that with conventional 1L ergometry but not from conventional 2L ergometry. Subsequently, the kinetic response of V̇O2 at the onset of moderate (,VT) and heavy (.VT) exercise was compared for motorized 1L and conventional 2L ergometry. METHODS tion (SD) of breath-by-breath fluctuation to the amplitude of the V̇O2 response (25). In the present study, the signalto-noise ratio was within 5%, which resulted in a SD of 62 s of the time constant. Each subject was given 15 min of rest before starting the next exercise transition. For the heavy WR tests, subjects normally performed three to five exercise transitions under the 1L condition and two to three exercise transitions under the 2L condition. Only one heavy exercise transition was performed on any single day. Measurements Subjects Six male subjects participated in the study. After a detailed explanation of the study, informed consent was obtained. The study was approved by the Human Subjects Committee of Kobe Design University. Description of the Cycle Ergometry For the 1L experiments, an electric motor was connected to the left side of the crankshaft of the cycle ergometer. A reduction gear assembly was utilized to match motor speed (1,800 rpm) to that of the subject (60 rpm). A special cam was designed for the motor shaft, which activated a switch to turn on the motor when the right pedal was at bottom dead center and turn it off when the pedal reached top dead center. During the exercise, the subject performed the down stroke on the right pedal with his right leg; at bottom dead center, the motor would be switched on by the cam and return the pedal to the top of the stroke. Throughout the entire exercise bout, the left leg rested on a footrest next to the ergometer. The positions of the ergometer handlebar and the saddle were standardized between the two exercise modes to minimize any difference in O2 cost for body stabilization. Protocol Subjects breathed through a low-resistance valve (HansRudolph, dead space 5 90 ml) connected to two pneumotachographs for measurement of inspiratory and expiratory flows, as previously described (22–24). Each system was calibrated repeatedly by inputting known volumes of room air at various mean flows and flow profiles. Respired gases were analyzed by mass spectrometry (model MGA-1100, Perkin Elmer) from a sample drawn continuously from the mouthpiece. Precision-analyzed gas mixtures were used for calibration. Alveolar gas-exchange variables were calculated breath by breath according to the algorithms of Beaver et al. (6). Heart rate (HR) was monitored continuously via a threelead electrocardiogram. In separate experiments in four of the original subjects, the EMG during constant WR exercise was recorded from bipolar surface electrodes from the rectus femoris, vastus lateralis, biceps femoris, tibialis anterior, and gastrocnemius muscles of the right leg of the subjects. EMG signals were amplified and digitized at a sampling rate of 1 kHz. The raw EMG activity patterns were rectified and triggered at the top dead center of each pedal cycle and averaged over 1-s intervals. In addition, the integrated EMG (iEMG) was calculated over 1-s periods. Analysis Incremental exercise tests. Ramp exercise protocols, preceded by 2-min unloaded cycling on a cycle ergometer, were utilized to estimate VT and peak V̇O2 for each exercise mode for each individual. The ramp exercise protocols were designed to produce fatigue within 10–15 min, with WR increases of 25 W/min for 2L and 6 W/min for 1L cycling exercise; pedal frequency was held constant at 60 rpm. Responses to 1L and 2L conditions were tested on separate days. The V̇O2 at the VT was estimated as the break point in the plot of CO2 output against V̇O2 (V-slope method). Constant WR exercise tests. Exercise transition tests were conducted under each exercise condition (1L vs. 2L exercise) on separate days. Each constant WR exercise test was performed for 6 min. The moderate WR used for both exercise conditions corresponded to a V̇O2 of ;90% of the VT estimated for each exercise condition, whereas the heavy exercise WR was estimated to require a V̇O2 equal to ;50% of the difference (D) between the subject’s VT and peak V̇O2, i.e., a value of VT 1 0.50D, based on the initial V̇O2-WR observed during the ramp exercise in each exercise condition. The exercise was preceded by 3 min of unloaded cycling at a pedal frequency of 60 rpm. To minimize random noise and to enhance the underlying response patterns for the moderate WR tests, subjects performed a total of four to seven repetitions of the exercise transition under each exercise condition. A greater number of transitions were performed in the 1L exercise than during the 2L exercise tests to improve the signal-to-noise ratio, in light of the smaller amplitude V̇O2 response with the small muscle mass exercise. The number of repetitions was determined according to the ratio of standard devia- Individual responses during the baseline-to-exercise transitions were time interpolated to 1-s intervals and averaged across each transition for each subject and condition. To further reduce the breath-to-breath noise so as to enhance the underlying characteristics, each average response was smoothed with a five-point moving-average filter. For the on transients, the response curve of V̇O2 was fit by a threeterm exponential function that included amplitudes, time constants, and time delays, using nonlinear least-squares regression techniques (4, 5, 12, 13, 20, 24). The computation of best-fit parameters was chosen by a computer program (KaleidaGraph, version 3) so as to minimize the sum of the squared differences between the fitted function and the observed response. The first exponential term started with the onset of exercise, and the second and third terms began after independent time delays V̇O2~t! 5 V̇O2(b) 1A0z (12e2t/t0) phase 1 (initial component) 1A1 z @1 2 e 2 ~t 2 TD1!/t1# phase 2 (fast, primary component) 1 A2 z @1 2 e 2 ~t 2 TD2!/t2# phase 3 (slow component) where V̇O2(b) is the unloaded cycling baseline value; A0, A1, and A2 are the asymptotic values for the exponential terms; t0, t1, and t2 are the time constants; and TD1, and TD2 are the time delays. The phase 1 V̇O2 at the start of phase 2 (i.e., at TD1) was assigned the value for that time (A90) A90 5 A 0 z ~1 2 e 2 TD1/t 0! The physiologically relevant amplitude of the fast primary exponential component during phase 2 (A91) was defined as Downloaded from journals.physiology.org/journal/jappl (054.081.105.228) on December 7, 2022. ˙ O KINETICS AND MUSCLE MASS V 2 the sum of A90 1 A1. Because of concerns regarding the validity of using the extrapolated asymptotic value for the slow component (A2) for comparisons, we used the value of the slow exponential function at the end of exercise, defined as A92. Because the V̇O2 response during moderate-intensity exercise (,VT) reaches a new steady state within 3 min after the onset of exercise in normal subjects, the slow exponential term invariably dropped out during the iterative-fitting procedure. In addition, to facilitate comparison across the subjects and different absolute WRs, the gain of the fast primary response (G1 5 A91/WR) and relative contribution of slow component to the overall increase in V̇O2 at end-exercise [A92/(A911 A92)] were calculated. Furthermore, the increment in V̇O2 between the 3rd and 6th min of the transition (DV̇O2 6–3) was calculated as an index of the slow component of the V̇O2 kinetics. The overall kinetics of the V̇O2 and HR responses were determined from mean response time (MRT). They were calculated by fitting the response data to a monoexponential function that included a single amplitude, time constant, and time delay, starting from the onset of the transition. From this, a summary statistic for the kinetics (MRT 5 time constant 1 time delay) was calculated. Statistics Data are presented as means 6 SD. The data were analyzed using repeated-measures analysis of variance design. Significant results were further analyzed by Scheffé’s post hoc test. Significance was set at P , 0.05. The slope of the 463 V̇O2-WR relationship during ramp exercise was determined by least-squares regression. RESULTS EMG Profile Typical EMG activity patterns at a WR of 100 W are shown in a representative subject in Fig. 1. With increasing WR, the iEMG increased for 1L and 2L cycle exercise, as expected (Fig. 2). However, there was a greater activation of the rectus femoris and tibialis anterior during conventional 1L exercise compared with that in 2L exercise. In contrast, the iEMG profile of the active muscles during motorized 1L exercise was not discernibly altered from that during 2L exercise. This is particularly evident within some of the major muscles (rectus femoris, vastus lateralis, biceps femoris, tibialis anterior) for the WR up to 100 W (Fig. 2). This indicates that we were successful in minimizing muscular contractions during the knee flexion (pedalup) phase for the motorized 1L exercise and matching closely the muscle contraction pattern for 2L exercise. Incremental Exercise The response of V̇O2 as a function of WR during the ramp exercise tests is shown in Fig. 3 for a represen- Fig. 1. Electromyogram (EMG) activity patterns of the right leg at a work rate of 100 W in a representative subject. The rectified EMG was triggered at the top dead center of each pedal cycle and averaged over 1-s intervals. Note the greater muscle activation of rectus femoris and tibialis anterior during conventional one-leg (1L) cycle exercise (C-1L) compared with that in two-leg (2L) exercise. In contrast, the EMG profile of the active muscles during motorized 1L cycle exercise (M-1L) was not discernibly altered from that during 2L exercise. Downloaded from journals.physiology.org/journal/jappl (054.081.105.228) on December 7, 2022. 464 ˙ O KINETICS AND MUSCLE MASS V 2 V̇O2-WR below the inflection point for 1L was significantly higher than for 2L exercise (1L 5 21.2 6 2.8 ml z min21 z W21; 2L 5 10.1 6 1.3 ml z min21 z W21). Beyond the inflection point, V̇O2 gain (ml z min21 z W21) was increased significantly from 21.2 to 33.1 for 1L, whereas the slope remained constant for 2L exercise. Constant WR Exercise The response for V̇O2 from baseline to exercise is shown in a representative subject for the two conditions in Fig. 4. To facilitate comparison of relative increase in V̇O2 between the two exercise conditions, V̇O2 responses were normalized to the difference between baseline V̇O2 and end-exercise V̇O2. The V̇O2 kinetics were the same for the two exercise conditions and elicited similar time constants (as t1) and MRT but higher gains (G1) for the fast component of V̇O2 for 1L compared with 2L exercise (Tables 2 and 3). The absolute amplitude of the slow component per single leg (A92 /leg, i.e., A92 for 1L and A92 /2 for 2L) was not different for the 1L vs. 2L exercise. The DV̇O2 6–3 tended to be smaller for the 1L than for the 2L exercise (P 5 0.06). However, the DV̇O2 6–3 per single leg was not different for the two exercise modes. HR Responses Fig. 2. Group mean values of the integrated EMG (iEMG) as a function of work rate. The conventional 1L exercise (E) substantially increased the iEMG compared with 2L exercise (■). In contrast, the iEMG profile of the active muscles during motorized 1L cycle exercise (F) was not discernibly altered from that during 2L exercise. This is particularly evident within the major muscles for work rates up to 100 W. tative subject, and mean summary responses are presented in Table 1. The inflection point in the plot of V̇O2 against WR seen for 1L but not for 2L exercise was determined by computer analysis. The slope of the The response for HR from baseline to exercise for each of the exercise conditions is shown in Table 4. The end-exercise values of HR were significantly lower for 1L than for 2L during moderate and heavy exercise. There was no significant difference in MRT of HR kinetics between the 1L and 2L exercise during moderate exercise. However, the MRT of HR was faster for 1L than for 2L during heavy exercise. DISCUSSION We had hypothesized that V̇O2 kinetics would be faster during the 1L exercise if the speed of the V̇O2 kinetics were limited by the rapidity of the cardiovascular response during the 2L exercise. However, V̇O2 kinetics after the onset of exercise were not speeded by recruitment of a smaller muscle mass for either moderate or heavy WR. Furthermore, the relative contribution of the slow component of V̇O2 to the overall V̇O2 increment was also not significantly different for the Table 1. Incremental exercise responses to 1L and 2L exercise Peak work rate, W Peak V̇O2, l/min Peak HR, beats/min V̇O2 at VT, l/min Slope 1, ml z min21 z W21 Slope 2, ml z min21 z W21 Fig. 3. The responses of O2 uptake (V̇O2) as a function of work rate during the ramp exercise tests under conditions of motorized 1L (E) vs. 2L exercise (F) in a representative subject. As work rate approached the maximum, V̇O2 slope was significantly higher for 1L exercise both below and above the inflection point. 1L 2L 95 6 13 2.34 6 0.46 155.0 6 14.9 1.10 6 0.26 21.2 6 2.8 33.1 6 9.6 292 6 31* 3.34 6 0.55* 183.5 6 2.3* 1.75 6 0.49* 10.1 6 1.3* 9.7 6 2.1* Values are means 6 SD; n 5 6 subjects. 1L, one-leg cycle exercise; 2L, two-leg cycle exercise; V̇O2, O2 uptake; HR, heart rate; VT, ventilatory threshold; slope 1, slope of V̇O2 vs. lower work rate; slope 2, slope of V̇O2 vs. higher work rate. * Significantly different from 1L, P , 0.05. Downloaded from journals.physiology.org/journal/jappl (054.081.105.228) on December 7, 2022. ˙ O KINETICS AND MUSCLE MASS V 2 465 Table 3. V̇O2 response parameters for heavy exercise Work rate, W Baseline, l/min A90, l/min A91, l/min t1, s TD1, s A92, l/min TD2, s G1, ml/min/W A92/(A91 1 A92) A92/leg, l/min MRT, s D V̇O2 6-3, l/min D V̇O2 6-3/leg, l/min 1L 2L 62 6 18 0.41 6 0.04 0.36 6 0.24 1.27 6 0.37 26.8 6 12.0 22.5 6 6.7 0.11 6 0.11 146.6 6 37.7 20.9 6 3.6 0.09 6 0.06 0.11 6 0.11 48.1 6 17.6 0.09 6 0.05 0.09 6 0.05 190 6 30* 0.56 6 0.05* 0.53 6 0.19 1.93 6 0.33* 27.8 6 16.1 22.3 6 8.3 0.25 6 0.06* 124.1 6 62.3 10.1 6 0.7* 0.12 6 0.02 0.13 6 0.03 49.7 6 12.2 0.14 6 0.06 (P 5 0.06) 0.07 6 0.03 Values are means 6 SD; n 5 6 subjects. A92/(A91 1 A92), relative contribution of slow component to net increase in V̇O2 at end exercise; A92/leg, absolute amplitude of the slow component per leg (i.e., A92 for 1L and A92/2 for 2L); D V̇O2 6-3, the increment in V̇O2 between 3rd and 6th min of exercise. * Significantly different from 1L, P , 0.05. Fig. 4. The relative increase in V̇O2 responses for the transition from unloaded cycling to moderate exercise (A) and heavy exercise (B) in a representative subject under conditions of motorized 1L (solid lines) and 2L exercise (dashed lines). During both moderate and heavy exercise, V̇O2 kinetics (i.e., time delays and time constants of the fast component of V̇O2) were not significantly different for the 2 exercise conditions. Furthermore, the characteristics of the slow component during heavy exercise were not significantly different for the 2 exercise modes. two modes of exercise. These results represent the first quantitative comparison of V̇O2 kinetics between 1L and 2L cycle exercise. In addition, the present study furthers our understanding of V̇O2 kinetics during 2L cycle exercise, which has been utilized as a standard exercise mode for recruitment of a large muscle mass. In particular, for the upright 2L cycle exercise condition in healthy humans, the present finding supports Table 2. V̇O2 response parameters for moderate exercise Work rate, W Baseline, l/min A90, l/min A91, l/min t1, s TD1, s G1, ml z min21 z W21 MRT, s 1L 2L 36 6 5 0.39 6 0.04 0.23 6 0.07 0.71 6 0.20 16.8 6 8.4 30.7 6 10.7 19.8 6 4.5 37.6 6 10.1 93 6 16* 0.55 6 0.06* 0.25 6 0.15 0.94 6 0.18* 18.4 6 8.1 26.4 6 6.5 10.1 6 0.5* 38.8 6 10.6 Values are means 6 SD; n 5 6 subjects. A90 and A91, amplitudes of response; t1, time constant; TD1, time delay; G1, gain of the fast component response ( A91/work rate); MRT, mean response time. * Significantly different from 1L, P , 0.05. the notion that those factors that determine the primary component of pulmonary and muscle V̇O2 kinetics for both ,VT and .VT WRs are limited by the rapidity of factors intrinsic to the skeletal muscles, such as microvascular O2 delivery-to-O2 requirement mismatch or oxidative enzyme inertia, rather than the cardiovascular response. Incremental Exercise Peak V̇O2 of 1L exercise averaged 70% of 2L exercise. Previous studies reported that the peak V̇O2 ratio between conventional (i.e., nonmotorized) 1L and 2L exercise ranged between 70 and 85% (11, 16, 21). The slopes of the V̇O2-WR relationship for 2L exercise agree closely with literature values (30, 31). However, the slope of the V̇O2-WR below the inflection point for 1L exercise was significantly higher than for 2L exercise. Specifically, the slopes were 21.2 and 10.1 ml z min21 z W21 for 1L and 2L exercise, respectively. Our results are similar to those found for 1L knee extension exercise (i.e., 15–17 ml z min21 z W21) (1, 31, 33). Moreover, as WR approached the maximum, V̇O2 per watt began to rise even further for 1L exercise. This profile was markedly different from the linear increase in V̇O2 seen for 2L exercise. The greater V̇O2 Table 4. HR exercise responses 1L Moderate work (,VT) Baseline, beats/min 76.7 6 8.2 End-exercise HR, beats/min 99.9 6 10.1 MRT, s 25.0 6 9.5 Heavy work (.VT) Baseline, beats/min 73.6 6 11.9 End-exercise HR, beats/min 120.3 6 21.4 MRT, s 44.8 6 20.6 2L 80.6 6 12.4 110.5 6 10.8* 29.9 6 10.7 84.4 6 12.9 156.0 6 11.9* 60.2 6 17.0* Values are means 6 SD; n 5 6 subjects. HR, heart rate. * Significantly different from 1L, P , 0.05. Downloaded from journals.physiology.org/journal/jappl (054.081.105.228) on December 7, 2022. ˙ O KINETICS AND MUSCLE MASS V 2 466 per watt seen for 1L exercise above the inflection point might reflect an increased O2 cost of metabolic processes of exercising leg muscles (see greater iEMG for 1L exercise than for 2L at WR 5 150 W in Fig. 2) and muscles for postural support (including contralateral leg muscle V̇O2 for body stabilization work) during exercise with a small muscle mass (1, 30, 31, 33). It is unclear why the 1L exercise did not achieve a maximum WR per leg (i.e., 95 and 146 W per leg for 1L and 2L exercise, respectively) similar to that for the 2L exercise, despite a muscle contraction pattern that closely matched that for 2L exercise. Before the start of the study, during calibration of the 1L ergometer, we had confirmed the ability of the electrical motor to substitute for the contralateral leg motion (the left leg) to rotate the crank axis and the fly wheel against WRs up to 350 W. The lower maximal performance with the 1L exercise may have been the consequence of postural instability (particularly of the hips and thorax) at very high WRs compared with the 2L exercise because the subjects were required to minimize body sway without moving the contralateral leg. Constant WR Exercise V̇O2 fast component. As explained above, we had hypothesized that V̇O2 kinetics would be faster during the 1L exercise if the V̇O2 kinetics were cardiovascular O2 delivery dependent in the control condition (i.e., the 2L exercise) and the cardiovascular responses to exercise were unchanged. However, V̇O2 kinetics after the onset of exercise were not speeded by recruitment of a smaller muscle mass for either moderate or heavy WR. The kinetics of V̇O2 can be slowed by decreasing CaO2 and/or arterial O2 delivery (9, 12, 19, 24, 26, 38). However, to date, there is no compelling evidence that increased muscle O2 delivery can speed the kinetics of V̇O2 during moderate exercise in healthy humans. Recently, Grassi et al. (17) demonstrated that faster adjustment of O2 delivery did not affect V̇O2 kinetics during submaximal contractions in isolated canine muscle, suggesting that the kinetics were determined principally by some intramuscular process(es) under these conditions. In humans, MacDonald et al. (27) demonstrated acceleration of V̇O2 kinetics (faster MRT) in heavy exercise by hyperoxia and a prior bout of heavy exercise. However, this could be attributed to a reduction of the slow component without a speeding of the phase 2 time constant. The reduction of the slow component without speeding of the phase 2 time constant during heavy exercise that follows prior heavy exercise has been confirmed in recent studies (13, 36). The present finding of an unaltered phase 2 time constant in the face of greatly different recruited muscle mass suggests that those factors that determine the primary component of pulmonary and muscle V̇O2 kinetics, at least for the upright cycle exercise condition in healthy humans, were not affected by muscle mass. For non-cycling-type exercise, pulmonary V̇O2 kinetics during moderate leg exercise with a small muscle mass yields response features that are quantitatively similar to those evidenced by large muscle mass exercise (3, 10, 28). For example, Barstow et al. (3) and Chilibeck et al. (10) reported no significant difference of phase 2 time constants of pulmonary V̇O2 during moderate exercise with different muscle mass (upright 2L cycling vs. ankle plantar flexion in young adult subjects). Furthermore, Rossiter et al. (34) showed close agreement of the time constants for phase 2 V̇O2 and for phosphocreatine determined simultaneously during prone knee extension exercise. Collectively, these findings imply that phase 2 V̇O2 during moderate exercise reflects muscle oxidative phosphorylation kinetics in the face of adequate O2 delivery to the muscle (2), despite differences in muscle mass. However, caution should be exercised when interpreting these data, since V̇O2 kinetics have been shown to vary with the type of exercise or muscle group and body position, e.g., arm cranking vs. leg cycling (7, 9, 22), knee extension vs. cycling (37), and supine vs. upright cycling (9, 19, 24). We found the gain of the fast V̇O2 component during the 1L exercise (;20 ml z min21 z W21) to be higher than that observed for the 2L exercise (;10 ml z min21 z W21) for both moderate and heavy WRs. These results are in contrast to the findings of Gleser (16), who found similar V̇O2 per watt for 1L cycling as for 2L, when the former was performed by two subjects, each cycling with one leg. However, our results are compatible with the O2 cost reported for 1L knee extension exercise (15–17 ml z min21 z W21) (1, 31, 33). The reasons for these discrepancies in findings for 1L exercise are currently unclear and require further investigation. Recognizing that, to a certain extent, the slope of the V̇O2-WR relationship can be a function of the rate of WR increase (39), the V̇O2-WR slope was determined for ramp increases of 6 and 12 W/min for 1L exercise. We found that the V̇O2-WR slope was not different between the two protocols (Koga S, Barstow TJ, Shiojiri T, Takaishi T, Fukuba Y, Kondo N, Shibasaki M, and Poole DC, unpublished observations). It is entirely feasible that proportionally higher O2 costs of metabolic “support” processes outside the exercising muscles contribute to the greater V̇O2 per watt gain for 1L exercise, particularly at very high WRs beyond the inflection point in the V̇O2-WR relationship (Fig. 3) (1, 30, 31, 33). However, it is also possible that the specific neuromuscular recruitment patterns necessary to yield a cycling efficiency commensurate with a V̇O2 of ;10 ml z min21 z W21 are peculiar to 2L cycling exercise. If this is the case, EMG analysis as used herein may not be sufficiently sensitive to detect such differences. V̇O2 slow component. It has been proposed that the slower V̇O2 kinetics and the presence of a slow component during 2L heavy exercise are likely to be associated with an inadequate O2 delivery to the working muscles (15, 20, 24, 26, 27, 39). Consistent with this, previous studies demonstrated the reduction of the slow component of V̇O2, under conditions in which muscle O2 delivery may have been increased (and mean capillary O2 pressure certainly was increased) (13, 15, 23, 27, 36). Therefore, if 1L exercise created a Downloaded from journals.physiology.org/journal/jappl (054.081.105.228) on December 7, 2022. ˙ O KINETICS AND MUSCLE MASS V 2 condition in which perfusion and O2 delivery to the working muscles at the onset of heavy exercise with a small muscle mass were facilitated compared with that for large muscle mass exercise, this should have resulted in a smaller slow component of V̇O2 during 1L heavy exercise. Because the primary origin of the V̇O2 slow component appears to be the working muscles (2, 4, 14, 29, 32) and thus the size of the slow component depends on the size of the exercising musculature, we normalized the amplitude of the slow component to recruited muscle mass performing the exercise (i.e., A92 and DV̇O2 6–3 for 1L; A92/2 and DV̇O2 6–3/2 for 2L). No difference was observed between the 1L and the 2L exercise in this respect. One putative explanation for the unaltered relative magnitude of the slow component of V̇O2 for the 1L compared with 2L exercise might be that any improved perfusion-related decrease in the slow component may have been offset by an augmented V̇O2, due to factors such as the O2 cost for energetic processes within the exercising muscles and for body stabilization (11, 16, 35), such that the net result was no measurable change in the slow component. Alternatively, the mechanisms responsible for the slow component may not have been sensitive to any improvement in flow-dependent O2 delivery during the 1L exercise, in contrast to previous manipulations that had resulted in reduction of the slow component, i.e., prior heavy exercise, increased muscle temperature, and hyperoxia (13, 15, 23, 27, 36). Similar to a previous study conducted for the 2L cycle exercise (32), direct measurement of the leg muscle V̇O2 is required to isolate unequivocally leg muscle responses from those occurring within the rest of the body. In conclusion, when iEMG profiles are unaltered, sentinel features of the V̇O2 kinetics response to moderate (TD1, t1) and heavy (TD1, t1, TD2, t2) exercise are independent of the size of the muscle mass recruited. The lower maximal performance with the 1L exercise may have been the unavoidable consequence of postural instability at very high WRs compared with the 2L exercise. 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