High levels of physiological function are a prerequisite for high-level performance in 2000-m rowing ergometer time trials, with strong associations observed with peak oxygen uptake (V˙O2peak), r = 0.85-0.96; power associated with V˙O2peak (WV˙O2peak), r = 0.97; and V˙O2 at lactate threshold (LT), r = 0.93 (7,12,25). A large capability to resynthesize ATP via oxidative pathways is, thus, of key importance to rowing performance.
A faster V˙O2 kinetic response may be important for performance by reducing the initial oxygen deficit and, thus, the concomitant accumulation of fatiguing by-products. Thus, there is tighter metabolic control, such that the same V˙O2 is attained with less perturbation of the phosphorylation and redox potentials (14). A number of studies have observed improvement in the V˙O2 kinetic response with training in running and cycling. It has been noted that for subjects with higher existing cardiorespiratory fitness levels and for untrained subjects after a period of training, the V˙O2 response is/becomes faster (4,6,17,26). In contrast, the time constant of the primary component during moderate- and heavy-intensity exercise has been shown to remain unchanged after 6 wk of training despite improvements in V˙O2peak and LT (4). In the same study, the authors note a shortening of the primary-component time constant in a subgroup of less-fit subjects.
Training studies have observed an attenuation of the V˙O2 slow component (4), suggesting that the fitter individual is more metabolically efficient at a greater range of work intensities. It has been proposed that the relative V˙O2 slow component is negatively correlated to V˙O2max and/or the percentage of slow-twitch motor units of the working muscle (1). It also has been reported that well-trained endurance runners display no V˙O2 slow-component response (2). The assessment of V˙O2 slow-component magnitude, by the subtraction of V˙O2 at 3 min into exercise from V˙O2 at 6 min, may not fully elucidate the magnitude of the V˙O2 slow component. Nevertheless, these studies have developed the rationale that either a speeding of V˙O2 onset or a reduction in the V˙O2 slow component are associated with the tolerance of exercise work rates (13). The continuum of improved V˙O2 kinetic responses has been explored in untrained and trained subjects and with single observations in highly elite cycling and running athletes, demonstrating, in particular, a rapid time constant response of 8-10 s (14,17). It is not clear whether the shorter time constant responses are systematically observed for a cohort of highly elite athletes, further from the sport of rowing. Accordingly, this study sought to test the hypothesis that elite rowers would possess a faster, more economic oxygen uptake response than club standard counterparts, and to explore their relationship with performance.
After approval from the local ethics committee, 16 willing participants provided written informed consent and completed a health questionnaire. Subjects were sorted into two groups by standard of competitive rowing achievement. Elite-level rowers (ELITE, N = 8; mean ± SD: age 25.8 ± 2.3 yr; body mass 96.3 ± 5.2 kg; height 193.2 ± 2.9 cm) were winners of an Olympic title in the year of the study. Club-level subjects (CLUB, N = 8; mean ± SD: age 25.0 ± 1.5 yr; body mass 89.5 ± 5.4 kg; height 186.8 ± 5.0 cm) were characterized as having never represented their country at a senior level. Subjects were assessed 20 wk into the training off-season period. ELITE subjects performed approximately 190 km·wk−1, of which 90% was performed below LT (≤1.5mM). CLUB subjects performed approximately 140 km·wk−1, of which 40% was performed below LT.
Subjects reported to the laboratory in a rested, fully hydrated state, at least 2 h after eating, having avoided strenuous exercise in the 24 h before a test session. Laboratory conditions were held constant at 20°C and at a relative humidity of 40-45%. All rowing exercise tests were performed on an air-braked rowing ergometer (Concept II C, Nottingham, UK) with a drag factor of 138-140 (in accordance with the British International Rowing guidelines for ergometer testing). The first test was used to determine the LT and V˙O2peak (coefficients of variation for this laboratory: 3.5 and 2.2%, respectively). Subjects revisited the laboratory to perform repetitions of square-wave transitions from rest to exercise. All tests were completed within a 10-d period.
Measurement of LT and V˙O2peak.
After a 10-min self-paced warm-up period, subjects performed an incremental test with five to six stages, each 4 min in duration. Exercise intensity increased by 25 W and by two strokes per minute for each stage. Prescribed power was maintained accurately (SD: ± 1.4 W, N = 11; trials N = 55; range 150-330 W). The 4-min stages were separated by 30-s breaks for blood sampling. Subjects rested for 2.5 min after the final incremental stage before initiating a 4-min maximal effort. To aid evaporative cooling, an oscillating fan was placed 1 m behind the ergometer and was directed at the head and shoulders.
Earlobe capillary blood samples of 20-25 μL were collected at the end of each stage and were assayed for blood lactate concentration ([BLa−]) using a GM7 Analox analyzer (Analox, London, UK), which had been calibrated using an 8 and 2.6 mM pyruvate solution. Calibration procedures were completed before each test. LT (power at LT, W LT) was determined by two experienced, independent reviewers as the breakpoint in the profile of [BLa−] against V˙O2 at which a marked, sustained increase in [BLa−] of 1 mM was observed from baseline. Throughout the incremental test, pulmonary gas exchange was measured breath-by-breath as described below. Peak V˙O2 was determined as the highest value recorded for any 30-s period during the 4-min maximum test. Solving the regression equation describing V˙O2 and power for the five incremental workloads calculated the power associated with V˙O2peak (WV˙O2peak).
On subsequent test days, subjects performed a series of square-wave transitions from rest to exercise, of 6-min duration, at either a moderate-intensity (80% V˙O2 at LT) or a heavy-intensity (50% of the difference in V˙O2 between LT and V˙O2peak) power output. All exercise transitions were preceded by 2 min of seated rest. Two moderate-intensity exercise transitions were followed by 6 min of rest, before a single heavy transition (3). This routine of exercise transitions was then repeated on a second day, giving a total of four moderate and two heavy exercise transitions. At the start of exercise, subjects were instructed to immediately increase the power output to the desired level (achieved in < 3 s) and to hold that level of work throughout the 6 min. Stroke rate, 500-m split time, and power output were recorded stroke by stroke using a computer-linked data-logging PCi monitor (Nottingham, UK). Heart rate was recorded telemetrically (Polar Electro Oy, Finland) for each stage or transition. Maximum heart rate was defined as the highest recorded 5-s average. Capillary blood samples were drawn after each square-wave effort and were analyzed for [BLa−].
Pulmonary gas exchange.
Gas exchange and minute ventilations were continuously monitored breath-by-breath during all testing sessions. Subjects wore a nose clip and breathed through a low-dead space (90 mL), low-resistance (0.1 kPa·L−1·s−1 at 15 L·s−1) mouthpiece throughout each test. Air was sampled through a 2-m small-bore (0.5 mm) capillary line at a rate of 60mL·min−1 and was analyzed for O2 by a differential paramagnetic analyzer and for CO2 concentrations by a sidestream infrared analyzer (Oxycon Alpha, Viasys, UK), which were calibrated before each test with gases of known concentration. Expiratory volumes were determined using a precision-engineered turbine volume transducer (Viasys, UK) that was calibrated before each test using a 3-L syringe. A computer integrated the volume and concentration signals, accounting for the gas transit delay through the capillary. Respiratory gas exchange variables (V˙O2, V˙CO2, V˙E) were calculated and displayed for every breath.
Oxygen uptake kinetic data.
For each exercise transition, the breath-by-breath data were interpolated to give second-by-second values. Transitions for each exercise domain were then time aligned to the start of exercise and were averaged to enhance the underlying response characteristics and to assist in the reduction of breath-by-breath noise often observed during rowing exercise and caused by the adjustment of ventilatory volume to the phase of the rowing stroke. Pilot investigations showed that more than four transitions for moderate exercise and two for heavy exercise resulted in no further reduction in the residual sum of squares of the modeled response. Nonlinear regression techniques were used to fit the V˙O2 data after the onset of exercise with an exponential function. A reiterative process ensured that the sum of squared error was minimized. The mathematical model consisted of two (for moderate-intensity exercise) or three (heavy-intensity exercise) exponential terms, each representing a phase of the response (1). The first exponential term started with the onset of exercise (time = 0), whereas each other term began after independent time delays based on the asymptotic value of the previous component.
where V˙O2 (b) is the resting baseline value; Ac, A PC, and A SC are the asymptotic amplitudes for the exponential term; τ c, τPC, and τSC are the time constants; and TDPC and TDSC are the time delays. Amplitudes expressed per unit of work are expressed as gain in V˙O2 above baseline: gainC, gainPC, and gainSC. The cardiodynamic-component term was terminated at the start of the primary component (i.e., at TDPC) and assigned the value for that time (Ac′).
The V˙O2 at the end of phase 1 (Ac′) and the amplitude of the primary component (A PC′) were summed to calculate the amplitude of the primary component (A PC′). The V˙O2 slow component at the end of exercise (A SC′) was calculated and is used in preference to the asymptotic value.
Ergometer 2000-m time trial performance.
All 2000-m ergometer time trial tests were performed as a criterion assessment for the domestic sporting governing body on designated, well-serviced Concept II C ergometers with a drag factor of 138-140. All 2000-m tests were performed within 10 d of the first laboratory visit.
The two groups were compared using two-tailed independent t-tests. The probability level of P < 0.05 was accepted as statistically significant. Pearson's product-moment correlation was employed to examine the relationship between individual physiological variables and 2000-m rowing speed. Data are presented as mean ± SD.
ELITE rowers were heavier (P = 0.02) than CLUB rowers, but they were of the same age (P = 0.44). ELITE subjects performed the maximal 2000-m ergometer row in a shorter time than CLUB subjects (P < 0.001). Peak V˙O2, WV˙O2peak, and markers of the blood lactate response (W LT, W 4mM) were all significantly greater in ELITE compared with CLUB rowers (P < 0.001). Peak [BLa−] was 1.5 mM greater (P = 0.007) in CLUB than in ELITE rowers. Ratio and allometric scaling of V˙O2peak, WV˙O2peak, and W LT (19) reinforced the greater aerobic function in the ELITE group (P < 0.01) (Table 1).
V˙O2 kinetic response.
The V˙O2 response kinetics to moderate- and heavy-intensity rowing for CLUB and ELITE subjects are summarized in Table 1 and are illustrated in (Figures 1 and 2. The τPC was faster for the ELITE group compared with the CLUB group for moderate- (P = 0.04 -intensity (P = 0.03) exercise. There were no differences between the groups for TDPC or TDSC. The absolute amplitude of the primary component (A PC′) was greater (P < 0.001) for ELITE than for CLUB subjects, owing to greater power outputs performed during exercise transitions. Relative to work rate (gainPC′), the ELITE group consumed less oxygen per watt for moderate (P = 0.02) and heavy (P = 0.005) exercise. The absolute V˙O2 slow component was greater (A SC′, P = 0.009) for ELITE compared with CLUB subjects, but significance was lost when expressed per watt (gainSC′; P = 0.14). For moderate-intensity exercise, end-exercise V˙O2 per watt is identical to gainPC′; however, for heavy-intensity exercise, the ELITE group consumed less oxygen per watt (1.2 mL·min−1·W−1; P = 0.02) than the CLUB group.
A significant intergroup correlation was observed between speed and τPC (r = −0.59, P = 0.02, Fig. 3) and between V˙O2max and τPC (r = −0.68, P < 0.01) recorded during heavy-intensity exercise. A significant (r = −0.74, P = 0.04) negative correlation existed for the gainSC′ and performance for the CLUB group, but not significantly so for the ELITE group (r = 0.50, P = 0.2); the intergroup relationship did not fully support intragroup associations (r = 0.18 P = 0.53). All other intra- and intergroup associations indices of the V˙O2 kinetics showed no significant relation to performance.
This study compared the physiological characteristics, particularly the V˙O2 kinetics, of ELITE and CLUB rowers, revealing that the ELITE rowers possessed a faster time constant and smaller gain of the V˙O2 primary component. It was hypothesized that the V˙O2 slow component would be smaller in ELITE subjects; however, the results of this study do not support this tenet. A contrast between groups was achieved by recruiting Olympic gold medalists for the year of the study. Although the ELITE subjects were significantly larger when physiological variables were normalized for body mass, the differences between the groups remained (Table 2).
It was hypothesized that the ELITE subjects would have a faster time constant for the primary component (τPC) than the CLUB rowers. In the present study, this was demonstrated (P < 0.05) for moderate- and high-intensity exercise. Comparison with other studies examining the on-transient response in relation to the fitness standard of subjects is problematic because of the varying modeling techniques, particularly the calculation of mean response time encompassing the V˙O2 slow component (26). However, subjects with no rowing experience are reported to possess a slower τPC than both the trained groups in the current work (24). Others have found τPC to remain unchanged for moderately fit subjects after 6 wk of training, despite improvements in V˙O2peak and LT, but those authors note a speeding of the primary component in a subgroup of less-fit subjects (4). Koppo and colleagues (17) have noted a significantly shorter primary time constant in well-trained cyclists compared with untrained controls. Further, a quick time constant of 8-10 s has been noted for the female world-record marathon runner, which compares with the 5.6 s observed in the current study for a multiple-Olympic champion oarsman. Dupont et al. (9) have demonstrated a strong correlation between τPC and the percent decrement in sprint performance; however, the current study is the first to show a significant intergroup association (r = −0.59, P = 0.02) between τPC (during heavy-intensity exercise) and time trial performance. V˙O2max and the percentage of type I muscle fibers are also reported to be significantly correlated with τPC (1,23). In the current study, muscle fiber type was not quantified, but it has been reported to be as high as 88% type I fibers in elite rowers (18,20). V˙O2peak was significantly correlated to τPC (r = −0.68, P < 0.01) in the current work, offering potential support to previously suggested mechanistic explanations. These observations are limited by the risk that using groups with divergent performance standards might cause an abnormal distribution of data, as indicated by nonsignificant intragroup associations.
An economic profile was observed in the ELITE subjects, as indicated by end-exercise V˙O2 amplitude (above baseline) expressed per watt. The results of this study suggest that economy of movement may be an important physiological characteristic of performance, as highlighted by the comparison of distinct groups, compared with studies that have considered similarly trained groups (12). Whether economy could independently influence performance or by reducing the regression slope to WV˙O2peak is not clear from the current data. Only one study has examined V˙O2 kinetics in rowing; that study suggests that in rowing, a greater primary gain was observed compared with cycling (24). On the rowing ergometer, the elite athlete achieves a higher work rate primarily by producing a higher power per stroke, thereby possessing better gross efficiency. The improvement of gross efficiency has been associated with the number of years spent training or total training volume and, concomitantly, with the reduction in the proportional cost of unloaded ergometer rowing (11). The ELITE subjects are full-time rowers and, consequently, would have performed a greater total amount of training than the CLUB subjects (190 vs 140 km·wk−1, respectively), facilitating the development of gross mechanical efficiency in the ELITE subjects (23.4 ± 0.6 vs 21.6 ± 0.4%, P = 0.01). The previously reported, untrained novice rower will not have undergone such extensive technical and physiological training associated with improved economy (12). Further, the untrained group is unlikely to possess the presupposed high proportions of type I muscle fibers that have been shown in highly trained rowers (18) and that have been linked to reduced oxygen costs of exercise (8).
During moderate-intensity exercise, ELITE subjects consumed 1.3 mL·min−1·W−1 less O2 compared with CLUB subjects, but this margin was reduced during heavy-intensity exercise to 1.2 mL·min−1·W−1 because of the development of the V˙O2 slow component during heavy work rates. It was hypothesized that the ELITE subjects would have a smaller slow component than the CLUB subjects. All subjects demonstrated a slow component that, in absolute terms, was greater in the ELITE subjects because of the greater power outputs performed. Although significant difference is lost when the amplitude of the slow component is expressed per watt, it is clear that theELITE subjects did not have a smaller gainSC′ than the CLUB subjects, as hypothesized. This finding is consistent with the work of Koppo et al. (17), who also show no differences between untrained and trained groups. Studies indicate that the V˙O2 slow component can be reduced with training (4,5). Further, the size of the V˙O2 slow component has been shown to correlate well (r = −0.64 to −0.83) with the percentage of type I fibers (1,23) but not with performance. In contrast to the current study, some researchers (2) have suggested that highly trained endurance athletes have no V˙O2 slow component. This conclusion, however, may be misleading because of the use of the 6minute-3minute method of assessing the V˙O2 slow component. If a fitter subject has a faster on-transient response (6,22), and the V˙O2 slow component can emerge as early as 90 s in the current work, then such methods (2) may not be sensitive enough to detect the V˙O2 slow component precisely. Moreover, in relation to differing training backgrounds showing similar V˙O2 slow-component sizes, the time delay of the slow-component onset has been found to occur earlier in trained subjects (17). There was a trend for earlier TDSC in the ELITE subjects (90 vs 107 s) that did not reach significance (P = 0.08), whereas τSC was not different between groups.
The size of the V˙O2 slow component has been shown to correlate well (r = −0.64 to −0.83) with the percentage of type I fibers (1,23). Although muscle fiber-type proportions were not measured in the current work, previously recorded morphological characteristics of high-performing rowers, showing a high proportion of type I fibers, would not be consistent with the differences observed in slow-component magnitudes in the current work. In addition, blood lactate has been linked with slow-component size, although this link has not been found to be causative (21). A further intramuscular mechanism for the V˙O2 slow component is a reduction of P-O coupling efficiency with augmented temperature. Whereas ELITE subjects possess greater body dimensions and, thus, would store more heat than their smaller CLUB counterparts, it has been shown that elevated temperature is unlikely to be responsible for increased V˙O2 (16). That ELITE athletes do not, as hypothesized, have a smaller gainSC than CLUB subjects may be related to the training performed before the study. The CLUB subjects had a background of higher-intensity training (~60% > LT [BLa−]) compared with the ELITE subjects (90% sub LT/< 1.5 mM [BLa−]). Greater training intensities in CLUB subjects may result in type II units being more frequently involved; thus, the stimulus for these units to adopt oxidative qualities specific to the intensity of work would be greater.
A greater V˙O2 slow component is said to indicate a greater inefficiency (10,13,15). On the other hand, it has been speculated that the V˙O2 slow component may represent, in part, the cost of recovery and other metabolic processes incurred in the initially recruited motor units that have become fatigued (13). To suggest that the ELITE subjects had more fatigable musculature than the CLUB subjects would seem misplaced. Moreover, irrespective of isolated phase 3 V˙O2 response, the ELITE subjects demonstrated a more economic total response; this should not be overlooked. A superior economy of movement has a higher global relevance and is more consistently associated with performance speed, because any given work rate would be performed at a lower percentage of V˙O2peak.
In conclusion, this study shows that the ELITE subjects possessed a faster τPC than the CLUB subjects, indicating a significant relationship with performance speed. Economy, defined as the gain of the primary component, was more favorable in the ELITE subjects during moderate- and heavy-intensity exercise. The ELITE subjects demonstrated a V˙O2 slow component that was no different than that of the CLUB subjects. This study has examined, for the first time, the V˙O2 kinetic responses of elite and club-level rowers.
The authors wish to thank the support of the British Olympic Medical Trust.
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Keywords:©2007The American College of Sports Medicine
TIME CONSTANT; SLOW COMPONENT; ECONOMY; ELITE ATHLETES