Physiology and Biochemistry
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Influence of Light Additional Arm Cranking Exercise ˙ O2 in Severe Cycling Exercise on the Kinetics of V V. L. Billat1, 2, L. Hamard 2, V. Bocquet3, S. Demarie1, M. Beroni 2, B. Petit 2, J. P. Koralsztein 2 1
Laboratoire d'étude de la motrictié humaine, Université Lille 2, Lille, France 2 Centre de Médicine du Sport CCAS, Paris, France 3 Université Paris 5, Paris, France
Billat VL, Hamard L, Bocquet V, Demarie S, Beroni M, Petit B, Koralsztein JP. Influence of Light Additional Arm Cranking Exercise on the Kinetics of V˙O2 in Severe Cycling Exercise. Int J Sports Med 2000; 21: 344 – 350 Accepted after revision: December 31, 1999
■■■■ This study examined the influence of light additional arm ˙ O2 slow component observed during cranking exercise on the V severe cycling exercise. During incremental tests, eleven triathletes exercised to exhaustion cycling with leg, cranking with arm and combined arm and leg cranking and cycling (arm work-rates being set at the third of leg work rates) to determine arm, leg ˙ O2max. After and combined arm and leg lactate threshold and V these incremental tests subjects performed in random order severe exercises until exhaustion at work-rates corresponding to the lactate threshold + 50 % of the difference to the work rate ˙ O2max and the lactate threshold, i.e., ∆50: 1) associated with V with legs only (leg ∆50) 2) leg ∆50 plus a very light arm cranking ˙ O2 exercise at 25 % of the arm lactate threshold (L∆50 + A25). V ˙ O2 (in ml × min–1) beslow component was the increase of V ˙ O2 6 – tween the third and the sixth minute of exercise (∆V 3 min). Results showed 1) Nine of the eleven triathletes had a ˙ O2 slow component in arm ∆50; 2) a light cycle arm exercise V (25 % of lactate threshold) added to a severe leg cycle exercise did not decrease time to exhaustion in severe exercise (493 ± 154 s vs 418 ± 84, P = 0.4); 3) For the five subjects who ˙ O2 slow component in leg cycling, the addition of a light had a V ˙ O2 slow compoarm exercise (25 % of arm LT) decreased the V nent significantly (from 457 ± 173 ml × min–1 for leg ∆50 to 111 ± 150 ml × min–1 for L∆50 + A25, Z = – 2.0, P = 0.04). In con˙O2 slow clusion, light additional arm cranking decreases the V component in severe cycling. Further studies are needed to confirm the hypothesis that extra work due to an increasing hand˙ O2 slow compogrip on the handlebars may contribute to the V nent in cycling. ˙ O2 slow component, arm cranking, leg cycling. ■ Key words: V
Int J Sports Med 2000; 21: 344 – 350 © Georg Thieme Verlag Stuttgart · New York ISSN 0172-4622
Introduction For arm exercise (as for leg), at work rates that elicit a lactic acidosis, an additional slow phase of V˙O2 (V˙O2 slow component) is superimposed upon the underlying V˙O2 kinetics [14, 22]. Poole et al. [24] demonstrated that the majority of the V˙O2 slow component is attributable to factors within the working limbs. However, recent studies reported in severe exercise an absence of the V˙O2 slow component during running in long-distance runners on level treadmill [9,10]. These studies reported a larger [14] slow component in cycling (tenfold) than in running at the same relative exercise intensity (i.e. between the lactate threshold and V˙O2max intensities of each exercise (∆50) [9,10]. In fact, the metabolic origins on the V˙O2 slow component observed during cycling are not well understood. Nagle et al. [21] focusing on high intensity cycling exercise leading to fatigue, demonstrated that the upper-body stabilising effort in conventional cycling incremental test (leg cycling with hands on the handlebars) contributes approximately 10 – 20 % to inducing V˙O2max at the end of exercise. Therefore, we hypothesised that the arm participation could influence the V˙O2 slow component in cycling. This study was designed to delete or at least decrease the increase of the arm “extra work” and the inducing “extra V˙O2” due to handgrip on the handlebars, which increases with fatigue during cycling. Therefore, the specific aim of this study was to yield further insight into the relative contribution of the arms to the V˙O2 slow component in severe cycling exercise. For this reason, we controlled the arm exercise by adding a very light arm exercise, a quarter of the arm lactate threshold work-rate, to the severe leg cycling exercise. We hypothesize that the V˙O2 slow component will be significantly decreased when this extra handgrip on the handlebars is replaced by a light sub-lactate threshold dynamic exercise carried out together with the severe cycling leg exercise.
˙O2 Kinetics in Leg Cycling Additional Arm Cranking and V Table 1
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Physical characteristics, triathlon experience, and training regimen data of the 11 triathletes
Subjects
Age (yr)
Weight (kg)
Height (cm)
Triathlon Experience (yr)
Triathlon Competitions (number)
Mean Training Distance (km × wk–1) Run Bike Swim
1
23
72
181
4
16
50
200
8
2
39
78
185
7
23
40
180
10
3
28
78
186
5
18
40
150
6
4
29
69
178
5
16
60
240
8
5
27
67
175
4
13
70
200
6
6
22
58
185
3
9
40
150
6
7
22
75
176
4
14
70
200
6
8
22
71
177
3
10
40
180
8
9
22
85
194
3
13
60
200
12
10
30
60
167
5
21
40
200
8
11
23
71
171
4
15
50
150
8
Mean
26
71
179
4
15
51
186
8
5
8
7
1
4
12
27
2
SD
Methods
Preliminary measurement
Subjects
Each subject performed tests at the same time of day in a climate-controlled laboratory (21 to 22 8C). Subjects were instructed not to train hard, or ingest food and beverages containing caffeine three days before testing. Each subject undertook three preliminary incremental tests, one with arms, one with legs and one with arms (1/3 of work-rate) and legs (2/3 of work-rate), on the cyclo-ergometers, to determine 1) V˙O2peak, 2) the work-rate associated with V˙O2peak and 3) the fraction of V˙O2peak at which the lactate threshold occurred. The respective fraction of arm and leg work was set in accordance with Bergh et al. [5] to attain the highest V˙O2peak.
Eleven well-trained triathletes gave their informed consent and volunteered to participate in this study, which was approved by the Paris Ethical Committee. The physical characteristics of the subjects are presented in Table 1. All subjects were highly motivated and familiar with combined leg and arm exercise on the ergometer and with the sensation and symptoms of fatigue during heavy exhaustive cycling and running exercise.
Material The subjects performed arm, leg, or combined arm-leg ergometry in standing-up (for arm) and in sitting position (for leg and arm-leg exercise) using a Monark weight cycle ergometer (Mod 90664 Monark, Varbeg, Sweden): one modified (elevated with shorter cranks) for arm and one conventional for leg cycling. Respiratory and pulmonary gas exchange variables were measured using a MedGraphics CPMax cart (Medical Graphics, St. Paul, MN, USA) which was calibrated prior to each test according to the manufacturer’s instructions. Breath-by-breath data were averaged every 15 s (with discrete time-bins). ECG was monitored from a three leads configuration (Marquette Electronics, Milwaukee, Wl, USA) and the output signal was fed to the CPX Medical Graphics system for computation of HR. V˙O2peak was the highest V˙O2 reached in the incremental test in two successive 15 s measurements. To be certain that subjects reached their V˙O2peak other criteria were used: 1) the respiratory exchange ratio above 1.1, 2) the measured maximal heart rate higher than 95 % of theoretical maximal heart rate [30] and 3) the inability of the subjects to maintain the pedalling speed. Blood samples were analysed for blood lactate concentration (Lab) using a purpose-built analyser YSI 27 (Yellow Springs Instruments, Ohio, USA).
These three incremental tests (arm cranking, leg cycling, and both arm and leg cycling) were performed to exhaustion two days apart and in a randomised order. The three continuous incremental tests were similar regarding the warm-up (6 min) and stages (2 min) duration. Cadence was set at 60 rpm for all exercises. Work-rates were respectively set at 30, 60 watts for separated arm and leg exercises and at 90 watts for combined exercise (30 watts for arms and 60 watts for legs). The poweroutput was then respectively increased by 15 (+ 250 gr) and 30 watts (+ 500 gr) for separated arm and leg exercises and by 45 watts for combined exercise (15 watts for arms and 30 watts for legs). The work-rate associated with V˙O2peak (Wr V˙O2peak ) for each of the three incremental tests (arm, leg and combined cycling) was defined as the minimal work-load at which V˙O2peak occurred [10] . All subjects were verbally encouraged and gave a maximum effort. Blood samples were obtained from the earlobe at the end of each 3 min-stage, immediately after the end of the exercise test and then 8 minutes into the recovery period. In this study, the lactate threshold (LT) was defined as the V˙O2 corresponding to the starting point of an accelerated lactate accumulation between the range of 3 – 5 mmol × l–1 (around
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4 mmol × l–1) [2] . Lactate threshold was expressed in % V˙O2peak. This point was closer in definition to the onset of blood lactate accumulation defined by Sjodin and Jacobs [29], than to the lactate threshold of Farrel et al. [15]. Although using an incremental test does not allow precise determination of the maximal blood lactate steady-state [7], the incremental test gave us a useful index to determine the range at which blood lactate starts to dramatically accumulate in the blood. To be sure that the triathletes would exercise in the range of severe-intensity exercise (where neither V˙O2 nor blood lactate can be stabilized and at which a consequent V˙O2 slow component appeared) [18], the work rate for both modes of exercise was set at 50 % of the work rate difference between those at the lactate threshold and at V˙O2peak determined in the incremental test exercise described above. This work rate was calculated to be half way between the lactate threshold and V˙O2 (∆50, equal to LT + 0.5 × [work rate at V˙O2peak – work rate at LT]) which was designated to be a severe intensity all-out exercise bout that produced fatigue at 10 to 15 minutes [18] . This power output was used in previous studies which have examined the V˙O2 slow component process [3, 4].
Experimental design and protocols The subjects cycled to exhaustion at ∆50, in random order: with leg or arms only, (Leg ∆50 and Arm ∆50), and then, with combined legs and arms cranking to exhaustion at Leg ∆50 + arms slightly exercising, i.e. 25 % of the arm lactate threshold (L ∆50 + A25). Each of these tests was separated by one week. After a fifteen minute warm-up period at 50 % of the work rate associated with V˙O2peak (Wr V˙O2peak) (which was below the lactate threshold for all subjects), the work-rate was increased to the supra-threshold exercise within 20 s. All subjects were given verbal encouragement throughout each trial. The time at which the subject was no longer able to maintain the required power-output was set as time to exhaustion (time limit) and was recorded to the nearest second. Blood samples were obtained from the earlobe before the warm-up run, during the last 30 seconds of the warm-up, every 3 min of all-out supra-threshold exercise and immediately after the end of the exercise test and then 8 minutes into the recovery period.
Data analysis As generally referenced in the literature [33, 34], the V˙O2 slow component was measured between the third and the sixth minute. A Student’s t -test for paired data compared the effect of additional arm work on the V˙O2 slow component. Results are presented as means ± standard deviation (SD). For the five out of eleven subjects who had a V˙O2 slow component in leg cycling, the comparison of this V˙O2 slow component in leg cycling vs the V˙O2 slow component in L ∆50 + A25 (leg cycling plus a light arm exercise equal to 25 % of arm lactate threshold) was done with the non parametric Wilcoxon test. The level of statistical significance was set at P = 0.05. Time delay for reaching the V˙O2 steady state was computed as follows:
Billat VL et al
Time delay calculation The time course of alveolar V˙O2 after the onset of exercise was described in terms of an exponential function that was fitted to the data with the use of non linear regression techniques in which minimising the sum of squared error was the criterion of convergence. The data were fitted with a logarithm-fitting package within the Sigma Plot software (SPSS, Chicago, II, USA). The method used is the Levenberg-Marquardt’s algorithm [20]. We started with a mono-exponential equation: y = y0+ a ×(1 – e(–b×[t–c])) (eq. 1). Where y is V˙O2 (ml/min) at any time (t in seconds), y0 is V˙O2 baseline at the end of the warm-up at 50 % of lactate threshold. The parameter “a” is the equation’s amplitude (∆ V˙O2 after the start of exercise), and the parameter “b” is the rate constant of the curve (the V˙O2 increase for every second of exercise). The parameter “c” verifies whether the test’s beginning starts actually at t = 0 (time 0). The time constant (τ) in accordance with Barstow and Mole [3], is the inverse function of the parameter b. Therefore equation (1) can be written: V˙O2 (t) = V˙O2baseline + ∆V˙O2 × (1 – e (–[t–δ]/τ])) (eq. 1’) Then we added three further parameters to express a double exponential function, thus: y = y0+ a × (1 – e (b×[t–c])) + d × (1 – e (–f×[t–g])) (eq. 2) The parameter “d” (second amplitude) and “f” (second slope) are the symmetric parameters of the mono-exponential. “g” indicates the time at which the additional V˙O2 increase begins. Initial estimates of the parameter values are made by inspection of the experimental V˙O2-time points. After defining variables, the Sigma plot program gives a value for all parameters with their significance. We can accept an equation if all its parameters are significant. One exception concerns the parameter named “d”. Indeed, this parameter must have the value equal to 0 normally, so if the program defines the parameter “d” close or equal to 0 with a P value close to 1, we can accept this equation. If both equations (1’ and 2) fit well the data, we choose, according to Akaike [1] criterion, the simplest equation (mono exponential rather than double exponential for instance). Moreover we calculated the time delay to reach a plateau of V˙O2 (at 98 % of V˙O2 plateau) (TD plateau) [30] according to the equation: V˙O2(t) = V˙O2baseline + ∆V˙O2 × (1 – e –4) = V˙O2baseline + 0.98 × ∆ V˙O2 (eq. 3)
˙O2 Kinetics in Leg Cycling Additional Arm Cranking and V
Int J Sports Med 2000; 21
Table 2 Maximal values of metabolic and cardiorespiratory parameters (mean ± SD) during the incremental tests for cycling and cranking Variables
Arm Cranking
Leg Cycling
Arm and Leg Cranking and Cycling
˙O2peak V (l × min–1) ˙O2peak V (l × kg–1 × min–1)
3.60 ± 0.54*#
4.68 ± 0.51§
4.54 ± 0.36§
#
§
§
50.5 ± 7.7*
65.5 ± 7.2
63.6 ± 5.1
Heart Rate (beats × min–1)
178 ± 15
184 ± 14
188 ± 12
[La] (mmol × l–1)
6.0 ± 1.6#
8.4 ± 2.5*§
6.7 ± 0.8#
Lactate Threshold ˙O2peak) (% WrV
80.6 ± 7.3
79.6 ± 4.1
75.5 ± 6.0
§ significantly different from arm cranking; # significantly different from leg cycling; * significantly different from arm cranking and leg cycling
bined exercise) (Table 2). Therefore, when setting the workrates for arm or leg severe square wave exercise, arm ∆50 and leg ∆50 were comparable (90.3 ± 2 and 89.8 ± 2.1 % WrV˙O2peak, respectively).
Constant work rate tests Since relative lactate threshold was similar in arm and leg exercise, work-rates for arm or leg severe square wave exercise (arm ∆50 and leg ∆50) were comparable (90.3 ± 2 and 89.8 ± 2.1 % WrV˙O2peak, respectively). Combined arm and leg exercise (L∆50 + A25) represented 86.4 ± 3.9 of WrV˙O2peak of combined arm and leg V˙O2peak. As mentioned in the “Methods” section, the selected warm-up period was below the lactate threshold (50 % of WrV˙O2peak). At the end of the fifteenminute warm-up period, triathletes were actually at 51 ± 2 % V˙O2max for all constant work rate exercises.
Time to fatigue Times to exhaustion were not significantly different between leg cycling and the same leg cycling work + light arm exercise performed at 25 % (L ∆50 + A25) even though the difference between the two work rates was as much as 23 % (Table 3).
Results
Incremental tests Table 2 shows the V˙O2peak, heart rate and blood lactate values, reached at the end of the incremental tests in leg, arm and combined cycling. There was no significant difference between triathletes’ V˙O2peak values during leg and combined arm and leg cycling exercises (65.5 ± 7.2 and 63.6 ± 5 ml × min–1 × kg–1, respectively), despite a significant difference of 56 watts between the two exercises (334 ± 57 watts vs 390 ± 184 watts for leg and combined cycling, P = 0.01). Maximal V˙O2 during leg cycling and arm cycling were both correlated (r = 0.60, P = 0.05). The lactate threshold expressed in percentage of the work-rate associated with V˙O2peak (WrV˙O2peak) is not significantly different between exercises (arm cranking, leg cycling and com-
V˙O2 kinetics: maximal V˙O2 attained in the severe all-out exercise Table 3 shows the parameter estimates for V˙O2 of severe exercises performed with arm ∆50, Leg ∆50, L∆50 + A25. The response of V˙O2 to the imposition of the work was well described by a single-exponential model for all the triathletes tested. Moreover, parameters of the double exponential did not meet the significance level. As shown in Table 3, all V˙O2 kinetic parameters, (i.e. time constant of V˙O2, the V˙O2 slow component, the time delay in all constant load severe exercises) were not significantly different between L ∆50 + A25 and leg ∆50. Slower kinetics were expressed during arm ∆50 (Table 3).
Table 3 Delay before exhaustion (tlim), Oxygen kinetics, and maximal values of metabolic and cardiorespiratory parameters (mean ± SD) during the constant workload tests for cycling and cranking Variables
Arm Cranking ∆50
Leg Cycling ∆50
Leg Cycling ∆50 + Arm25
tlim (min, sec)
10 min 54 s ± 5 min 10 s*
8 min 13 s ± 2 min 34 s§
6 min 58 s ± 1 min 24 s§
#
§#
337 ± 31*§
work rate (watts)
167 ± 34*
300 ± 53
˙O2peak) in relative work rate (% WrV incremental arm, leg or in incremental arm and leg exercise (for L ∆50 + A25) ˙O2 (l × min–1) V
90.3 ± 3.6
89.8 ± 2.0
86.4 ± 3.9
4.49 ± 0.47§
4.59 ± 0.60§
3.83 ± 0.45*#
˙O2 (l × kg–1 × min–1) V ˙O2 (% V ˙O2max) relative V
54.0 ± 6.4*
Heart Rate (beats × min–1)
178 ± 13
#
107 ± 9.4*
§
64.6 ± 8.4§
§
97.6 ± 8.1
101.2 ± 10.3
186 ± 13
183 ± 14
63.2 ± 6.6
[La] (mmol × l–1)
6.6 ± 2.5
7.5 ± 2.2
6.9 ± 2.4
∆[La] end – 3 min (mmol × l–1) ˙O26 – 3 min (ml × min–1) ∆V
2.3 ± 1.1
3.2 ± 1.6
2.9 ± 1.6
248 ± 307#
153 ± 382#
˙O2 plateau (seconds) Time delay to V
313 ± 169
205 ± 130
205 ± 175
τ (seconds)
121 ± 65∆
84 ± 52
87 ± 66
#§* Significantly different from leg ∆50 + Arm25, arm, and leg ∆50 respectively.
34 ± 284§*
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Billat VL et al
Table 4 Individual data of oxygen slow component and blood lactate accumulation between the third and the sixth minute; end value of blood lactate concentration during the constant workload tests for cranking and cycling
Subject
arm ∆50
˙O2 (6 – 3) (ml × min–1) ∆V leg ∆50 + arm25 leg ∆50
∆ Lactate (6 – 3) (mM) and (End blood lactate concentration, mM) arm ∆50 leg ∆50 leg ∆50 + arm25
1
576
– 37
– 146
1.3 (5.1)
2.8 (8.1)
1.4 (7.9)
2
553
537
– 47
1.0 (4.1)
0.9 (5.3)
1.1 (4.3)
3
117
157
86
1.1 (3.5)
2.0 (5.8)
1.1 (3.5)
4
358
552
131
1.1 (8.9)
1.8 (9.6)
4.4 (8.9)
5
462
576
288
1.3 (5.7)
2.1 (7.4)
1.7 (5.7)
6
165
30
224
1.4 (8.7)
3.9 (10.5)
4.0 (10.2)
7
– 510
465
270
1.5 (6.3)
0.3 (9.3)
3.8 (7.0)
8
426
– 262
298
– 3.1 (11.7)
4.5 (10.2)
4.3 (10.5)
9
180
– 77
– 688
1.1 (8.3)
0.5 (6.7)
2.0 (4.4)
10
360
– 91
18
0.6 (5.1)
1.3 (4.3)
2.1 (5.7)
11
43
– 403
– 64
1.6 (5.4)
0.0 (5.4)
4.1 (7.8)
0.8 ± 1.3# (6.6 ± 2.5)
1.8 ± 1.5 (7.5 ± 2.2)
2.7 ± 1.4 (6.9 ± 2.4)
Mean ± SD
248 ± 308
153 ± 382
34 ± 284
# Significantly different from leg ∆50 + Arm25; no significant difference between end blood lactate concentration (F = 1.6, P = 0.22). No significant difference be˙O2 (6 – 3) (because of large standard deviation). For the 5 subjects (no. 2, 3, 4, 5, 7) who have V ˙O2 slow component in leg, this decreased signifitween the ∆V cantly with the additional arm work (Z = – 2.0, P = 0.04).
For the five subjects who had a V˙O2 slow component in leg cycling (Table 4), the addition of a light arm exercise (25 % of arm LT) decreased the V˙O2 slow component significantly (from 457 ± 173 ml × min–1 for leg ∆50 to 111 ± 150 ml × min–1 for L + A25, Z = – 2.0, P = 0.04). Nine of the eleven triathletes had a V˙O2 slow component in arm ∆50.
not surprising since it is reported that the arm has a greater proportion of type II muscle fibres than the leg in the same subject [31]. Moreover, Barstow et al. [4] have demonstrated that the amplitude of the V˙O2 slow component was positively correlated with the percentage of type II (fast-twitch) fibres in the contracting muscles.
The decrease of the amplitude of the V˙O2 slow component between the severe leg cycling (leg ∆50) and the same leg cycling with the additional light arm exercise (L ∆50 + A25) is not correlated with arm V˙O2 slow component (r = 0.10).
In fact, it has been suggested that the V˙O2 slow component may primarily be related to motor unit recruitment patterns during exercise depending upon the contribution of less efficient, fast twitch motor units [3, 4,19, 25, 34]. Recently, Bohnert et al. [11] reported that the increase of lactate and the decrease of pH induced in a second leg supra threshold bout was smaller when preceded by prior leg exercise than prior arm exercise inducing the same blood lactate concentration. It was, therefore, concluded that while metabolic acidaemia induced at a site remote from legs is associated with a less prominent slow phase of the V˙O2 kinetics for high-intensity leg exercise, a component specific to the involved contractile units appears to exert the dominant effect.
Discussion The results showed that severe arm cranking induced a slow component of V˙O2 in most of the triathletes (9/11) and in half (5/11) of them when they performed the same relative power output (Wr∆50) with legs. It may be probable that the subjects who did not have a slow component of V˙O2 in cycling, even if they were above their lactate threshold work rate, were not above the critical power. This last one which is the horizontal asymptote of the power rate-time relationship has been described as the upper limit for which V˙O2 can maintain a steady-state [18]. These present data show also that in the subjects who have a slow component of V˙O2 in cycling, a very light arm exercise (25 % of the arm lactate threshold i.e. 35 w) added to the same ∆50 leg cycling, decreases the induced slow component of V˙O2.
V˙O2 slow component in arm severe exercise in trained endurance arm subjects The data reported here for severe arm exercise were in accordance with previous works performed with arm exercise in untrained subjects. In fact, for arms also, a slow kinetic response of V˙O2 has been described for work rates above lactate threshold by Pendergast et al. [22, 23] and Casaburi et al. [14]. That is
Even if there is a suggestion that the V˙O2 slow component originates in the “exercising-muscles” [24], to our knowledge no data are available in the literature to provide an answer to the question if the difference in V˙O2 kinetics for arm vs leg in high work-rates (above LT) could be accounted for by a difference in percentage of fast twitch fibres between arm and leg, especially in triathletes [6,16, 31]. The group of subjects consisted of triathletes. These trained triathletes’ arm V˙O2max was higher than that obtained in untrained subjects (78 % vs less than 65 % of leg maximal V˙O2) according to Reybrouck et al. [26] and lower than kayakers [8,13]. This arm V˙O2 maximal value was obtained in a standing-up position that has been demonstrated not to be significantly different from a sitting position [32]. A maximal V˙O2 plateau was observed in 8 of the eleven triathletes. Maximum heart rates reached in all the three incremental tests (arm, leg
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Int J Sports Med 2000; 21
and combined exercise) were not significantly different, in accordance with Vokac et al. [32]. Therefore, we can be sure that the calibration of arm severe exercise was accurate and in the severe range intensity, which was confirmed by the blood lactate at the end of the constant-load arm exercise (about 7 mM); this was not different from the leg ∆50 and from L ∆50 + A25.
duced a V˙O2 slow component in all subjects and light arm exercises added to the severe leg cycling decreased V˙O2 slow component and accelerated the V˙O2 kinetics. The blood lactate end values obtained in the four severe exercises performed (arm, leg and combined exercise) were comparable to those found in the previous study in severe ∆50 cycling and running with triathletes [10] .
It is also possible to argue, as Casaburi et al. [14] did, that the extra V˙O2 at this higher output comes from an isometric exercise component required for torso stabilization. In fact, we suggest that in the standing-up position, muscles of the lower limbs assume stabilisation. In severe arm exercise, we think that postural muscles, and legs in particular, are not responsible for the slow onset progressive 500 ml/min of V˙O2 increase over the last 3 min of exercise. As already stated, the severe arm cranking (167 ± 34 W) represented only half the work-rate of the associated leg WrV˙O2max (334 ± 57 W). Moreover, the initial oxygen cost per watt of arm cranking measured below the lactate threshold was only 135 % of oxygen cost per watt of leg cycling. This value is in accordance with the literature whatever the test position [17, 28]. However, it seems that the large V˙O2 increase with time in severe arm cranking should be taken into consideration in arm ergometry and training, even for subjects well-trained in arm exercise. However, even if these triathletes had good arm V˙O2peak values they were not trained to arm cycling. Arm V˙O2 slow component could be compared between two groups with the same arm V˙O2peak values both of which are either used to cranking or not (e.g. swimmers vs kayakers).
Conclusion
Arm light cranking added to severe leg cycling decrease the V˙O2 slow component Most of the studies that have reported a V˙O2 slow component were performed during cycling [12,18, 27, 34]. However, a recent study showed that thirteen high level runners (V˙O2max 74.9 ± 3.0 ml/min/kg) were able to maintain a V˙O2 steady-state at 91 % of V˙O2max for 17 minutes with an end blood lactate of 6.5 ± 2.1 mM [9]. They ran at 90 % of the velocity associated with V˙O2max (vV˙O2max), a velocity above their critical velocity (86 ± 1.5 % vV˙O2max ). In another recent study comparing cycling and running V˙O2 slow component in severe square wave exercise, ten triathletes performed exhaustive exercise on a treadmill and on a cycloergometer at a work rate corresponding to 90 % of work rate at V˙O2peak. This exercise was carried out until exhaustion and was well above the lactate threshold which was similar for both types of exercise in absolute (V˙O2) and relative intensity (82 % WrV˙O2peak) [10]. Moreover, the duration of the tests before exhaustion was superimposable for both types of exercise and comparable to the present study (about 10 min), with blood lactate levels at the end of the tests which were similar both for running (7.2 ± 1.9 mmol/1) and cycling (7.3 ± 2.4 mmol/l). However, the V˙O2 slow component was significantly lower during running compared to cycling (20.9 ± 2 ml/min versus 268.8 ± 24 ml/min, p < 0.02). That is why, in the present study, we examined the hypothesis that this V˙O2 slow component could be due, in part, to the progressive participation of the arms in the exercise towards the point of fatigue (defined as the inability to sustain a given workrate). We found that arm cranking and leg cycling in-
We hypothesize that arm participation could influence the V˙O2 slow component in cycling. An addition of a light arm exercise (35 W, i.e. a quarter of the arm lactate threshold) negates this V˙O2 slow component by accelerating the V˙O2 kinetics. Further studies are needed to confirm the hypothesis that extra work due to an increasing hand-grip on the handlebars may contribute to the V˙O2 slow component in cycling.
Acknowledgements This study was supported by grants from Caisse Centrale des Activités Sociales d’Electricité et Gaz de France.
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Billat VL et al
Corresponding Author: Véronique Billat, Ph.D. Centre de Médicine du Sport CCAS 2 avenue Richerand 75010 Paris France Phone.: Fax.: E-mail:
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