Recent works have shown that repeated 6-s bouts of intensive exercise against increasing braking forces on cycle ergometer with a resting recovery (force-velocity test: FV test) induce a high blood-lactate accumulation (20,22), indicating an imbalance between lactate production, lactate removal, and/or other tissue lactate utilization. Moreover, the rise in blood lactate concentration ([La]) has been shown to level off when peak anaerobic power (PAnP) is achieved(22). If the repetition of intensive exercise bouts starts with a heavy braking force, PAnP increases more, up to a comparable[La], than it does if the test is started with a light braking force(21). Furthermore, 2-chloropropionate, which decreases lactate production by an activation of pyruvate dehydrogenase, increases PAnP as measured by the FV test (20). It was thus assumed that the FV test induced a marked imbalance in lactate exchanges, reflected by the high blood lactate accumulation, that may contribute to the limitation in anaerobic performance as measured during this test. Indeed, results obtained from several investigations suggest that work performance is adversely affected by the elevated [La] (14,18), which may retard the rate of muscular glycolysis by inhibiting the activity of glycolytic enzymes (8,15). Lactate removal from the blood following exercise therefore appears to be of great importance in improving the subsequent performance, particularly when the exercise is repeated at high intensity. Although lactate accumulated in the blood from exercise may be removed by various organs, tracer studies with14 C-Lactate have shown that a significant proportion of lactate is taken up by skeletal muscle and then metabolized via its reconversion to pyruvate, which is subsequently oxidized in the Krebs cycle with energy production (7,13). Moreover, numerous investigations have reported that blood lactate level is lower during continuous aerobic work than during resting recovery(4,11,25,28). Based on these findings, we hypothesized that an active recovery that accelerates blood lactate removal would reduce the plasma lactate accumulation induced by the repetition of intensive exercise bouts and consequently improve the anaerobic performance measured during the force-velocity test.
To verify this hypothesis we investigated the effects of an active recovery on plasma lactate concentration and subsequent anaerobic power output following repeated intensive exercise bouts during the force-velocity test.
MATERIAL AND METHODS
Ten healthy male volunteers (age, 27.3 ± 2.4 yr; weight, 70.6± 3 kg; height, 174.8 ± 2.2 cm) participated in this study. No subject was known to be suffering from any chronic disease and none was on any regular medication. The aim and protocol of the study were explained and written consent was obtained.
Exercise testing. An incremental aerobic exercise test and two FV tests were performed by all subjects on the same cycle ergometer (864, Monark-Crescent AB, Varberg, Sweden). During the aerobic test, respiratory variables and gas exchanges were measured with a breath by breath automated exercise metabolic system (CPX Medical Graphics, Saint Paul, MN). Briefly, subjects breathed via a low-resistance breathing valve (2700 Hans-Rudolph, Inc., KS). Expiratory airflow was measured with a pneumotachograph (Type 3,3800, Hans-Rudolph, Inc.) connected to a pressure transducer (DP 250-14, Validyne Engineering Corp., CA). Expiratory gases were analyzed for O2 with a zirconia solid electrolyte O2 analyzer and for CO2 with an infrared analyzer. Before each test, the volume was calibrated by five inspiratory strokes with a 3-1 pump; the gas analyzer, with two mixtures of gases of known oxygen and carbon dioxyde concentrations.
The FV test consisted of repeated bouts of intensive exercise against increasing braking forces (F) with a 5-min between-bout recovery period(27). The bout duration was fixed at 6 s, the maximum time it took for a highly motivated subject to attain his maximal peak velocity (V) after the starting signal. Each FV test was performed with the subject in a sitting position. Subjects started the test against an F of 2 kg, and recovered for 5 min before repeating the same bout of intensive exercise against an F increased by 2 kg. The subjects generally performed four or five intensive exercise bouts in the session. At the end of the test, when the pedaling frequency was less than 130 rpm, F was increased by 1 kg in order to obtain a PAnP as precise as possible. We assumed that the subject attained the F corresponding to his PAnP if an additional braking force induced a power decrease. The force-velocity relationships were calculated by an automatic system (22) that allowed, for each exercise bout, the determination of V from the measurement of pedal frequency and for each F, the power corresponding to the product of F and V. The accuracy of the pedal revolution duration was 3.3 ms. As pointed out by Vandewalle et al.(27), the relationship between F and V can be expressed as follows: V = b - aF or V = V0 - V0F/F0 = V0 (1- F/F0) where V0 is the intercept with the velocity axis, i.e., the maximal V for an F equal to zero; and F0, the intercept with the force axis, i.e., the maximal F for a V equal to zero. These relationships were calculated by extrapolation from the linear relation linking F and V at a pedaling frequency greater than 90 rpm. Given the linear F·V relationship, there is a parabolic relationship between braking force and power output calculated from peak velocity during the FV test(27). The highest power value calculated was defined as the peak anaerobic power (PAnP). In Figure 1, the forcevelocity relationship obtained for one subject is shown as an example.
Blood samples and plasma lactate analysis. Blood samples were drawn from a 32-mm catheter (Cathlon IV 4426) placed in a superficial forearm vein. A three-way tap was placed on the catheter to allow rinsing with a syringe containing a mixture of heparin and physiological saline (250 UI·ml-1) and then blood sampling with a dry syringe after the catheter had been cleared of saline. Blood samples for plasma lactate determination were collected in Vacutainer tubes (Becton Dickinson, NJ) containing fluoride/ethylenediaminetetraacetic acid (fluoride/EDTA) and placed immediately on ice. Plasma was obtained via centrifugation (5 min at 3000 rpm at 4°C) in a refrigerated centrifuge (PR-J, Beckman Instruments). The decanted plasma was then separated and frozen at -15°C until assayed. All the plasma lactate concentrations were determined within 48 h by a fully enzymatic method (reagent kit from Boehringer). To measure plasma lactate with this method (23), the reaction was carried out with an excess of NAD, leading thus to the formation of pyruvate and NADH. To force this reaction to completion in this direction, the formed pyruvate was trapped by carbonate buffer L-glutamate. The increased absorbance at 340 nm due to NADH formation became a measure of the lactate originally present. The different readings were taken by a centrifugal analyzer (Cobas Bio, Roche, France).
One week before the experiment, all subjects received standardized instructions as to the testing procedure. On the first day, clinical interviews and examinations were conducted with height, body mass, and resting 12-lead ECG tracing recorded. Preliminary force-velocity and incremental aerobic exercise tests were then performed on separate days. The preliminary FV test allowed the subjects to familiarize themselves with the procedure, equipment, and laboratory environment. The incremental aerobic exercise test enabled us to determine the individualized exercise intensity to be used during the active recovery. The aerobic test started with a 3-min 30 W warm-up period. The workload was then increased by 30 W each minute. When the subjects were close to their maximal oxygen uptake values (˙VO2max), the incrementload was reduced to 20 or 10 W to improve the accuracy of the individual maximal aerobic power (MAP) values. The criteria used to ensure that the subjects had reached their ˙VO2max were the following: stability of ˙VO2 in spite of the increase in work load; stability of the heart rate at a value close to the theoretical maximal heart rate (220- age) ± 10%; a respiratory exchange ratio of 1.1; and an inability to maintain the required pedaling frequency (60 rpm). The power corresponding to˙VO2max was considered to be maximal aerobic power (MAP). After completion of the incremental aerobic exercise test, the anaerobic threshold was determined for each subject from gas exchange measurements (Vth) using the V-slope method of Beaver et al. (2). This method involves the analysis of ˙VCO2 behavior as a function of ˙VO2 and assumes that the Vth corresponds to the last point before a nonlinear increase in ˙VCO2 in relation to ˙VO2.
During the following week, in a randomized crossover design, each subject performed two FV tests separated by a 3-d interval, once with a 5-min passive recovery after each intensive exercise bout (PR) and once with a 5-min active recovery at 32% of MAP intensity (AR). On these days, an identical standard breakfast without coffee was served 2 h before exercise testing (2 wheat muffins, 50 g of cheese, 300 ml of unsweetened orange juice, totaling approximately 1600 kJ). Twenty minutes after arrival at the laboratory, a Teflon catheter (Cathlon IV 4426) was placed into a forearm vein for blood sampling. The subjects rested for 10 min just before FV exercise testing. To ensure that flywheel acceleration during AR did not influence bout performance, each successive bout was always begun from a dead stop. Blood samples were drawn at rest 5 min before the test, for each F when the subject stopped pedaling (S1) and then at the end of each 5-min between-bout recovery period (S2). A three-lead ECG (DII, V2, V5) was monitored with cardioscope (Quinton Q 3000, WA) during all exercise tests and allowed us to determine heart rate (HR). During the aerobic exercise test, HR was determined at rest, at each step of the exercise, and each minute during the 5-min recovery period. During the FV test, HR was determined at rest, at each F when the subject stopped pedaling, and at the end of each 5-min between-bout recovery period.
During the FV test with PR and AR, delta [La] was determined for the common braking forces and for the force corresponding to PAnP by subtracting the [La] measured at S2 from that obtained at S1.
Values are reported as mean ± SEM. To be sure that the exercise intensity used during AR wad lower than that corresponding to the Vth, the values, expressed as workload were compared using a paired Student'st-test (Table 1). A two-way analysis of variance for repeated measures (two-way ANOVA) was applied to each set of PR and AR measurements. When the ANOVA F-ratio was significant, a Newman-Keuls multiple comparison test was performed to determine the location of the differences, and the means were compared thereafter using the contrast method(29). A linear correlation was done to attempt to determine a relationship between power and [La]. The limit for statistical significance was always set at P < 0.05.
The mean cardiorespiratory variables measured during the incremental aerobic exercise test and the exercise intensity used during the FV test with AR are summarized in Table 1. Figure 2 represents the mean values of HR during the FV tests at S1 and S2. No significant difference was obtained in the HR values measured at S1 between the FV test with PR and AR. However, significantly higher values of HR were noted at S2 for the FV test with AR (F = 37.59, P < 0.01).
Venous Plasma Lactate Concentration
The time course of the plasma [La] during the FV tests at the common braking forces (2 kg, 4 kg, 6 kg) and at the force corresponding to PAnP and PAnP + 1 kg, measured at S1 and S2 with PR and AR, are shown inFigure 3. During the FV test with PR, [La] increased significantly when measured at S1 (F = 25.76, P < 0.001), and S2(F = 18.08, P < 0.001); the increase between PAnP and PAnP + 1 kg, however, was not significant. From the beginning of the exercise to the PAnP, a significant positive correlation between the increase in power output and the increase in [La] measured at S2 (r = 0.82, P < 0.01) was obtained.
During the FV test with AR, [La] measured at S1 for each F was not significantly different from PR, except for PAnP + 1 kg. Measured at S2, however, [La] was significantly lower with AR than with PR (F = 10.32,P < 0.05), especially for high braking forces (6 kg: P< 0.01 and PAnP: P < 0.01). The time course of delta [La] is represented in Figure 4. Delta [La] was significantly lower for AR at 6 kg (P < 0.05) and PAnP (P < 0.05).
For all subjects, power outputs were obtained for each F at velocities greater than 90 rpm, in the linear portion of the force-velocity relationship. The mean values of power output obtained for common loads and the loads corresponding to PAnP and PAnP + 1 kg during PR and AR are shown inFigure 5. For lower forces (2 kg and 4 kg) the mean power output values with AR were not significantly different from those with PR. However, the mean power output values at 6 kg (P < 0.01) and PAnP(P < 0.01) were significantly higher with AR.
This study shows that active recovery during repeated bouts of intensive exercise (the force-velocity test) attenuates the plasma lactate concentration measured at high braking forces. Moreover, this decrease in concentration with active recovery was accompanied by a parallel increase in the power output at these braking forces.
Few tests allow the evaluation of a subject's anaerobic fitness. Perhaps the best known is the Wingate test, which is performed against one standard braking force. As Vandewalle et al. (27) have shown, this test measures peak anaerobic power well only if the braking force is optimal. The FV test, consisting of incremental braking forces, was therefore chosen for this study in order to evaluate peak anaerobic power with greater accuracy. The exercise intensity used during AR in the present study was based on Belcastro and Bonen's work (4), which investigated the blood lactate level at various intensities of exercise recovery and assumed that the optimal lactate reduction occurs at 32% of ˙VO2max. The use of this light workload (32% of ˙VO2max) for the recovery period is based on the notion that higher workload will result in an increased imbalance between the rate of lactate appearance and disappearance. Indeed, it has been shown that recovery performed at great intensity may increase lactate production. Accordingly, previous studies reveal that exercise recovery at workloads below the lactate threshold (LT) is more effective, with respect to lactate reduction, than above LT (25,28). Similarly, the AR exercise intensity used in this study, expressed as workload(Table 1) and heart rate (Fig. 2), was always lower than that corresponding to the individual Vth.
The result of this study shows that the power outputs obtained with high braking forces were increased with AR. Nevertheless, the interpretation of the change in power output observed in this study may be limited to the experimental procedure used. As other investigators have done(3,9), we used the early definition of Vandewalle et al. (27) to calculate power output, i.e., the product of braking force and peak velocity, without taking into account the flywheel inertia. Indeed, using the Wingate test, Lakomy (19) showed that on a mechanically braked cycle ergometer, maximal power was achieved before peak velocity and was 30%-40% higher than the power calculated when peak velocity was reached. However, because each successive bout following AR was begun from a dead stop and the calculation of power output was the same for AR and PR, the values obtained represent a valid index for investigating the effect of AR on anaerobic performance. Furthermore, because the order of testing was randomized and all subjects were familiarized with the FV test before experimentation, the changes in power output do not seem to be the effect of day-to-day variation or learning.
Our results show also that AR decreased blood lactate concentrations following repeated exercise bouts. The lower levels of plasma lactate obtained with AR in this study are in agreement with several investigations; however, the mechanisms involved are not well known. Brooks (6) showed that an important mechanism for lactate disappearance during exercise is the oxidation in skeletal muscles. This author indicated, that lactate, which is produced as a result of Type IIb fiber recruitment, is transported into Type I or IIa fibers, where it is oxidized. Indeed, a relationship exists between lactate removal and the percentage of slow twitch fiber (% ST), which is related to the metabolic and anatomic features of these fibers. Specifically, the greater capillary density around the ST fibers(1) and their enriched H-LDH isozyme content (LDH-1 + LDH-2) (16) suggest that the delivery, uptake, and subsequent oxidation of lactate is facilitated here. With active recovery, the functional significance of the ST fibers for lactate removal becomes more evident, since these fibers are employed during low-intensity exercise and can therefore rely on lactate as a substrate. Other factors, such the rate of blood flow, which influence lactate efflux from skeletal muscle, should also be considered in lowered lactate concentration (10). In our study we have shown that the heart rate values during AR were higher than that obtained with PR. This result indicate that cardiac output and leg blood flow were also higher during AR. The increased blood flow may expedited the lactate translocation from the muscle cell to the blood and allows an increased rate of lactate removal in other sites consuming lactate.
In this study, the AR resulted in lower lactate concentration for high braking forces. At first view, it appears surprising that plasma lactate and delta [La] concentrations after AR were significantly lower only for high braking forces (6 kg and PAnP). However, this finding is in accordance with Bonen et al. (5), who found that the effect of AR becomes significant only for high blood lactate concentration. Similarly, our results show that only the power outputs obtained at these high braking forces wre increased with the AR protocol. This increase in power output with AR associated with a lower concentration in plasma [La] probably indicates attenuation of lactic acidosis. Previous studies conducted with the FV test with PR have indicated that the repetition of exercise bouts induces a recruitment of lactic anaerobic metabolism(3,20,22). Indeed, we observed a substantial increase in plasma lactate concentration from the first braking force, which leveled off when PAnP was achieved. In addition, a high correlation coefficient was obtained between plasma [La] and power output. Furthermore, recent study from our laboratory using localized nuclear magnetic resonance during FV test with PR observed that muscle lactate rises significantly at PAnP when venous plasma lactate levels off (personal data). Moreover, PAnP decreased for each subject after muscle lactate rose. This indicates that repeated bouts of intense exercise during the FV test induces an imbalance between lactate production and lactate removal which could induce muscle H+ accumulation. The consequence of this this H+ accumulation in the muscle involved during the FV test may be therefore one of the limiting factors of anaerobic performance. Indeed, at low pH, both phosphorylase and phosphofructokinase will be inhibited (15), leading to a reduction in the rate of glycolysis and hence a reduction in the rate of ATP production (14,26). Consequently, less power can be developed. In this study, however, only venous lactate concentration was measured and thus it was difficult to assess the effect of the lactate removal due to AR on metabolic muscle disorders. This requires further investigations using either biochemical measurements on muscle biopsy samples or measurements of high-energy phosphates, metabolites, and intramuscular lactate by31 P and 1H nuclear magnetic resonance(17,24).
In summary, this study showed that when repeated bouts of intensive exercise, i.e., the force-velocity test, were followed by active recovery periods, plasma lactate concentration was lower compared with passive recovery levels. In addition, higher power outputs were observed with the active recovery protocol. These findings, however, were significant only at high braking forces. Further studies are needed to assess the effects of AR on lactate exchange induced during the force-velocity test.
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