Effect of soccer training on the running speed and the blood lactate concentration at the lactate minimum test

Tegtbur et al. [23] devised a new method able to estimate the intensity at maximal lactate steady state termed lactate minimum test. According to Billat et al. [7], no studies have yet been published on the affect of training on highest blood lactate concentration that can be maintained over time without continual blood lactate accumulation. Therefore, the aim of the present study was to verify the effect of soccer training on the running speed and the blood lactate concentration (BLC) at the lactate minimum test (Lac(min)). Thirteen Brazilian male professional soccer players, all members of the same team playing at National level, volunteered for this study. Measurements were carried out before (pre) and after (post) eight weeks of soccer training. The Lac(min) test was adapted to the procedures reported by Tegtbur et al. [23]. The running speed at the Lac(min) test was taken when the gradient of the line was zero. Differences in running speed and blood lactate concentration at the Lac(min) test before (pre) and after (post) the training program were evaluated by Student's paired t-test. The training program increased the running speed at the Lac(min) test (14.94 +/- 0.21 vs. 15.44 +/- 0.42* km(.)h(-1)) and the blood lactate concentration (5.11 +/- 2.31 vs. 6.93 +/- 1.33* mmol(.)L(-1)). The enhance in the blood lactate concentration may be explained by an increase in the lactate/H+ transport capacity of human skeletal muscle verified by other authors.

Determination of anaerobic threshold in rats using the lactate minimum test

The break point of the curve of blood lactate vs exercise load has been called anaerobic threshold (AT) and is considered to be an important indicator of endurance exercise capacity in human subjects. There are few studies of AT determination in animals. We describe a protocol for AT determination by the lactate minimum test in rats during swimming exercise. The test is based on the premise that during an incremental exercise test, and after a bout of maximal exercise, blood lactate decreases to a minimum and then increases again. This minimum value indicates the intensity of the AT. Adult male (90 days) Wistar rats adapted to swimming for 2 weeks were used. The initial state of lactic acidosis was obtained by making the animals jump into the water and swim while carrying a load equivalent to 50% of body weight for 6 min (30-s exercise interrupted by a 30-s rest). After a 9-min rest, blood was collected and the incremental swimming test was started. The test consisted of swimming while supporting loads of 4.5, 5.0, 5.5, 6.0 and 7.0% of body weight. Each exercise load lasted 5 min and was followed by a 30-s rest during which blood samples were taken. The blood lactate minimum was determined from a zero-gradient tangent to a spline function fitting the blood lactate vs workload curve. AT was estimated to be 4.95 ± 0.10% of body weight while interpolated blood lactate was 7.17 ± 0.16 mmol/l. These results suggest the application of AT determination in animal studies concerning metabolism during exercise.

Protocols for hyperlactatemia induction in the lactate minimum test adapted to swimming rats

The lactate minimum test (LACmin) has been considered an important indicator of endurance exercise capacity and a single session protocol can predict the maximal steady state lactate (MLSS). The objective of this study was to determine the best swimming protocol to induce hyperlactatemia in order to assure the LACmin in rats (Rattus norvegicus), standardized to four different protocols (P) of lactate elevation. The protocols were PI: 6 min of intermittent jumping exercise in water (load of 50% of the body weight - bw); P2: two 13% bw load swimming bouts until exhaustion (thin); P3: one thin 13% bw load swimming bout; and P4: two 13% bw load swimming bouts (1st 30 s, 2nd to thin), separated by a 30 s interval. The incremental phase of LACmin beginning with initial loads of 4% bw, increased in 0.5% at each 5 min. Peak lactate concentration was collected after 5, 7 and 9 min (mmol L-1) and differed among the protocols P 1 (15.2 +/- 0.4, 14.9 +/- 0.7, 14.8 +/- 0.6) and P2 (14.0 +/- 0.4, 14.9 +/- 0.4, 15.5 +/- 0.5) compared to P3 (5.1 +/- 0.1, 5.6 +/- 0.3, 5.6 +/- 0.3) and P4 (4.7 +/- 0.2, 6.8 +/- 0.2, 7.1 +/- 0.2). The LACmin determination success rates were 58%, 55%, 80% and 91% in P1, P2, P3 and P4 protocols, respectively. The MLSS did not differ from LACmin in any protocol. The LACmin obtained from P4 protocol showed better assurance for the MLSS identification in most of the tested rats. (c) 2007 Elsevier B.V. All rights reserved.

The Lactate Minimum Test protocol provides valid measures of cycle ergometer VO2 peak

Aim. The aim of the present study was to investigate the validity of the Lactate Minimum Test (LMT) for the determination of peak VO2 on a cycle ergometer and to determine the submaximal oxygen uptake (VO2) and pulmonary ventilation (VE) responses in an incremental exercise test when it is preceded by high intensity exercise (i.e., during a LMT).Methods. Ten trained male athletes (triathletes and cyclists) performed 2 exercise tests in random order on an electromagnetic cycle ergometer: 1) Control Test (CT): an incremental test with an initial work rate of 100 W, and with 25 W increments at 3-min intervals, until voluntary exhaustion; 2) LMT: an incremental test identical to the CT, except that it was preceded by 2 supramaximal bouts of 30-sec (similar to120% VO(2)peak) with a 30-sec rest to induce lactic acidosis. This test started 8 min after the induction of acidosis.Results. There was no significant difference in peak VO2 (65.6+/-7.4 ml.kg(-1).min(-1); 63.8+/-7.5 ml.kg(-1).min(-1) to CT and LMT, respectively). However, the maximal power output (POmax) reached was significantly higher in CT (300.6+/-15.7 W) than in the LMT (283.2+/-16.0 W).VO2 and VE were significantly increased at initial power outputs in LMT.Conclusion. Although the LMT alters the submaximal physiological responses during the incremental phase (greater initial metabolic cost), this protocol is valid to evaluate peak VO2, although the POmax reached is also reduced.

Validation of the lactate minimum test as a specific aerobic evaluation protocol for table tennis players

The purpose of this study was to validate the lactate minimum test as a specific aerobic evaluation protocol for table tennis players. Using the frequency of 72 balls·min-1 for 90 sec, an exercise-induced metabolic acidosis was determined in 8 male table tennis players. The evaluation protocol began with a frequency of 40 balls·min-1 followed by an increase of 8 balls·min-1 every 3 min until exhaustion. The mean values that corresponded to the subjects' lactate minimum (Lacmin) were equal to 53.1 ± 1.5 balls·min-1 [adjusted for the time test (Lacmin_time)] and 51.6 ± 1.6 balls·min-1 [adjusted for the frequency of balls (Lacmin_Freq)], which resulted in a high correlation between the two forms of adjustment (r = 0.96 and (P = 0.01). The mean maximum lactate steady state (MLSS) was 52.6 ± 1.6 balls·min-1. Pearson's correlations between Lacmin_time vs. MLSS and Lacmin_freq vs. MLSS were statistically significant (P = 0.03 and r = 0.86, P = 0.03 and r = 0.85, respectively). These findings indicate that the Lacmin test predicts MLSS. Therefore, it is an excellent method to obtain the athletes' anaerobic threshold. Also, there is the advantage that it can be performed in 1 day in the game area. However, the Lacmin value does not depend on the Lacpeak value.

Maximal Oxygen uptake cannot be determined in the incremental phase of the lactate minimum test on a cycle ergometer

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Effect of an acute β-adrenergic blockade on the blood glucose response during lactate minimum test

The aim of this study was to determine the relationship between blood lactate and glucose during an incremental test after exercise induced lactic acidosis, under normal and acute β-adrenergic blockade. Eight fit males (cyclists or triathletes) performed a protocol to determine the intensity corresponding to the individual equilibrium point between lactate entry and removal from the blood (incremental test after exercise induced lactic acidosis), determined from the blood lactate (Lacmin) and glucose (Glucmin) response. This protocol was performed twice in a double-blind randomized order by ingesting either propranolol (80 mg) or a placebo (dextrose), 120 min prior to the test. The blood lactate and glucose concentration obtained 7 minutes after anaerobic exercise (Wingate test) was significantly lower (p<0.01) with the acute β-adrenergic blockade (9.1±1.5 mM; 3.9±0.1 mM), respectively than in the placebo condition (12.4±1.8 mM; 5.0±0.1 mM). There was no difference (p>0.05) between the exercise intensity determined by Lacmin (212.1±17.4 W) and Glucmin (218.2±22.1 W) during exercise performed without acute β-adrenergic blockade. The exercise intensity at Lacmin was lowered (p<0.05) from 212.1±17.4 to 181.0±15.6 W and heart rate at Lacmin was reduced (p<0.01) from 161.2±8.4 to 129.3±6.2 beats min-1 as a result of the blockade. It was not possible to determine the exercise intensity corresponding to Glucmin with β-adrenergic blockade, since the blood glucose concentration presented a continuous decrease during the incremental test. We concluded that the similar pattern response of blood lactate and glucose during an incremental test after exercise induced lactic acidosis, is not present during β-adrenergic blockade suggesting that, at least in part, this behavior depends upon adrenergic stimulation.

The response of the lactate minimum test to a 12-week swimming training

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Effect of the passive recovery period on the lactate minimum speed in sprinters and endurance runners

The objective of this study was to verify the effect of the passive recovery time following a supramaximal sprint exercise and the incremental exercise test on the lactate minimum speed (LMS). Thirteen sprinters and 12 endurance runners performed the following tests: 1) a maximal 500 m sprint followed by a passive recovery to determine the time to reach the peak blood lactate concentration; 2) after the maximal 500 m sprint, the athletes rested eight mins, and then performed 6 x 800 m incremental test, in order to determine the speed corresponding to the lower blood lactate concentration (LMS1) and; 3) identical procedures of the LMS1, differing only in the passive rest time, that was performed in accordance with the time to peak lactate (LMS2). The time (min) to reach the peak blood lactate concentration was significantly higher in the sprinters (12.76+/-2.83) than in the endurance runners (10.25+/-3.01). There was no significant difference between LMS1 and LMS2, for both endurance (285.7+/-19.9; 283.9+/-17.8 m/min; r= 0.96) and sprint runners (238.0+/-14.1; 239.4+/-13.9 m/min; r= 0.93), respectively. We can conclude that the LMS is not influenced by a passive recovery period longer than eight mins (adjusted according with the time to peak blood lactate), although blood lactate concentration may differ at this speed. The predominant type of training (aerobic or anaerobic) of the athletes does not seem to influence the phenomenon previously described.

Blood glucose responses in humans mirror lactate responses for individual anaerobic threshold and for lactate minimum in track tests

The equilibrium point between blood lactate production and removal (La-min(-)) and the individual anaerobic threshold (IAT) protocols have been used to evaluate exercise. During progressive exercise, blood lactate [La-](b), catecholamine and cortisol concentrations, show exponential increases at upper anaerobic threshold intensities. Since these hormones enhance blood glucose concentrations [Glc](b), this study investigated the [Glc] and [La-](b) responses during incremental tests and the possibility of considering the individual glucose threshold (IGT) and glucose minimum;(Glc(min)) in addition to IAT and La-min(-) in evaluating exercise. A group of 15 male endurance runners ran in four tests on the track 3000 m run (v(3km)); IAT and IGT- 8 x 800 m runs at velocities between 84% and 102% of v(3km); La-min(-) and Glc(min) - after lactic acidosis induced by a 500-m sprint, the subjects ran 8 x 800 m at intensities between 87% and 97% of v(3km); endurance test (ET)- 30 min at the velocity of IAT. Capillary blood (25 mu l) was collected for [La-](b) and [Glc](b) measurements. The TAT and IGT were determined by [La-](b) and [Glc](b) kinetics during the second test. The La-min(-) and Glc(min) were determined considering the lowest [La-] and [Glc](b) during the third test. No differences were observed (P < 0.05) and high correlations were obtained between the velocities at IAT [283 (SD 19) and IGT 281 (SD 21)m. min(-1); r = 0.096; P < 0.001] and between La,, [285 (SD 21)] and Glc(min) [287 (SD 20) m. min(-1) = 0.77; P < 0.05]. During ET, the [La-](b) reached 5.0 (SD 1.1) and 5.3 (SD 1.0) mmol 1(-1) at 20 and 30 min, respectively (P > 0.05). We concluded that for these subjects it was possible to evaluate the aerobic capacity by IGT and Glc(min), as well as by IAT and La-min(-).

Relationships and significance of lactate minimum, critical velocity, heart rate deflection and 3 000 m track-tests for running

The running velocities associated to lactate minimum (V-lm), heart rate deflection (V-HRd), critical velocity (CV), 3000 M (V-3000) and 10000 m performance (V-10km) were compared. Additionally the ability of V-lm and VHRd on identifying sustainable velocities was investigated.Methods. Twenty runners (28.5 +/- 5.9 y) performed 1) 3000 m running test for V3000; 2) an all-out 500 in sprint followed by 6x800 m incremental bouts with blood lactate ([lac]) measurements for V-lm; 3) a continuous velocity-incremented test with heart rate measurements at each 200 m for V-HRd; 4) participants attempted to 30 min of endurance test both at V-lm(ETVlm) and V-HRd(ETVHRd). Additionally, the distance-time and velocity-1/time relationships produced CV by 2 (500 m and 3000 m) or 3 predictive trials (500 m, 3000 m and distance reached before exhaustion during ETVHRd), and a 10 km race was recorded for V-10km.Results. The CV identified by different methods did not differ to each other. The results (m(.)min(-1)) revealed that V-.(lm) (281 +/- 14.8)< CV (292.1 +/- 17.5)=V-10km (291.7 +/- 19.3)< V-HRd (300.8 +/- 18.7)=V-3000 (304 +/- 17.5) with high correlation among parameters (P < 0.001). During ETVlm participants completed 30 min of running while on the ETVHRd they lasted only 12.5 +/- 8.2 min with increasing [lac].Conclusion. We evidenced that CV and Vim track-protocols are valid for running evaluation and performance prediction and the parameters studied have different significance. The V-lm reflects the moderate-high intensity domain (below CV), can be sustained without [lac] accumulation and may be used for long-term exercise while the V-HRd overestimates a running intensity that can be sustained for long-time. Additionally, V-3000 and V-HRd reflect the severe intensity domain (above CV).

Minimum blood lactate and muscle protein of rats during swimming exercise

Few studies dealing with effort intensity during swimming exercise in rats have been reported in the literature. Recently, with the use of the lactate minimum test (LMT), our group estimated the minimum blood lactate (MBL) of rats during swimming exercises. This information allowed accurate evaluation of the effort intensity developed by rats during swimming exercise. The present study was designed to evaluate the effects of swimming exercise sessions in below, equivalent and above intensities to MBL, on protein metabolism of rats. Adult (90 days) sedentary male Wistar rats were used in the present study. Mean values of MBL, in the present study, were obtained at blood concentration of 6.7 +/- 0.4 mmol/L with a load of 5% bw. The animals were sacrificed at rest (R) or immediately after a single swimming session (30 min) supporting loads below (3.5% bw), equivalent (5.0% bw) and high load (6.5% bw) to AT. Blood samples were collected each 5 min of exercise for lactate determination. Soleus muscle protein synthesis (amount of L-[C-14] fenil alanyn incorporation to protein) and breakdown (tyrosin release) rates were evaluated. Blood lactate concentrations (mmol/L) stabilized with the below (5.4 +/- 0.01) and equivalent (6.4 +/- 0.006) to MBL but increased, progressively, with the high load. There were no differences in protein synthesis (pmol/mg.h) among rest values (65.2 +/- 3.4) and after-exercise supporting the loads below (61.5 +/- 1.3) and the equivalent (60.7+/-1.7) to MBL but there was a decrease with the high load (36.6+/-2.0). Protein breakdown rates (pmol/g.h) increase after exercise supporting the loads below (227.0 +/- 6.1), equivalent (227.9 +/- 6.0) and high (363.6 +/- 7.1) to MBL in relation to the rest (214.3 +/- 6.0). The results indicate the viability of the application of LMT in studies with rats since it detected alterations imposed by exercise.

Effect of an acute β-adrenergic blockade on exercise intensity corresponding to the lactate minimum

β-Adrenoreceptor blockade is reported to impair endurance, power output and work capacity in healthy subjects and patients with hypertension. The purpose of this study was to investigate the effect in eighth athletic males of an acute β-adrenergic blockade with propranolol on their individual power output corresponding to a defined lactate minimum (LM). Eight fit males (cyclist or triathlete) performed a protocol to determine the power output corresponding to their individual LM (defined from an incremental exercise test after a rapidly induced exercise lactic acidosis). This protocol was performed twice in a double-blind randomized order by each athlete first ingesting propranolol (80mg) and in a second trial a placebo, 120 minutes respectively prior to the test sequence. The blood lactate concentration obtained 7 minutes after anaerobic exercise (a Wingate test) was significantly lower after acute β-adrenergic blockade (8.6 ± 1.6mM) than under the placebo condition (11.7 ± 1.6mM). The work rate at the LM was lowered from 215.0 ± 18.6 to 184.0 ± 18.6 watts and heart rate at the LM was reduced from 165 ± 1.5 to 132 ± 2.2 beats/minute as a result of the blockade. There was a non-significant correlation (r = 0.29) between the power output at the LM with and without acute β-adrenergic blockade. In conclusion, since the intensity corresponding to the LM is related to aerobic performance, the results of the present study, are able to explain in part, the reduction in aerobic power output produced during β-adrenergic blockade.

Comparison of the lactate minimum speed and the maximal lactate steady state to determine aerobic capacity in purebred Arabian horses

AIM: To compare five different protocols for estimating the lactate minimum speed (LMS) with that for estimating the maximal lactate steady state (MLSS) in Arabian horses, in order to obtain a more rapid method for monitoring aerobic capacity and prescribing training schedules. METHODS: Eight purebred Arabian horses were conditioned to exercise on a treadmill for 12 days then submitted to three to five exercise sessions to determine the MLSS. Blood samples were collected from a jugular catheter at specific intervals for measurement of lactate concentrations. The MLSS was the velocity maintained during the last 20 minutes of constant submaximal exercise, at which the concentration of lactate increased by no more than 1.0 mmol/L. The LMS test protocols (P1 - P5) included a warm-up period followed by a high-intensity gallop. The speed was then reduced to 4 m/s, and the incremental portion of the test was initiated. In P1, P2, and P3, the velocity increment was 0.5 m/s, and the duration of each incremental stage was three, five and seven minutes, respectively. In P4 and P5, the velocity increments were 1.0 and 1.5 m/s, respectively, and the duration of the stages was fixed at five minutes each. A second-degree polynomial function was fitted to the lactate-velocity curve, and the velocity corresponding to the lowest concentration of lactate was the LMS. RESULTS: Only the mean LMS determined by P1 and P2 did not differ from the velocity determined by the MLSS test (p > 0.1). There was a strong correlation (r >0.6) between P1 and the MLSS velocity. A limits of agreement plot revealed that the best agreement occurred between the MLSS test and P1 (mean bias = 0.14 m/s), followed by P2 (bias = -0.22 m/s). The lactate concentrations associated with the various LMS protocols did not differ. CONCLUSIONS: This study shows the variation between protocols of the LMS test for determining the onset of blood lactate accumulation but also reveals that, at least for Arabian horses, the P1 protocol of the LMS has good agreement with the MLSS. © 2013 Copyright New Zealand Veterinary Association.