Low dose of dichloroacetate infusion reduces blood lactate after submaximal exercise in horses

The acute administration of an indirect activator of the enzyme pyruvate dehydroge-nase (PDH) in human athletes causes a reduction in blood lactate level during and after exercise. A single IV dose (2.5m.kg-1) of dichloroacetate (DCA) was administered before a submaximal incremental exercise test (IET) with five velocity steps, from 5.0 m.s-1 for 1 min to 6.0, 6.5, 7.0 and 7.5m.s-1 every 30s in four untrained mares. The blood collections were done in the period after exercise, at times 1, 3, 5, 10, 15 and 20 min. Blood lactate and glucose (mM) were determined electro-enzymatically utilizing a YSI 2300 automated analyzer. There was a 15.3% decrease in mean total blood lactate determined from the values obtained at all assessment times in both trials after the exercise. There was a decrease in blood lactate 1, 3, 5, 10, 15 and 20 min after exercise for the mares that received prior DCA treatment, with respective mean values of 6.31±0.90 vs 5.81±0.50, 6.45±1.19 vs 5.58±1.06, 6.07±1.56 vs 5.26±1.12, 4.88±1.61 vs 3.95±1.00, 3.66±1.41 vs 2.86±0.75 and 2.75±0.51 vs 2.04±0.30. There was no difference in glucose concentrations. By means of linear regression analysis, V140, V160, V180 and V200 were determined (velocity at which the rate heart is 140, 160, 180, and 200 beats/minute, respectively). The velocities related to heart rate did not differ, indicating that there was no ergogenic effect, but prior administration of a relatively low dose of DCA in mares reduced lactatemia after an IET.

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(-).

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.

Effect of the aerobic capacity on the validity of the anaerobic threshold for determination of the maximal lactate steady state in cycling

The maximal lactate steady state (MLSS) is the highest blood lactate concentration that can be identified as maintaining a steady state during a prolonged submaximal constant workload. The objective of the present study was to analyze the influence of the aerobic capacity on the validity of anaerobic threshold (AT) to estimate the exercise intensity at MLSS (MLSS intensity) during cycling. Ten untrained males (UC) and 9 male endurance cyclists (EC) matched for age, weight and height performed one incremental maximal load test to determine AT and two to four 30-min constant submaximal load tests on a mechanically braked cycle ergometer to determine MLSS and MLSS intensity. AT was determined as the intensity corresponding to 3.5 mM blood lactate. MLSS intensity was defined as the highest workload at which blood lactate concentration did not increase by more than 1 mM between minutes 10 and 30 of the constant workload. MLSS intensity (EC = 282.1 ± 23.8 W; UC = 180.2 ± 24.5 W) and AT (EC = 274.8 ± 24.9 W; UC = 187.2 ± 28.0 W) were significantly higher in trained group. However, there was no significant difference in MLSS between EC (5.0 ± 1.2 mM) and UC (4.9 ± 1.7 mM). The MLSS intensity and AT were not different and significantly correlated in both groups (EC: r = 0.77; UC: r = 0.81). We conclude that MLSS and the validity of AT to estimate MLSS intensity during cycling, analyzed in a cross-sectional design (trained x sedentary), do not depend on the aerobic capacity.

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.

PHYSIOLOGICAL and PERCEIVED EXERTION RESPONSES AT INTERMITTENT CRITICAL POWER and INTERMITTENT MAXIMAL LACTATE STEADY STATE

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

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.

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).

The validity of critical speed determined from track cycling for identification of the maximal lactate steady state

The objective of this study was to determine the critical speed (CS) for track cycling and to assess whether a lactate steady state occurs at this speed. Fourteen competitive cyclists performed the following tests on an official cycling track (333.3 m): 1) incremental test for determination of the intensity corresponding to 4 mM of blood lactate (onset of blood lactate accumulation, OBLA) and maximal oxygen uptake (VO(2)max); 2) CS: 3 maximal bouts for distances of 2, 4 and 6 km executed in random order and with a period of recovery of 40 to 50 min between bouts. CS was determined for each subject from the linear regression between the distance and the time taking to cycle it; 3) Endurance test in which subjects were instructed to pedal at 100% of their individually determined CS for 30 min. At the 10(th) and 30(th) min (or upon exhaustion), 25 mul of blood were collected from ear lobe for later analysis of blood lactate [Lac]b. An increase less than or equal to1 mM between 10 and 30 min of exercise was considered as the criterion for the occurrence of the lactate steady state. CS (49.6 +/- 8.6 ml.kg(-1).min(-1); 36.9 +/- 2.7 km.h(-1)) was significantly higher than OBLA (43.7 8.0 ml.kg(-1).min(-1); 35.24 +/- 2.6 km.h(-1)) although the two parameters were highly correlated (r=0.97). During the endurance test, only 8 of the 14 subjects completed the 30 min period at CS. of these 8 subjects, only 2 presented a lactate steady state. Time to exhaustion at CS was 20.3 +/- 1.6 min for the remaining 6 subjects. The 12 subjects who did not reach a lactate steady state presented mean [Lac]b values of 7.4 +/- 1.3 mM at 10 min and of 9.4 +/- 1.9 mM at the end of the test (exhaustion), characterizing an exercise intensity of high lactacidemia. on the basis of the present results, we can conclude that CS determined by a track cycling test seems to overestimate the intensity of the maximal lactate steady state for most subjects.

Maximal lactate steady state in running mice: Effect of exercise training

1. Maximal lactate steady state (MLSS) corresponds to the highest blood lactate concentration (MLSSc) and workload (MLSSw) that can be maintained over time without continual blood lactate accumulation and is considered an important marker of endurance exercise capacity. The present study was undertaken to determine MLSSw and MLSSc in running mice. In addition, we provide an exercise training protocol for mice based on MLSSw.2. Maximal lactate steady state was determined by blood sampling during multiple sessions of constant-load exercise varying from 9 to 21 m/min in adult male C57BL/6J mice. The constant-load test lasted at least 21 min. The blood lactate concentration was analysed at rest and then at 7 min intervals during exercise.3. The MLSSw was found to be 15.1 +/- 0.7 m/min and corresponded to 60 +/- 2% of maximal speed achieved during the incremental exercise testing. Intra- and interobserver variability of MLSSc showed reproducible findings. Exercise training was performed at MLSSw over a period of 8 weeks for 1 h/day and 5 days/week. Exercise training led to resting bradycardia (21%) and increased running performance (28%). of interest, the MLSSw of trained mice was significantly higher than that in sedentary littermates (19.0 +/- 0.5 vs 14.2 +/- 0.5 m/min; P = 0.05), whereas MLSSc remained unchanged (3.0 mmol/L).4. Altogether, we provide a valid and reliable protocol to improve endurance exercise capacity in mice performed at highest workload with predominant aerobic metabolism based on MLSS assessment.

Maximal lactate steady state concentration independent of pedal cadence in active individuals

The maximal lactate steady state (MLSS) is defined as the highest blood lactate concentration that can be maintained over time without a continual blood lactate accumulation. The objective of the present study was to analyze the effects of pedal cadence (50 vs. 100 rev min(-1)) on MLSS and the exercise workload at MLSS (MLSSworkload) during cycling. Nine recreationally active males (20.9 +/- 2.9 years, 73.9 +/- 6.5 kg, 1.79 +/- 0.09 m) performed an incremental maximal load test (50 and 100 rev min(-1)) to determine anaerobic threshold (AT) and peak workload (PW), and between two and four constant submaximal load tests (50 and 100 rev min(-1)) on a mechanically braked cycle ergometer to determine MLSSworkload and MLSS. MLSSworkload was defined as the highest workload at which blood lactate concentration did not increase by more than 1 mM between minutes 10 and 30 of the constant workload. The maximal lactate steady state intensity (MLSSintensity) was defined as the ratio between MLSSworkload and PW. MLSSworkload (186.1 +/- 21.2 W vs. 148.2 +/- 15.5 W) and MLSSintensity (70.5 +/- 5.7% vs. 61.4 +/- 5.1%) were significantly higher during cycling at 50 rev min(-1) than at 100 rev min(-1), respectively. However, there was no significant difference in MLSS between 50 rev min(-1) (4.8 +/- 1.6 mM) and 100 rev min(-1) (4.7 +/- 0.8 mM). We conclude that MLSSworkload and MLSSintensity are dependent on pedal cadence (50 vs. 100 rev min(-1)) in recreationally active individuals. However, this study showed that MLSS is not influenced by the different pedal cadences analyzed.

MAXIMAL LACTATE STEADY-STATE INDEPENDENT of RECOVERY PERIOD DURING INTERMITTENT PROTOCOL

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Influence of exercise mode and maximal lactate-steady-state concentration on the validity of OBLA to predict maximal lactate-steady-state in active individuals

The aim of this study was to analyze the effects of exercise mode on the validity of onset of blood lactate accumulation (OBLA-3.5-mM fixed blood lactate concentration) to predict the work-rate at maximal lactate steady state (MLSSwork-rate). Eleven recreationally active mates (21.3 +/- 2.9 years, 72.8 +/- 6.7 kg, 1.78 +/- 0.1 m) performed randomly incremental tests to determine OBLA (stage duration of 3 min), and 2 to 4 constants work-rate exercise tests to directly determine maximal lactate steady state parameters on a cycle-ergometer and treadmill. For both exercise modes, the OBLA was significantly correlated to MLSSwork-rate, (cycling: r = 0.81 p = 0.002; running: r = 0.94, p < 0.001). OBLA (156.2 +/- 41.3 W) was lower than MLSSwork-rate (179.6 +/- 26.4 W) during cycling exercise (p = 0.007). However, for running exercise, there was no difference between OBLA (3.2 +/- 0.6 m s(-1)) and MLSSwork-rate (3.1 +/- 0.4 m s(-1)). The difference between OBLA and MLSSworkrate on the cycle-ergometer (r = 0.86; p < 0.001) and treadmill (r = 0.64; p = 0.048) was significantly related to the specific MLSS. We can conclude that the validity of OBLA on predicting MLSSwork-rate is dependent on exercise mode and that its disagreement is related to individual variations in MLSS. (C) 2007 Sports Medicine Australia. Published by Elsevier Ltd. All rights reserved.

Is maximal lactate steady state during intermittent cycling different for active compared with passive recovery?

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

A kinetic model of phosphorus metabolism in growing goats

The effect of increasing phosphorus (P) intake on P utilization was investigated in balance experiments using 12 Saanen goats, 4 to 5 mo of age and weighing 20 to 30 kg. The goats were given similar diets with various concentrations of P, and 32P was injected to trace the movement of P in the body. A P metabolism model with four pools was developed to compute P exchanges in the system. The results showed that P absorption, bone resorption, and excretion of urinary P and endogenous and fecal P all play a part in the homeostatic control of P. Endogenous fecal output was positively correlated to P intake (P < .01). Bone resorption of P was not influenced by intake of P, and P recycling from tissues to the blood pool was lesser for low P intake. Endogenous P loss occurred even in animals fed an inadequate P diet, resulting in a negative P balance. The extrapolated minimum endogenous loss in feces was .067 g of P/d. The minimum P intake for maintenance in Saanen goats was calculated to be .61 g of P/ d or .055 g of P/(kg.75·d) at 25 kg BW. Model outputs indicate greater P flow from the blood pool to the gut and vice versa as P intake increased. Intake of P did not significantly affect P flow from bone and soft tissue to blood. The kinetic model and regressions could be used to estimate P requirement and the fate of P in goats and could also be extrapolated to both sheep and cattle.