Determination of the anaerobic threshold and maximal lactate steady state speed in equines using the lactate minimum speed protocol

Maximal blood lactate steady state concentration (MLSS) and anaerobic threshold (AT) have been shown to accurately predict long distance events performance and training loads, as well, in human athletes. Horse endurance races can take up to 160 km and, in practice, coaches use the 4 mM blood lactate concentration, a human based fixed concentration to establish AT, to predict training loads to horse athletes, what can lead to misleading training loads. The lactate minimum speed (LMS) protocol that consists in an initial elevation in blood lactate level by a high intensity bout of exercise and then establishes an individual equilibrium between lactate production and catabolism during progressive submaximal efforts, has been proposed as a nonfixed lactate concentration, to measure individual AT and at the same time predicts MLSS for human long distance runners and basketball players as well. The purpose of this study was to determine the reliability of the LMS protocol in endurance horse athletes. Five male horses that were engaged on endurance training, for at least 1 year of regular training and competition, were used in this study. Animals were submitted to a 500 m full gallop to determine each blood lactate time to peak (LP) after these determinations, animals were submitted to a progressive 1000 m exercise, starting at 15 km h(-1) to determine LMS, and after LMS determination animals were also submitted to two 10,000 m running, first at LMS and then 10% above LMS to test MLSS accuracy. Mean LP was 8.2+/-0.7 mM at approximately 5.8+/-6.09 min, mean LMS was 20.75+/-2.06 km h(-1) and mean heart rate at LMS was 124.8+/-4.7 BPM. Blood lactate remained at rest baseline levels during 10,000 m trial at LMS, but reached a six fold significantly raise during 10% above LMS trial after 4000 and 6000 m (p<0.05) and (p<0.01) after 8000 and 10,000 m. In conclusion, our adapted LMS protocol for horse athletes proposed here seems to be a reliable method to state endurance horse athletes LT and MLSS.     

Comparison of blood and saliva lactate level after maximum intensity exercise

Several studies have described high correlation of salivary and blood lactate level during exercise. Measuring the effectiveness and intensity of training, lactate concentration in blood, and lately in saliva are used.The aim of our study was to evaluate the correlation between the concentration and timing of salivary and blood lactate level in endurance athletes and non-athletes after a maximal treadmill test, and to identify physiological and biochemical factors affecting these lactate levels.Sixteen volunteers (8 athletes and 8 non-athletes) performed maximal intensity (Astrand) treadmill test. Anthropometric characteristics, body composition and physiological parameters (heart rate, RR-variability) were measured in both studied groups. Blood and whole saliva samples were collected before and 1, 4, 8, 12, 15, 20 min after the exercise test. Lactate level changes were monitored in the two groups and two lactate peaks were registered at different timeperiods in athletes. We found significant correlation between several measured parameters (salivary lactate - total body water, salivary lactate - RR-variability, maximal salivary lactate - maximal heart rate during exercise, salivary- and blood lactate -1 min after exercise test). Stronger correlation was noted between salivary lactate and blood lactate in athletes, than in controls.     

The relationship between selected blood lactate thresholds and match performance in elite soccer referees

The aim of this study was to examine the relationship between selected blood lactate thresholds and competitive match activities in elite soccer referees. Eight elite-level referees (mean age, 37.6 +/- 3.4 years) were each observed during 2 Serie A matches (n = 16), and the mean of each match activity was used for analysis. Match activities were monitored using a technology similar to that reported by Ohashi and others. Blood lactate thresholds were assessed under field conditions during a progressive multistage protocol. Running velocities attained at selected blood lactate concentrations (2 and 4 mmol x L(-1), V2 and V4, respectively) were chosen because these are commonly used to assess endurance performance. Analyses of correlations were performed considering V2 and V4 values as independent variables and total distance, maximal velocity distance (runs performed at velocities faster than 24 km x h(-1)) and high-intensity activity distance (runs performed at velocities faster than 18 km x h(-1)) as dependent variables. Significance was set at p 相似文献   

Plasma LDH and CK activities after 400 m sprinting by well-trained sprint runners

Blood lactate concentration and the activities of plasma LDH and CK were determined in 13 well-trained middle distance runners after a 400-m sprint. It was found that there is a significant relationship between mean velocity in the 400-m sprint and plasma CK activity (r = -0.56, P less than 0.05), but the mean sprint velocity did not correlate with peak blood lactate concentration (r = -0.09) or plasma LDH activity (r = -0.40). There was a significant negative correlation between mean sprint velocity and H type LDH isozyme activity (r = -0.66, P less than 0.05), and a significant positive correlation with M type LDH isozyme activity (r = 0.66, P less than 0.05). These results suggest that the magnitude of enzyme efflux from tissue into blood may be depressed by training, and that in well-trained sprinters plasma CK and LDH isozyme activities may be better indicators of physical training and/or physical performance than peak blood lactate or plasma LDH activities.     

The relationship of plasma ammonia and lactate concentrations to perceived exertion in trained and untrained women

The purpose of this study was to investigate the covariance between perceived exertion (recorded using Borg's category-ratio scale CR-10) and the relative oxygen uptake, and lactate and ammonia concentrations in blood from a peripheral vein. Ratings of perceived exertion (RPE) at 25%, 50%, 75% and 90% maximal oxygen uptake and lactate and ammonia concentrations were compared in well-trained women distance runners (n = 22) and untrained women (n = 10). Ammonia concentrations in peripheral venous blood were significantly correlated with RPE (P less than 0.05), both in the trained and untrained women. Differences between the trained and untrained subjects occurred when the ammonia concentration increased to 148 mumol.l-1 in both groups investigated; similarly, the mean RPE correlated significantly with the lactate concentration (P less than 0.05), both in the trained and untrained women and there was a difference in RPE between groups when lactate concentration in the blood had risen to 4.4 mmol.l-1. It would seem that the correlation of blood ammonia and lactate concentrations with RPE during exercise could be a useful indicator of the development of fatigue.     

Blood lactate changes during isocapnic buffering in sprinters and long distance runners

This study was carried out to compare blood lactate changes in isocapnic buffering phase in an incremental exercise test between sprinters and long distance runners, and to seek the possibility for predicting aerobic or anaerobic potential from blood lactate changes in isocapnic buffering phase. Gas exchange variables and blood lactate concentration ([lactate]) in six sprinters (SPR) and nine long distance runners (LDR) were measured during an incremental exercise test (30 W.min-1) up to subject's voluntary exhaustion on a cycle ergometer. Using a difference between [lactate] at lactate threshold (LT) and [lactate] at the onset of respiratory compensation phase (RCP) and the peak value of [lactate] obtained during a recovery period from the end of the exercise test, the relative increase in [lactate] during the isocapnic buffering phase ([lactate]ICBP) was assessed. The [lactate] at LT (mean +/- SD) was similar in both groups (1.36 +/- 0.27 for SPR vs. 1.24 +/- 0.24 mmol.l-1 for LDR), while the [lactate] at RCP and the peak value of [lactate] were found to be significantly higher in SPR than in LDR (3.61 +/- 0.33 vs. 2.36 +/- 0.45 mmol.l-1 for RCP, P < 0.001, 10.18 +/- 1.53 vs. 8.10 +/- 1.61 mmol.l-1 for peak, P < 0.05). The [lactate]ICBP showed a significantly higher value in SPR (22.5 +/- 5.9%, P < 0.05) compared to that in LDR (14.2 +/- 5.0%) as a result of a twofold greater increase of [lactate] from LT to RCP (2.25 +/- 0.49 for SPR vs. 1.12 +/- 0.39 mmol.l-1 for LDR). In addition, the [lactate]ICBP inversely correlated with oxygen uptake at LT (VO2LT, r = -0.582, P < 0.05) and maximal oxygen uptake (VO2max, r = -0.644, P < 0.01). The results indicate that the [lactate]ICBP is likely to give an index for the integrated metabolic, respiratory and buffering responses at the initial stage of metabolic acidosis derived from lactate accumulation.     

The relationship between onset of blood lactate accumulation, critical velocity, and maximal lactate steady state in soccer players

The objective of this study was to analyze the validity of the velocity corresponding to the onset of blood lactate accumulation (OBLA) and critical velocity (CV) to determine the maximal lactate steady state (MLSS) in soccer players. Twelve male soccer players (21.5 +/- 1.0 years) performed an incremental treadmill test for the determination of OBLA. The velocity corresponding to OBLA (3.5 mM of blood lactate) was determined through linear interpolation. The subjects returned to the laboratory on 7 occasions for the determination of MLSS and CV. The MLSS was determined from 5 treadmill runs of up to 30-minute duration and defined as the highest velocity at which blood lactate did not increase by more than 1 mM between minutes 10 and 30 of the constant velocity runs. The CV was determined by 2 maximal running efforts of 1,500 and 3,000 m performed on a 400-m running track. The CV was calculated as the slope of the linear regression of distance run versus time. Analysis of variance revealed no significant differences between OBLA (13.6 +/- 1.4 km.h(-1)) and MLSS (13.1 +/- 1.2 km.h(-1)) and between OBLA and CV (14.4 +/- 1.1 km.h(-1)). The CV was significantly higher than the MLSS. There was a significant correlation between MLSS and OBLA (r = 0.80), MLSS and CV (r = 0.90), and OBLA and CV (r = 0.80). We can conclude that the OBLA can be utilized in soccer players to estimate the MLSS. In this group of athletes, however, CV does not represent a sustainable steady-state exercise intensity.     

Relationship between uphill running performance at altitude and blood metabolite levels

Venous blood samples were obtained from 18 marathon runners before and after the 27 km uphill portion of a 46 km transmountain race at altitudes of 1,950-3,400 m. There was an inverse correlation between blood lactate levels and running time (r = -0.83), with the runners with higher lactate levels completing the race in less time. The faster half of the group had higher blood levels of glucose and lactate and lower free fatty acid levels at 26 km distance and 3,400 m elevation. The elevated lactate concentrations in the blood of the faster runners suggest that anaerobic metabolism can contribute significantly to total energy production during prolonged exercise at high altitude.     

Blood lactate and ammonium ion accumulation during graded exercise in humans

The purpose of this study was to determine the pattern of blood lactate and ammonium ion (NH+4) accumulation during graded exercise in humans. Six adult volunteers performed a maximum O2 uptake (VO2 max) test on a bicycle ergometer. Blood samples were collected each minute of the test. Both blood lactate (r = 0.92) and NH4+ (r = 0.70) increased exponentially in relation to increased work. However, closer examination of individual curves revealed that both metabolites remained near resting levels during mild exercise (less than 40% VO2 max) and then demonstrated abrupt upward break points at increased work loads (greater than 50% VO2 max). There was a significant linear relationship (r = 0.96) between the work load at which the lactate break point (LBP) and NH4+ break point (ABP) occurred in each subject. In addition, there was a significant linear relationship (r = 0.82) between the blood concentrations of NH4+ and lactate during exercise. The results suggest a connection between NH4+ production and glycolytic energy metabolism during exercise. Several possible explanations are offered; however, further work at the cellular level is needed before the exact relationship between NH4+ and lactate can be determined.     

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 (v3km); IAT and IGT - 8 x 800 m runs at velocities between 84% and 102% of v3km; La-(min) and Glc(min) - after lactic acidosis induced by a 500-m sprint, the subjects ran 6 x 800 m at intensities between 87% and 97% of v3km; endurance test (ET) - 30 min at the velocity of IAT. Capillary blood (25 microl) was collected for [La-]b and [Glc]b measurements. The IAT 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. x min(-1); r = 0.096; P < 0.001] and between La-(min) [285 (SD 21)] and Glc(min) [287 (SD 20) m. x min(-1) r = 0.77; P < 0.05]. During ET, the [La-]b reached 5.0 (SD 1.1) and 5.3 (SD 1.0) mmol x l(-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).     

Cardiovascular reflexes during sustained handgrip exercise: role of muscle fibre composition, potassium and lactate

Six healthy men performed sustained static handgrip exercise for 2 min at 40% maximal voluntary contraction followed by a 6-min recovery period. Heart rate (fc), arterial blood pressures, and forearm blood flow were measured during rest, exercise, and recovery. Potassium ([K+]) and lactate concentrations in blood from a deep forearm vein were analysed at rest and during recovery. Mean arterial pressure (MAP) and fc declined immediately after exercise and had returned to control levels about 2 min into recovery. The time course of the changes in MAP observed during recovery closely paralleled the changes in [K+] (r = 0.800, P < 0.01), whereas the lactate concentration remained elevated throughout the recovery period. The close relationship between MAP and [K+] was also confirmed by experiments in which a 3-min arterial occlusion period was applied during recovery to the exercised arm by an upper arm cuff. The arterial occlusion affected MAP while fc recovered at almost the same rate as in the control experiment. Muscle biopsies were taken from the brachioradialis muscle and analysed for fibre composition and capillary supply. The MAP at the end of static contraction and the [K+] appearing in the effluent blood immediately after contraction were positively correlated to the relative content of fast twitch (% FT) fibres (r = 0.886 for MAP vs % FT fibres, P < 0.05 and r = 0.878 for [K+] vs % FT fibres, P < 0.05). Capillary to fibre ratio showed an inverse correlation to % FT fibres (r = -0.979, P < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

Electro-mechanical failures and lactate production during fatigue

The electrical and mechanical failures observed during sustained and intermittent electrically triggered (30 Hz) contractions of human flexor carpi ulnaris were compared with the blood lactate concentration. The changes recorded during contractions sustained for 60 s were compared with those observed during a series of sixty 1 s contractions separated by 1 s intervals, and also with the changes during the first 30 min of recovery. No significant (P less than 0.05) difference in force reduction or maximal venous lactate concentration was observed in either fatigue test, although electrical failure differed significantly (P less than 0.05). The recovery of electrical failure was poorly correlated with the reduction in lactate concentration following both sustained (r = -0.70) and intermittent contractions (r = 0.72). In contrast, the recovery in tetanic tension, rate of tension development and time to half relaxation correlated closely with the reduction in venous lactate concentration (r = -0.95, -0.93 and 0.96 respectively). It is suggested that, of the peripheral processes which appear to play a dominant role in peripheral fatigue, lactate production controls mechanical failure directly.     

Disposal of blood [1-13C]lactate in humans during rest and exercise

Lactate irreversible disposal (RiLa) and oxidation (RoxLa) rates were studied in six male subjects during rest (Re), easy exercise [EE, 140 min of cycling at 50% of maximum O2 consumption (VO2max)] and hard exercise (HE, 65 min at 75% VO2max). Twenty minutes into each condition, subjects received a Na+-L(+)-[1-13C]lactate intravenous bolus injection. Blood was sampled intermittently from the contralateral arm for metabolite levels, acid-base status, and enrichment of 13C in lactate. Expired air was monitored continuously for determination of respiratory parameters, and aliquots were collected for determination of 13C enrichment in CO2. Steady-rate values for O2 consumption (VO2) were 0.33 +/- 0.01, 2.11 +/- 0.03, and 3.10 +/- 0.03 l/min for Re, EE, and HE, respectively. Corresponding values of blood lactate levels were 0.84 +/- 0.01, 1.33 +/- 0.05, and 4.75 +/- 0.28 mM in the three conditions. Blood lactate disposal rates were significantly correlated to VO2 (r = 0.78), averaging 123.4 +/- 20.7, 245.5 +/- 40.3, and 316.2 +/- 53.7 mg X kg-1 X h-1 during Re, EE, and HE, respectively. Lactate oxidation rate was also linearly related to VO2 (r = 0.81), and the percentage of RiLa oxidized increased from 49.3% at rest to 87.0% during exercise. A curvilinear relationship was found between RiLa and blood lactate concentration. It was concluded that, in humans, 1) lactate disposal (turnover) rate is directly related to the metabolic rate, 2) oxidation is the major fate of lactate removal during exercise, and 3) blood lactate concentration is not an accurate indicator of lactate disposal and oxidation.     

Effect of expertise on postmaximal long sprint blood metabolite responses

The aim of this study was to describe and compare the blood metabolic responses obtained after a single maximal exercise in elite and less-successful athletes and to investigate whether these responses are related to sprint performance. Eleven elite (ELI) and 14 regional (REG) long sprint runners performed a 300-m running test as fast as possible. Blood samples were taken at rest and at 4 minutes after exercise for measurements of blood lactate concentration [La] and acid-base status. The blood metabolic responses of ELI subjects compared to those of REG subjects for pH (7.07 ± 0.05 vs. 7.14 ± 1.5), sodium bicarbonate concentration ([HCO(3)(-)], 8.1 ± 1.5 vs. 9.8 ± 1.8 mmol·L(-1)), hemoglobin O(2) saturation (SaO(2)) (94.7 ± 1.8 vs. 96.2 ± 1.6%) were significantly lower (p < 0.05), and [La] was significantly higher in ELI (21.1 ± 2.9 vs. 19.1 ± 1.2 mmol·L(-1), p < 0.05). The 300-m performance (in % world record) was negatively correlated with pH (r = -0.55, p < 0.01), SaO2 (r = -0.64, p < 0.001), [HCO(3)(-)] (r = -0.40, p < 0.05), and positively correlated with [La] (r = 0.44, p < 0.05). In conclusion, for the same quantity of work, the best athletes are able to strongly alter their blood acid-base balance compared to underperforming runners, with larger acidosis and lactate accumulation. To obtain the pH limits with acute maximal exercise, coaches must have their athletes perform a distance run with duration of exercise superior to 35 seconds. The blood lactate accumulation values (mmol·L(-1)·s(-1)) recorded in this study indicate that the maximal glycolysis rate obtained in the literature from short sprint distances is maintained, but not increased, until 35 seconds of exercise.     

Lactate extraction during net lactate release in legs of humans during exercise

Lactate metabolism was studied in six normal males using a primed continuous infusion of lactate tracer during continuous graded supine cycle ergometer exercise. Subjects exercised at 49, 98, 147, and 196 W for 6 min at each work load. Blood was sampled from the brachial artery, the iliac vein, and the brachial vein. Arteriovenous differences were determined for chemical lactate concentration and L-[1-14C]-lactate. Tracer-measured lactate extraction was determined from the decrease in lactate radioactivity per volume of blood perfusing the tissue bed. Net lactate release was determined from the change in lactate concentration across the tissue bed. Total lactate release was taken as the sum of tracer-measured lactate extraction and net (chemical) release. At rest the arms and legs showed tracer-measured lactate extraction, as determined from the isotope extraction, despite net chemical release. Exercise elicited an increase in both net lactate release and tracer-measured lactate extraction by the legs. For the legs the total lactate release (net lactate release + tracer-measured lactate extraction) was roughly equal to twice the net lactate release under all conditions. The tracer-measured lactate extraction by the exercising legs was positively correlated to arterial lactate concentration (r = 0.81, P less than 0.001) at the lower two power outputs. The arms showed net lactate extraction during exercise, which was correlated to the arterial concentration (r = 0.86). The results demonstrate that exercising skeletal muscle extracts a significant amount of lactate during net lactate release and that the working skeletal muscle appears to be a major site of blood lactate removal during exercise.     

Physiological changes in hemostasis associated with acute exercise

Acute exercise enhances fibrinolytic (FA), factor VIII coagulant and factor VIII ristocetin cofactor activities, and increases the concentration of factor VIII-related antigen. Little is known concerning the mechanisms of these changes. To investigate possible relationships between exercise-induced changes in blood lactate, 2,3-diphosphoglycerate (DPG), and the hemostatic variables, a branching multistage treadmill protocol was used to exercise male volunteers to a maximum effort. Blood samples were drawn before, immediately post-, and 8 min postexercise. All hemostatic variables were significantly (P less than 0.05) increased postexercise. Highest values for factor VIII coagulant, factor VIII-related antigens and factor VIII ristocetin cofactor were observed at 8 min postexercise. Significant (P less than 0.001) correlations were found postexercise for lactate with factor VIII coagulant (r = 0.64), while no association between pre-, post-, or 8 min postexercise. Postexercise lactate demonstrated a significant correlation (r = +0.81), which was strengthened by including the preexercise high-density lipoprotein (HDL) concentrations (r = +0.87). Consequently, the expected postexercise FA may be calculated from the observed values for postexercise lactate and preexercise HDL. The correlations of lactate with postexercise FA and with postexercise factor VIII coagulant may reflect a common stimulus for these exercise-induced changes.     

Anaerobic threshold and maximal steady-state blood lactate in prepubertal boys

To elucidate further the special nature of anaerobic threshold in children, 11 boys, mean age 12.1 years (range 11.4-12.5 years), were investigated during treadmill running. Oxygen uptake, including maximal oxygen uptake (VO2max), ventilation and the "ventilatory anaerobic threshold" were determined during incremental exercise, with determination of maximal blood lactate following exercise. Within 2 weeks following this test four runs of 16-min duration were performed at a constant speed, starting with a speed corresponding to about 75% of VO2max and increasing it during the next run by 0.5 or 1.0 km.h-1 according to the blood lactate concentrations in the previous run, in order to determine maximal steady-state blood lactate concentration. Blood lactate was determined at the end of every 4-min period. "Anaerobic threshold" was calculated from the increase in concentration of blood lactate obtained at the end of the runs at constant speed. The mean maximal steady-state blood lactate concentration was 5.0 mmol.l-1 corresponding to 88% of the aerobic power, whereas the mean value of the conventional "anaerobic threshold" was only 2.6 mmol.l-1, which corresponded to 78% of the VO2max. The correlations between the parameters of "anaerobic threshold", "ventilatory anaerobic threshold" and maximal steady-state blood lactate were only poor. Our results demonstrated that, in the children tested, the point at which a steeper increase in lactate concentrations during progressive work occurred did not correspond to the true anaerobic threshold, i.e. the exercise intensity above which a continuous increase in lactate concentration occurs at a constant exercise intensity.     

Criterion and longitudinal validity of a fixed-distance incremental running test for the determination of lactate thresholds in field settings

The aim of this study was to examine the criterion validity of 2 lactate thresholds (LTs, intensity corresponding to 1 mmol·L(-1) above baseline; onset of blood lactate accumulation, intensity at 4 mmol·L(-1)) determined with a fixed-distance incremental field test by assessing their correlation with those obtained using a traditional fixed-time laboratory protocol. A second aim was to verify the longitudinal validity by examining the relationships between the changes in LTs obtained with the 2 protocols. To determine the LTs, 12 well-trained male middle and long distance amateur and competitive runners training from 4 to 7 d·wk(-1) (age 25 [5] years, body mass 66 [5] kg, estimated VO(2)max 58.6 [4.9] ml·min(-1)·kg(-1), SD in parentheses) performed in 2 separate sessions an incremental running test on the field starting at 12 km·h(-1) and increasing the speed by 1 km·h(-1) every 1,200 m (FixD test) and an incremental treadmill test in the laboratory starting at 12 km·h(-1) and increasing the speed by 1 km·h(-1) every 6 minutes. The 2 tests were repeated after 6-12 weeks. A nearly perfect relationship was found between the running speeds at LTs determined with the 2 protocols (r = 0.95 [CI95% 0.83-0.99]; p < 0.001). The correlations between longitudinal changes in LTs were very large (0.78 [0.32-0.95; p = 0.006]). The heart rate corresponding to the LTs were not significantly different. This study showed the criterion and longitudinal validity of LTs determined with a protocol consisting of fixed-distance intervals performed in field setting.     

Monocarboxylate transporters, blood lactate removal after supramaximal exercise, and fatigue indexes in humans.

The present study investigated whether muscular monocarboxylate transporter (MCT) 1 and 4 contents are related to the blood lactate removal after supramaximal exercise, fatigue indexes measured during different supramaximal exercises, and muscle oxidative parameters in 15 humans with different training status. Lactate recovery curves were obtained after a 1-min all-out exercise. A biexponential time function was then used to determine the velocity constant of the slow phase (gamma(2)), which denoted the blood lactate removal ability. Fatigue indexes were calculated during 1-min all-out (FI(AO)) and repeated 10-s (FI(Sprint)) cycling sprints. Biopsies were taken from the vastus lateralis muscle. MCT1 and MCT4 contents were quantified by Western blots, and maximal muscle oxidative capacity (V(max)) was evaluated with pyruvate + malate and glutamate + malate as substrates. The results showed that the blood lactate removal ability (i.e., gamma(2)) after a 1-min all-out test was significantly related to MCT1 content (r = 0.70, P < 0.01) but not to MCT4 (r = 0.50, P > 0.05). However, greater MCT1 and MCT4 contents were negatively related with a reduction of blood lactate concentration at the end of 1-min all-out exercise (r = -0.56, and r = -0.61, P < 0.05, respectively). Among skeletal muscle oxidative indexes, we only found a relationship between MCT1 and glutamate + malate V(max) (r = 0.63, P < 0.05). Furthermore, MCT1 content, but not MCT4, was inversely related to FI(AO) (r = -0.54, P < 0.05) and FI(Sprint) (r = -0.58, P < 0.05). We concluded that skeletal muscle MCT1 expression was associated with the velocity constant of net blood lactate removal after a 1-min all-out test and with the fatigue indexes. It is proposed that MCT1 expression may be important for blood lactate removal after supramaximal exercise based on the existence of lactate shuttles and, in turn, in favor of a better tolerance to muscle fatigue.     

Nitric oxide synthase activity in blood vessels of spontaneously hypertensive rats: antioxidant protection by gamma-tocotrienol.

Involvement of free radicals and nitric oxide (NO) has long been implicated to the pathogenesis of essential hypertension. Several studies using antioxidants as the radical scavenger have shown to confer protection against free radical mediated diseases. This study is designed to investigate the role of antioxidant gamma-tocotrienol on endothelial nitric oxide synthase (NOS) activity in spontaneously hypertensive rats (SHR). SHR's were divided into four groups namely untreated SHR (HC), treatment with 15 mg gamma-tocotrienol/kg diet (gammal), 30 mg gamma-tocotrienol/kg diet (gamma2) and 150 mg gamma-tocotrienol/kg diet (gamma3) and studied for three months. Wister Kyoto (WKY) rats were used as the control (C). Blood pressure was recorded every fortnightly by tail plethysmography. Animals were sacrificed and NOS activity in blood vessels was measured by [3H]arginine radioactive assay. Nitrite concentration in plasma was determined by Greis assay and lipid peroxides in the blood vessels by spectrofluorometry. This study showed that gamma-tocotrienol significantly reduced systolic blood pressure (SBP) in SHRs with a maximum reduction in group treated with gamma-tocotrienol 15 mg/kg diet (HC: 210 +/- 9 mmHg, gammal:123 +/- 19 mmHg). Blood vessels from untreated SHR showed a reduced NOS activity compare to that of WKY rats (C: 1.54 +/- 0.26 pmol/mg protein, HC: 0.87 +/- 0.23 pmol/mg protein; p<0.001). Gamma-tocotrienol improves NOS activity in all the groups with more significance in group gamma2 (p<0.001) and gamma3 (p<0.05). Plasma level of nitrite was reduced in SHR from 55 +/- 3 microM/ml in WKY to 26+/-2 muM/ml (p<0.001). Plasma nitrite level was reversed by treatment with gamma-tocotrienol. (gammal: p<0.001, gamma2: p<0.005, gamma3: p<0.001, respectively). In all the treatment groups, NOS activity showed significant negative correlation with blood pressure (gammal: r=-0.716, p<0.05; gamma2: r=-0.709, p<0.05; gamma3: r=-0.789, p<0.05). For plasma nitrite, although it shows a negative correlation with blood pressure it was significant only in gammal (r=-0.676, p<0.05) and gamma2 (r=-0.721, p<0.05). From this study we found that compared to WKY rats, SHR has lower NOS activity in blood vessels, which upon treatment with antioxidant gamma-tocotrienol increased the NO activity and concomitantly reduced the blood pressure. These findings further strengthen the hypothesis that free radicals and NO play critical role in pathogenesis of essential hypertension.