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.     

Maximal lactate steady state in rats submitted to swimming exercise.

The higher concentration during exercise at which lactate entry in blood equals its removal is known as 'maximal lactate steady state' (MLSS) and is considered an important indicator of endurance exercise capacity. The aim of the present study was to determine MLSS in rats during swimming exercise. Adult male Wistar rats, which were adapted to water for 3 weeks, were used. After this, the animals were separated at random into groups and submitted once a week to swimming sessions of 20 min, supporting loads of 5, 6, 7, 8, 9 or 10% of body wt. for 6 consecutive weeks. Blood lactate was determined every 5 min to find the MLSS. Sedentary animals presented MLSS with overloads of 5 and 6% at 5.5 mmol/l blood lactate. There was a significant (P<0.05) increase in blood lactate with the other loads. In another set of experiments, rats of the same strain, sex and age were submitted daily to 60 min of swimming with an 8% body wt. overload, 5 days/week, for 9 weeks. The rats were then submitted to a swimming session of 20 min with an 8% body wt. overload and blood lactate was determined before the beginning of the session and after 10 and 20 min of exercise. Sedentary rats submitted to the same acute exercise protocol were used as a control. Physical training did not alter the MLSS value (P<0.05) but shifted it to a higher exercise intensity (8% body wt. overload). Taken together these results indicate that MLSS measured in rats in the conditions of the present study was reproducible and seemed to be independent of the physical condition of the animals.     

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.     

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 P1: 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 (tlim); P3: one tlim 13% bw load swimming bout; and P4: two 13% bw load swimming bouts (1st 30 s, 2nd to tlim), 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 P1 (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.     

Cardiorespiratory and lactate responses to a 1-hour submaximal running at the lactate threshold

Cardiorespiratory and blood lactate (La) responses to prolonged submaximal running at an intensity relative to lactate threshold (LT) were examined in 15 recreational runners, aged 19 to 32. In test 1 where treadmill speed was progressively incremented by 10-20m/min until exhaustion, oxygen uptake at the LT (VO2 @ LT: 2.34 +/- 0.331/min or 41.6 +/- 5.7 ml/kg/min) and VO2max (3.58 +/- 0.341/min or 63.6 +/- 5.5 ml/kg/min) were measured. In test 2, the subject was required to run on the treadmill for 1 hour at a fixed velocity (Vt) which corresponded to his Vt @ LT. As expected, mean VO2 ranged during the 1-h submaximal running from 2.31 +/- 0.411/min or 63.0 +/- 7.8% VO2max at min 10-20 to 2.52 +/- 0.351/min or 69.2 +/- 6.2% VO2max at min 50-60, both of which were close to VO2 @ LT (65.2 +/- 4.4% VO2max). The slight decrease in blood La was found from min 20 to min 60, and this was accompanied by a parallel decline in respiratory exchange ratio. Shifts in the energy substrate toward a reliance on fat oxidation may occur during the course of 1-h running at Vt @t LT. The small oxygen debt observed after the 1-h running may confirm the assumption that prolonged running at Vt at LT would be performed in an almost fully aerobic steady state. We conclude that prolonged running at Vt @ LT may possibly maximize health-related benefits in the healthy adult.     

Determination of the lactate threshold and maximal blood lactate steady state intensity in aged rats

The reliability of the lactate threshold (LT) determined in aged rats and its validity to identify an exercise intensity corresponding to the maximal blood lactate steady state (MLSS) were analyzed. Eighteen male aged Wistar rats (～365 days) were submitted to two incremental swimming tests until exhaustion, consisting of an initial load corresponding to 1% of body mass (BM) and increments of 1% BM at each 3‐min with blood lactate ([lac]) measurements. The LT was determined by visual inspection (LT_V) as well by applying a polynomial function on the [lac]/workload ratio (LT_P) by considering the vertices of the curve. For the MLSS, twelve animals were submitted, on different days, to 3–4 exercise sessions of 30‐min with workload corresponding to 4, 5 or 6% BM. The MLSS was considered the highest exercise intensity at which the [lac] variation was not higher than 0.07 mM.min^?1 during the last 20‐min. No differences were observed for the test‐retest results (4.9 ± 0.7 and 5.0 ± 0.8 %BM for LTv; and 6.0 ± 0.6 and 5.8 ± 0.6 %BM for LTp) that did not differ from the MLSS (5.4 ± 0.5 %BM). The LT identified for aged rats in swimming, both by visual inspection and polynomial function, was reliable and did not differ from the MLSS. Copyright © 2009 John Wiley & Sons, Ltd.     

Method for diagnosis and control of aerobic training in rats based on lactate threshold

We propose a protocol for determination of lactate threshold (LT) and test the validity of one aerobic training based on LT in rats. In group I, V(LTi) (velocity at LT before training) was determined in all rats (n=10), each rat training at its own V(LTi) and in group II, animals (n=7) ran at 15 m min(-1), the mean V(LTi) of group I. The training consisted of daily runs at V(LTi) for 50 min, 5 days/week, for 4 weeks. In group I, this program increased V(LT) (V(LTi) 14.90+/-1.49 m min(-1) and V(LTf), after training, 22.60+/-1.17 m min(-1)) and the velocity at exhaustion (19.50+/-1.63 m min(-1) and 27.60+/-1.17 m min(-1)). [Lactate] at LT (2.62+/-0.43 mmol L(-1) versus 2.11+/-0.15 mmol L(-1)) and relative values of LT (76+/-3% versus 82+/-2%) stayed unaltered. In group II the V(LTf) was 20+/-1.8 m.mim(-1), the [lactate] at the LT, 2.02+/-0.17 mmol.L(-1); the exhaustion speed, 23.57+/-2.11 m.mim(-1) and relative value of LT, 82.71+/-2.29%. There were no significant differences in these parameters between groups I and II. Thus, this protocol based on LT is effective and the mean V(LT) determined in a small number of healthy untrained rats can be used for aerobic training in a larger group of healthy animals of same gender and age.     

Maximal lactate steady-state prediction through quadratic modeling of selected stages of the lactate minimum test

In this study, we compared the maximal lactate steady state (MLSS) with lactate minimal (LM) intensities determined visually and through a quadratic polynomial function of selected stages of LM test. Eleven male recreational cyclists (27.7 +/- 4.5 years, 175.7 +/- 5.6 cm, 69.5 +/- 10.8 kg, and 12.0 +/- 5.5% body fat) performed one LM test under previous induction of hyperlactaemia with an initial intensity of 75 W with 30-W increments every 3 minutes with blood lactate concentration (HLa) and rating of perceived exertion (RPE) measurements. The LM intensity was determined visually (VLM) and by modeling the lactate response through polynomial function by using: 1) all stages (LMP); 2) the first stage, the stage corresponding to RPE-13 and the last stage/exhaustion (LMP3max); 3) the three lowest lactate concentration stages (LMP3adj); and 4) the initial, RPE-13, and RPE-16 stages (LMP3sub). The MLSS was determined as the highest intensity at a variation not greater than 0.05 mmol.l.min of HLa during the last 20 minutes of a 30-minute exercise session. The MLSS (204.0 +/- 16.0 W), VLM (198.6 +/- 15.2 W), LMP3adj (190.4 +/- 12.9 W), and LMP3sub (192.1 +/- 27.2 W) were not different, well correlated, and in agreement to each other. In conclusion, the polynomial modeling of HLa response to three submaximal stages produced exercise intensities that did not differ from MLSS.     

Variations in running activity and enzymatic adaptations in voluntary running rats

The running behavior and biochemical markers of oxidative and glycolytic activities associated with voluntary running activity were studied in male Sprague-Dawley rats after 6 wk of training in exercise wheel cages. Twenty-four-hour recordings of running activity were used to quantify the number of individual running bouts, their duration and running speed, and the distance run per day. We then established three categories of voluntary running activity based on the mean distance run per day during the last 3 wk of training: low-activity runners averaged 2-5 km/day, medium runners 6-9 km/day, and high runners greater than 11 km/day. Each group demonstrated an intermittent, nocturnal running pattern, at relatively high intensities, with a similar mean running speed for all groups (avg approximately 45 m/min). Differences in total distance run per day were the result of variations in both the number and duration of individual running bouts. Specifically, high runners (n = 7) had 206 +/- 30 individual running bouts per 24 h, each lasting 87 +/- 7 s; medium runners (n = 7) 221 +/- 22 running bouts, lasting 47 +/- 5 s; and low runners (n = 7) 113 +/- 7 bouts, each lasting 40 +/- 7 s. Voluntary running depressed the rate of body weight gain compared with sedentary control rats, despite an increased food and water intake for all runners. Furthermore, drinking activity was temporally associated with running periods.(ABSTRACT TRUNCATED AT 250 WORDS)     

Reverse lactate threshold test accurately predicts maximal lactate steady state and 5 km performance in running

This study evaluated the accuracy of the reverse lactate threshold (RLT) and the onset of blood lactate accumulation (OBLA; 4 mmol·L^-1) to determine the running speed at the maximal lactate steady state (MLSS) and 5 km running performance in a field test approach. Study 1: 16 participants performed an RLT test, and 2 or more constant-speed tests, lasting 30 minutes each, to determine running speed at the MLSS. Study 2: 23 participants performed an RLT test and a 5000 m all-out run as an indicator of performance. The RLT test consisted of an initial lactate-priming segment, in which running speed was increased stepwise up to ~5% above the estimated MLSS, followed by a reverse segment in which speed was decreased by 0.1 m·s^-1 every 180 s. RLT was determined using the highest lactate equivalent ([La^-]/running speed) during the reverse segment. OBLA was determined during the priming segment and was set at a value of 4 mmol∙L¹. The mean difference in MLSS was +0.06 ± 0.05 m·s^-1 for RLT, and +0.13 ± 0.23 m·s^-1 for OBLA. OBLA showed a good concordance with the MLSS (ICC = 0.83), whereas RLT revealed excellent concordance with the MLSS with an ICC = 0.98. RLT showed a very high correlation with 5000 m speed (r = 0.97). The RLT exhibited exceptional agreement to MLSS and 5000 m running performance. Due to this high accuracy, especially concerning the small intraindividual differences, the RLT test may be superior to common threshold concepts. Further research is needed to evaluate its sensitivity during the training process.     

Insulin-induced hypoglycemia in fed and fasted exercising rats.

To determine running performance and hormonal and metabolic responses during insulin-induced hypoglycemia, fed and fasted male rats (315 +/- 3 g) were infused with insulin (100 mU/ml, 1.5 ml/h) or saline (1.5 ml/h) for 60 min and then killed at rest or after running on the treadmill (21 m/min, 15% grade). Insulin-infused fed rats ran poorly during the second 10 min of a 20-min exercise test. They were capable of running a total of 43 +/- 5 min, compared with 138 +/- 6 min for saline-infused fed rats. Fasted insulin-infused rats were able to run only 12.8 +/- 0.8 min, compared with 122 +/- 15 min for fasted saline-infused rats. In fasted rats, blood glucose was 1.6 +/- 0.1 mM after 60 min of insulin infusion and 1.2 +/- 0.1 mM after running to exhaustion. Artificial increase of plasma free fatty acids had no effect on performance. Intravenous infusion of glucose at the time of fatigue produced an immediate recovery, allowing the formerly fatigued rats to run 20 min without development of fatigue. These results provide evidence that severe hypoglycemia can be a significant cause of fatigue, even if it occurs early in the course of an exercise bout.     

Metabolic and physiological response of the rabbit to continuous and intermittent treadmill exercise

Our knowledge of the effects of exercise on the heart is limited by the predominant use of rats as an animal model. The rabbit has many advantages over the rat as an animal model to study. However, little work has characterized its capacity to exercise. The purposes of the present study were to determine if the rabbit could (i) learn to run on a motor-driven treadmill at relatively high speeds using different exercise protocols, and (ii) characterize the various physiological and metabolic responses of the rabbit to acute bouts of exercise. We found that female New Zealand white rabbits had the capacity to run continuously on the treadmill for up to 21 min at 20 m/min until exhausted. Continuous, endurance-type exercise resulted in significant elevations in body temperature, heart rate, and plasma lactate levels. Plasma triglyceride concentration decreased as a function of this type of running whereas plasma glucose levels were unchanged. Twenty-four hours after a bout of running, plasma creatine phosphokinase activity was significantly elevated. The rabbits also had the capacity to learn to run using an intermittent, higher speed protocol. These physically untrained animals could achieve speeds of up to 70 m/min for 10 bouts of 15 s run/30 s rest. Their metabolic and physiological responses to this protocol were similar to those of continuous running with the following exceptions. The decrease in plasma triglyceride was less marked and the increase in plasma lactate was greater after intermittent exercise. Glycogen content of the rabbit vastus lateralis muscle was also significantly depleted after exhaustive, intermittent exercise.(ABSTRACT TRUNCATED AT 250 WORDS)     

Enhanced mitochondrial sensitivity to creatine in rats bred for high aerobic capacity.

Qualitative and quantitative measures of mitochondrial function were performed in rats selectively bred 15 generations for intrinsic aerobic high running capacity (HCR; n = 8) or low running capacity (LCR; n=8). As estimated from a speed-ramped treadmill exercise test to exhaustion (15 degrees slope; initial velocity of 10 m/min, increased 1 m/min every 2 min), HCR rats ran 10 times further (2,375+/-80 m) compared with LCR rats (238+/-12 m). Fiber bundles were obtained from the soleus and chemically permeabilized. Respiration was measured 1) in the absence of ADP, 2) in the presence of a submaximally stimulating concentration of ADP (0.1 mM ADP, with and without 20 mM creatine), and 3) in the presence of a maximally stimulating concentration of ADP (2 mM). Although non-ADP-stimulated and maximally ADP-stimulated rates of respiration were 13% higher in HCR compared with LCR, the difference was not statistically significant (P>0.05). Despite a similar rate of respiration in the presence of 0.1 mM ADP, HCR rats demonstrated a higher rate of respiration in the presence of 0.1 mM ADP+20 mM creatine (HCR 33% higher vs. LCR, P<0.05). Thus mitochondria from HCR rats exhibit enhanced mitochondrial sensitivity to creatine (i.e., the ability of creatine to decrease the Km for ADP). We propose that increased respiratory sensitivity to ADP in the presence of creatine can effectively increase muscle sensitivity to ADP during exercise (when creatine is increased) and may be, in part, a contributing factor for the increased running capacity in HCR rats.     

A physiological description of critical velocity

Although critical velocity (CV) provides a valid index of aerobic function, the physiological significance of CV is not known. Twelve individuals performed exhaustive runs at 95% to 110% of the velocity at which VO2max was attained in an incremental test. VO2max was elicited in each run. Using the time to exhaustion at each velocity, CV was calculated for each participant. Using the time to achieve VO2max at each velocity, which was shorter at higher velocities, a parameter we have designated as CV' was calculated for each participant. During exercise at or below CV', VO2max cannot be elicited. CV (238+/-24 m x min(-1)) and CV' (239+/-25 m x min(-1)) were equal (t = 0.60, p = 0.56) and correlated (r = 0.97, p < 0.01). These results demonstrate that CV is the threshold intensity above which exercise of sufficient duration will lead to attainment of VO2max.     

Evaluation of cellular energetics by the Pasteur effect in intact cardiomyoblasts and isolated perfused hearts

This work aims at exploring changes in cellular energetics by exploiting the Pasteur effect. We assumed that lactate overproduction arising from antimycin A-induced inhibition of mitochondrial respiration (delta-lactate = stimulated [lactate] -basal [lactate]) is indicative of the energy provided aerobically by the cell. Rat embryonal cardiomyocytes (H9c2), incubated with 2 micromol/L antimycin A, increased about 6 fold their lactate production in a manner linear with time and cell number. Antimycin A was also delivered to Langendorff-perfused rat hearts under control aerobic conditions or after 20 min-ischemia and 30 min-reperfusion. The test started at the end of each perfusion and lactate was measured into perfusate collected for further 25 min. A cardioplegic solution was also delivered during the test to exclude that lactate production was influenced by cardiac contraction. Control delta-lactate was 20.9 +/- 2.31 (S.E.M.) microg/mL and markedly decreased after reperfusion (7.66 +/- 0.51, p < 0.001), showing that energy production was impaired of about 70%. The determination of oxygen consumption by mitochondria isolated from reperfused hearts also suggested that the damage to the respiratory chain was similar to that evaluated by lactate overproduction (Respiratory Control Index: 75% lower than control, p < 0.001). Moreover, when delta-lactate was referred to the estimated cells which remained viable at the end of reperfusion (49.9%), it was 25% lower than control (p < 0.05). Therefore, we proposed this test as a tool for quantifying both physiological and pathological energetic modifications in living intact cardiomyocytes and in isolated and perfused hearts.     

Short-term training attenuates muscle TCA cycle expansion during exercise in women.

Muscle glycogenolytic flux and lactate accumulation during exercise are lower after 3-7 days of "short-term" aerobic training (STT) in men (e.g., Green HJ, Helyar R, Ball-Burnett M, Kowalchuk N, Symon S, and Farrance B. J Appl Physiol 72: 484-491, 1992). We hypothesized that 5 days of STT would attenuate pyruvate production and the increase in muscle tricarboxylic acid cycle intermediates (TCAI) during exercise, because of reduced flux through the reaction catalyzed by alanine aminotransferase (AAT; pyruvate + glutamate <--> 2-oxoglutarate + alanine). Eight women [22 +/- 1 yr, peak oxygen uptake (Vo2 peak) = 40.3 +/- 4.6 ml. kg-1. min-1] performed seven 45-min bouts of cycle exercise at 70% Vo2 peak over 9 days (1 bout/day; rest only on days 2 and 8). During the first and last bouts, biopsies (vastus lateralis) were obtained at rest and after 5 and 45 min of exercise. Muscle glycogen concentration was approximately 50% higher at rest after STT (493 +/- 38 vs. 330 +/- 20 mmol/kg dry wt; P 相似文献   

Improved running economy in elite runners after 20 days of simulated moderate-altitude exposure.

To investigate the effect of altitude exposure on running economy (RE), 22 elite distance runners [maximal O(2) consumption (Vo(2)) 72.8 +/- 4.4 ml x kg(-1) x min(-1); training volume 128 +/- 27 km/wk], who were homogenous for maximal Vo(2) and training, were assigned to one of three groups: live high (simulated altitude of 2,000-3,100 m)-train low (LHTL; natural altitude of 600 m), live moderate-train moderate (LMTM; natural altitude of 1,500-2,000 m), or live low-train low (LLTL; natural altitude of 600 m) for a period of 20 days. RE was assessed during three submaximal treadmill runs at 14, 16, and 18 km/h before and at the completion of each intervention. Vo(2), minute ventilation (Ve), respiratory exchange ratio, heart rate, and blood lactate concentration were determined during the final 60 s of each run, whereas hemoglobin mass (Hb(mass)) was measured on a separate occasion. All testing was performed under normoxic conditions at approximately 600 m. Vo(2) (l/min) averaged across the three submaximal running speeds was 3.3% lower (P = 0.005) after LHTL compared with either LMTM or LLTL. Ve, respiratory exchange ratio, heart rate, and Hb(mass) were not significantly different after the three interventions. There was no evidence of an increase in lactate concentration after the LHTL intervention, suggesting that the lower aerobic cost of running was not attributable to an increased anaerobic energy contribution. Furthermore, the improved RE could not be explained by a decrease in Ve or by preferential use of carbohydrate as a metabolic substrate, nor was it related to any change in Hb(mass). We conclude that 20 days of LHTL at simulated altitude improved the RE of elite distance runners.