Anaerobic energy provision does not limit Wingate exercise performance in endurance-trained cyclists

[EN] The aim of this study was to evaluate the effects of severe acute hypoxia on exercise performance and metabolism during 30-s Wingate tests. Five endurance- (E) and five sprint- (S) trained track cyclists from the Spanish National Team performed 30-s Wingate tests in normoxia and hypoxia (inspired O(2) fraction = 0.10). Oxygen deficit was estimated from submaximal cycling economy tests by use of a nonlinear model. E cyclists showed higher maximal O(2) uptake than S (72 +/- 1 and 62 +/- 2 ml x kg(-1) x min(-1), P < 0.05). S cyclists achieved higher peak and mean power output, and 33% larger oxygen deficit than E (P < 0.05). During the Wingate test in normoxia, S relied more on anaerobic energy sources than E (P < 0.05); however, S showed a larger fatigue index in both conditions (P < 0.05). Compared with normoxia, hypoxia lowered O(2) uptake by 16% in E and S (P < 0.05). Peak power output, fatigue index, and exercise femoral vein blood lactate concentration were not altered by hypoxia in any group. Endurance cyclists, unlike S, maintained their mean power output in hypoxia by increasing their anaerobic energy production, as shown by 7% greater oxygen deficit and 11% higher postexercise lactate concentration. In conclusion, performance during 30-s Wingate tests in severe acute hypoxia is maintained or barely reduced owing to the enhancement of the anaerobic energy release. The effect of severe acute hypoxia on supramaximal exercise performance depends on training background.

La lattatemia nel puledro neonato sottoposto a terapia intensiva

Admission blood lactate concentration has been shown to be a useful indicator of disease severity in human medicine and numerous studies have associated hyperlactatemia with patients at high risk of death who should be treated aggressively regardless of the cause of the lactate generation. The degree and duration of hyperlactacidaemia also have been correlated with the subsequent development of organ failure. Similarly, in a small number of studies about equine colic, blood lactate concentration has been investigated as a useful prognostic variable . In neonatal foals blood lactate was studied first by Magdesian (2003) who described venous blood lactate concentration in 14 normal foals during the initial 48 hours post-partum. A preliminary study about lactate concentration in foals presenting to a neonatal intensive care unit reported that surviving foals had earlier lactate clearance. The measurement of blood lactate concentration is traditionally available with a wet chemistry laboratory method or with blood-gas analyzers, for clinicians working at university or large private hospital. But this methods may not be easily accessible to many practitioners in field conditions. Several relatively inexpensive, easy to use and rapid pocket size monitors to measure lactate concentration have been validated in human patients and athletes. None of these portable lactate analyzer have been evaluated in clinically normal neonatal foals or in foals referred to a neonatal intensive care unit. The aims of this study were to validate the Lactate Scout analyzer in neonatal foals, investigating the correlation between lactate concentration in whole blood measured with the portable monitor and measured in plasma with the reference laboratory analyzer. The effect of hematocrit (Hct) on the accuracy of Lactate Scout was also evaluated. Further, we determined the utility of venous lactate measurement in critically-ill foals, describing lactate values in the most frequent neonatal pathologies, evaluating serial blood lactate measurements during hospitalization and investigating its prognostic value. The study also describes normal range for lactate in healthy neonatal foals during the first 72 hours of life.

Bicarbonato ingestion has no ergogenic effect on consecutive all out sprint test in MWX elite cyclists

The aim of the present study was to examine the effect of sodium bicarbonate ingestion on consecutive "all out" sprint tests, analyzing the acid-base status and its influence on performance and perceived effort. Ten elite bicycle motocross (BMX) riders (20.7 ± 1.4 years, training experience 8-12 years) participated in this study which consisted of two trials. Each trial consisted of three consecutive Wingate tests (WTs) separated by 15 min recovery. Ninety minutes prior to exercise subjects ingested either NaHCO(3) (-) (0.3 g kg(-1) body weight) or placebo. Blood samples were collected for the assessment of blood acid-base status: bicarbonate concentration ([HCO(3) (-)]), pH, base excess (BE) and blood lactate concentration ([La(-)]). Performance variables of peak power (PP), mean power (MP), time to peak power and fatigue index were calculated for each sprint. Significant differences (p < 0.05) were observed in acid-base variables [pH before WT1: 7.47 ± 0.05 vs. 7.41 ± 0.03; [HCO(3) (-)] before WT1: 29.08 ± 2.27 vs. 22.85 ± 0.24 mmol L(-1) (bicarbonate vs. placebo conditions, respectively)], but there were not significant differences in performance variables between trials [PP WT1: 1,610 ± 373 vs. 1,599 ± 370 W; PP WT2: 1,548 ± 460 vs. 1,570 ± 428 W; PP WT3: 1,463 ± 361 vs. 1,519 ± 364 W. MP WT1: 809 ± 113 vs. 812 ± 108 W; MP WT2: 799 ± 135 vs. 799 ± 124 W; MP WT3: 762 ± 165 vs. 782 ± 118 W (bicarbonate vs. placebo conditions, respectively)]. Rating of perceived effort (RPE) was not influenced nor ratings of perceived readiness. Sodium bicarbonate ingestion modified significantly the blood acid-base balance, although the induced alkalosis did not improve the Wingate test performance, RPE and perceived readiness across three consecutive WTs in elite BMX cyclists.

Locomotor Muscle Fatigue Does Not Alter Oxygen Uptake Kinetics during High-Intensity Exercise

The V˙O2 slow component (V˙O2sc) that develops during high-intensity aerobic exercise is thought to be strongly associated with locomotor muscle fatigue. We sought to experimentally test this hypothesis by pre-fatiguing the locomotor muscles used during subsequent high-intensity cycling exercise. Over two separate visits, eight healthy male participants were asked to either perform a non-metabolically stressful 100 intermittent drop-jumps protocol (pre-fatigue condition) or rest for 33 min (control condition) according to a random and counterbalanced order. Locomotor muscle fatigue was quantified with 6-s maximal sprints at a fixed pedaling cadence of 90 rev·min−1. Oxygen kinetics and other responses (heart rate, capillary blood lactate concentration and rating of perceived exertion, RPE) were measured during two subsequent bouts of 6 min cycling exercise at 50% of the delta between the lactate threshold and V˙O2max determined during a preliminary incremental exercise test. All tests were performed on the same cycle ergometer. Despite significant locomotor muscle fatigue (P = 0.03), the V˙O2sc was not significantly different between the pre-fatigue (464 ± 301 mL·min−1) and the control (556 ± 223 mL·min−1) condition (P = 0.50). Blood lactate response was not significantly different between conditions (P = 0.48) but RPE was significantly higher following the pre-fatiguing exercise protocol compared with the control condition (P < 0.01) suggesting higher muscle recruitment. These results demonstrate experimentally that locomotor muscle fatigue does not significantly alter the V˙O2 kinetic response to high intensity aerobic exercise, and challenge the hypothesis that the V˙O2sc is strongly associated with locomotor muscle fatigue.

Quantifying the physical demands of a musical performance and their effects on performance quality

This study investigated the effects of fatigue on performance quality induced by a prolonged musical performance. Ten participants prepared 10 min of repertoire for their chosen wind instrument that they played three times consecutively. Prior to the performance and within short breaks between performances, researchers collected heart rate, respiratory rate, blood pressure, blood lactate concentration, rating of perceived exertion (RPE), and rating of anxiety. All performances were audio recorded and later analysed for performance errors. Reliability in assessing performance errors was assessed by typical error of measure (TEM) of 15 repeat performances. Results indicate all markers of physical stress significantly increased by a moderate to large amount (4.6 to 62.2%; d = 0.50 to 1.54) once the performance began, while heart rate, respirations, and RPE continued to rise by a small to large amount (4.9 to 23.5%; d = 0.28 to 0.93) with each performance. Observed changes in performance between performances were well in excess of the TEM of 7.4%. There was a significant small (21%, d = 0.43) decrease in errors after the first performance; after the second performance, there was a significant large increase (70.4%, d = 1.14). The initial increase in physiological stress with corresponding decrease in errors after the first performance likely indicates "warming up," while the continued increase in markers of physical stress with dramatic decrement in performance quality likely indicates fatigue. Musicians may consider the relevance of physical fitness to maintaining performance quality over the duration of a performance.

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.

Is the formula of Traub still up to date in antemortem blood glucose level estimation?

According to the hypothesis of Traub, also known as the 'formula of Traub', postmortem values of glucose and lactate found in the cerebrospinal fluid or vitreous humor are considered indicators of antemortem blood glucose levels. However, because the lactate concentration increases in the vitreous and cerebrospinal fluid after death, some authors postulated that using the sum value to estimate antemortem blood glucose levels could lead to an overestimation of the cases of glucose metabolic disorders with fatal outcomes, such as diabetic ketoacidosis. The aim of our study, performed on 470 consecutive forensic cases, was to ascertain the advantages of the sum value to estimate antemortem blood glucose concentrations and, consequently, to rule out fatal diabetic ketoacidosis as the cause of death. Other biochemical parameters, such as blood 3-beta-hydroxybutyrate, acetoacetate, acetone, glycated haemoglobin and urine glucose levels, were also determined. In addition, postmortem native CT scan, autopsy, histology, neuropathology and toxicology were performed to confirm diabetic ketoacidosis as the cause of death. According to our results, the sum value does not add any further information for the estimation of antemortem blood glucose concentration. The vitreous glucose concentration appears to be the most reliable marker to estimate antemortem hyperglycaemia and, along with the determination of other biochemical markers (such as blood acetone and 3-beta-hydroxybutyrate, urine glucose and glycated haemoglobin), to confirm diabetic ketoacidosis as the cause of death.

Lactate sequestration by osteoderms of the broad-nose caiman, Caiman latirostris, following capture and forced submergence

Lactate accumulation in osteoderms; of the broad-nose caiman, Caiman latirostris, was determined following capture and surgery and after a period of forced submergence and related to concurrent values in blood. Control samples of bone and blood were taken after recovery from surgery and before submergence. In addition, samples of osteoderm were incubated in a lactate solution to determine equilibrium concentration, and additional samples were analyzed for elemental and CO2 concentrations. The composition of the osteoderms closely resembles that of typical vertebrate bone, with a high concentration of calcium and phosphate. Plasma and osteoderm lactate concentrations were both elevated following surgery and decreased significantly after 1 day of recovery. Submergence produced a typical lactate pattern in the plasma, with only a modest increase during the dive and then a sharp increase during recovery to a peak of 31.2 +/- 1.9 mumol ml(-1) after 1 h. When caimans were anesthetized 2 h after submergence, osteoderm lactate in the same animals was significantly increased to 14.8 mumol g(-1) wet mass. The ratio of the osteoderm: plasma lactate concentration after submergence was similar to the ratio observed in the incubated samples, suggesting that osteoderm lactate concentrations in vivo were equilibrated with circulating plasma levels. We conclude that caiman osteoderms sequester lactate during lactic acidosis and that the time course is fast enough to have benefit to these animals following normal anaerobic burst activity.

Serum cortisol, lactate and creatinine concentrations in Thoroughbred fillies of different ages and states of training

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

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(-).

Lactate in Bitches with Pyometra

Lactate is a compound produced by the anaerobic metabolism of glucose, and hyperlactataemia occurs when the rate of production of lactate exceeds the rate of elimination. This occurs in situations of hypoxia and tissue hypoperfusion. Lactate has been considered a useful prognostic indicator in critically ill patients. Pyometra is a disease of adult female dogs characterized by inflammation of the uterus with an accumulation of exudate, which occurs during the luteal phase. It is one of the most common diseases that occur in the genital tract of female dogs. A total of 31 dogs were diagnosed with pyometra. The diagnosis was confirmed at ultrasonography. of the 31 dogs, 25 females had open cervix pyometra and six had closed cervix pyometra. Plasma lactate concentrations were determined by an enzymatic colorimetric method. The average concentration (+/- SD) of plasma lactate in all 31 bitches with pyometra was 3.55 +/- 0.46 mm. Healthy dogs had plasma lactate concentrations between 0.3 and 2.5 mm (mean +/- SD). Concentrations ranged from 0.8 to 2.9 mm when plasma lactate was measured with a portable device and 0.42.6 mm with the blood gas analyser. Even though plasma lactate values vary between several studies and equipment used to measure concentrations, our results for dogs with pyometra are higher indicating hyperlactataemia (Thorneloe et al. , Can Vet J 48, 283288). Plasma lactate in dogs with closed cervix pyometra was mean +/- SD and in dogs with open cervix pyometra, it was mean +/- SD. The plasma lactate concentration in dogs with pyometra was higher than in healthy bitches, and there was no influence of patency of the cervix on the concentration of plasma lactate concentrations. Plasma lactate concentrations were similar for animals with open and closed pyometra (3.54 +/- 0.52 to 3.64 +/- 1.03 mm).

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. © 2001 Elsevier B.V. All rights reserved.

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.

HYPERLACTEMIA INDUCTION MODES AFFECT THE LACTATE MINIMUM POWER AND PHYSIOLOGICAL RESPONSES IN CYCLING

Zagatto, AM, Padulo, J, Muller, PTG, Miyagi, WE, Malta, ES, and Papoti, M. Hyperlactemia induction modes affect the lactate minimum power and physiological responses in cycling. J Strength Cond Res 28(10): 2927-2934, 2014The aim of this study was to verify the influence of hyperlactemia and blood acidosis induction on lactate minimum intensity (LMI). Twenty recreationally trained males who were experienced in cycling (15 cyclists and 5 triathletes) participated in this study. The athletes underwent 3 lactate minimum tests on an electromagnetic cycle ergometer. The hyperlactemia induction methods used were graded exercise test (GXT), Wingate test (WAnT), and 2 consecutive Wingate tests (2 x WAnTs). The LMI at 2 x WAnTs (200.3 +/- 25.8 W) was statistically higher than the LMI at GXT (187.3 +/- 31.9 W) and WAnT (189.8 +/- 26.0 W), with similar findings for blood lactate, oxygen uptake, and pulmonary ventilation at LMI. The venous pH after 2 x WAnTs was lower (7.04 +/- 0.24) than in (p <= 0.05) the GXT (7.19 +/- 0.05) and WAnT (7.19 +/- 0.05), whereas the blood lactate response was higher. In addition, similar findings were observed for bicarbonate concentration [HCO3] (2 x WAnTs lower than WAnT; 15.3 +/- 2.6 mmol center dot L-1 and 18.2 +/- 2.7 mmol center dot L(-)1, respectively) (p <= 0.05). However, the maximal aerobic power and total time measured during the incremental phase also did not differ. Therefore, we can conclude that the induction mode significantly affects pH, blood lactate, and [HCO3] and consequently they alter the LMI and physiological parameters at LMI.

Specific determination of maximal lactate steady state in soccer players

The aim of this study was to establish the validity of the anaerobic threshold (AT) determined on the soccer-specific Hoff circuit (AT(Hoff)) to predict the maximal lactate steady-state exercise intensity (MLSSHoff) with the ball. Sixteen soccer players (age: 16.0 +/- 0.5 years; body mass: 63.7 +/- 9.0 kg; and height: 169.4 +/- 5.3 cm) were submitted to 5 progressive efforts (7.0-11.0 km.h(-1)) with ball dribbling. Thereafter, 11 players were submitted to 3 efforts of 30 minutes at 100, 105, and 110% of AT(Hoff). The AT(Hoff) corresponded to the speed relative to 3.5 mmol.L-1 lactate concentration. The speed relative to 4.0 mmol.L-1 was assumed to be AT(Hoff4.0), and the AT(HoffBI) was determined through bisegmented adjustment. For comparisons, Student's t-test, intraclass correlation coefficient (ICC), and Bland and Altman analyses were used. For reproducibility, ICC, typical error, and coefficient of variation were used. No significant difference was found between AT test and retest determined using different methods. A positive correlation was observed between AT(Hoff) and AT(Hoff4.0). The MLSSHoff (10.6 +/- 1.3 km.h(-1)) was significantly different compared with AT(Hoff) (10.2 +/- 1.2 km.h(-1)) and AT(HoffBI) (9.5 +/- 0.4 km.h(-1)) but did not show any difference from LAn(Hoff4.0) (10.7 +/- 1.4 km.h(-1)). The MLSSHoff presented high ICCs with AT(Hoff) and AT(Hoff4.0) (ICC = 0.94; and ICC = 0.89; p <= 0.05, respectively), without significant correlation with AT(HoffBI). The results suggest that AT determined on the Hoff circuit is reproducible and capable of predicting MLSS. The AT(Hoff4.0) was the method that presented a better approximation to MLSS. Therefore, it is possible to assess submaximal physiological variables through a specific circuit performed with the ball in young soccer players.