952 resultados para lactate minimum


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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.

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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

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Objective. The aim of this study was to verify the possibility of lactate minimum (LM) determination during a walking test and the validity of such LM protocol on predicting the maximal lactate steady-state (MLSS) intensity. Design. Eleven healthy subjects (24.2 ± 4.5 yr; 74.3 ± 7.7 kg; 176.9 ± 4.1 cm) performed LM tests on a treadmill, consisting of walking at 5.5 km h -1 and with 20-22% of inclination until voluntary exhaustion to induce metabolic acidosis. After 7 minutes of recovery the participants performed an incremental test starting at 7% incline with increments of 2% at each 3 minutes until exhaustion. A polynomial modeling approach (LMp) and a visual inspection (LMv) were used to identify the LM as the exercise intensity associated to the lowest [bLac] during the test. Participants also underwent to 24 constant intensity tests of 30 minutes to determine the MLSS intensity. Results. There were no differences among LMv (12.6 ± 1.7 %), LMp (13.1 ± 1.5 %), and MLSS (13.6 ± 2.1 %) and the Bland and Altman plots evidenced acceptable agreement between them. Conclusion. It was possible to identify the LM during walking tests with intensity imposed by treadmill inclination, and it seemed to be valid on identifying the exercise intensity associated to the MLSS. Copyright © 2012 Guilherme Morais Puga et al.

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

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O Limiar Anaeróbio (Lan) pode ser determinado por protocolos que utilizam concentrações fixas de lactato sanguíneo como o OBLA (Onset of Blood Lactate Accumulation) e os que utilizam procedimentos mais individualizados, como o Lactato Mínimo (Lacmin). Independente do método, a mensuração da capacidade aeróbia através do Lan nesses casos exige a utilização de equipamentos sofisticados, além do elevado custo por atleta, o que torna sua aplicação limitada. Como alternativa, um dos testes não invasivos mais empregados no meio esportivo é o de 12 minutos proposto por Cooper. O objetivo principal do presente estudo foi comparar a intensidade de exercício obtida pelo teste de 12min com as intensidades correspondentes ao Lan obtido pelo protocolo adaptado ao de Tegtbur et al. (1993) (Lac minat) e pelo OBLA em futebolistas profissionais. Para tanto participaram 16 atletas pertencentes a uma equipe profissional filiada à série A3 do futebol paulista. Cada atleta foi avaliado nos três protocolos, com intervalo mínimo de 48 e máximo de 72 horas. Os resultados mostraram diferença (p < 0,05) entre as velocidades (km.h-1) obtidas pelo teste de Cooper (15,09 ± 0,94) e OBLA (14,28 ± 1,02); entretanto, esses testes apresentaram correlação significativa. Cooper e OBLA não apresentaram correlação com o Lac minat, mas as velocidades foram similares com esse protocolo. Dessa maneira, a partir da análise de regressão entre os valores de Cooper e OBLA foi possível determinar uma equação de correção que permita, através do teste de Cooper, a obtenção da intensidade correspondente ao Lan determinado pelo OBLA em futebolistas profissionais.

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

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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

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O objetivo deste estudo foi comparar a intensidade de exercício no lactato mínimo (LACmin), com a intensidade correspondente ao limiar de lactato (LL) e limiar anaeróbio (LAn). Participaram do estudo, 11 atletas do sexo masculino (idade, 22,5 + 3,17 anos; altura, 172,3 + 8,2 cm; peso, 66,9 + 8,2kg; e gordura corporal, 9,8 + 3,4%). Os indivíduos foram submetidos, em uma bicicleta eletromagnética (Quinton - Corival 400), a dois testes: 1) exercício contínuo de cargas crescentes - carga inicial de 100W, com incrementos de 25W a cada três min. até a exaustão voluntária; e 2) teste de lactato mínimo - inicialmente os indivíduos pedalaram duas vezes 425W (+ 120%max) durante 30 segundos, com um min. de intervalo, com o objetivo de induzir o acúmulo de lactato. Após oito min. de recuperação passiva, os indivíduos iniciaram um teste contínuo de cargas progressivas, idêntico ao descrito anteriormente. O LL e o LAn foram identificados como sendo o menor valor entre a razão - lactato sanguíneo (mM) / intensidade de exercício (W), e a intensidade correspondente a 3,5mM de lactato sanguíneo, respectivamente. O LACmin foi identificado como sendo a intensidade correspondente a menor concentração de lactato durante o teste de cargas progressivas. Não foi observada diferença significante entre a potência do LL (197,7 + 20,7W) e do LACmin (201,6 + 13,0W), sendo ambas significantemente menores do que do LAn (256,7 + 33,3W). Não foram encontradas também diferenças significantes para o (ml.kg-1.min-1) e a FC (bpm) obtidos no LL (43,2 + 5,01; 152,0 + 13,0) e no LACmin (42,1 + 3,9; 159,0 + 10,0), sendo entretanto significantemente menores do que os obtidos para o LAn (52,2 + 8,2; 174,0 + 13,0, respectivamente). Pode-se concluir que o teste de LACmin, nas condições experimentais deste estudo, pode subestimar a intensidade de MSSLAC (estimada indiretamente pelo LAn), o que concordacom outros estudos que determinaram a MSSLAC diretamente. Assim, são necessários mais estudos que analisem o possível componente tempo-dependente (intensidade inicial) que pode existir no protocolo do LACmin.

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O objetivo principal deste estudo foi verificar se diferentes formas de indução à acidose interferem na determinação da intensidade do lactato mínimo (LACmin) em corredores de longa distância. Desse modo, 14 corredores de provas fundas do atletismo participaram do estudo. Os atletas realizaram três protocolos: 1) teste incremental em esteira rolante, com incrementos de 1km.h-1 a cada três minutos até a exaustão, para a determinação das intensidades de limiar anaeróbio (OBLA), de limiar aeróbio (Laer), consumo máximo de oxigênio (VO2max) e intensidade de consumo máximo de oxigênio (vVO2max); 2) teste de lactato mínimo em pista de atletismo (LACminp), que consistiu de dois esforços máximos de 233m na pista de atletismo com intervalo de um minuto entre cada repetição, com oito minutos de recuperação passiva, seguido de um teste incremental semelhante ao do protocolo 1; e 3) teste de lactato mínimo em esteira rolante (LACmine), constituído de dois esforços máximos de um minuto e 45 segundos com intervalo de um minuto, na intensidade de 120% da vVO2max, seguido dos mesmos procedimentos do protocolo 2. Foram coletadas amostras de sangue do lóbulo da orelha ao final de cada estágio em todos os protocolos e no 7º minuto de recuperação passiva dos testes de LACmine e LACminp. A análise de variância (ANOVA) mostrou que ocorreram diferenças significativas entre as intensidades de LACmine (13,23 ± 1,78km.h-1) e OBLA (14,67 ± 1,44km.h-1). Dessa maneira, a partir dos resultados obtidos no presente estudo, é possível concluir que a determinação da intensidade correspondente ao lactato mínimo é dependente do protocolo utilizado para a indução à acidose. Além disso, o LACmine subestimou a intensidade correspondente ao OBLA, não podendo ser utilizado para a mensuração da capacidade aeróbia de corredores fundistas.

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The present study was designed to determine the exercise intensity equivalent to the metabolic aerobic/anaerobic transition of alloxan diabetic rats, through lactate minimum test (LMT), and to evaluate the effects of swimming exercise at this intensity (LM) on the glucose and protein metabolism of these animals. Adult male Wistar rats received alloxan (SD, alloxan-injected rats that remained sedentary) intravenously (30 mg kg(-1) body weight) for diabetes induction. As controls (SC, vehicle-injected rats that remained sedentary), vehicle-injected rats were utilized. Two weeks later, the animals were submitted to oral glucose tolerance test (oGTT) and LMT. After the tests, some of the animals were submitted to swimming exercise training [TC (vehicle-injected rats that performed a 6-week exercise program) and TD (alloxan-injected rats that performed a 6-week exercise program)] for I h day(-1), 5 days week(-1), with an overload equivalent to LM determined by LMT, for 6 weeks. At the end of the experiment, the animals were submitted to a second LMT and oGTT, and blood and skeletal muscle assessments (protein synthesis and degradation in the isolated soleus muscle) were made. The overload equivalent to LM at the beginning of the experiment was lower in the SID group than in the SC group. After training, the overload equivalent to LM was higher in the TC and TD groups than in the SC and SD groups. The blood glucose of TD rats during oGTT was lower than that of SD rats. Protein degradation was higher in the SD group than in other groups. We conclude that LMT was sensitive to metabolic and physiologic alterations caused by uncontrolled diabetes. Training at LM intensity improved aerobic condition and the glucose and protein metabolism of alloxan diabetic rats. (C) 2007 Elsevier B.V. All rights reserved.

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To evaluate the effect of acute exercise and exercise training at the anaerobic threshold (AT) intensity on aerobic conditioning and insulin secretion by pancreatic islets, adult male Wistar rats were submitted to the lactate minimum test (LMT) for AT determination. Half of the animals were submitted to swimming exercise training (trained), 1 h/day, 5 days/week during 8 weeks, with an overload equivalent to the AT. The other half was kept sedentary. At the end of the experimental period, the rats were submitted to an oral glucose tolerance test and to another LMT. Then, the animals were sacrificed at rest or immediately after 20 minutes of swimming exercise at the AT intensity for pancreatic islets isolation. At the end of the experiment mean workload (% bw) at AT was higher and blood lactate concentration (mmol/L) was lower in the trained than in the control group. Rats trained at the AT intensity showed no alteration in the areas under blood glucose and insulin during OGTT test. Islet insulin content of trained rats was higher than in the sedentary rats while islet glucose uptake did not differ among the groups. The static insulin secretion in response to the high glucose concentration (16.7 mM) of the sedentary group at rest was lower than the sedentary group submitted to the acute exercise and the inverse was observed in relation to the trained groups. physical training at the AT intensity improved the aerobic condition and altered insulin secretory pattern by pancreatic islets. © 2010 Landes Bioscience.

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Aim. The purpose of this study was to compare the anaerobic threshold speed (AT) obtained from fixed lactate blood concentrations (AT 4 mM and AT 3.5 mM), lactate minimum speed (LM) and critical speed (CS), determined from different distances in fifteen Brazilian national level swimmers (10 boys = 14.8 ± 0.6 years old and 5 girls = 14.6 ±0.8 year-old). Methods. The tests to determine the AT 4 mM, AT 3.5 mM, LM and CS were performed in a 25 m swimming pool and consisted of 7 or 8 evaluations separated by 24-48 h intervals. Data were submitted to analysis of variance (ANOVA) for repeated measures, followed by the post hoc Scheffé test and Pearson correlation coefficients. Significance was set at P<0.01. Results. There were no significant differences among the values for AT 4 mM and CS1 (1.34 ± 0.05 vs. 1.33 ± 0.05 m.s -1, respectively). However, AT 4 mM and CS1 were significantly higher than AT 3.5 mM (1.28 ± 0.04 m.s -1), LM (1.27 ± 0.05 m.s -1), CS2 (1.26 ± 0.06 m.s -1), CS3 (1.27 ± 0.06 m.s -1) and CS4 (1.25 ± 0.07 m.s -1). There were no significant differences among the values for AT 3.5 mM, LM, CS2, CS3 and CS4. Conclusion. The results obtained in this study suggest that the anaerobic threshold determined by a fixed lactate concentration of 3.5 mM, as well as the LM and the CS methods determined by different distances, seem to be the most appropriate indexes for the evaluation of aerobic capacity in adolescent swimmers.

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This study was undertaken to characterize the effects of monotonous training at lactate minimum (LM) intensity on aerobic and anaerobic performances; glycogen concentrationsin the soleus muscle, the gastrocnemius muscle and the liver; and creatine kinase (CK), free fatty acids and glucose concentrations in rats. The rats were separated into trained (n =10), baseline (n = 10) and sedentary (n=10) groups. The trained group was submitted to the following: 60 min/day, 6 day/week and intensity equivalent to LM during the 12-week training period. The training volume was reduced after four weeks according to a sigmoid function. The total CK (U/L) increased in the trained group after 12 weeks (742.0±158.5) in comparison with the baseline (319.6±40.2) and the sedentary (261.6+42.2) groups. Free fatty acids and glycogen stores (liver, soleus muscle and gastrocnemius muscle) increased after 12 weeks of monotonous training but aerobic and anaerobic performances were unchanged in relation to the sedentary group. The monotonous training at LM increased the level of energy substrates, unchanged aerobic performance, reduced anaerobic capacity and increased the serum CK concentration; however, the rats did not achieve the predicted training volume.

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Background: Obesity, oxidative stress and inflammation, by triggering insulin resistance, may contribute to the accumulation of hepatic fat, and this accumulation by lipotoxicity can lead the organ to fail. Because obesity is growing at an alarming rate and, worryingly, in a precocious way, the present study aimed to investigate the effects of moderate physical training performed from childhood to adulthood on liver fat metabolism in rats. Methods. Twenty rats that were 28days old were divided into two groups: control (C) and trained (T). The C Group was kept in cages without exercise, and the T group was submitted to swimming exercise for 1hour/day, 5days/week from 28 to 90days of age (8weeks) at 80% of the anaerobic threshold determined by the lactate minimum test. At the end of the experiment, the body weight gain, insulin sensitivity (glucose disappearance rate during the insulin tolerance test), concentrations of free fatty acids (FFA) and triglycerides (TG) and hepatic lipogenic rate were analyzed. For the statistical analysis, the Student t-test was used with the level of significance preset at 5%. Results: The T group showed lower body weight gain, FFA concentrations, fat accumulation, hepatic lipogenic rate and insulin resistance. Conclusion: The regular practice of moderate physical exercise from childhood can contribute to the reduction of obesity and insulin resistance and help prevent the development of accumulation of hepatic fat in adulthood. © 2013de Moura et al; licensee BioMed Central Ltd.