183 resultados para lactate threshold


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This study investigated the effect of a calcium lactate pre-rinse on sodium fluoride protection in an in vitro erosion-remineralization model simulating two different salivary flow rates. Enamel and dentin specimens were randomly assigned to 6 groups (n = 8), according to the combination between rinse treatments - deionized water (DIW), 12 mm NaF (NaF) or 150 mm calcium lactate followed by NaF (CaL + NaF) and unstimulated salivary flow rates - 0.5 or 0.05 ml/min simulating normal and low salivary flow rates, respectively. The specimens were placed into custom-made devices, creating a sealed chamber on the specimen surface connected to a peristaltic pump. Citric acid was injected into the chamber for 2 min, followed by artificial saliva (0.5 or 0.05 ml/min) for 60 min. This cycle was repeated 4x/day for 3 days. Rinse treatments were performed daily 30 min after the 1st and 4th erosive challenges, for 1 min each time. Surface loss was determined by optical profilometry. KOH-soluble fluoride and structurally bound fluoride were determined in specimens at the end of the experiment. Data were analyzed by 2-way ANOVA and Tukey tests (alpha = 0.05). NaF and CaL + NaF exhibited significantly lower enamel and dentin loss than DIW, with no difference between them for normal flow conditions. The low salivary flow rate increased enamel and dentin loss, except for CaL + NaF, which presented overall higher KOH-soluble and structurally bound fluoride levels. The results suggest that the NaF rinse was able to reduce erosion progression. Although the CaL prerinse considerably increased F availability, it enhanced NaF protection against dentin erosion only under hyposalivatory conditions. (C) 2014 S. Karger AG, Basel

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

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

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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.

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The objective of this study was to compare the power corresponding to maximal lactate steady state determined through continuous (MLSSC) and intermittent protocol with active recovery (MLSSI). Ten trained male cyclists (25 ± 4 yr, 72.5 ± 10.6 kg, 178.5 ± 4.0 cm), performed the following tests on different days on a cycle ergometer: (1) incremental test in order to determine the anaerobic threshold (AT) and maximal power (Pmax); (2) two to five constant workload tests to determine MLSSC, and; 3) two to three constant workload tests to determine MLSSI, consisting on 8 x 4 minutes bouts interspersed by two minutes of active recovery at 50% Pmax (i.e., 46 min of exercise protocol). MLSS intensity was defined as the highest workload at which blood lactate concentration did not increase by more than 1 mM between minutes 10 and 30 of the constant workload. The workload corresponding to MLSSC (273.2 ± 21.4 W) was significantly lower than that corresponding to MLSSI (300.5 ± 23.9 W). With base on these data, it can be verified that the intermittent exercise mode utilized in this study, allows an increase of 10% approximately, in the exercise intensity corresponding to MLSS.

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Exercise physiology has attempted to reproduce the experimental exercise in the laboratory using mainly rats. The swimming exercise has emerged as one of the leading research in these type ergometers. Thus, this research consisted of a literature review addressing the key issues which involve the exercise of swimming in the model rats. Training of aerobic and anaerobic swimming, evaluation models and models of periodization were the topics suggested in this research. In several studies, models of aerobic and anaerobic training have been proposed with the aim of studying their effect on normal and abnormal physiological parameters. However, earlier studies lacked methods of analysis aiming to determine the exercise intensity in the animal model. For this reason, in the last decade, assessment models have been adapted for humans to animals, especially rats. The maximal lactate steady state (MLSS) and lactate minimum (LM) are among the various techniques used to measure the amount of effort produced by swimming exercise in rats. Thereafter, based on biochemical parameters such as lactate, swimming exercise in rats has become the highest-rated, ie, using as reference the anaerobic threshold (AT). In another aspect, an entirely new line of research has tried to understand and promising swimming training in a periodized and its effects on some biochemical parameters. But this is an area little researched so far. Thus, the experimental model of swimming has proved an important resource of exercise physiology. From this model, it becomes possible to study the exercise, especially swimming, in more accurate, based on invasive and incisive analysis of the rat

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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

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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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Power-counting arguments are used to organize the interactions contributing to the NN-->d pi,pn pi reactions near threshold. We estimate the contributions from the three formally leading mechanisms: the Weinberg-Tomozawa (WT) term, the impulse term, and the Delta-excitation mechanism. Subleading but potentially large mechanisms, including S-wave pion rescattering, the Galilean correction to the WT term, and short-ranged contributions are also examined. The WT term is shown to be numerically the largest, and the other contributions are found to approximately cancel. Similarly to the reaction pp-->pp pi(0), the computed cross sections are considerably smaller than the data. We discuss possible origins of this discrepancy.