Comparison of aerobic capacity determined by the lactate minimum test among guard, forward and forward-center positions in basketball players

To aim of this study was to verify the aerobic capacity by lactate minimum test (LM) among different positions in professional basketball players. Twelve high performance basketball players (12 Major National Leagues, 26.7± 3.2 years) were evaluated by LM. The method of lactate elevation consisted of 6 maximum sprints of 35 m separated by 10 s of recovery each (Running Anaerobic Sprint Test). The progressive phase in LM consisted of 4 periods of 3 min each at 8, 10, 11 and 12 Km/h. After lactate elevation phase and progressive periods, 25μL samples of blood were collected to determine peak lactate (PL) concentration and relative lactate minimum concentration (LACc) respectively. The running speed at the LM was taken when the gradient of the line was zero. Anova one-way statistical was utilized to compare the intensity corresponding LM, LACc and PL (p≤0.05). The velocity (Km/h) of LM did not differ among positions: Guard LM= 9.46±0.17 Km/h; Forward LM= 9.60±0.68 Km/h and Forward-Center LM= 9.64±0.25 Km/h. The LACc did not differ: Guard LM= 3.55±0.51 mmol/L; Forward LM= 3.48±1.63 mmol/L and Forward-Center LM= 4.00±0.43 mmol/L. No changes occurred in PL: Guard LM= 8.35±1.41 mmol/L; Forward LM= 8.16±1.47 mmol/L and Forward-Center LM= 8.76±1.20 mmol/L. The aerobic capacity determined by LM did not differ among guard, forward and forward center basketball players

Determination of Force Corresponding to Maximal Lactate Steady State in Tethered Swimming

The main aim of the present investigation was to verify if the aerobic capacity (AC) measured in tethered swimming corresponds to the maximal lactate steady state (MLSS) and its correlation with 30 min and 400m free style swimming. Twenty-five swimmers were submitted to an incremental tethered swimming test (ITS) with an initial load of 20N and increments of 10N each 3min. After each stage of 3min, the athletes had 30s of interval to blood sample collections that were used to measure blood lactate concentrations ([La-]). The ACBI was determined by the abrupt increase in [La-] versus force (F). The points obtained between [La-] versus force (N) were adjusted by an exponential curve model to determine AC corresponding to 3.5mmol.l-1 (AC3.5) and 4.0mmol.l-1 (AC4.0). After these procedures, the swimmers performed maximal efforts of 30min and 400m in free style swimming. We used the distance performed in 30min and the time performed in 400m to calculate the median velocities (i.e. V30 and V400) of these protocols. After one week, in order to measure the MLSS, nine athletes performed three 30-min tethered swimming efforts with intensities of 90, 100, and 110% of ACBI. The ANOVA one-way was used to compare the ACBI, AC3.5 and AC4.0. Correlations between ACs, and between ACs and V30 and V400 (p\u3c0.05) were determined using the Pearson’s correlation coefficient. The intensity corresponding to 100% of ACBI was similar to the MLSS. It was observed significant correlations of the aerobic capacities (i.e. ACBI, AC3.5 and AC4.0) with V30 (r\u3e0.91) and V400 (r\u3e0.63). According to our results, it is possible to conclude that the ACBI corresponds to the MLSS, and both the AC - individually determined - and the AC - determined using fixed blood lactate concentrations of 3.5 and 4.0mmol.l-1 - can be used to predict the mean velocity of 30min and 400m in free style swimming. In addition to that, the tethered swimming system can be used for aerobic development in places where official sized swimming pools are not available, such as rehabilitation clinics and health clubs

Molecular hydrogen downregulates acute exhaustive exercise-induced skeletal muscle damage

Physical exercise-induced skeletal muscle damage may be characterized by increased oxidative stress, inflammation, and apoptosis which may be beneficial when exercise is regular, but it is rather harmful when exercise is exhaustive and performed acutely by unaccustomed individuals. Molecular hydrogen (H2) has emerged as a potent antioxidant, anti-inflammatory, and anti-apoptotic agent, but its action on the deleterious effects of acute exhaustive exercise in muscle damage remain unknown. Therefore, we tested the hypothesis that H2 decreases acute exhaustive exercise-induced skeletal muscle damage of sedentary rats. Rats ran to exhaustion on a sealed treadmill inhaling an H2-containing mixture or the control gas. We measured oxidative stress (SOD, GSH, and TBARS), inflammatory (TNF-α, IL-1β, IL-6, IL-10, and NF-kB phosphorylation) and apoptotic (expression of caspase-3, Bcl-2, and HSP70) markers. Exercise caused no changes in SOD activity but increased TBARS levels. H2 caused increases in exercise-induced SOD activity and blunted exercise-induced increased TBARS levels. We observed exercise-induced TNF-α and IL-6 surges as well as NF-kB phosphorylation, which were blunted by H2. Exercise increased cleaved caspase-3 expression, and H2 reduced this response. In conclusion, H2 effectively downregulates muscle damage, reducing oxidative stress, inflammation, and apoptosis after acute exhaustive exercise performed by an unaccustomed organism.The accepted manuscript in pdf format is listed with the files at the bottom of this page. The presentation of the authors' names and (or) special characters in the title of the manuscript may differ slightly between what is listed on this page and what is listed in the pdf file of the accepted manuscript; that in the pdf file of the accepted manuscript is what was submitted by the author

Acute physical exercise increases leptin‐induced hypothalamic extracellular signal‐regulated kinase1/2 phosphorylation and thermogenesis of obese mice

The obesity is a result of energy imbalance and the increase in thermogenesis seems an interesting alternative for the treatment of this disease. The mechanism of energy expenditure through thermogenesis is tightly articulated in the hypothalamus by leptin. The hypothalamic extracellular signal‐regulated kinase‐1/2 (ERK1/2) is a key mediator of the thermoregulatory effect of leptin and mediates the sympathetic signal to the brown adipose tissue (BAT). In this context, physical exercise is one of the main interventions for the treatment of obesity. Thus, this study aimed to verify the effects of acute physical exercise on leptin‐induced hypothalamic ERK1/2 phosphorylation and thermogenesis in obese mice. Here we showed that acute physical exercise reduced the fasting glucose of obese mice and increased leptin‐induced hypothalamic p‐ERK1/2 and uncoupling protein 1 (UCP1) content in BAT ( P < 0.05). These molecular changes are accompanied by an increased oxygen uptake (VO 2) and heat production in obese exercised mice ( P < 0.05). The increased energy expenditure in the obese exercised animals occurred independently of changes in spontaneous activity. Thus, this is the first study demonstrating that acute physical exercise can increase leptin‐induced hypothalamic ERK1/2 phosphorylation and energy expenditure of obese mice1201697704CNPQ - Conselho Nacional de Desenvolvimento Científico e TecnológicoFAPESP – Fundação de Amparo à Pesquisa Do Estado De São Paulo306535/2017‐32016/18488‐8OCR