Protective effects of whey protein concentrate admixtured of curcumin on metabolic control, inflammation and oxidative stress in Wistar rats submitted to exhaustive exercise.

This work aimed to evaluate the effects of whey protein concentrate (WPC) admixtured of curcumin on metabolic control, inflammation and oxidative stress in Wistar rats submitted to exhaustive exercise. A total of forty-eight male rats were divided into six experimental groups (n 8): standard diet group (AIN-93M), standard diet submitted to exhaustion test group (AIN-93M ET), WPC admixtured of curcumin group (WPC + CCM), WPC + CCM submitted to exhaustion test group (WPC + CCM ET), CCM group and CCM subjected to exhaustion test group (CCM ET). The swimming exhaustion test was performed after 4 weeks of experiment. The consumption of WPC + CCM as well as isolated CCM did not alter the biometric measurements, the animals' food consumption and the hepatic and kidney function, as well as the protein balance of the animals (P > 0·05), but reduced the glycaemia and the gene expression of TNF-α and IL-6 and increased the expression of IL-10 (P < 0·05). The animals that were submitted to the exhaustion test (AIN-93M ET) showed higher aspartate aminotransferase values when compared to the animals that did not perform the exercise (AIN-93 M) (P < 0·05). WPC + CCM reduced the concentration of nitric oxide, carbonylated protein and increased the concentration of catalase (P < 0·05). Both (WPC + CCM and CCM) were able to increase the concentrations of superoxide dismutase (P < 0·05). We concluded that the WPC admixtured of CCM represents a strategy capable of decreasing blood glucose and oxidative and inflammatory damage caused by exhaustive physical exercise in swimming.

Core temperature circadian rhythm across aging in Spontaneously Hypertensive Rats.

The purpose of this study was to evaluate the circadian rhythm of core temperature (Tcore) across aging in Spontaneously Hypertensive Rats (SHR) with comparison to the two rat strains often used as their normotensive control animals, namely, Wistar (WIS) and Wistar Kyoto (WKY). METHODS: WIS, WKY and SHR rats were subdivided into three different groups according their age: WIS16, WIS48, WIS72, WKY16, WKY48, WKY72, SHR16, SHR48 and SHR72 weeks-old. Body mass and blood pressure were periodically measured along the experiments. All animal group had their circadian rhythm of Tcore evaluated over three consecutive days (72 h) by telemetry using an implanted temperature sensor. The Tcore circadian rhythm was averaged in 1-h blocks and analyzed using the cosinor method. RESULTS: Sixteen-week-old SHR (SHR16) presented higher Tcore than WIS16 (from 06am to 06pm) and WKY16 (from 07am to 06pm). Both normotensive groups exhibited increases in Tcore during circadian rhythm with aging. The cosinor analysis showed no differences between strains and ages for the acrophase. An age effect on the SHR strain (SHR16 < SHR72) was observed regarding the amplitude. SHR16 had higher values regarding MESOR compared to WIS16 and WKY16. In addition, WIS72 and WKY72 showed higher values than WIS16 and WKY16, respectively. Finally, no differences were observed in the strength rhythm analysis. CONCLUSIONS: SHR presented impaired thermoregulatory control at only 16 weeks of age when showing a higher body temperature during the activity phase, while other circadian rhythm parameters showed no differences across aging. Therefore, in taking our results as a whole we can conclude that WIS and WKY are appropriate Wistar strains to be used as normotensive controls for SHR.

ß-hydroxy-ß-methylbutyrate supplementation benefits the effects of resistance training on body fat reduction via increased irisin expression in white adipose tissue.

The effects of resistance training (RT) associated with calcium ß-hydroxyß-methylbutyrate (CaHMB) supplementation on the body composition and gene expression of cytokines related to skeletal muscle hypertrophy and adipose tissue metabolism were studied in rats. Male Wistar rats were divided into four groups of 12 animals: sedentary control (SC); sedentary supplemented (SS); resistance training control (RTC) and resistance training supplemented (RTS). Rats from RTC and RTS groups were submitted to an RT programme and those from SS and RTS groups received 1 mL of CaHMB (320 mg kg-1 day-1) by gavage, for 8 weeks. We evaluated: body composition; plasma lipid profile; the gene expression of interleukin (IL)-6, IL-10, IL-15 and fibronectin type III domain-containing protein 5 (FNDC-5) in skeletal muscle, and IL-6, mitochondrial uncoupling protein 1 (UCP-1) in white adipose tissue (WAT); and the concentration of irisin in WAT. Compared to RTC alone, the combination of CaHMB with RT (RTS) further reduced abdominal circumference (5.3%), Lee index (2.4%), fat percentage (24.4%), plasma VLDL cholesterol (16.8%) and triglycerides (17%) and increased the gene expression of FNDC-5 (78.9%) and IL-6 (47.4%) in skeletal muscle and irisin concentration (26.9%) in WAT. Neither RT nor CaHMB affected the protein percentage or the gene expression of IL-6 and UCP-1 in WAT and IL-10, IL-15 in skeletal muscle. In conclusion, CaHMB supplementation increased the beneficial effects of RT on body fat reduction and was associated with muscular genic expression of IL-6 and FNDC-5 and irisin concentration in WAT, despite the lack of change in protein mass and maximal strength.

Could pre-infection exercise training improve the efficacy of specific antiparasitic chemotherapy for Chagas disease?

Considering a potential exercise-drug interaction, we investigated whether exercise training could improve the efficacy of specific antiparasitic chemotherapy in a rodent model of Chagas disease. Wistar rats were randomized into five groups: sedentary and uninfected (CT); sedentary and infected (SI); sedentary, infected and treated (SIT); trained and infected (TI); trained, infected and treated (TIT). After 9-weeks running training, the animals were infected with T. cruzi and followed up for 4 weeks, receiving 100 mg kg-1 day-1 benznidazole. No evidence of myocarditis was observed in CT animals. TI animals exhibited reduced parasitemia, myocarditis, and reactive tissue damage compared to SI animals, in addition to increased IFN-γ, IL-4, IL-10, heart non-protein antioxidant (NPA) levels and glutathione-s transferase activity (P < 0.05). The CT, SIT and TIT groups presented similar reductions in parasitemia, cytokines (IFN-γ, TNF-α, IL-4, IL-10, IL-17 and MCP-1), inflammatory infiltrate, oxidative heart damage and antioxidant enzymes activity compared to SI and TI animals, as well as reduced heart microstructural remodeling (P < 0.05). By modulating heart inflammation and redox metabolism, exercise training exerts a protective effect against T. cruzi infection in rats. However, the antiparasitic and cardioprotective effects of benznidazole chemotherapy are more pronounced, determining similar endpoints in sedentary and trained T. cruzi-infected rats.

Spontaneously hypertensive rats have greater impairments in regulating abdominal temperature than brain cortex temperature following physical exercise.

This study aimed to evaluate the changes in brain (Tbrain) and abdominal (Tabd) temperatures in spontaneously hypertensive rats (SHRs) following fatiguing exercise. Male normotensive Wistar rats (NWRs) and SHRs were used at 16 weeks of age. Their arterial pressure was measured by tail plethysmography prior to the experiments to confirm the hypertensive status of the SHRs. Then, the rats underwent implantation of an abdominal temperature sensor to measure Tabd and a guide cannula in the frontal cortex to enable the insertion of a thermistor to measure Tbrain. After a familiarization period, each animal was subjected to incremental speed exercises until fatigue in either a temperate (25 °C) or warm (32 °C) environment, followed by a 60-min post-exercise period at the same temperature at which they exercised. Tbrain, Tabd and tail-skin temperature (Tskin) were measured every min throughout the experiments. SHRs exhibited higher Tabd values than NWRs, and these higher values were transiently and persistently observed at 25 °C and 32 °C, respectively. For example, at 32 °C, Tabd was 0.84 °C higher in SHRs at the 25th min (large effect size). In contrast, regardless of the ambient temperature, SHRs exhibited similar Tbrain values as NWRs, indicating preserved Tbrain regulation following exercise in hypertensive rats. SHRs presented higher Tskin during the last half of the post-exercise period at 25 °C, whereas no inter-group differences were observed at 32 °C. In conclusion, the present results highlight that SHRs, an animal model that mimics uncontrolled essential hypertension in humans, exhibited greater impairments in regulating Tabd than Tbrain during the post-exercise period.

Acute paraquat exposure determines dose-dependent oxidative injury of multiple organs and metabolic dysfunction in rats: impact on exercise tolerance.

This study investigated the pathological morphofunctional adaptations related to the imbalance of exercise tolerance triggered by paraquat (PQ) exposure in rats. The rats were randomized into four groups with eight animals each: (a) SAL (control): 0.5 ml of 0.9% NaCl solution; (b) PQ10: PQ 10 mg/kg; (c) PQ20: PQ 20 mg/kg; and (d) PQ30: PQ 30 mg/kg. Each group received a single injection of PQ. After 72 hours, the animals were subjected to an incremental aerobic running test until fatigue in order to determine exercise tolerance, blood glucose and lactate levels. After the next 24 h, lung, liver and skeletal muscle were collected for biometric, biochemical and morphological analyses. The animals exposed to PQ exhibited a significant anticipation of anaerobic metabolism during the incremental aerobic running test, a reduction in exercise tolerance and blood glucose levels as well as increased blood lactate levels during exercise compared to control animals. PQ exposure increased serum transaminase levels and reduced the glycogen contents in liver tissue and skeletal muscles. In the lung, the liver and the skeletal muscle, PQ exposure also increased the contents of malondialdehyde, protein carbonyl, 8-hydroxy-2'-deoxyguanosine, superoxide dismutase and catalase, as well as a structural remodelling compared to the control group. All these changes were dose-dependent. Reduced exercise tolerance after PQ exposure was potentially influenced by pathological remodelling of multiple organs, in which glycogen depletion in the liver and skeletal muscle and the imbalance of glucose metabolism coexist with the induction of lipid, protein and DNA oxidation, a destructive process not counteracted by the upregulation of endogenous antioxidant enzymes.

Voluntary exercise delays heart failure onset in rats with pulmonary artery hypertension.

Increased physical activity is recommended for the general population and for patients with many diseases because of its health benefits but can be contraindicated if it is thought to be a risk for serious cardiovascular events. One such condition is pulmonary artery hypertension (PAH). PAH and right ventricular failure was induced in rats by a single injection of monocrotaline (MCT). MCT rats with voluntary access to a running wheel ran on average 2 km/day. The time for half the animals to develop heart failure signs (median survival time) was 28 days (exercise failure group), significantly longer than sedentary animals (sedentary failure group, 23 days). The contractility of single failing myocytes in response to increasing demand (stimulation frequency) was significantly impaired compared with that in both sedentary control and exercising control myocytes. However, myocytes from exercising MCT rats, tested at 23 days (exercise + MCT group), showed responses intermediate to the control (sedentary control and exercising control) and failing (sedentary failure and exercise failure) groups. We conclude that voluntary exercise is beneficial to rats with heart failure induced by PAH, and this is evidence to support the consideration of appropriate exercise regimes for potentially vulnerable groups.

Basal and ß-adrenergic cardiomyocytes contractility dysfunction induced by dietary protein restriction is associated with downregulation of SERCA2a expression and disturbance of endoplasmic reticulum Ca2+ regulation in rats.

BACKGROUND: The mechanisms responsible for the cardiac dysfunction associated with dietary protein restriction (PR) are poorly understood. Thus, this study was designed to evaluate the effects of PR on calcium kinetics, basal and ß-adrenergic contractility in murine ventricular cardiomyocytes. METHODS: After breastfeeding male Fisher rats were distributed into a control group (CG, n = 20) and a protein-restricted group (PRG, n = 20), receiving isocaloric diets for 35 days containing 15% and 6% protein, respectively. Biometric and hemodynamic variables were measured. After euthanasia left ventricles (LV) were collected for histopathological evaluation, SERCA2a expression, cardiomyocytes contractility and Ca(2+)sparks analysis. RESULTS: PRG animals showed reduced general growth, increased heart rate and arterial pressure. These animals presented extracellular matrix expansion and disorganization, cardiomyocytes hypotrophy, reduced amplitudes of shortening and maximum velocity of contraction and relaxation at baseline and after ß-adrenergic stimulation. Reduced SERCA2a expression as well as higher frequency and lower amplitude of Ca(2+)sparks were observed in PRG cardiomyocytes. CONCLUSION: The observations reveal that protein restriction induces marked myocardial morphofunctional damage. The pathological changes of cardiomyocyte mechanics suggest the potential involvement of the ß-adrenergic system, which is possibly associated with changes in SERCA2a expression and disturbances in Ca(2+) intracellular kinetics.

Temperature Control of Hypertensive Rats during Moderate Exercise in Warm Environment.

The control of body temperature in Spontaneously Hypertensive Rat (SHR) subjected to exercise in warm environment was investigated. Male SHR and Wistar rats were submitted to moderate exercise in temperate (25°C) and warm (32°C) environments while body and tail skin temperatures, as well as oxygen consumption, were registered. Total time of exercise, workload performed, mechanical efficiency and heat storage were determined. SHR had increased heat production and body temperature at the end of exercise, reduced mechanical efficiency and increased heat storage (p < 0.05). Furthermore, these rats also showed a more intense and faster increase in body temperature during moderate exercise in the warm environment (p < 0.05). The lower mechanical efficiency seen in SHR was closely correlated with their higher body temperature at the point of fatigue in warm environment (p < 0.05). Our results indicate that SHR exhibit significant differences in body temperature control during moderate exercise in warm environment characterized by increased heat production and heat storage during moderate exercise in warm environment. The combination of these responses result in aggravated hyperthermia linked with lower mechanical efficiency. Key PointsThe practice of physical exercise in warm environment has gained importance in recent decades mainly because of the progressive increases in environmental temperature;To the best of our knowledge, these is the first study to analyze body temperature control of SHR during moderate exercise in warm environment;SHR showed increased heat production and heat storage that resulted in higher body temperature at the end of exercise;SHR showed reduced mechanical efficiency;These results demonstrate that when exercising in a warm environment the hypertensive rat exhibit differences in temperature control.

Protein restriction after weaning modifies the calcium kinetics and induces cardiomyocyte contractile dysfunction in rats.

Protein restriction (PR) is associated with cardiovascular diseases. The purpose of this study was to investigate the effects on single ventricular cardiomyocyte contractile function of a short-term PR after weaning. Male Fischer rats that were 28 days old were randomly divided into a control group (CG, n = 16) and a protein-restricted group (PRG, n = 16). After weaning, CG and PRG animals received isocaloric diets containing 15 and 6% protein, respectively, for 35 days. Biometric parameters were then measured, and the hearts were removed for the analysis of contractile function and calcium transient in isolated cardiomyocytes of the left ventricule (LV), and the quantification of calcium and collagen fibers in LV myocardium. PRG animals had lower body weight (BW) and LV weight (LVW), an increased LVW to BW ratio and a higher proportion of collagen fibers than CG animals. PRG animals exhibited reduced tissue levels of calcium, reduced the length, width and volume of cardiomyocytes and their sarcomere length compared to CG animals. Cardiomyocytes from PRG animals had a lower amplitude of shortening, a slower time to the peak of shortening and a longer time to half-relaxation than those from the CG. Cardiomyocytes from PRG animals also presented a lower peak of calcium transient and a longer calcium transient decay time than CG animals. Taken together, the results indicate that short-term PR after weaning induces a marked structural remodeling of the myocardium parenchyma and stroma that coexists with contractile dysfunctions in single LV cardiomyocytes of rats, which is probably associated with pathological changes of the intracellular calcium kinetics, rather than inadequate available amounts of this mineral in cardiac tissue.

Chronic exercise partially restores the transmural heterogeneity of action potential duration in left ventricular myocytes of spontaneous hypertensive rats.

Hypertension leads to electrophysiological changes in the heart. Chronic exercise induced by a treadmill-running programme (TRP) is considered a potential non-pharmacological treatment for hypertension and may have implications in heart remodelling. However, it is not known whether the TRP is able to improve the electrophysiological properties of the heart in spontaneously hypertensive rats (SHR). In the present study, we investigated whether TRP affects the electrical properties of left ventricular (LV) myocytes isolated from different layers of the LV wall of SHR. Male SHR were divided into exercised (chronic treadmill running for 8 weeks; CEX-SHR) and sedentary (SED-SHR) groups. Age-matched normotensive Wistar male rats served as controls. Action potentials (AP) and transient outward potassium current (I(to) ) were recorded in subepicardial (EPI) and subendocardial (ENDO) LV myocytes. In normotensive controls, AP duration (APD) was longer in ENDO cells than in EPI cells. This sort of transmural heterogeneity in the LV was not observed in sedentary SHR and was partially restored in SHR subject to chronic exercise. This partial recovery was associated with an increase in I(to) density in EPI cells but not in ENDO cells. The electrophysiological changes observed in the CEX-SHR group were not accompanied by either amelioration of systolic blood pressure or a reduction in heart hypertrophy. These findings imply that a TRP is able to improve the electrophysiological parameters of isolated cardiac myocytes in SHR. This sort of adaptation contributes to the overall improvement of heart physiology in this model.

3,4-Dihydroxycinnamic acid attenuates the fatigue and improves exercise tolerance in rats.

3,4-Dihydroxycinnamic acid (3,4-DA) is a natural compound with high antioxidant potential found in various foods. This study found that animals administered with 3,4-DA had higher exercise tolerance, reduced blood lactate, and markers of hepatic oxidation. Blood glucose and antioxidant enzymes were not affected by this treatment. 3,4-DA may have applicability in reducing the fatigue associated with exercise.

Pre-game hydration status, sweat loss, and fluid intake in elite Brazilian young male soccer players during competition.

In this study, we assessed the pre-game hydration status and fluid balance of elite young soccer players competing in a match played in the heat (temperature 31.0 ± 2.0 ° C, relative humidity 48.0 ± 5.0%) for an official Brazilian soccer competition. Fluid intake was measured during the match, as were urine specific gravity and body mass before and after the game to estimate hydration status. Data were obtained from 15 male players (age 17.0 ± 0.6 years, height 1.78 ± 0.06 m, mass 65.3 ± 3.8 kg); however, data are only analysed for 10 players who completed the full game. The mean (± s) sweat loss of players amounted to 2.24 ± 0.63 L, and mean fluid intake was 1.12 ± 0.39 L. Pre-game urine specific gravity was 1.021 ± 0.004, ranging from 1.010 to 1.025. There was no significant correlation between sweat loss and fluid intake (r = 0.504, P = 0.137) or between urine specific gravity and fluid intake (r = -0.276, P = 0.440). We conclude that young, native tropical soccer players started the match hypohydrated and replaced about 50% of the sweat lost. Thus, effective strategies to improve fluid replacement are needed for players competing in the heat.

Heart rate monitoring in soccer: interest and limits during competitive match play and training, practical application.

The identification of physiological loads imposed by soccer training or match play reveals essential information, which may help improve training and recovery strategies. Until today, the use of heart rate (HR) monitoring is not standardized in soccer. Thus, the aim of this review was to analyze, determine and compare the exercise intensity (EI) monitored by HR in professional, youth, and recreational soccer players during matches and training sessions using a meta-analysis. Heart rate is one of the most common physiological variables used to determine exercise internal training load. The mean EI recorded during competitive matches was described as 70-80% of VO2max or 80-90% of maximal heart rate (HRmax), independent of the playing level. With respect to HR training zones, approximately 65% of the total match duration is spent at intensity of 70-90% HRmax and rarely below 65% HRmax. However, although HRmax is mostly employed in the literature, monitoring EI should be expressed in relation to reserve heart rate, as it was described as a more reliable indicator of HR, allowing interindividual comparisons. The HR response according to the playing position indicates that midfielders are characterized by the highest EI, followed by forwards and fullbacks. Moreover, in the second half of the match, the EI is lower than that observed during the first half; this reduction could be correlated with the level of the player's physical conditioning. Consequently, coaches may favor the use of interval training or small-sided training games because these are shown to improve both aerobic capacity and the ability to repeat high-intensity actions. Small-sided games allow reaching similar HR responses to those found during interval training and match play but with greater heterogeneity values. Future investigations should include a larger sample of players with special reference to playing position and the expression of EI in percentage of the reserve heart rate, analyzing the possible intergender differences in HR response.

Effects of moderate-continuous and high-intensity interval aerobic training on cardiac function of spontaneously hypertensive rats.

The aim of this study was to verify the effects of moderate-intensity continuous (MICT) and high-intensity interval (HIIT) aerobic training on cardiac morphology and function and the mechanical properties of single cardiomyocytes in spontaneously hypertensive rats (SHR) in the compensated phase of hypertension. Sixteen-week-old male SHR and normotensive Wistar (WIS) rats were allocated to six groups of six animals each: SHR CONT or WIS CONT (control); SHR MICT or WIS MICT (underwent MICT, 30 min/day, five days per week for eight weeks); and SHR HIIT or WIS HIIT (underwent HIIT, 30 min/day, five days per week for eight weeks). Total exercise time until fatigue and maximum running speed were determined using a maximal running test before and after the experimental period. Systolic (SAP), diastolic (DAP), and mean (MAP) blood pressures were measured using tail plethysmography before and after the experimental period. Echocardiographic evaluations were performed at the end of the experimental period. The rats were euthanized after in vivo assessments, and left ventricular myocytes were isolated to evaluate global intracellular Ca2+ transient ([Ca2+]i) and contractile function. Cellular measurements were performed at basal temperature (~37°C) at 3, 5, and 7 Hz. The results showed that both training programs increased total exercise time until fatigue and, consequently, maximum running speed. In hypertensive rats, MICT decreased SAP, DAP, MAP, interventricular septal thickness during systole and diastole, and the contraction amplitude at 5 Hz. HIIT increased heart weight and left ventricular wall thickness during systole and diastole and reduced SAP, MAP, and the time to peak [Ca2+]i at all pacing frequencies. In conclusion, both aerobic training protocols promoted beneficial adaptations to cardiac morphology, function, and mechanical properties of single cardiomyocytes in SHR.

L-NAME treatment enhances exercise-induced content of myocardial heat shock protein 72 (Hsp72) in rats.

BACKGROUND/AIM: Nitric oxide (NO) modulates the expression of the chaperone Hsp72 in the heart, and exercise stimulates both NO production and myocardial Hsp72 expression. The main purpose of the study was to investigate whether NO interferes with an exercise-induced myocardial Hsp72 expression. METHODS: Male Wistar rats (70-100 days) were divided into control (C, n=12), L-NAME-treated (L, n=12), exercise (E, n=13) and exercise plus L-NAME-treated (EL, n=20) groups. L-NAME was given in drinking water (700 mg·L(-1)) and the exercise was performed on a treadmill (15-25 m·min(-1), 40-60 min.day(-1)) for seven days. Left ventricle (LV) protein Hsp content, NOS and phosphorylated-NOS (p-NOS) isoforms were measured using Western blotting. The activity of NOS was assayed in LV homogenates by the conversion of [(3)H]L-arginine to [(3)H]L-citrulline. RESULTS: Hsp72 content was increased significantly (223%; p < 0.05) in the E group compared to the C group, but exercise alone did not alter the NOS content, p-NOS isoforms or NOS activity. Contrary to our expectation, L-NAME enhanced (p < 0.05) the exercise-induced Hsp72 content (EL vs. C, L and E groups = 1019%, 548% and 457%, respectively). Although the EL group had increased stimulatory p-eNOS(Ser1177) (over 200%) and decreased inhibitory p-nNOS(Ser852) (ñ50%) compared to both the E and L groups (p < 0.05), NOS activity was similar in all groups. CONCLUSIONS: Our results suggest that exercise-induced cardiac Hsp72 expression does not depend on NO. Conversely, the in vivo L-NAME treatment enhances exercise-induced Hsp72 production. This effect may be due to an increase in cardiac stress.

Effects of Trypanosoma cruzi infection on myocardial morphology, single cardiomyocyte contractile function and exercise tolerance in rats.

The aim of this study was to investigate the effects of Trypanosoma cruzi (T. cruzi) infection on myocardial morphology, single cardiomyocyte contractile function and exercise tolerance in rats. Adult Wistar rats were randomized into control (n = 14) and infected (n = 14) groups. Infected animals were inoculated with T. cruzi Y strain (300,000 trypomastigotes/50 g body weight). After 9 weeks, the animals were subjected to a treadmill running protocol. Then, the right atrium (RA) and left ventricle (LV) were removed for morphological and cell contractile evaluation. The infected animals exhibited a significant reduction in distance travelled, total time to fatigue and workload. In addition, these animals had hypertrophy, increased myocardial cellularity, and an increase in the proportion of collagen and blood vessels. RA and LV myocytes from infected animals showed marked contractile dysfunction under basal conditions and a reduced contractile response to ß-adrenergic stimulation. The workload of infected animals was correlated closely with the amplitude of cell shortening of RA and LV myocytes. T. cruzi infection influenced the myocardial morphology and the mechanical properties of RA and LV single myocytes negatively and reduced exercise tolerance. Single cardiomyocyte contractile dysfunction could constitute an additional mechanism of cardiac impairment and reduced exercise tolerance in this infection.

Fluid balance of elite Brazilian youth soccer players during consecutive days of training.

In this study we investigated pre-training hydration status, fluid intake, and sweat loss in 20 elite male Brazilian adolescent soccer players (mean ± s: age 17.2 ± 0.5 years; height 1.76 ± 0.05 m; body mass 69.9 ± 6.0 kg) on three consecutive days of typical training during the qualifying phase of the national soccer league. Urine specific gravity (USG) and body mass changes were evaluated before and after training sessions to estimate hydration status. Players began the days of training mildly hypohydrated (USG > 1.020) and fluid intake did not match fluid losses. It was warmer on Day 1 (33.1 ± 2.4°C and43.4 ± 3.2% relative humidity; P < 0.05) and total estimated sweat losses (2822 ± 530 mL) and fluid intake (1607 ± 460 mL) were significantly higher (P < 0.001) compared with Days 2 and 3. Data also indicate a significant correlation between the extent of sweat loss and the volume of fluid consumed (Day 1: r = 0.560, P = 0.010; Day 2: r = 0.445, P = 0.049; Day 3: r = 0.743, P = 0.0001). We conclude that young, native tropical soccer players arrive hypohydrated to training and that they exhibit voluntary dehydration; therefore, enhancing athletes' self-knowledge of sweat loss during training might help them to consume sufficient fluid to match the sweat losses.

Exercise intensity and technical demands of small-sided games in young Brazilian soccer players: effect of number of players, maturation, and reliability.

The aims of this study were to examine in young soccer players (a) the effect of varying the number of players on exercise intensity (EI) and technical actions during small-sided games (SSGs), (b) the reliability of EI and technical actions, and (c) the influence of the players' maturation on EI and involvements with the ball (IWBs). Sixteen male soccer players (mean ± SD; age 13.5 ± 0.7 years, height 164 ± 7 cm, and weight 51.8 ± 8 kg) completed 2 bouts of 3 vs. 3 (SSG3), 4 vs. 4 (SSG4), and 5 vs. 5 (SSG5) training. Exercise intensity was measured using heart rate and expressed as a percentage of maximal heart rate (%MHR). Technical actions were quantified from video recordings. Maturation stage was determined with the Tanner scale. Exercise intensity in SSG3 (89.8 ± 2%MHR) was higher (p < 0.003) than that in SSG5 (86.9 ± 3%MHR). The EI in the first set (86.8 ± 4%MHR) was lower (p < 0.001) than that in the second (89.1 ± 3%MHR) and in the third set (89.4 ± 3%MRH). No effects of number of players were found in IWB, passes, target passes, tackles, and headers. Significantly more crosses, dribbling, and shots on goal were observed during SSG3 compared to during SSG4 or SSG5 (p < 0.05). The typical error for EI, expressed as coefficient of variation, ranged from 2.2 to 3.4%. The reliability for the most frequent technical actions ranged from 6.8 to 19.3%. The level of maturation was not correlated with either EI or IWB. These results extend previous findings with adult players suggesting that SSGs can provide an adequate training stimulus for young players and are feasible for groups with heterogeneous maturation levels.

Changes in cellular contractility and cytokines profile during Trypanosoma cruzi infection in mice.

Trypanosoma cruzi, an intracellular protozoan parasite infecting a wide variety of vertebrates, is the agent responsible for Chagas' disease. This pathology often results in severe inflammatory heart condition and it is one of the major causes of dilated cardiomyopathy leading to heart failure in Latin America. Nevertheless, little is known about the changes in isolate cardiac myocytes contractility during the development of this pathology. Here we report a relationship between cytokines profile of mice infected with T. cruzi and the modifications in the cellular contractility pattern. We found that cellular contractility, measured as fractional shortening, showed a complex behavior. The changes were evaluated during the acute phase (15, 30 and 45 dpi) and chronic phase (>90 dpi). The time to half contraction and relaxation were lengthier despite the number of days after infection or the heart region evaluated. The maximal contraction and relaxation velocities were significantly slower. The observed changes in cellular contractility were correlated with the presence of circulating IFN-gamma, TNF-alpha and MCP-1/CCL2 during the course of infection. Together, our data demonstrate that cellular contractility is altered in the three heart regions studied, and these alterations are observed at the very beginning of the parasitism and they remained until the chronic phase has been reached. Indeed, we propose a role for IFN-gamma, TNF-alpha and MCP-1/CCL2 in the mechanical heart remodeling during experimental Chagas' disease.