Antônio José Natali

Heart Rate Monitoring in Soccer: Interest and Limits During Competitive Match Play and Training, Practical Application.

Abstract Alexandre, D, Da Silva, C, Hill-Haas, S, Wong, DP, Natali, AJ, De Lima, JRP, Filho, MGB, Marins, JCB, Garcia, ES, and Chamari, K. Heart rate monitoring in soccer: Interest and limits during competitive match play and training–Practical application. J Strength Cond Res 26(10): 2890–2906, 2012—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 V[Combining Dot Above]O2max 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 players 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.

Red but not white meat consumption is associated with metabolic syndrome, insulin resistance and lipid peroxidation in Brazilian middle-aged men

Background The influence of diet on metabolic syndrome and oxidative stress are not completely known. Design This cross-sectional study assessed the association of red meat and white meat consumption with metabolic syndrome, insulin resistance and lipid peroxidation in Brazilian middle-aged men. Methods A total of 296 subjects (age: 50.5 ± 5.0 years, body mass index: 25.8 ± 3.5 kg/m2) were evaluated. Anthropometry, lifestyle features, blood biochemical parameters, diagnosis of metabolic syndrome, homeostatic model assessment for insulin resistance, a lipid peroxidation marker (oxidized low-density lipoprotein) and triglycerides:high-density lipoprotein cholesterol ratio were assessed. Dietary intake was estimated by a food frequency questionnaire. Results The subjects included in the highest tertile red meat (≥81.5 g/d) and saturated fatty acid from red meat consumption (≥4.3 g/d) had higher occurrence of central obesity (nearly 60%, p < 0.01), hypertriglyceridaemia (nearly 43%, p < 0.01) and metabolic syndrome (35%, p < 0.01). They also had higher values of homeostatic model assessment for insulin resistance, oxidized low-density lipoprotein, and triglycerides:high-density lipoprotein cholesterol ratio, regardless of interfering factors. There were no associations of highest white meat tertile (≥39.4 g/d) and saturated fatty acid from white meat (≥1.0 g/d) consumption with the assessed parameters (p > 0.05). Conclusions Red meat consumption was cross-sectionally associated with the occurrence of central obesity, hypertriglyceridaemia, and metabolic syndrome as well as with higher homeostatic model assessment for insulin resistance, oxidized low-density lipoprotein concentrations and triglycerides:high-density lipoprotein cholesterol ratio. The content of saturated fatty acid from red meat consumption may be a factor that contributed to this relationship, while white meat consumption was not associated with metabolic syndrome and the assessed biomarkers.

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

Abstract 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.

Trypanosoma cruzi infection induces morphological reorganization of the myocardium parenchyma and stroma, and modifies the mechanical properties of atrial and ventricular cardiomyocytes in rats

BACKGROUND This study investigates morphofunctional adaptations of the heart stroma and parenchyma in rats that are chronically infected with Trypanosoma cruzi. METHODS Four-month-old male Wistar rats were randomized into control (n=14) and infected (n=14) groups. Infected animals were inoculated with T. cruzi Y strain. After 9 weeks, the animals were euthanized, and the right atrium (RA) and left ventricle (LV) were removed for biochemical, stereological, and cardiomyocyte mechanical analyses. RESULTS Infected animals presented cardiomyocyte atrophy and myocardial fibrosis. For these animals, the total volume, length, surface area, and cross-sectional area of cardiomyocytes were significantly reduced, and the total interstitial and collagen volumes were significantly increased in the RA and LV compared to the controls. The total volume and length of blood vessels were significantly increased in the LV, and the total blood vessel surface area was significantly higher in the RA of infected animals. RA and LV cardiomyocytes from infected animals exhibited a significant reduction in cell shortening (43.02% and 24.98%, respectively), prolongation of the time to the peak of contraction (17.09%) and the time to half relaxation (23.68%) compared to non-infected animals. Lipid hydroperoxides, but not mineral concentrations, were significantly increased in the RA and LV from infected animals, showing an inverse correlation with cell shortening. CONCLUSIONS T. cruzi infection induces global structural remodeling of the RA and LV in rats. This remodeling coexists with cardiomyocyte contractility dysfunction, which is possibly related to the abnormal organization of the myocardial stroma and increased cellular lipid peroxidation.

Exercise capacity is related to calcium transients in ventricular cardiomyocytes

The aim of the present study was to evaluate the Ca2+ handling and contractility properties of cardiomyocytes isolated from rats with high intrinsic aerobic exercise capacity. Standard-performance (SP) and high-performance (HP) rats were categorized with a treadmill progressive exercise test according to the exercise time to fatigue (TTF). The SP group included rats with TTF between 16.63 and 46.57 min, and the HP group included rats with TTF>46.57 min. Isolated ventricular cardiomyocytes were dissociated from the hearts of SP and HP rats, and intracellular global Ca2+ ([Ca2+]i) transients were measured. The [Ca2+]i transient peak was increased in the HP group relative to the SP group (5.54+/-0.31 vs. 4.18+/-0.12 F/F0; P<or=0.05) and was positively correlated with the TTF attained during the progressive test (r=0.81). We also performed contractility measurements in isolated cardiomyocytes and found higher amplitude of contraction in the HP group compared with the SP group (6.7+/-0.2 vs. 6.0+/-0.3% resting cell length; P<or=0.05). To reinforce the intrinsic differences between SP and HP rats, we performed Western blot experiments and observed increased expression of sarco(endo)plasmic reticulum Ca2+-ATPase type 2a (1.30+/-0.07 vs. 1.74+/-0.18 arbitrary units; P<or=0.05) and ryanodine receptor type 2 (1.86+/-0.13 vs. 3.57+/-0.12 arbitrary units; P<or=0.05) in HP rats. In summary, our data showed important intrinsic differences in cardiomyocyte properties that could explain some of the divergence observed in rats with high intrinsic aerobic exercise capacity.

The benefits of endurance training in cardiomyocyte function in hypertensive rats are reversed within four weeks of detraining

The aim of the present study was to verify the effects of low-intensity endurance training and detraining on the mechanical and molecular properties of cardiomyocytes from spontaneously hypertensive rats (SHRs). Male SHRs and normotensive control Wistar rats at 16-weeks of age were randomly divided into eight groups of eight animals: NC8 and HC8 (normotensive and hypertensive control for 8weeks); NT8 and HT8 (normotensive and hypertensive trained at 50-60% of maximal exercise capacity for 8weeks); NC12 and HC12 (normotensive and hypertensive control for 12weeks); NDT and HDT (normotensive and hypertensive trained for 8weeks and detrained for 4weeks). The total exercise time until fatigue (TTF) was determined by a maximal exercise capacity test. Resting heart rate (RHR) and systolic arterial pressure (SAP) were measured. After the treatments, animals were killed by cervical dislocation and left ventricular myocytes were isolated by enzymatic dispersion. Isolated cells were used to determine intracellular global Ca(2+) ([Ca(2+)]i) transient and cardiomyocyte contractility (1Hz; ~25°C). [Ca(2+)]i regulatory proteins were measured by Western blot, and the markers of pathologic cardiac hypertrophy by quantitative real-time polymerase chain reaction (q-RT-PCR). Exercise training augmented the TTF (NC8, 11.4±1.5min vs. NT8, 22.5±1.4min; HC8, 11.7±1.4min vs. HT8, 24.5±1.3min; P<0.05), reduced RHR (NT8initial, 340±8bpm vs. NT8final, 322±10bpm; HT8initial, 369±8bpm vs. HT8final, 344±10bpm; P<0.05), and SBP in SHR animals (HC8, 178±3mmHg vs. HT8, 161±4mmHg; P<0.05). HC8 rats showed a slower [Ca(2+)]i transient (Tpeak, 83.7±1.8ms vs. 71.7±2.4ms; T50%decay, 284.0±4.3ms vs. 264.0±4.1ms; P<0.05) and cell contractility (Vshortening, 86.1±6.7μm/s vs. 118.6±6.7μm/s; Vrelengthening, 57.5±7.4μm/s vs. 101.3±7.4μm/s; P<0.05), and higher expression of ANF (300%; P<0.05), skeletal α-actin (250%; P<0.05) and a decreased α/β-MHC ratio (70%; P<0.05) compared to NC8. Exercise training increased [Ca(2+)]i transient (NC8, 2.39±0.06F/F0 vs. NT8, 2.72±0.06F/F0; HC8, 2.28±0.05F/F0 vs. HT8, 2.82±0.05F/F0; P<0.05), and cell contractility (NC8, 7.4±0.3% vs. NT8, 8.4±0.3%; HC8, 6.8±0.3% vs. HT8, 7.8±0.3%; P<0.05). Furthermore, exercise normalized the expression of ANF, skeletal α-actin, and the α/β-MHC ratio in HT8 rats, augmented the expression of SERCA2a (NC8, 0.93±0.15 vs. NT8, 1.49±0.14; HC8, 0.83±0.13 vs. HT8, 1.32±0.14; P<0.05) and PLBser16 (NC8, 0.89±0.18 vs. NT8, 1.23±0.17; HC8, 0.77±0.17 vs. HT8, 1.32±0.16; P<0.05), and reduced PLBt/SERCA2a (NC8, 1.21±0.19 vs. NT8, 0.50±0.21; HC8, 1.38±0.17 vs. HT8, 0.66±0.21; P<0.05). However, all these adaptations returned to control values within 4weeks of detraining in both SHR and normotensive control animals. In conclusion, low-intensity endurance training induces positive benefits to left ventricular myocyte mechanical and molecular properties, which are reversed within 4weeks of detraining.

Long-term aerobic swimming training by rats reduces the number of aberrant crypt foci in 1,2-dimethylhydrazine-induced colon cancer

We determined the effect of long-term aerobic swimming training regimens of different intensities on colonic carcinogenesis in rats. Male Wistar rats (11 weeks old) were given 4 subcutaneous injections (40 mg/kg body weight each) of 1,2-dimethyl-hydrazine (DMH, dissolved in 0.9% NaCl containing 1.5% EDTA, pH 6.5), at 3-day intervals and divided into three exercise groups that swam with 0% body weight (EG1, N = 11), 2% body weight (EG2, N = 11), and 4% body weight of load (EG3, N = 10), 20 min/day, 5 days/week for 35 weeks, and one sedentary control group (CG, N = 10). At sacrifice, the colon was removed and counted for tumors and aberrant crypt foci. Tumor size was measured and intra-abdominal fat was weighed. The mean number of aberrant crypt foci was reduced only for EG2 compared to CG (26.21 +/- 2.99 vs 36.40 +/- 1.53 crypts; P < 0.05). Tumor incidence was not significantly different among groups (CG: 90%; EG1: 72.7%; EG2: 90%; EG3: 80%). Swimming training did not affect either tumor multiplicity (CG: 2.30 +/- 0.58; EG1: 2.09 +/- 0.44; EG2: 1.27 +/- 0.19; EG3: 1.50 +/- 0.48 tumors) or size (CG: 1.78 +/- 0.24; EG1: 1.81 +/- 0.14; EG2: 1.55 +/- 0.21; EG3: 2.17 +/- 0.22 cm(3)). Intra-abdominal fat was not significantly different among groups (CG: 10.54 +/- 2.73; EG1: 6.12 +/- 1.15; EG2: 7.85 +/- 1.24; EG3: 5.11 +/- 0.74 g). Aerobic swimming training with 2% body weight of load protected against the DMH-induced preneoplastic colon lesions, but not against tumor development in the rat.

Resistance training regulates cardiac function through modulation of miRNA-214.

Aims: To determine the effects of resistance training (RT) on the expression of microRNA (miRNA)-214 and its target in sarcoplasmic reticulum Ca2+-ATPase (SERCA2a), and on the morphological and mechanical properties of isolated left ventricular myocytes. Main methods: Male Wistar rats were divided into two groups (n = 7/group): Control (CO) or trained (TR). The exercise-training protocol consisted of: 4 × 12 bouts, 5×/week during 8 weeks, with 80% of one repetition maximum. Key findings: RT increased the left ventricular myocyte width by 15% and volume by 12%, compared with control animals (p < 0.05). The time to half relaxation and time to peak were 8.4% and 4.4% lower, respectively, in cells from TR group as compared to CO group (p < 0.05). RT decreased miRNA-214 level by 18.5% while its target SERCA2a expression were 18.5% higher (p < 0.05). Significance: Our findings showed that RT increases single left ventricular myocyte dimensions and also leads to faster cell contraction and relaxation. These mechanical adaptations may be related to the augmented expression of SERCA2a which, in turn, may be associated with the epigenetic modification of decreased miRNA-214 expression.

Treinamento físico para indivíduos HIV positivo submetidos à HAART: efeitos sobre parâmetros antropométricos e funcionais

introduction: The use of highly active antiretroviral therapy (HAART) has improved the prog nosis of HiV-infected individuals. However, HAART has been associated with the development of metabolic and fat distribution abnormalities, known as HiV-associated lipodystrophy syndrome (HiVAlS). Objective: This study investigated the impact of 24 weeks of resistance exercise with aerobic component (REAC) on anthropometric and functional parameters in HiV-infected patients undergoing HAART. Methods: n inety- nine HiV-infected patients were randomly allocated into four groups: exercise and lipodystrophy (n = 24; Ex + lip); exercise without lipodystrophy (n = 21; Ex + nolip); control and lipodystrophy (n = 27; noEx + lip); control without lipodystrophy (n = 27; noEx + nolip). Subjects from exercised groups (Ex+lip and Ex+nolip) participated in a 24-week REAC program. Anthropometric, strength and cardiorespiratory fitness tests were assessed at baseline and 24 weeks after intervention. Results: Body circumferences (p < 0.0001) and waist-hip ratio (p = 0.017) changed after 24 weeks of REAC in both exercised groups. The sum of seven skinfolds assessed, body fat percentage, body fat mass, total fat, central fat and peripheral subcutaneous fat reduced (p < 0.0001) in response to REAC. l ean body mass increased (p < 0.0001) in exercised groups, regardless of the outcome (lip or nolip). Strength and cardiorespiratory fitness increased (p < 0.0001) in both exercised groups in response to REAC. Conclusion: 24 weeks of REAC prevented the manifestation of changes arising from HiVldS and contributed to their reduction.

Exercise training prior to myocardial infarction attenuates cardiac deterioration and cardiomyocyte dysfunction in rats

OBJECTIVES: The present study was performed to investigate 1) whether aerobic exercise training prior to myocardial infarction would prevent cardiac dysfunction and structural deterioration and 2) whether the potential cardiac benefits of aerobic exercise training would be associated with preserved morphological and contractile properties of cardiomyocytes in post-infarct remodeled myocardium. METHODS: Male Wistar rats underwent an aerobic exercise training protocol for eight weeks. The rats were then assigned to sham surgery (SHAM), sedentary lifestyle and myocardial infarction or exercise training and myocardial infarction groups and were evaluated 15 days after the surgery. Left ventricular tissue was analyzed histologically, and the contractile function of isolated myocytes was measured. Students t-test was used to analyze infarct size and ventricular wall thickness, and the other parameters were analyzed by the Kruskal-Wallis test followed by Dunns test or a one-way analysis of variance followed by Tukeys test (p<0.05). RESULTS: Myocardial infarctions in exercise-trained animals resulted in a smaller myocardial infarction extension, a thicker infarcted wall and less collagen accumulation as compared to myocardial infarctions in sedentary animals. Myocardial infarction-induced left ventricular dilation and cardiac dysfunction, as evaluated by +dP/dt and -dP/dt, were both prevented by previous aerobic exercise training. Moreover, aerobic exercise training preserved cardiac myocyte shortening, improved the maximum shortening and relengthening velocities in infarcted hearts and enhanced responsiveness to calcium. CONCLUSION: Previous aerobic exercise training attenuated the cardiac dysfunction and structural deterioration promoted by myocardial infarction, and such benefits were associated with preserved cardiomyocyte morphological and contractile properties.