Wellington Lunz

Reproducibility of heart rate variability parameters measured in healthy subjects at rest and after a postural change maneuver

Heart rate variability (HRV) provides important information about cardiac autonomic modulation. Since it is a noninvasive and inexpensive method, HRV has been used to evaluate several parameters of cardiovascular health. However, the internal reproducibility of this method has been challenged in some studies. Our aim was to determine the intra-individual reproducibility of HRV parameters in short-term recordings obtained in supine and orthostatic positions. Electrocardiographic (ECG) recordings were obtained from 30 healthy subjects (20-49 years, 14 men) using a digital apparatus (sampling ratio = 250 Hz). ECG was recorded for 10 min in the supine position and for 10 min in the orthostatic position. The procedure was repeated 2-3 h later. Time and frequency domain analyses were performed. Frequency domain included low (LF, 0.04-0.15 Hz) and high frequency (HF, 0.15-0.4 Hz) bands. Power spectral analysis was performed by the autoregressive method and model order was set at 16. Intra-subject agreement was assessed by linear regression analysis, test of difference in variances and limits of agreement. Most HRV measures (pNN50, RMSSD, LF, HF, and LF/HF ratio) were reproducible independent of body position. Better correlation indexes (r > 0.6) were obtained in the orthostatic position. Bland-Altman plots revealed that most values were inside the agreement limits, indicating concordance between measures. Only SDNN and NNv in the supine position were not reproducible. Our results showed reproducibility of HRV parameters when recorded in the same individual with a short time between two exams. The increased sympathetic activity occurring in the orthostatic position probably facilitates reproducibility of the HRV indexes.

Long-term use of low-dose spironolactone in spontaneously hypertensive rats: Effects on left ventricular hypertrophy and stiffness

The aim of the present study was to evaluate the effect of low-dose spironolactone initiated during the early stages of hypertension development and to assess the effects of chronic pressure overload on ventricular remodeling in rats. Male spontaneously hypertensive rats (SHRs) (4 weeks) were randomized to receive daily spironolactone (20 mg/kg) or vehicle (mineral oil) from 4 weeks to 8 months of age. Systolic blood pressure was measured non-invasively by tail-cuff pletysmography at baseline, 4 and 8 months. Hemodynamic assessment was performed at the end of treatment by arterial and ventricular catheterization. An in situ left ventricular pressure-volume curve was created to evaluate dilatation and wall stiffness. Systolic blood pressure at 1 month of age was higher in SHRs than in the Wistar group; it increased throughout the follow-up period and remained elevated with treatment (Wistar: 136 ± 2, SHR: 197 ± 6.8, SHR-Spiro: 207 ± 7.1 mmHg; p < 0.05). Spironolactone reduced cardiac hypertrophy (Wistar: 1.25 ± 0.03 SHR: 1.00 ± 0.03, SHR-Spiro: 0.86 ± 0.02 g; p < 0.05) and left ventricular mass normalized to body weight (Wistar: 2.51 ± 0.06, SHR: 2.70 ± 0.08, 2.53 ± 0.07 mg/g; p < 0.05). Moreover, the left ventricular wall stiffness that was higher in SHRs was partially reduced by spironolactone treatment (Wistar: 0.370 ± 0.032; SHR: 0.825 ± 0.058; SHR-Spiro: 0.650 ± 0.023 mmHg/ml; p < 0.05). Our results show that long-term spironolactone treatment initiated at the early stage of hypertension development reduces left ventricular hypertrophy and wall stiffness in SHRs.

Effects of chronic treadmill training on body mass gain and visceral fat accumulation in overfed rats

This study evaluated the effects of chronic treadmill training on body mass gain and visceral fat accumulation in overfed rats. Overfeeding was induced by reducing the litter size to 3 male pups per mother during the suckling period. The litter size of control rats was adjusted to 10 male pups per mother. Seven weeks after birth overfed and normally fed rats were selected and assigned to a sedentary protocol or to a low-intensity treadmill training protocol (60 min, 5 times/week, for 9 weeks). Four groups (overfed sedentary, N = 23; normally fed sedentary, N = 32; overfed exercised, N = 18, and normally fed exercised, N = 18) were evaluated at 18 weeks. Data are reported as means +/- SEM. Initial body weight was similar in control and overfed rats [8.0 +/- 0.2 g (N = 42) vs 8.0 +/- 0.1 g (N = 50); P > 0.05] and body weight gain during the suckling period was higher in the overfed rats (30.6 +/- 0.9 vs 23.1 +/- 0.3 g; P < 0.05). Exercise attenuated the body weight gain of overfed compared to sedentary rats (505 +/- 14 vs 537 +/- 12 g; P < 0.05). The sedentary overfed rats showed higher visceral fat weight compared to normally fed animals (31.22 +/- 2.08 vs 21.94 +/- 1.76 g; P < 0.05). Exercise reduced visceral fat by 36.5% in normally fed rats and by 35.7% in overfed rats. Exercise attenuated obesity in overfed rats and induced an important reduction of visceral fat.

Kinetics of cardiac and vascular remodeling by spontaneously hypertensive rats after discontinuation of long-term captopril treatment

Angiotensin-converting enzyme inhibitors reduce blood pressure and attenuate cardiac and vascular remodeling in hypertension. However, the kinetics of remodeling after discontinuation of the long-term use of these drugs are unknown. Our objective was to investigate the temporal changes occurring in blood pressure and vascular structure of spontaneously hypertensive rats (SHR). Captopril treatment was started in the pre-hypertensive state. Rats (4 weeks) were assigned to three groups: SHR-Cap (N = 51) treated with captopril (1 g/L) in drinking water from the 4th to the 14th week; SHR-C (N = 48) untreated SHR; Wistar (N = 47) control rats. Subgroups of animals were studied at 2, 4, and 8 weeks after discontinuation of captopril. Direct blood pressure was recorded in freely moving animals after femoral artery catheterism. The animals were then killed to determine left ventricular hypertrophy (LVH) and the aorta fixed at the same pressure measured in vivo. Captopril prevented hypertension (105 + or - 3 vs 136 + or - 5 mmHg), LVH (2.17 + or - 0.05 vs 2.97 + or - 0.14 mg/g body weight) and the increase in cross-sectional area to luminal area ratio of the aorta (0.21 + or - 0.01 vs 0.26 + or - 0.02 microm(2)) (SHR-Cap vs SHR-C). However, these parameters increased progressively after discontinuation of captopril (22nd week: 141 + or - 2 mmHg, 2.50 + or - 0.06 mg/g, 0.27 + or - 0.02 microm(2)). Prevention of the development of hypertension in SHR by using captopril during the prehypertensive period prevents the development of cardiac and vascular remodeling. Recovery of these processes follows the kinetic of hypertension development after discontinuation of captopril.

Long-term intense resistance training in men is associated with preserved cardiac structure/function, decreased aortic stiffness, and lower central augmentation pressure.

Objective: There have been contradictory reports regarding resistance exercise and central arterial compliance. The American Heart Association has recommended its use in preventing/treating cardiovascular diseases. We examined the effects of long-term endurance running and intense resistance training on central hemodynamics, compared with healthy control (CON). Methods: Sixty-nine male participants, 25–50 years [19 intense resistance trained (IRT) group, 21 endurance runners, and 29 CON] were investigated by radial tonometry-pulse wave analysis, pulse wave velocity (PWV), and echocardiogram. Data were expressed as mean ± SE (median). Differences were tested by analysis of variance and analysis of covariance was used to adjust for confounding variables. Results: There were no differences among groups regarding age, height (Ht), brachial and central blood pressure. Resting heart rate (HR) was lower and high-density lipoprotein cholesterol (HDL-C) higher in endurance runners. Weight, peripheral pulse pressure, and pulse pressure amplification were higher and HDL-C lower in the IRT group. Left ventricular mass and creatine phosphokinase were higher in trained participants. Relative wall thickness was similar among groups. The ratio of the velocity of peak E and A waves (E/A) was higher and PWV significantly lower in endurance runners (7.2 ± 0.14 m/s) and IRT (7.5 ± 0.14 m/s) as compared with CON (8.2 ± 0.16 m/s) even after adjustments for age, Ht, HR and mean arterial pressure (MAP), or mean systolic pressure. Differences in central augmentation pressure (cAP) adjusted for age, height, systolic or MAP, PWV, and HR (IRT equal to 0.08 ± 0.9, CON equal to 3.4 ± 0.9 and endurance running equal to 3.6 ± 1) were no longer significant after further adjustments to aortic diameter or weight. Conclusion: Long-term resistance training in men is associated with preserved cardiac structure/function, decreased aortic stiffness, and lower cAP.

Comparação da resposta autonômica cardiovascular de praticantes de musculação, corredores de longa distância e não praticantes de exercício

The aim of the study was to compare the cardiovascular autonomic response (CAR) of recreational weight trainers, long distance runners and non-exercised subjects. Men, 21 to 55 years old, were grouped in: recreational weight trainers (W, n = 31), long distance runners (R, n = 28) and non-exercised (C, n = 35). Four strategies of evaluation of the CAR were selected: Resting heart rate (RHR), cold pressor test (CPT), heart rate variability (HRV) and heart rate recovery (HHR) following maximal exercise test. The RHR was lower (R = 54 ± 2; W = 62 ± 2; C= 65 ± 2 bpm; mean ± SE) and the HHR 60s post exercise was larger in the R group (R = 34 ± 3; W = 23 ± 1; C = 24 ± 2 bpm). The R group presented larger high-frequency (HF; 55.1 ± 4.0 n.u) and smaller low-frequency (LF; 43.1 ± 4.0 n.u) components of HRV than C group (HF = 40.7 ± 3.3; LF = 56.7 ± 3.5 n.u.). The W group did not show any differences compared to C group. The studys conclusion was that long-term weight-training program, unlike of long-term running training, it is not able to alter significantly the regulatory pattern of CAR.

Transição metabólica no teste progressivo de pessoas treinadas com musculação e corrida

INTRODUCCION: La especificidad de las adaptaciones cardiorrespiratorias y metabolicas del entrenamiento aerobico y de fuerza evoca diferentes respuestas durante la prueba de esfuerzo cardiopulmonar (PECP). Objetivo: Describir el comportamiento cardiorrespiratorio durante la transicion metabolica (TM) de la PECP, de corredores y culturistas, en comparacion con un grupo control. METODOS: Hombres entre 21 y 55 anos fueron agrupados de la siguiente manera: grupo corredores (GC; n = 30), grupo culturistas (GCU; n = 23) y grupo control (GCON; n = 38). Los participantes se sometieron a evaluacion antropometrica y PECP, con el analisis de umbral anaerobico ventilatorio (UAV) y el punto de compensacion respiratoria (PCR). Se calculo la economia de carrera mediante la relacion entre VO2 y velocidad de la prueba (ECINCLINA). RESULTADOS: En la transicion metabolica, la carga (km/h) fue mayor en el GC (4,2 ± 1,6) vs. GCON (2,7 ± 1,6) y GCU (2,8 ± 1,0); P < 0,05. El GC presento mayor VO2UAV; VO2RCPy VO2MAX. (36 ± 8; 46 ± 8; 51 ± 8 vs. 24 ± 6; 35 ± 5; 40 ± 6 y 26 ± 6; 35 ± 6; 40 ± 7 ml.kg-1.min-1; P < 0,05), en comparacion con GCON y GCU, respectivamente, incluso despues de la correccion alometrica. La FCREP fue menor entre GD y GCON (GC = 52 ± 6; GCON = 60 ± 8 bpm; P < 0,05). La fase de TM en el GC presento mayor aumento de carga de trabajo y menos cambios en el pulso de oxigeno en comparacion con GCON y GCU. El VO2 durante la TM no difirio entre los grupos. El GC mostro menor ECINCLINA en los momentos finales de la prueba en comparacion con GCON y GCU. CONCLUSION: El GC mostro una mayor eficiencia metabolica en las transiciones progresivas de esfuerzo en comparacion con GCON y GCU, y GCU no muestra una mayor capacidad de transicion en el PECP, incluso en comparacion con los individuos sedentarios.

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 [3H]L-arginine to [3H]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-eNOSSer1177 (over 200%) and decreased inhibitory p-nNOSSer852 (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.

Marcadores hematológicos de corredores amadores do município de Vitória/ES

Abstract Introduction: The immune system presents close relationship to physical exercise. Meanwhile, few studies have verified the ...

Colon cancer and swimming exercise: effect on wistar rat testes

ABSTRACT This study was undertaken to determine whether colon cancer (CC) and chronic swimming exercise alter rat testis. Eleven weeks old rats were distributed into control group (n=6) and the groups that were induced to develop CC by dimethylhydrazine injections (nEG, EG0, EG2 and EG4; n=10 each group). In the group nEG, the rats did not swim, whereas groups EG0, EG2 and EG4, underwent a swimming program with distinct loads (0, 2 and 4% of body mass, respectively) for 35 weeks. The morphometry, stereology and cell counts showed damage caused by the CC on the germ epithelium. These results were noteworthy since this was the first report to associate the CC with testicular damage. Swimming exercise had no significant role in reducing, or increasing the CC effects on the testis, despite having slightly improved the testis structure of the exercised rats without load. In conclusion, CC caused testis impairment, which could not be avoided by the swimming exercise. Key words: 1,2-dimethylhydrazine, fertility, reproduction, spermatogenesis