Sleep quality and regular physical activity in reducing cardiac risk.

BACKGROUND: Adolescents with sedentary behavior, spending many hours in front of the television and electronic devices, develop early involvement of cardiovascular disease and obesity. These sedentary behaviors increased significantly in this age group during the pandemic of 2020/2021. Sleep directly influences aspects of health, such as blood pressure and cardiac autonomic balance and exercise has a protective effect on these same physiological parameters. OBJECTIVE: This study aimed to examine whether or not physically active adolescents positively influence HRV and cardiovascular parameters despite poor sleep quality. METHODS: This is an analytic and transversal study. Sleep quality, physical activity levels, blood pressure, and heart rate variability (HRV) were measured. Two-way ANOVA and Tuckey post hoc test evaluated the difference between groups. RESULTS: Among 352 adolescents entrolled, mean age was 15.8 ± 0.24 years. It was observed that compared to the physically active group with poor sleep quality, the sedentary poor sleep quality group presented a more significant deficit in blood pressure and autonomic parameters such as pNN50, SD1, and HF. CONCLUSION: Adolescents who practiced physical activity regularly have shown better HRV and sleep quality compared with sedentary adolescents.

Exercise Training Plus Sildenafil Treatment: Role on Autonomic and Inflammatory Markers.

The current study aimed to determine the effects of sildenafil-associated aerobic exercise training (ET) on the physical performance, hemodynamic, autonomic and inflammatory parameters of rats. Male Wistar rats were randomly assigned to: sedentary rats placebo-treated (SP); sedentary rats sildenafil-treated (SS); trained rats placebo-treated (TP); and trained rats sildenafil-treated (TS). Sildenafil treatment consisted of 8 weeks of daily oral gavage (1.5 mg/kg), one hour before the session of ET (60-75% of maximal running speed, 5 days/week, for 8 weeks). After ET period, physical capacity, hemodynamic, autonomic and skeletal muscle inflammatory profile were assessed. Chronic sildenafil treatment causes an additional increase of physical capacity in aerobically trained rats. However, these beneficial effects were accompanied by unwanted alterations, as increased of arterial pressure and peripheral sympathetic modulation, as well as exacerbated inflammatory status on skeletal muscle of rats. Taken together, these data suggest the positive and negative effects of sildenafil chronic administration, associated to aerobic ET, at doses used in clinical practice. This report stresses the importance of paying greater attention to the indiscriminate use of this substance in high-performance sports.

Aerobic exercise training delays cardiac dysfunction and improves autonomic control of circulation in diabetic rats undergoing myocardial infarction.

BACKGROUND: Exercise training (ET) has been used as a nonpharmacological strategy for treatment of diabetes and myocardial infarction (MI) separately. We evaluated the effects ET on functional and molecular left ventricular (LV) parameters as well as on autonomic function and mortality in diabetics after MI. METHODS AND RESULTS: Male Wistar rats were divided into control (C), sedentary-diabetic infarcted (SDI), and trained-diabetic infarcted (TDI) groups. MI was induced after 15 days of streptozotocin-diabetes induction. Seven days after MI, the trained group underwent ET protocol (90 days, 50-70% maximal oxygen consumption-VO(2)max). LV function was evaluated noninvasively and invasively; baroreflex sensitivity, pulse interval variability, cardiac output, tissue blood flows, VEGF mRNA and protein, HIF1-α mRNA, and Ca(2+) handling proteins were measured. MI area was reduced in TDI (21 ± 4%) compared with SDI (38 ± 4%). ET induced improvement in cardiac function, hemodynamics, and tissue blood flows. These changes were probable consequences of a better expression of Ca(2+) handling proteins, increased VEGF mRNA and protein expression as well as improvement in autonomic function, that resulted in reduction of mortality in TDI (33%) compared with SDI (68%) animals. CONCLUSIONS: ET reduced cardiac and peripheral dysfunction and preserved autonomic control in diabetic infarcted rats. Consequently, these changes resulted in improved VO(2)max and survival after MI.

ACUTE TRANSCRANIAL DIRECT CURRENT STIMULATION (tDCS) IMPROVES VENTILATORY VARIABILITY AND AUTONOMIC MODULATION IN RESISTANT HYPERTENSIVE PATIENTS.

Here, we assessed the impact of one session of transcranial direct current stimulation (tDCS) or SHAM (20 min, each) on ventilatory responses to cardiopulmonary exercise test, central and peripheral blood pressure (BP), and autonomic modulation in resistant hypertensive (RHT) patients. RHT subjects (n = 13) were randomly submitted to SHAM and tDCS crossing sessions (1 week of "washout"). Patients and a technician who set the tDCS/Sham room up were both blind. After brain stimulation, patients were submitted to a cardiopulmonary exercise test to evaluate ventilatory and cardiovascular response to exercise. Hemodynamic (Finometer®, Beatscope), and autonomic variables were measured at baseline (before tDCS/Sham) and after incremental exercise. RESULTS: Our study shows that tDCS condition improved heart rate recovery, VO2 peak, and vagal modulation (after cardiopulmonary exercise test); attenuated the ventilatory variability response, central and peripheral blood pressure well as sympathetic modulation (after cardiopulmonary exercise test) in comparison with SHAM. These data suggest that acute tDCS sessions prevented oscillatory ventilation behavior during the cardiopulmonary exercise test and mitigated the increase of systolic blood pressure in RHT patients. After the exercise test, tDCS promotes better vagal reentry and improved autonomic modulation, possibly reducing central blood pressure and aortic augmentation index compared to SHAM. Brazilian Registry of Clinical Trials (ReBEC): https://ensaiosclinicos.gov.br/rg/RBR-8n7c9p.

Carvacrol reduces blood pressure, arterial responsiveness and increases expression of MAS receptors in spontaneously hypertensive rats.

AIM: To analyze the effect of the use of carvacrol in the cardiovascular system of spontaneously hypertensive rats (SHR). METHODS: Methods: Twenty animals were allocated in four groups, one group control Wistar receiving only sorbitol, used as vehicle of administration of the carvacrol (Wistar-Vehicle), one control group SHR, also receive only sorbitol (SHR-Vehicle), a third, treated with losartan (SHR-Losartan/50 mg/kg), and the fourth, treated with carvacrol (SHR - Carvacrol/20 mg/kg). Sorbitol, losartan and carvacrol were administered by oral gavage daily for 30-day. Hemodynamic variables, vascular reactivity, biochemical parameters, and expression of Mas and AT1 receptors in kidney tissues were analyzed. RESULTS: SHR- Carvacrol group showed a maximal effect of inhibition of 56% in the curve of norepinephrine. The Emax of the curves with Ca2+ were smaller in the groups SHR-losartan (40.17%) and SHR-carvacrol (35.71%) when compared to the SHR-Vehicle. The carvacrol increased the expression of the MAS receptors in kidney tissue. CONCLUSION: Thirty days of treatment with carvacrol showed an antihypertensive effect associated with less peripheral vascular resistance. Also, treatment with carvacrol increased the expression of MAS receptors in kidney tissue.

Ace gene dosage influences the development of renovascular hypertension.

1. Clinical and experimental evidence highlights the importance of the renin-angiotensin system in renovascular hypertension. Furthermore, genetic factors affecting angiotensin-converting enzyme (ACE) could influence the development of renovascular hypertension. 2. To test the effect of small gene perturbations on the development of renovascular hypertension, mice harbouring two or three copies of the Ace gene were submitted to 4 weeks of two-kidney, one-clip (2K1C) hypertension. Blood pressure (BP), cardiac hypertrophy, baroreflex sensitivity and blood pressure and heart rate variability were assessed and compared between the different groups. 3. The increase in BP induced by 2K1C was higher in mice with three copies of the Ace gene compared with mice with only two copies (46 vs 23 mmHg, respectively). Moreover, there was a 3.8-fold increase in the slope of the left ventricle mass/BP relationship in mice with three copies of the Ace gene. Micewith three copies of the Ace gene exhibited greater increases in cardiac and serum ACE activity than mice with only two copies of the gene. Both baroreflex bradycardia and tachycardia were significantly depressed in mice with three copies of the Ace gene after induction of 2K1C hypertension. The variance in basal systolic BP was greater in mice with three copies of the Ace gene after 2K1C hypertension compared with those with only two copies of the gene (106 vs 54%, respectively). In addition, the low-frequency component of the pulse interval was higher mice with three copies of the Ace gene after 2K1C hypertension compared with those with only two (168 vs 86%, respectively). Finally, in mice with three copies of the Ace gene, renovascular hypertension induced a 6.1-fold increase in the sympathovagal balance compared with a 3.2-fold increase in mice with only two copies of the gene. 4. Collectively, these data provide direct evidence that small genetic disturbances in ACE levels per se have an influence on haemodynamic, cardiac mass and autonomic nervous system responses in mice under pathological perturbation.

Dose-related Effects of Resveratrol in Different Models of Pulmonary Arterial Hypertension: A Systematic Review.

BACKGROUND: Pulmonary Arterial Hypertension (PAH) is a severe and progressive disease of pulmonary arterioles. This pathology is characterized by elevation of the pulmonary vascular resistance and pulmonary arterial pressure, leading to right heart failure and death. Studies have demonstrated that resveratrol possesses a protective effect on the mechanisms related to the genesis of the PAH-induced by different models. OBJECTIVE: This study aimed to investigate the dose-related effects of resveratrol in different models of pulmonary arterial hypertension. METHODS: To identify eligible papers, we performed a systematic literature search on Scielo, Pub- Med, and Scholar Google. The research was limited to articles written in English in the last 10 years. We used the following descriptors to search: Pulmonary Arterial Hypertension and Resveratrol, OR Resveratrol, and Animal models of Pulmonary Arterial Hypertension, OR Resveratrol, and in vitro models of Pulmonary Arterial Hypertension. RESULTS: 1724 studies were identified through the descriptors used, fifty-five studies with different models of pulmonary arterial hypertension were selected for the full review, forty-four were excluded after application of exclusion and inclusion criteria, totalizing eleven studies included in this systematic review. CONCLUSION: The results showed that resveratrol, at low and high doses, protects in a dosedependent manner against the development of PAH induced through monocrotaline, normoxia and hypoxia models. In addition to having chemopreventive, anti-inflammatory, antioxidant and antiproliferative properties. In the case of PAH-related myocardial injury, resveratrol protects cells from apoptosis, thus working as an antiapoptotic agent.

Pyridostigmine Improves the Effects of Resistance Exercise Training after Myocardial Infarction in Rats.

Myocardial infarction (MI) remains the leading cause of morbidity and mortality worldwide. Exercise training and pharmacological treatments are important strategies to minimize the deleterious effects of MI. However, little is known about the effects of resistance training combined with pyridostigmine bromide (PYR) treatment on cardiac and autonomic function, as well as on the inflammatory profile after MI. Thus, in the present study, male Wistar rats were randomly assigned into: control (Cont); sedentary infarcted (Inf); PYR - treated sedentary infarcted rats (Inf+P); infarcted rats undergoing resistance exercise training (Inf+RT); and infarcted rats undergoing PYR treatment plus resistance training (Inf+RT+P). After 12 weeks of resistance training (15-20 climbs per session, with a 1-min rest between each climb, at a low to moderate intensity, 5 days a week) and/or PYR treatment (0.14 mg/mL of drink water), hemodynamic function, autonomic modulation, and cytokine expressions were evaluated. We observed that 3 months of PYR treatment, either alone or in combination with exercise, can improve the deleterious effects of MI on left ventricle dimensions and function, baroreflex sensitivity, and autonomic parameters, as well as systemic and tissue inflammatory profile. Furthermore, additional benefits in a maximal load test and anti-inflammatory state of skeletal muscle were found when resistance training was combined with PYR treatment. Thus, our findings suggest that the combination of resistance training and PYR may be a good therapeutic strategy since they promote additional benefits on skeletal muscle anti-inflammatory profile after MI.

Maximal exercise test is a useful method for physical capacity and oxygen consumption determination in streptozotocin-diabetic rats.

BACKGROUND: The aim of the present study was to investigate the relationship between speed during maximum exercise test (ET) and oxygen consumption (VO2) in control and STZ-diabetic rats, in order to provide a useful method to determine exercise capacity and prescription in researches involving STZ-diabetic rats. METHODS: Male Wistar rats were divided into two groups: control (CG, n = 10) and diabetic (DG, n = 8). The animals were submitted to ET on treadmill with simultaneous gas analysis through open respirometry system. ET and VO2 were assessed 60 days after diabetes induction (STZ, 50 mg/Kg). RESULTS: VO2 maximum was reduced in STZ-diabetic rats (72.5 +/- 1 mL/Kg/min-1) compared to CG rats (81.1 +/- 1 mL/Kg/min-1). There were positive correlations between ET speed and VO2 (r = 0.87 for CG and r = 0.8 for DG), as well as between ET speed and VO2 reserve (r = 0.77 for CG and r = 0.7 for DG). Positive correlations were also obtained between measured VO2 and VO2 predicted values (r = 0.81 for CG and r = 0.75 for DG) by linear regression equations to CG (VO2 = 1.54 * ET speed + 52.34) and DG (VO2 = 1.16 * ET speed + 51.99). Moreover, we observed that 60% of ET speed corresponded to 72 and 75% of VO2 reserve for CG and DG, respectively. The maximum ET speed was also correlated with VO2 maximum for both groups (CG: r = 0.7 and DG: r = 0.7). CONCLUSION: These results suggest that: a) VO2 and VO2 reserve can be estimated using linear regression equations obtained from correlations with ET speed for each studied group; b) exercise training can be prescribed based on ET in control and diabetic-STZ rats; c) physical capacity can be determined by ET. Therefore, ET, which involves a relatively simple methodology and low cost, can be used as an indicator of cardio-respiratory capacity in future studies that investigate the physiological effect of acute or chronic exercise in control and STZ-diabetic male rats.

Effects of soccer training during preseason on physical and physiological variables in youth soccer players

Abstract Aim: This study aimed to explore the effects of a training program during the pre-season on aerobic and anaerobic performance, hemodynamics, autonomic variables, and sleep quality in youth soccer players. Methods: Nineteen athletes, with an average age of 17 ± 1 years, participated in the study. The multicomponent training protocol was divided into technical, tactical, and physical practice for four weeks. The cardiac autonomic modulation was obtained through an electrocardiogram and blood pressure values were measured by a sphygmomanometer. The athletes answered the Pittsburgh questionnaire that assessed sleep patterns and issues. The VO2max was analyzed using the Intermittent Recovery Test Yo-Yo level 1. The RAST test was used to assess anaerobic power. Results: There was improvement in Heart Rate Variability (HRV) indicated by the increase in indexes, mean square root of the differences between normal cycles (RMSSD), low frequency increase (LF) (p = 0.04; d = 0.70), high frequency decrease (HF) (p = 0.01; d = 1.02) and the LF / HF sympathovagal index (p = 0.03; d = 0.70), variables related to faster recovery. An improvement in the components of sleep duration (p = 0.03) and quality (p = 0.02) of baseline and post-intervention sleep was also observed. Conclusion: The four-week multicomponent protocol contributed to improving VO2max, improving fatigue rates, quality of sleep, and maximum power. Additionally, we observe that youth soccer athletes had physiological and hemodynamic adaptations that resulted in an improvement in cardiac autonomic modulation and sleep patterns after four weeks of training.

Low intensity resistance training improves systolic function and cardiovascular autonomic control in diabetic rats.

AIMS: We evaluated the effects of low intensity resistance training (RT) on left ventricular (LV) function, baroreflex sensitivity (BRS), and cardiovascular autonomic control of streptozotocin-induced diabetic rats. METHODS: Male Wistar rats were divided into (n=8 each group): sedentary control (SC), trained control (TC), sedentary diabetic (SD), and trained diabetic (TD). Trained groups underwent low intensity RT (40%-50% 1 repetition maximum) for 10 weeks. Echocardiographic evaluation, arterial pressure (AP), heart rate (HR), BRS, and autonomic measurements were performed. RESULTS: Diabetes induced an increase in glycemia and a reduction in body weight in diabetics when compared with control animals. Diabetic rats displayed cardiac dysfunction, reduced systolic AP and HR, impaired BRS and autonomic derangement when compared to control rats. RT improved ejection fraction (SD: 68%±1.3% vs. TD: 75%±3.0%) and velocity of circumferential fiber shortening (SD: 0.32±0.02 vs. TD: 0.40±0.01 circ/seg.10(-4)). Trained diabetic rats presented increased AP (+10.2%), HR (+10.4%), and BRS after RT protocol. CONCLUSIONS: Low intensity RT induced an increase in systolic function in diabetic rats. This may be due to positive LV remodeling and BRS improvement, which may have played an important role in the attenuation of hemodynamic impairment and cardiac autonomic neuropathy in streptozotocin-diabetic rats.

Impact of myocardial infarction on cardiac autonomic function in diabetic rats.

AIMS: We evaluated autonomic and hemodynamic parameters and maximal oxygen consumption (VO(2)max) as possible determinants of mortality in streptozotocin (STZ) diabetic rats after myocardial infarction (MI). METHOD: Male Wistar rats were divided into (n=8 of each): control sham (CS), diabetes sham (DS), MI (I), and diabetes+MI (DI). MI was induced 15 days after STZ induction. VO(2)max was measured at 3 (basal), 30, 60, and 91 days after MI. Hemodynamic and autonomic parameters were evaluated 92 days after MI. RESULTS: MI area was similar in infarcted groups (~44%). Mortality rate increased in the DI (70%) compared with I (53%) group. Cardiopulmonary baroreflex, sympathetic (48%) and vagal (33%) tonus, low frequency (LF) band (57%), and LF/high frequency (HF) band ratio (53%) were reduced in DI compared with I animals. Furthermore, cardiac output (CO), peripheral vascular resistance (PVR) impairment, and VO(2)max reductions were observed in the DI compared with the I group. CONCLUSIONS: Our data suggest that the CO and PVR changes as well as VO(2)max reduction were probably associated with additional cardiac autonomic control impairment, and, consequently, increased mortality rate in diabetic rats after a chronic myocardial infarction.

Effect of simvastatin in the autonomic system is dependent on the increased gain/sensitivity of the baroreceptors.

A number of mechanisms have been proposed to explain the pleiotropic effect of statin therapy to reduce sympathetic outflow in cardiovascular disease. We tested the hypothesis that statin treatment could improve baroreflex gain-sensitivity triggered by morphological adaptations in the mechanoreceptor site, thus reducing sympathetic activity, regardless of arterial pressure (AP) level reduction. Male spontaneously hypertensive rats (SHR) were divided into control (SHR, n = 8) and SHR-simvastatin (5 mg/kg/day, for 7 days) (SHR-S, n = 8). After treatment, AP, baroreflex sensitivity (BRS) in response to AP-induced changes, aortic depressor nerve activity, and spectral analyses of pulse interval (PI) and AP variabilities were performed. Internal and external carotids were prepared for morphoquantitative evaluation. Although AP was similar between groups, sympathetic modulation, represented by the low frequency band of PI (SHR: 6.84 ± 3.19 vs. SHR-S: 2.41 ± 0.96 msec(2)) and from systolic AP variability (SHR: 3.95 ± 0.36 vs. SHR-S: 2.86 ± 0.18 mmHg(2)), were reduced in treated animals. In parallel, simvastatin induced an increase of 26% and 21% in the number of elastic lamellae as well as a decrease of 9% and 25% in the carotid thickness in both, external and internal carotid, respectively. Moreover, improved baroreceptor function (SHR: 0.78 ± 0.03 vs. SHR-S: 1.06 ± 0.04% mv/mmHg) was observed in addition to a 115% increase in aortic depressor nerve activity in SHR-S rats. Therefore, our data suggest that the reduction of sympathetic outflow in hypertension by simvastatin treatment may be triggered by structural changes in the carotid arteries and increased BRS in response to an improvement of the baroreceptors discharge and consequently of the afferent pathway of the baroreflex arch.

Exercise training reduces sympathetic modulation on cardiovascular system and cardiac oxidative stress in spontaneously hypertensive rats.

BACKGROUND: Spontaneously hypertensive rats (SHRs) show increased cardiac sympathetic activity, which could stimulate cardiomyocyte hypertrophy, cardiac damage, and apoptosis. Norepinephrine (NE)-induced cardiac oxidative stress seems to be involved in SHR cardiac hypertrophy development. Because exercise training (ET) decreases sympathetic activation and oxidative stress, it may alter cardiac hypertrophy in SHR. The aim of this study was to determine, in vivo, whether ET alters cardiac sympathetic modulation on cardiovascular system and whether a correlation exists between cardiac oxidative stress and hypertrophy. METHODS: Male SHRs (15-weeks old) were divided into sedentary hypertensive (SHR, n = 7) and exercise-trained hypertensive rats (SHR-T, n = 7). Moderate ET was performed on a treadmill (5 days/week, 60 min, 10 weeks). After ET, cardiopulmonary reflex responses were assessed by bolus injections of 5-HT. Autoregressive spectral estimation was performed for systolic arterial pressure (SAP) with oscillatory components quantified as low (LF: 0.2-0.75 Hz) and high (HF: 0.75-4.0 Hz) frequency ranges. Cardiac NE concentration, lipid peroxidation, antioxidant enzymes activities, and total nitrates/nitrites were determined. RESULTS: ET reduced mean arterial pressure, SAP variability (SAP var), LF of SAP, and cardiac hypertrophy and increased cardiopulmonary reflex responses. Cardiac lipid peroxidation was decreased in trained SHRs and positively correlated with NE concentrations (r = 0.89, P < 0.01) and heart weight/body weight ratio (r = 0.72, P < 0.01), and inversely correlated with total nitrates/nitrites (r = -0.79, P < 0.01). Moreover, in trained SHR, cardiac total nitrates/nitrites were inversely correlated with NE concentrations (r = -0.82, P < 0.01). CONCLUSIONS: ET attenuates cardiac sympathetic modulation and cardiac hypertrophy, which were associated with reduced oxidative stress and increased nitric oxide (NO) bioavailability.