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Objective: This study evaluated the impact of functional training (FT) on the ambulatory blood pressure and physical fitness of resistant hypertensive older adults., Method: This randomized clinical and controlled rehearsal involved 15 participants from Juazeiro do Norte-CE divided into two groups: a control group (CG), n = 7, without physical training, and an experimental group (EG), n = 8, subjected to 24 sessions of FT. The comparative analysis included ambulatory blood pressure (24 h mapping) and physical fitness (Senior Fitness Test), using an ANOVA of two factors, an alpha of 0.05, and a post hoc by Bonferroni where necessary. The dimension of the intervention effect was verified using Eta Squared., Results: The results show that FT promoted a significant reduction in systolic blood pressure (SAP) during the day and at night, as well as improving physical fitness, including the force/resistance of the lower and upper limbs, physical mobility, and aerobic resistance. The flexibility of the upper and lower limbs was not affected., Conclusion: It is concluded that FT is effective in reducing SAP and improving physical fitness in resistant older adults. However, this type of training may positively influence general physical fitness of older adults with resistant hypertension.

Background: Strength training has beneficial effects on kidney disease, in addition to helping improve antioxidant defenses in healthy animals., Objective: To verify if strength training reduces oxidative damage to the heart and contralateral kidney caused by the renovascular hypertension induction surgery, as well as to evaluate alterations in the activity of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) endogenous antioxidant enzymes., Methods: Eighteen male rats were divided into three groups (n=6/group): sham, hypertensive, and trained hypertensive. The animals were induced to renovascular hypertension through left renal artery ligation. Strength training was initiated four weeks after the induction of renovascular hypertension, continued for a 12-weeks period, and was performed at 70% of 1RM. After the training period, the animals were euthanized and the right kidney and heart were removed for quantitation of hydroperoxides, malondialdehyde and sulfhydryl groups, which are markers of oxidative damage. In addition, the activity of SOD, CAT, and GPx antioxidant enzymes was also measured. The adopted significance level was 5% (p < 0.05)., Results: After strength training, a reduction in oxidative damage to lipids and proteins was observed, as could be seen by reducing hydroperoxides and total sulfhydryl levels, respectively. Furthermore, an increased activity of superoxide dismutase, catalase, and glutathione peroxidase antioxidant enzymes was observed., Conclusion: Strength training is able to potentially reduce oxidative damage by increasing the activity of antioxidant enzymes. (Arq Bras Cardiol. 2021; 116(1):4-11).

Exercise therapy is a conservative strategy to manage hypertension. The aim of this study was to investigate the effects of a 12-week equipment-based Pilates training program on the hemodynamics of medication-controlled hypertensive women. Forty-five women were classified into two groups: medication-controlled hypertensive (n = 30) or control (n = 15). To be eligible for the hypertensive group, participants had to have a clinical diagnosis of hypertension, be taking medication to control their blood pressure and not to have done any exercise activity in the previous three months. In the control group, the participants needed to have normal blood pressure levels and not to have done any exercise activity in the previous three months. All women participated in a 12-week equipment-based Pilates training program (2 × 60min sessions per week). Systolic and diastolic blood pressure (SBP, DBP), heart rate (HR) and creatine kinase levels (CK) were assessed before and after the program. SBP, DBP and heart rate were also assessed before and after each session. There was no statistically significant difference after Pilates training for systolic (normotensive MD 4.1, 95%CI -9.2 to 17.5, hypertensive MD 3.8, 95%CI -5.3 to 13.1) and diastolic (normotensive MD 5.8, 95%CI -2.0 to 13.7, hypertensive MD 4.0, 95%CI -4.3 to 12.4) blood pressure. Heart rate was reduced after Pilates training in both normotensive (MD 4.5, 95%CI 1.1 to 7.8) and medication-controlled hypertensive (MD 7.9, 95%CI 4.4 to 11.4) women. Creatine kinase activity was reduced after Pilates training in medication-controlled hypertensive women (p = 0.019). Blood pressure was not altered, but heart rate and creatinine kinase activity were reduced following 12 weeks of Equipment-based Pilates training., Competing Interests: Declaration of competing interest None., (Copyright © 2020 Elsevier Ltd. All rights reserved.)

Background and objectives: The practice of physical exercise, especially resistance exercise, is important for the treatment and/or prevention of cardiovascular risk factors in adult individuals. However, there are few studies on its effects on adolescent individuals. Therefore, the aim of the present study was to evaluate the effects of applying a 12-week resistance training program on cardiovascular risk factors in adolescents. Materials and Methods: Thus, 122 adolescents aged 13-16 years of both genders participated in the study from school in the city of Lagarto, Sergipe (SE), Brazil, divided into two groups: Control Group (CG) and Group undergoing resistance training (RTG). Blood collection and anthropometric measurements were performed before and after the 12-week resistance training program (RTP). Results: After 12 weeks of the RTP in the adolescents, there was a reduction in the triglyceride variables (9.55%, p = 0.0286), Low-Density Lipoproteins (LDL) (5.42%, p = 0.0244), non-High-Density Lipoproteins (HDL) (5.40%, p = 0.0019), blood glucose (6.71%, p = 0.0040), systolic blood pressure (10.13%, p < 0.0001), as well as an increase in the body weight variable (1.73%, p = 0.0003). Conclusions: It was concluded that a 12-week RTP can prevent and/or alleviate the development of several chronic degenerative diseases in adulthood and that resistance training is important for maintaining the health of adolescents.

Aims: We evaluated the acute effects of different intensities of resistance exercise over endothelium-dependent vasodilatation, eNOSser1177 phosphorylation level and endothelial production of NO in superior mesenteric artery of healthy rats., Main Methods: Groups: control (Ct), resistance exercise in the intensities of 30% (Ex30%), 50% (Ex50%) and 70% (Ex70%) of the maximal load established by the maximal repetition test (1RM). Exercise protocol: 15 sets of 10 repetitions. The rings of mesenteric artery were mounted in an isometric system or were prepared for further implementation of Western blot and DAF-FM techniques., Key Findings: The maximal response of the relaxation induced by insulin was not altered in the animals of the Ex30% group when compared to the Ct group. However, the animals of the Ex50% and Ex70% groups presented an increase in this response when compared to the Ct group. The eNOSser1177 phosphorylation levels showed an increase in Ex50% and Ex70% groups when compared to the Ct (1.6-fold and 3.3-fold, respectively). In the endothelial production of NO, it was observed that the Ex30% group did not show alteration in the NO production when compared to the Ct group. On the other hand, the animals exercised in the Ex50% and Ex70% groups showed increase in the NO synthesis when compared to the animals in the Ct group., Significance: Our results suggest that the magnitude of these vascular endothelium adjustments is strongly related to the increase of the resistance exercise intensity from the intensity of 50% of 1 RM.

Background: Resistance exercise effects on cardiovascular parameters are not consistent., Objectives: The effects of resistance exercise on changes in blood glucose, blood pressure and vascular reactivity were evaluated in diabetic rats., Methods: Wistar rats were divided into three groups: control group (n = 8); sedentary diabetic (n = 8); and trained diabetic (n = 8). Resistance exercise was carried out in a squat device for rats and consisted of three sets of ten repetitions with an intensity of 50%, three times per week, for eight weeks. Changes in vascular reactivity were evaluated in superior mesenteric artery rings., Results: A significant reduction in the maximum response of acetylcholine-induced relaxation was observed in the sedentary diabetic group (78.1 ± 2%) and an increase in the trained diabetic group (95 ± 3%) without changing potency. In the presence of NG-nitro-L-arginine methyl ester, the acetylcholine-induced relaxation was significantly reduced in the control and trained diabetic groups, but not in the sedentary diabetic group. Furthermore, a significant increase (p < 0.05) in mean arterial blood pressure was observed in the sedentary diabetic group (104.9 ± 5 to 126.7 ± 5 mmHg) as compared to that in the control group. However, the trained diabetic group showed a significant decrease (p < 0.05) in the mean arterial blood pressure levels (126.7 ± 5 to 105.1 ± 4 mmHg) as compared to the sedentary diabetic group., Conclusions: Resistance exercise could restore endothelial function and prevent an increase in arterial blood pressure in type 1 diabetic rats.

Sildenafil is a selective inhibitor of cyclic guanosine monophosphate (cGMP)-specific phosphodiesterase type 5 (PDE-5). A patent was registered for this drug in 1990, which expired in 2010. Since expiration, the drug has been marketed under various trade names or as generic drugs. Numerous clinical trials have been conducted addressing the effectiveness of the drug for erectile dysfunction (ED) and its safety regarding the presence or absence of specific comorbidities. After over 20 years in the market, we need to ask: has the scientific community reached a general consensus as to the overall efficacy and safety of the drug? Can we firmly state that the benefits of the drug outweigh its risks? This review suggests that sildenafil is an effective and easily manageable treatment for erectile dysfunction, both in the absence and in the presence of comorbidities. After two decades of the emergence of sildenafil as a drug of choice for the treatment of ED (and the numerous studies and clinical trials undertaken during this time span), it is now possible to state that the benefits of the drug do outweigh the risks, and represent an significant improvement in the quality of life in men with ED.

Background: The increase in fructose consumption is paralleled by a higher incidence of metabolic syndrome, and consequently, cardiovascular disease mortality. We examined the effects of 8 weeks of low intensity exercise training (LET) on metabolic, hemodynamic, ventricular and vascular morphological changes induced by fructose drinking in male rats., Methods: Male Wistar rats were divided into (n = 8 each) control (C), sedentary fructose (F) and ET fructose (FT) groups. Fructose-drinking rats received D-fructose (100 g/l). FT rats were assigned to a treadmill training protocol at low intensity (30% of maximal running speed) during 1 h/day, 5 days/week for 8 weeks. Measurements of triglyceride concentrations, white adipose tissue (WAT) and glycemia were carried out together with insulin tolerance test to evaluate metabolic profile. Arterial pressure (AP) signals were directly recorded. Baroreflex sensitivity (BS) was evaluated by the tachycardic and bradycardic responses. Right atria, left ventricle (LV) and ascending aorta were prepared to morphoquantitative analysis., Results: LET reduced WAT (-37.7%), triglyceride levels (-33%), systolic AP (-6%), heart weight/body weight (-20.5%), LV (-36%) and aortic (-76%) collagen fibers, aortic intima-media thickness and circumferential wall tension in FT when compared to F rats. Additionally, FT group presented improve of BS, numerical density of atrial natriuretic peptide granules (+42%) and LV capillaries (+25%), as well as the number of elastic lamellae in aorta compared with F group., Conclusions: Our data suggest that LET, a widely recommended practice, seems to be particularly effective for preventing metabolic, hemodynamic and morphological disorders triggered by MS.

The aim of this study was to investigate metabolic and cardiovascular responses to walking in fructose-fed rats. Male Wistar rats were divided into control (C), sedentary fructose (SF) and walking fructose (WF). Fructose-fed rats received D-fructose (100 g/l). WF rats walked on a treadmill at constant load (0.3 km/h) during 1 h/day, 5 days/week for 8 weeks. Measurements of triglyceride concentrations, adipose tissue and glycemia were carried out together with insulin tolerance test to evaluate metabolic profile. Arterial pressure (AP) signals were directly recorded. Baroreflex sensitivity (BR) was evaluated by the reflex tachycardia (TR) and bradycardia (BR) to AP changes. The results showed that walking decreased the adipose tissue (SF: 6.5 ± 0.4; WF: 2.8 ± 0.1; C: 3.0 ± 0.3 g), blood triglyceride levels (SF: 291 ± 6.5; WF: 150 ± 8.1; C: 103 ± 4.5 mg/dl) and increased insulin sensitivity (SF: 2.5 ± 0.2; WF: 3.3 ± 0.32; C: 4.8 ± 0.4 %/min). Baroreflex sensitivity was improved in the WF group expressed by BR (SF: 0.75 ± 0.10; WF: 1.18 ± 0.10; C: 1.5 ± 0.14 ms/mmHg) and TR (SF: 0.80 ± 0.12; WF: 1.21 ± 0.10; C: 1.35 ± 0.11 ms/mmHg), as well as when verified by the alpha index. Although the WF group showed decreased AP when compared with the SF group, the values still enhanced in relation to C rats (SF: 137 ± 2; WF: 129 ± 1; C: 115 ± 6 mmHg). Our findings allow a better understanding of the effects of walking, a low-intensity exercise training, on the hemodynamic and metabolic aspects of male rats with metabolic syndrome and indicate that walking seems to be particularly effective in treating metabolic disturbances in this model.

Objectives: The aim of this study was to evaluate cardiovascular autonomic function in a rodent obesity model induced by monosodium glutamate injections during the first seven days of life., Method: The animals were assigned to control (control, n = 10) and monosodium glutamate (monosodium glutamate, n = 13) groups. Thirty-three weeks after birth, arterial and venous catheters were implanted for arterial pressure measurements, drug administration, and blood sampling. Baroreflex sensitivity was evaluated according to the tachycardic and bradycardic responses induced by sodium nitroprusside and phenylephrine infusion, respectively. Sympathetic and vagal effects were determined by administering methylatropine and propranolol., Results: Body weight, Lee index, and epididymal white adipose tissue values were higher in the monosodium glutamate group in comparison to the control group. The monosodium glutamate-treated rats displayed insulin resistance, as shown by a reduced glucose/insulin index (-62.5%), an increased area under the curve of total insulin secretion during glucose overload (39.3%), and basal hyperinsulinemia. The mean arterial pressure values were higher in the monosodium glutamate rats, whereas heart rate variability (>7 times), bradycardic responses (>4 times), and vagal (~38%) and sympathetic effects (~36%) were reduced as compared to the control group., Conclusion: Our results suggest that obesity induced by neonatal monosodium glutamate treatment impairs cardiac autonomic function and most likely contributes to increased arterial pressure and insulin resistance.

Activation of renin-angiotensin system has been linked to cardiovascular and autonomic dysfunctions in diabetes. Experiments were performed to investigate the effects of angiotensin-converting enzyme inhibitor (ACEI), enalapril, on cardiac and autonomic functions in diabetic rats. Diabetes was induced by streptozotocin (50 mg/kg), and rats were treated with enalapril (1 mg · kg(-1) · d(-1)). After 30 days, evaluations were performed in control, diabetic, and enalapril-treated groups. Cardiac function was evaluated by echocardiography and through cannulation of the left ventricle (at baseline and in response to volume overload). Heart rate and systolic blood pressure variabilities were evaluated in the time and frequency domains. Streptozotocin rats had left ventricular systolic and diastolic dysfunctions, expressed by reduced ejection fraction and increased isovolumic relaxation time. The ACEI prevented these changes, improved diastolic cardiac responses to volume overload and total power of heart rate variability, reduced the ACE1 activity and protein expression and cardiac angiotensin (Ang) II levels, and increased angiotensin-converting enzyme 2 activity, despite unchanged blood pressure. Correlations were obtained between Ang II content with systolic and diastolic functions and heart rate variability. These findings provide evidence that the low-dose ACEI prevents autonomic and cardiac dysfunctions induced by diabetes without changing blood pressure and associated with reduced cardiac Ang II and increased angiotensin-converting enzyme 2 activity.

Purpose: Cardiac aldosterone might be involved in the deleterious effects of nandrolone decanoate (ND) on the heart. Therefore, we investigated the involvement of cardiac aldosterone, by the pharmacological block of AT1 or mineralocorticoid receptors, on cardiac hypertrophy and fibrosis., Methods: Male Wistar rats were randomized into eight groups (n = 14 per group): Control (C), nandrolone decanoate (ND), trained (T), trained ND (TND), ND + losartan (ND + L), trained ND + losartan (TND + L), ND + spironolactone (ND + S), and trained ND + spironolactone (TND + S). ND (10 mg·kg(-1)·wk(-1)) was administered during 10 wk of swimming training (five times per week). Losartan (20 mg·kg(-1)·d(-1)) and spironolactone (10 mg·kg(-1)·d(-1)) were administered in drinking water., Results: Cardiac hypertrophy was increased 10% by using ND and 17% by ND plus training (P < 0.05). In both groups, there was an increase in the collagen volumetric fraction (CVF) and cardiac collagen type III expression (P < 0.05). The ND treatment increased left ventricle-angiotensin-converting enzyme I activity, AT1 receptor expression, aldosterone synthase (CYP11B2), and 11-β hydroxysteroid dehydrogenase 2 (11β-HSD2) gene expression and inflammatory markers, TGFβ and osteopontin. Both losartan and spironolactone inhibited the increase of CVF and collagen type III. In addition, both treatments inhibited the increase in left ventricle-angiotensin-converting enzyme I activity, CYP11B2, 11β-HSD2, TGFβ, and osteopontin induced by the ND treatment., Conclusions: We believe this is the first study to show the effects of ND on cardiac aldosterone. Our results suggest that these effects may be associated to TGFβ and osteopontin. Thus, we conclude that the cardiac aldosterone has an important role on the deleterious effects on the heart induced by ND.

The present study investigated the effects of exercise training on arterial pressure, baroreflex sensitivity, cardiovascular autonomic control and metabolic parameters on female LDL-receptor knockout ovariectomized mice. Mice were divided into two groups: sedentary and trained. Trained group was submitted to an exercise training protocol. Blood cholesterol was measured. Arterial pressure (AP) signals were directly recorded in conscious mice. Baroreflex sensitivity was evaluated by tachycardic and bradycardic responses to AP changes. Cardiovascular autonomic modulation was measured in frequency (FFT) and time domains. Maximal exercise capacity was increased in trained as compared to sedentary group. Blood cholesterol was diminished in trained mice (191+/-8mg/dL) when compared to sedentary mice (250+/-9mg/dL, p<0.05). Mean AP and HR were reduced in trained group (101+/-3mmHg and 535+/-14bpm, p<0.05) when compared with sedentary group (125+/-3mmHg and 600+/-12bpm). Exercise training induced improvement in bradycardic reflex response in trained animals (-4.24+/-0.62bpm/mmHg) in relation to sedentary animals (-1.49+/-0.15bpm/mmHg, p<0.01); tachycardic reflex responses were similar between studied groups. Exercise training increased the variance (34+/-8 vs. 6.6+/-1.5ms(2) in sedentary, p<0.005) and the high-frequency band (HF) of the pulse interval (IP) (53+/-7% vs. 26+/-6% in sedentary, p<0.01). It is tempting to speculate that results of this experimental study might represent a rationale for this non-pharmacological intervention in the management of cardiovascular risk factors in dyslipidemic post-menopause women.

The aging process is associated with alterations in the cardiovascular and autonomic nervous systems. Autonomic changes related to aging involve parasympathetic and sympathetic alterations leading to a higher incidence of cardiovascular disease morbidity and mortality. Several studies have suggested that physical exercise is effective in preventing deleterious changes. Chronic exercise in geriatrics seems to be associated with improvement in the cardiovascular system and seems to promote a healthy lifestyle. In this review, we address the major effects of aging on the autonomic nervous system in the context of cardiovascular control. We examine the use of chronic exercise to prevent cardiovascular changes during the aging process.

The renin-angiotensin system has been implicated in the etiology of the cardiovascular complications of diabetes. Our studies extend these findings to show a specific role for angiotensin AT1a receptors in mediating diabetes-induced hypertension. Male angiotensin AT1a knockout (AT1aKO) and wild-type (AT1aWT) mice with arterial telemetric catheters were injected with streptozotocin (STZ; 150 mg/kg ip). The STZ dose was selected on the basis of a dose-response experiment in C57/BL mice. Blood glucose, water intake, body weight, blood pressure (BP), and heart rate (HR) were measured over a 2-wk period. Estimates of BP and HR variance (BPV and HRV) and their low- and high-frequency domains were also determined. STZ induced similar levels of hyperglycemia and polydypsia in the groups. Mean arterial pressure (MAP) was increased from 100 +/- 6 to 124 +/- 6 mmHg in diabetic AT1aWT. MAP was unchanged in AT1aKO (80 +/- 4 vs. 85 +/- 5 mmHg, basal vs. STZ). Treatment with an ACE inhibitor, captopril, produced a greater reduction in MAP (-18%) in diabetic AT1aWT than in AT1aKO (-3.4%). BPV was lower in AT1aKO (19 +/- 0.5 vs. 9 +/- 2 mmHg(2), AT1aWT vs. AT1aKO). Diabetes reduced BPV but only in AT1aWT (19 +/- 0.5 vs. 8 +/- 1 mmHg(2), basal vs. STZ). There were no changes in HR in either group. In AT1aKO, STZ increased HRV and its high-frequency domain with no changes seen in AT1aWT. Results document that ANG AT1a receptors are critical in diabetes-induced hypertension and in cardiac autonomic responses.

Studies were conducted in rats to determine the effect of maternal diabetes and the consequent hyperglycemia on cardiovascular function in the offspring. Diabetes was induced in pregnant Wistar rats through streptozotocin injection (50 mg/kg). Cardiovascular parameters were measured in 2-mo-old offspring animals of diabetic (OD, n=12) and control rats (OC, n=8). Arterial pressure (AP), heart rate (HR), baroreflex sensitivity, and vascular responsiveness to phenylephrine (PH) and sodium nitroprusside (SN) were measured. Angiotensin-converting enzyme (ACE) activity in heart, kidney, and lung was determined. OD rats exhibited increases in systolic AP (138+/-8 vs. 119+/-6 mmHg, OD vs. OC), with no change in HR (342+/-21 vs. 364+/-39 beats per minute (bpm), OD vs. OC). The reflex tachycardia elicited by SN was reduced in OD rats, as indicated by the slope of the linear regression (-2.2+/-0.4 vs. -3.6+/-0.8 bpm/mmHg, OD vs. OC). Vascular responsiveness to PH was increased 63% in OD rats compared with OC. OD rats showed increases in ACE activity in heart, kidney, and lung (1.13+/-0.24, 3.04+/-0.86, 40.8+/-8.9 vs. 0.73+/-0.19, 1.7+/-0.45, 28.1+/-6 nmol His-Leu.min-1 mg protein-1, OD vs. OC). Results suggest that diabetes during pregnancy affects cardiovascular function in offspring, seen as hypertension, baroreflex dysfunction, and activation of tissue renin-angiotensin system.

Studies examined the role of angiotensin (ANG) AT1a receptors in cardiovascular autonomic control by measuring arterial pressure (AP) and heart rate (HR) variability and the effect of autonomic blockade in mice lacking AT1a receptors (AT1a -/-). Using radiotelemetry in conscious AT1a +/+ and AT1a -/- mice, we determined 1) AP and pulse interval (PI) variability in time and frequency (spectral analysis) domains, 2) AP response to alpha(1)-adrenergic and ganglionic blockade, and 3) intrinsic HR after ganglionic blockade. Pulsatile AP was recorded (5 kHz) for measurement of AP and PI and respective variability. Steady-state AP responses to prazosin (1 microg/g ip) and hexamethonium (30 microg/g ip) were also measured. AP was lower in AT1a -/- vs. AT1a +/+, whereas HR was not changed. Prazosin and hexamethonium produced greater decreases in mean AP in AT1a -/- than in AT1a +/+. The blood pressure difference was marked after ganglionic blockade (change in mean AP of -44 +/- 10 vs. -18 +/- 2 mmHg, AT1a -/- vs. AT1a +/+ mice). Intrinsic HR was also lower in AT1a -/- mice (431 +/- 32 vs. 524 +/- 22 beats/min, AT1a -/- vs. AT1a +/+). Beat-by-beat series of systolic AP and PI were submitted to autoregressive spectral estimation with variability quantified in low-frequency (LF: 0.1-1 Hz) and high-frequency (HF: 1-5 Hz) ranges. AT1a -/- mice showed a reduction in systolic AP LF variability (4.3 +/- 0.8 vs. 9.8 +/- 1.3 mmHg(2)), with no change in HF (2.7 +/- 0.3 vs. 3.3 +/- 0.6 mmHg(2)). There was a reduction in PI variability of AT1a -/- in both LF (18.7 +/- 3.7 vs. 32.1 +/- 4.2 ms(2)) and HF (17.7 +/- 1.9 vs. 40.3 +/- 7.3 ms(2)) ranges. The association of lower AP and PI variability in AT1a -/- mice with enhanced AP response to alpha(1)-adrenergic and ganglionic blockade suggests that removal of the ANG AT1a receptor produces autonomic imbalance. This is seen as enhanced sympathetic drive to compensate for the lack of ANG signaling.

Experiments were performed to investigate the influence of exercise training on cardiovascular function in mice. Heart rate, arterial pressure, baroreflex sensitivity, and autonomic control of heart rate were measured in conscious, unrestrained male C57/6J sedentary (n = 8) and trained mice (n = 8). The exercise training protocol used a treadmill (1 h/day; 5 days/wk for 4 wk). Baroreflex sensitivity was evaluated by the tachycardic and bradycardic responses induced by sodium nitroprusside and phenylephrine, respectively. Autonomic control of heart rate and intrinsic heart rate were determined by use of methylatropine and propranolol. Resting bradycardia was observed in trained mice compared with sedentary animals [485 +/- 9 vs. 612 +/- 5 beats/min (bpm)], whereas mean arterial pressure was not different between the groups (106 +/- 2 vs. 108 +/- 3 mmHg). Baroreflex-mediated tachycardia was significantly enhanced in the trained group (6.97 +/- 0.97 vs. 1.6 +/- 0.21 bpm/mmHg, trained vs. sedentary), whereas baroreflex-mediated bradycardia was not altered by training. The tachycardia induced by methylatropine was significantly increased in trained animals (139 +/- 12 vs. 40 +/- 9 bpm, trained vs. sedentary), whereas the propranolol effect was significantly reduced in the trained group (49 +/- 11 vs. 97 +/- 11 bpm, trained vs. sedentary). Intrinsic heart rate was similar between groups. In conclusion, dynamic exercise training in mice induced a resting bradycardia and an improvement in baroreflex-mediated tachycardia. These changes are likely related to an increased vagal and decreased sympathetic tone, similar to the exercise response observed in humans.

Several studies have reported impairment in cardiovascular function and control in diabetes. The studies cited in this review were carried out from a few days up to 3 months after streptozotocin administration and were concerned with the control of the circulation. We observed that early changes (5 days) in blood pressure control by different peripheral receptors were maintained for several months. Moreover, the impairment of reflex responses observed after baroreceptor and chemoreceptor stimulation was probably related to changes in the efferent limb of the reflex arc (sympathetic and parasympathetic), but changes also in the central nervous system could not be excluded. Changes in renal sympathetic nerve activity during volume expansion were blunted in streptozotocin-treated rats, indicating an adaptive natriuretic and diuretic response in the diabetic state. The improvement of diabetic cardiovascular dysfunction induced by exercise training seems to be related to changes in the autonomic nervous system. Complementary studies about the complex interaction between circulation control systems are clearly needed to adequately address the management of pathophysiological changes associated with diabetes.