Effects of exercise training on cardiovascular adrenergic system (original) (raw)
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Journal of applied physiology (Bethesda, Md. : 1985), 2002
To test whether changes in sympathetic nervous system (SNS) activity or insulin sensitivity contribute to the heterogeneous blood pressure response to aerobic exercise training, we used compartmental analysis of [3H]norepinephrine kinetics to determine the extravascular norepinephrine release rate (NE2) as an index of systemic SNS activity and determined the insulin sensitivity index (S(I)) by an intravenous glucose tolerance test, before and after 6 mo of aerobic exercise training, in 30 (63 +/- 7 yr) hypertensive subjects. Maximal O2 consumption increased from 18.4 +/- 0.7 to 20.8 +/- 0.7 ml x kg(-1) x min(-1) (P = 0.02). The average mean arterial blood pressure (MABP) did not change (114 +/- 2 vs. 114 +/- 2 mmHg); however, there was a wide range of responses (-19 to +17 mmHg). The average NE2 did not change significantly (2.11 +/- 0.15 vs. 1.99 +/- 0.13 microg x min(-1) x m(-2)), but there was a significant positive linear relationship between the change in NE2 and the change in ...
Heart Research - Open Journal, 2015
Autonomic dysfunction is closely related to the development of hypertension, which is characterized by increased sympathetic activity, decreased vagal tonus and baroreflex dysfunction. The hypertension-induced maladaptive changes progressively lead to heart failure, myocardial infarction and stroke. Hypertrophic remodeling of brain arterioles, chemoreceptors activation, blood-brain barrier abnormalities, oxidative stress and pro-inflammatory cytokines production in autonomic brain areas increase neuronal activity and sympathetic outflow. These responses, together with increased baroreflex dysfunction-induced pressure variability, reninangiotensin system hyperactivation and capillary rarefaction, increase blood pressure levels and act as a positive feedback mechanism to perpetuate hypertension and development of endorgan damage. Exercise training, a non-pharmacological tool, has been used as an adjuvant therapy to treat hypertension. Our recent data showed that moderate aerobic training in adult SHR completely normalizes oxidative stress and inflammation in autonomic brain areas involved in cardiovascular control and promptly corrects baroreflex dysfunction and increases cardiac vagal activity. The early (2-weeks) training-induced beneficial responses improve autonomic control even in the persistence of hypertension, since a partial reduction of pressure levels was observed after 8 weeks of exercise training, which was related to reversion of arteriolar hypertrophic remodeling and consequent decrease of peripheral vascular resistance.
American Journal of Hypertension, 2008
ARTICLES nature publishing group Norepinephrine (NE) is an important marker of sympathetic activity in many tissues. Previously, studies have demonstrated that sympathetic hyperactivity is related with the development and severity of cardiovascular disease. 1,2 Moreover, impaired autonomic balance is considered an important predictor of mortality. Spontaneously hypertensive rats (SHRs), an experimental model of essential hypertension, present high plasmatic NE concentrations associated with increased sympathetic activation. 4 Increased cardiac sympathetic stimulation may lead to cardiomyocyte hypertrophy, 5 cardiac damage, 6 and apopto-sis. 7 Reinforcing this idea, the use of β-blockers has decreased hypertension-induced cardiac hypertrophy 8 and cardiomyocyte apoptosis in heart failure. It is known that exercise training (ET) reduces sympathetic modulation of the cardiovascular system. 10 In fact, low-intensity ET attenuated cardiac sympathetic modulation in SHR, and reduced plasma NE and epinephrine concentrations in exercised rabbits with heart failure. 10,11 On the other hand, some studies have demonstrated that ET did not modify plasma NE concentrations. 12,13 During hypertension, it is well known that ET improves autonomic balance, decreases mean arterial pressure, and attenuates oxidative stress, 14 but there are no studies assessing ET-induced changes on cardiac NE concentrations in SHR.
Psychosomatic Medicine, 2013
Objective-Exercise has widely documented cardioprotective effects, but the mechanisms underlying these effects are not entirely known. Previously, we demonstrated that aerobic but not strength training lowered resting heart rate and increased cardiac vagal regulation, changes that were reversed by sedentary deconditioning. Here, we focus on the sympathetic nervous system and test whether aerobic training lowers levels of cardiovascular sympathetic activity in rest and that deconditioning would reverse this effect. Methods-We conducted a randomized controlled trial contrasting the effects of aerobic (A) versus strength (S) training on indices of cardiac (preejection period, or PEP) and vascular (lowfrequency blood pressure variability, or LF BPV) sympathetic regulation in 149 young, healthy, and sedentary adults. Participants were studied before and after conditioning, as well as after 4 weeks of sedentary deconditioning. Results-As previously reported, aerobic capacity increased in response to conditioning and decreased after deconditioning in the aerobic, but not the strength, training group. Contrary to prediction, there was no differential effect of training on either PEP (A: mean [SD] −0.83 [7.8] milliseconds versus S: 1.47 [6.69] milliseconds) or LF BPV (A: mean [SD] −0.09 [0.93] ln mm Hg 2 versus S: 0.06 [0.79] ln mm Hg 2) (both p values > .05). Conclusions-These findings, from a large randomized controlled trial using an intent-to-treat design, show that moderate aerobic exercise training has no effect on resting state cardiovascular indices of PEP and LF BPV. These results indicate that in healthy, young adults, the cardioprotective effects of exercise training are unlikely to be mediated by changes in resting sympathetic activity. Trial Registration-Clinicaltrials.gov identifier: NCT00358137.
Frontiers in Neuroscience, 2020
Exercise training is a cornerstone in reducing blood pressure (BP) and muscle sympathetic nerve activity (MSNA) in individuals with essential hypertension. Highintensity interval training (HIIT) has been shown to be a time efficient alternative to classical continuous training in lowering BP in essential hypertension, but the effect of HIIT on MSNA levels has never been investigated. Leg MSNA responsiveness to 6 weeks of HIIT was examined in 14 hypertensive men (HYP; age: 62 ± 7 years, night time BP: 136 ± 12/83 ± 8 mmHg, BMI: 28 ± 3 kg/m 2), and 10 age-matched normotensive controls (NORM; age: 60 ± 8 years, night time BP: 116 ± 2/68 ± 4 mmHg and BMI: 27 ± 3 kg/m 2). Before training, MSNA levels were not different between HYP and NORM (burst frequency (BF): 41.0 ± 10.3 vs. 33.6 ± 10.6 bursts/min and burst incidence (BI): 67.5 ± 19.7 vs. 64.2 ± 17.0 bursts/100 heart beats, respectively). BF decreased (P < 0.05) with training by 13 and 5% in HYP and NORM, respectively, whereas BI decreased by 7% in NORM only, with no difference between groups. Training lowered (P < 0.05) night-time mean arterial-and diastolic BP in HYP only (100 ± 8 vs. 97 ± 5, and 82 ± 6 vs. 79 ± 5 mmHg, respectively). The change in HYP was greater (P < 0.05) compared to NORM. Training reduced (P < 0.05) body mass, visceral fat mass, and fat percentage similarly within-and between groups, with no change in fat free mass. Training increased (P < 0.05)VO 2-max in NORM only. Six weeks of HIIT lowered resting MSNA levels in age-matched hyper-and normotensive men, which was paralleled by a significant reduction in BP in the hypertensive men.
Aerobic Exercise During Advance Stage of Uncontrolled Arterial Hypertension
Frontiers in Physiology
AimTo evaluate the influence of physical training on myocardial function, oxidative stress, energy metabolism, and MAPKs and NF-κB signaling pathways in spontaneously hypertensive rats (SHR), at advanced stage of arterial hypertension, which precedes heart failure development.MethodsWe studied four experimental groups: normotensive Wistar rats (W, n = 27), trained W (W-EX, n = 31), SHR (n = 27), and exercised SHR (SHR-EX, n = 32). At 13 months old, the exercise groups underwent treadmill exercise 5 days a week for 4 months. In vitro myocardial function was analyzed in left ventricular (LV) papillary muscle preparations. Antioxidant enzyme activity and energy metabolism were assessed by spectrophotometry. Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity was analyzed by lucigenin reduction and protein expression by Western blot. Statistical analyzes: ANOVA and Tukey or Kruskal–Wallis and Dunn tests.ResultsSHR-EX had a lower frequency of heart failure features than ...
Hypertension, 1999
Exercise training plays an important role in the reduction of high blood pressure. In this review, we discuss the effect of distinct intensities of exercise training on the reduction of high blood pressure in spontaneously hypertensive rats (SHR). In addition, we present some hemodynamic mechanisms and associated neural controls by which exercise training attenuates hypertension in SHR. Low-intensity exercise training is more effective in reducing high blood pressure than is high-intensity exercise training in SHR. The decrease in blood pressure is due to resting bradycardia, and in consequence, lower cardiac output. Sympathetic attenuation to the heart is the major explanation for the resting bradycardia. Recovery of the sensitivity of baroreflex control of heart rate, which is usually impaired in SHR, is an important neurogenic component involved in the benefits elicited by exercise training.
Frontiers in Physiology
Aerobic physical training reduces arterial pressure in patients with hypertension owing to integrative systemic adaptations. One of the key factors is the decrease in cardiac sympathetic influence. Thus, we hypothesized that among other causes, cardiac sympathetic influence reduction might be associated with intrinsic cardiac adaptations that provide greater efficiency. Therefore, 14 spontaneously hypertensive rats (SHR group) and 14 normotensive Wistar Kyoto rats (WKY group) were used in this study. Half of the rats in each group were trained to swim for 12 weeks. All animals underwent the following experimental protocols: double blockade of cardiac autonomic receptors with atropine and propranolol; echocardiography; and analysis of coronary bed reactivity and left ventricle contractility using the Langendorff technique. The untrained SHR group had a higher sympathetic tone, cardiac hypertrophy, and reduced ejection fraction compared with the untrained WKY group. In addition, reduc...