Adrenergic responsiveness and intrinsic sinoatrial automaticity of exercise-trained rats

Me, Schaefer; Ja, Allert; Hr, Adams; Mh, Laughlin

doi:10.1249/00005768-199208000-00010

Cited by 22 publications

(16 citation statements)

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“…In contrast to previous studies, in which resting bradycardia after running training was explained by a reduction in IHR (12,21) or reduced atrioventricular conduction (11) in man and rats, we provide evidence here for vagal-mediated resting bradycardia after swimming training in rats. In fact, a different cardiac adaptation after swimming training should be expected, since this training mode differs from running training with respect to body position in the water, water pressure and temperature regulation.…”

Section: Heart Rate Adaptationscontrasting

confidence: 99%

Swimming training increases cardiac vagal activity and induces cardiac hypertrophy in rats

Medeiros

Oliveira

Gianolla

et al. 2004

Braz J Med Biol Res

123

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The effect of swimming training (ST) on vagal and sympathetic cardiac effects was investigated in sedentary (S, N = 12) and trained (T, N = 12) male Wistar rats (200-220 g). ST consisted of 60-min swimming sessions 5 days/week for 8 weeks, with a 5% body weight load attached to the tail. The effect of the autonomic nervous system in generating training-induced resting bradycardia (RB) was examined indirectly after cardiac muscarinic and adrenergic receptor blockade. Cardiac hypertrophy was evaluated by cardiac weight and myocyte morphometry. Plasma catecholamine concentrations and citrate synthase activity in soleus muscle were also determined in both groups. Resting heart rate was significantly reduced in T rats (355 ± 16 vs 330 ± 20 bpm). RB was associated with a significantly increased cardiac vagal effect in T rats (103 ± 25 vs 158 ± 40 bpm), since the sympathetic cardiac effect and intrinsic heart rate were similar for the two groups. Likewise, no significant difference was observed for plasma catecholamine concentrations between S and T rats. In T rats, left ventricle weight (13%) and myocyte dimension (21%) were significantly increased, suggesting cardiac hypertrophy. Skeletal muscle citrate synthase activity was significantly increased by 52% in T rats, indicating endurance conditioning. These data suggest that RB induced by ST is mainly mediated parasympathetically and differs from other training modes, like running, that seems to mainly decrease intrinsic heart rate in rats. The increased cardiac vagal activity associated with ST is of clinical relevance, since both are related to increased life expectancy and prevention of cardiac events. Correspondence

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Section: Heart Rate Adaptationscontrasting

confidence: 99%

Swimming training increases cardiac vagal activity and induces cardiac hypertrophy in rats

Medeiros

Oliveira

Gianolla

et al. 2004

Braz J Med Biol Res

123

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“…Resting bradycardia usually occurs in trained humans (15, 31, 32) and exercise-trained rats (8,20,24,28) and is considered to be a hallmark of exercise training improvement (8,16,20,24,28). Our results verify that bradycardia is also a characteristic of training in mice as seen in a previous study (25).…”

Section: Discussionsupporting

confidence: 89%

“…In normal rats, the reduction in IHR (pacemaker mediated) after exercise training seems to be the causal mechanism for the resting bradycardia (24,28). Studies demonstrate that both sympathetic and parasympathetic input were reduced after a program of physical activity in normotensive rats (20,24).…”

Section: Discussionmentioning

confidence: 99%

Exercise training changes autonomic cardiovascular balance in mice

Angelis¹,

Wichi²,

Jesus³

et al. 2004

Journal of Applied Physiology

127

106

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. Exercise training changes autonomic cardiovascular balance in mice. J Appl Physiol 96: 2174-2178, 2004. First published January 16, 2004 10.1152/ japplphysiol.00870.2003.-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 ϭ 8) and trained mice (n ϭ 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 Ϯ 9 vs. 612 Ϯ 5 beats/min (bpm)], whereas mean arterial pressure was not different between the groups (106 Ϯ 2 vs. 108 Ϯ 3 mmHg). Baroreflex-mediated tachycardia was significantly enhanced in the trained group (6.97 Ϯ 0.97 vs. 1.6 Ϯ 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 Ϯ 12 vs. 40 Ϯ 9 bpm, trained vs. sedentary), whereas the propranolol effect was significantly reduced in the trained group (49 Ϯ 11 vs. 97 Ϯ 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. bradycardia; autonomic nervous system; baroreflex; blood pressure RESTING BRADYCARDIA, INDUCED by exercise training, has been well documented in humans and animals; however, the mechanisms underlying the effect are not well understood. Studies in humans suggest that increased vagal activity is responsible for the decrease in heart rate (HR) (31, 32). In contrast, in young trained rats the resting bradycardia was more likely due to alterations in cardiac pacemaker function, a regulator of intrinsic heart rate (IHR), rather than to increased vagal activity (24). Moreover, the improvement in baroreflex control of HR observed in trained animals (3, 10, 11) and humans (1, 26) may also play a role in the basal HR changes.Exercise training induces cardiovascular and metabolic changes that are dependent on exercise intensity and duration as well as physiological condition (1, 8-10, 26, 30). Studies in mice demonstrate that treadmill exercise resulted in linear increases in HR, maximum oxygen consumption (V O 2 max ), and respiratory exchange ratio, similar to that seen in larger species (11). A test of ␤-adrenergic stimulation suggested that sympathetic tone was not altered, whereas vagal input was reduced. Swimming (4-w...

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“…Resting bradycardia usually occurs in trained humans (1-3,11,24) and exercise-trained male (5,17,23,25) and female (19,26) rats and is considered to be a hallmark of exercise training improvement (4,5,17,23,25). Our results confirmed the occurrence of resting bradycardia in female rats.…”

Section: Discussionsupporting

confidence: 86%

“…In fact, the mechanisms underlying the cardiac adaptive responses to exercise training seem to be different for different species and genders. In normal male rats and humans, the reduction in IHR (pacemaker mediated) after exercise training seems to be the causal mechanism of the resting bradycardia (4,23,25). Studies have demonstrated that sympathetic and/or parasympathetic inputs were reduced in trained normotensive male rats or humans (4,5,23,27,28).…”

Section: Discussionmentioning

confidence: 99%

Tonic and reflex cardiovascular autonomic control in trained-female rats

Sanches

Sartori

Jorge

et al. 2009

Braz J Med Biol Res

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The effects of exercise training on cardiovascular and autonomic functions were investigated in female rats. After an aerobic exercise training period (treadmill: 5 days/week for 8 weeks), conscious female Wistar (2 to 3 months) sedentary (S, N = 7) or trained rats (T, N = 7) were cannulated for direct arterial pressure (AP) recording in the non-ovulatory phases. Vagal (VT) and sympathetic tonus (ST) were evaluated by vagal (atropine) and sympathetic (propranolol) blockade. Baroreflex sensitivity was evaluated by the heart rate responses induced by AP changes. Cardiopulmonary reflex was measured by the bradycardic and hypotensive responses to serotonin. Resting bradycardia was observed in T (332 ± 7 bpm) compared with S animals (357 ± 10 bpm), whereas AP did not differ between groups. T animals exhibited depressed VT and ST (32 ± 7 and 15 ± 4 bpm) compared to S animals (55 ± 5 and 39 ± 10 bpm). The baroreflex and cardiopulmonary bradycardic responses were lower in T (-1.01 ± 0.27 bpm/mmHg and -17 ± 6 bpm) than in the S group (-1.47 ± 0.3 bpm/mmHg and -41 ± 9 bpm). Significant correlations were observed between VT and baroreflex (r = -0.72) and cardiopulmonary (r = -0.76) bradycardic responses. These data show that exercise training in healthy female rats induced resting bradycardia that was probably due to a reduced cardiac ST. Additionally, trained female rats presented attenuated bradycardic responses to baro- and cardiopulmonary receptor stimulation that were associated, at least in part, with exercise training-induced cardiac vagal reduction

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Adrenergic responsiveness and intrinsic sinoatrial automaticity of exercise-trained rats

Cited by 22 publications

References 0 publications

Swimming training increases cardiac vagal activity and induces cardiac hypertrophy in rats

Swimming training increases cardiac vagal activity and induces cardiac hypertrophy in rats

Exercise training changes autonomic cardiovascular balance in mice

Tonic and reflex cardiovascular autonomic control in trained-female rats

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