Loss of resting bradycardia with detraining is associated with intrinsic heart rate changes

Abstract

The mechanisms underlying the loss of resting bradycardia with detraining were studied in rats. The relative contribution of autonomic and non-autonomic mechanisms was studied in 26 male Wistar rats (180-220 g) randomly assigned to four groups: sedentary (S, N = 6), trained (T, N = 8), detrained for 1 week (D1, N = 6), and detrained for 2 weeks (D2, N = 6). T, D1 and D2 were treadmill trained 5 days/week for 60 min with a gradual increase towards 50% peak VO 2 . After the last training session, D1 and D2 were detrained for 1 and 2 weeks, respectively. The effect of the autonomic nervous system in causing training-induced resting bradycardia and in restoring heart rate (HR) to pre-exercise training level (PET) with detraining was examined indirectly after cardiac muscarinic and adrenergic receptor blockade. T rats significantly increased peak VO 2 by 15 or 23.5% when compared to PET and S rats, respectively. Detraining reduced peak VO 2 in both D1 and D2 rats by 22% compared to T rats, indicating loss of aerobic capacity. Resting HR was significantly lower in T and D1 rats than in S rats (313 ± 6.67 and 321 ± 6.01 vs 342 ± 12.2 bpm) and was associated with a significantly decreased intrinsic HR (368 ± 6.1 and 362 ± 7.3 vs 390 ± 8 bpm). Two weeks of detraining reversed the resting HR near PET (335 ± 6.01 bpm) due to an increased intrinsic HR in D2 rats compared with T and D1 rats (376 ± 8.8 bpm). The present study provides the first evidence of intrinsic HR-mediated loss of resting bradycardia with detraining in rats. Endurance exercise training is generally defined as any regularly performed aerobic activity involving the use of large muscle groups for a sufficient duration and intensity to train the cardiorespiratory systems. In previously sedentary subjects, aerobic exercise training increases maximal exercise performance, as reflected by an increase in peak oxygen uptake (peak VO 2 ) (1). In addition, aerobic exercise training leads to an improvement of cardiovascular capacity, which is associated with lower resting and submaximal heart rates (HR) and increased ventricular weight and volume. These cardiovascular adaptations induced by aerobic exercise training are of clinical relevance since both are associated with increased life expectancy and decreased cardiovascular events (2).

O grau de melhora na função das células progenitoras endoteliais derivadas da medula óssea é dependente do volume de treinamento físico aeróbio

“…As observed, greater resting bradycardia in animals trained in swimming 20 than on treadmill 23 was found. In the present study, we observed that the groups submitted to the two ET protocols presented similar reduction in rest HR regardless of the exercise volume applied, when compared with its initial HR.…”

“…Among the autonomic and hemodynamic adaptations which will influence the cardiovascular system, resting bradycardia consists in a good functional parameter to verify the adaptation and efficiency of the aerobic ET; therefore, it is considered an ET physiological marker. This adaptation is observed both in experimentation animals 20,21,23 and humans 24 .…”

“…The mechanisms through which this bradycardia occurs seem to be strongly influenced by the type of ET. In normotensive rats, this resting bradycardia resulting from the aerobic ET on treadmill is associated with reduction in the intrinsic HR 23 , while the animals submitted to the swimming protocol seem to present resting bradycardia due to increase of vagal tonus 20 . The BP adaptation due to the ET seems to depend on the presence of risk factors and cardiovascular diseases.…”

“…The BP adaptation due to the ET seems to depend on the presence of risk factors and cardiovascular diseases. In fact, studies have shown that the BP response remains unchanged in normotensive humans and animals submitted to aerobic ET 20,21,[23][24][25] . In the present study, consistent with other ones previously mentioned, there was no significant difference in BP between the trained and sedentary groups, showing hence that ET with swimming does not alter rest BP.…”

Potencial do treinamento físico para a prevenção de distúrbios metabólicos induzidos por dieta hipercalórica

“…Dados prévios do nosso grupo (HIGA, 2012) e de outros (PANVELOSKI-COSTA et al, 2011;GOMES et al, 2012;MUBARAK et al, 2013;HODGSON et al, 2013) (MUNTZEL et al, 2012), o efeito modulador do treinamento físico sobre a frequência cardíaca, determinado pelo sistema nervoso parassimpático ou pela frequência cardíaca intrínseca (EVANGELISTA et al, 2005), pode ter sido parcialmente contraposto pela atividade nervosa simpática estimulada pela dieta hipercalórica. Embora a bradicardia de repouso não tenha sido observada, o fato de o grupo TFH apresentar aumento de desempenho no teste de esforço físico máximo confirma que o protocolo de treinamento físico utilizado foi eficaz para promover adaptações tipicamente aeróbias.…”