Low-Intensity Aerobic Exercise Mitigates Exercise-Induced Bronchoconstriction by Improving the Function of Adrenal Medullary Chromaffin Cells in Asthmatic Rats

Abstract

Exercise is one of the most common triggers of bronchoconstriction in patients with asthma. The low levels of circulating epinephrine produced by the adrenal medullary chromaffin cells (AMCCs) are associated with exercise-induced bronchoconstriction (EIB) in asthmatics. In the present study, we tested the hypothesis that low-intensity aerobic exercise may ameliorate EIB using a rat model of asthma. Male Sprague-Dawley rats at 7 weeks of age, sensitized with ovalbumin or treated with saline, were subjected to low or moderate exercise training (50 or 75% of maximum velocity) for one hour in a treadmill 30 min after ovalbumin or saline inhalation. The exercise capacity, airway responsiveness, lung morphology, the morphological changes and endocrine function of AMCCs were measured in both groups of rats after exercise training for 6 weeks. Either low-intensity or moderate-intensity exercise mitigated EIB and increased exercise capacity in ovalbumin-sensitized (asthmatic) rats. Low-intensity aerobic exercise reduced the vacuolar degeneration degrees, lipid contents, neuronal peripherin and neurofilament-68 expression, demolished neurites, but increased the chromaffin granule density, endocrine chromogranin A and phenylethanolamine N-methyltransferase expression in the adrenal medullary tissues, accompanied by increased levels of circulating epinephrine and corticosterone, but decreased nerve growth factor in asthmatic rats. Finally, low-intensity aerobic exercise significantly reduced the relative levels of phosphorylated extracellular signalregulated kinase and phosphorylated cAMP responsive element-binding protein and the relative mRNA expression levels of downstream molecules, including c-FOS and c-JUN in the adrenal medullary of asthmatic rats. We suggest that low-intensity aerobic exercise improves the endocrine dysfunction of AMCCs and mitigates EIB.

Long-term moderate intensity exercise alleviates myocardial fibrosis in type 2 diabetic rats via inhibitions of oxidative stress and TGF-β1/Smad pathway

“…However, long-term high expression of TGF-β1 can lead to excessive tissue repair and further generate fibrosis [39]. Cellular TGF-β1 is regulated by adrenal hormones, and lower intensity aerobic exercise may significantly reduce the level of adrenaline in the circulation of patients with hypertension and diabetes [40,41]. Therefore, exercise in the present study may decrease the expression of TGF-β1 in the myocardium of diabetic rats and reduce the degree of myocardial fibrosis by inhibiting the secretion of adrenaline in diabetic rats [42].…”

Exercise reverses OVA‐induced inhibition of glucocorticoid receptor and increases anti‐inflammatory cytokines in asthma

“…In addition, there is evidence demonstrating that asthmatic patients have increased vagal tone (Lewis et al., ); however, the effect of AT on this autonomic imbalance remains unknown. Lastly, endogenous cortisol is a natural, powerful anti‐inflammatory hormone (Barnes, 1998), and recent evidence suggests that AT increases the corticosteroid plasma levels in a rat asthma model (Qin et al., ). Based on these previous studies and our findings, we speculate that AT increases plasma cortisol levels and the GR expression that could potentiate the anti‐inflammatory effects induced by AT during asthma pathophysiology.…”

Intensity of swimming exercise influences tracheal reactivity in rats

“…Furthermore, low-intensity aerobic exercise has been associated with an increase in the levels of serum epinephrine mitigating EIB in asthmatic Sprague-Dawley rats (44). In these studies, the exercise attenuated the airway resistance in asthmatic rats, but not in normal rats, however, the species used in our study differs from theirs.…”