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Introduction: It is known that aerobic exercise (AE) training attenuates the development of lung emphysema induced by exposure to cigarette smoke (CS)1 and we also demonstrated that high fructose (HF) intake might induce lung emphysema in mice2. Objective: To evaluate whether AE training protects against the development of lung emphysema induced by HF intake in mice exposed or not to CS. Methods: Male C57Bl/6 mice were assigned to 8 groups: Control, CS, AE, CS+AE, Fructose (Fr), Fr+CS, Fr+AE and Fr+CS+AE (n=16-20/group). Groups were treated accordingly with AE training (1h/day, 5 days/week), Fr (20% in the drinking water daily) or CS (30min, twice/day, 5 days/week) for 12 weeks. After this period, the animals were anesthetized and euthanized for the collection of blood plasma, bronchoalveolar lavage fluid (BALF), lungs and quadriceps muscles for subsequent histology analysis and measures of cytokine levels, gene expression and oxidative stress. This study was approved by the Ethics Committee of the School of Medicine of the University of Sao Paulo (protocol 001/14). Results: HF intake induced lung emphysema comparable to that caused by exposure to CS (p<0,001). Combination of Fr+CS induced more severe lung emphysema compared to the other groups (p<0,01). Although there was no effect of AE training on cytokine levels analysis in BALF, oxidative stress measures, antioxidant genes expression and development of lung emphysema induced by HF intake, AE training inhibited the increase of interleukin (IL)-6, IL-10, IL-1β, tumor necrosis factor (TNF)-α, adiponectin and leptin levels in plasma and/or skeletal muscle (p<0,001). Conclusion: AE training does not protect against the development of lung emphysema induced by HF intake but attenuates systemic inflammation in mice.
References:
1 Sci Rep. 2019 Jun 27;9(1):9344.
2 Eur Respir J. 2012 Feb;39(2):254-64.
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