Exercise Prevents Diaphragm Wasting Induced by Cigarette Smoke through Modulation of Antioxidant Genes and Metalloproteinases.

Gracielle Vieira Ramos,Milton Arruda Martins,Tania Fátima Salvini,Clara Maria Pinheiro-Dardis,Alessandra Choqueta De Toledo-Arruda,João Luiz Quagliotti Durigan,Rodolfo Paula Vieira,Camila Liyoko Suehiro,Thiago Luiz De Russo

doi:10.1155/2018/5909053

Abstract

Background The present study aimed to analyze the effects of physical training on an antioxidant canonical pathway and metalloproteinases activity in diaphragm muscle in a model of cigarette smoke-induced chronic obstructive pulmonary disease (COPD). Methods Male mice were randomized into control, smoke, exercise, and exercise + smoke groups, which were maintained in trial period of 24 weeks. Gene expression of kelch-like ECH-associated protein 1; nuclear factor erythroid-2 like 2; and heme-oxygenase1 by polymerase chain reaction was performed. Metalloproteinases 2 and 9 activities were analyzed by zymography. Exercise capacity was evaluated by treadmill exercise test before and after the protocol. Results Aerobic training inhibited diaphragm muscle wasting induced by cigarette smoke exposure. This inhibition was associated with improved aerobic capacity in those animals that were submitted to 24 weeks of aerobic training, when compared to the control and smoke groups, which were not submitted to training. The aerobic training also downregulated the increase of matrix metalloproteinases (MMP-2 and MMP-9) and upregulated antioxidant genes, such as nuclear factor erythroid-2 like 2 (NRF2) and heme-oxygenase1 (HMOX1), in exercise + smoke group compared to smoke group. Conclusions Treadmill aerobic training protects diaphragm muscle wasting induced by cigarette smoke exposure involving upregulation of antioxidant genes and downregulation of matrix metalloproteinases.

Highlights

Chronic obstructive pulmonary disease (COPD) is associated with respiratory and peripheral muscle dysfunction
Little is known regarding the key role of extracellular matrix (ECM) remodeling associated with oxidative stress on respiratory muscles weakness in chronic obstructive pulmonary disease (COPD) during chronic cigarette smoke (CS) exposure
After 24 weeks of aerobic training, the exercise time on treadmill and the maximal speed were significantly greater in those groups that trained endurance exercise, when compared to the groups that were not trained

Summary

Introduction

Chronic obstructive pulmonary disease (COPD) is associated with respiratory and peripheral muscle dysfunction. The present study aimed to analyze the effects of physical training on an antioxidant canonical pathway and metalloproteinases activity in diaphragm muscle in a model of cigarette smoke-induced chronic obstructive pulmonary disease (COPD). Aerobic training inhibited diaphragm muscle wasting induced by cigarette smoke exposure This inhibition was associated with improved aerobic capacity in those animals that were submitted to 24 weeks of aerobic training, when compared to the control and smoke groups, which were not submitted to training. The aerobic training downregulated the increase of matrix metalloproteinases (MMP-2 and MMP-9) and upregulated antioxidant genes, such as nuclear factor erythroid-2 like 2 (NRF2) and heme-oxygenase (HMOX1), in exercise + smoke group compared to smoke group. Treadmill aerobic training protects diaphragm muscle wasting induced by cigarette smoke exposure involving upregulation of antioxidant genes and downregulation of matrix metalloproteinases

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Results

Conclusion