Pulmonary rehabilitation restores limb muscle mitochondria and improves the intramuscular metabolic profile

Author:

Qumu Shiwei1,Sun Weiliang2,Guo Jing2,Zhang Yuting2,Cai Lesi3,Si Chaozeng4,Xu Xia5,Yang Lulu16,Situ Xuanming7,Yang Tianyi7,He Jiaze16,Shi Minghui16,Liu Dongyan8,Ren Xiaoxia1,Huang Ke1,Niu Hongtao1,Li Hong2,Yu Chang’An9,Chen Yang10,Yang Ting1

Affiliation:

1. Department of Pulmonary and Critical Care Medicine, Center of Respiratory Medicine, National Center for Respiratory Medicine, National Clinical Research Center for Respiratory Diseases, China-Japan Friendship Hospital, Beijing 100029, China; Institute of Respiratory Medicine, Chinese Academy of Medical Science, Beijing 100029, China

2. Institute of Clinical Medical Sciences, China-Japan Friendship Hospital, Beijing 100029, China

3. National Anti-Drug Laboratory Beijing Regional Center, Beijing 100164, China

4. Department of Information Management, China–Japan Friendship Hospital, Beijing 100029, China

5. Department of Immunology, School of Basic Medical Sciences, Capital Medical University, Beijing 100005, China

6. Capital Medical University, Beijing 100069, China

7. Department of Rehabilitation, China–Japan Friendship Hospital, Beijing 100029, China

8. Tsinghua University School of Medicine, Beijing 100084, China

9. Department of Cardiology, China–Japan Friendship Hospital, Beijing 100029, China

10. The State Key Laboratory of Medical Molecular Biology, Department of Biochemistry and Molecular Biology, Institute of Basic Medical Sciences, School of Basic Medicine, Chinese Academy of Medical Science and Peking Union Medical College, Beijing 100005, China.

Abstract

Abstract Background: Exercise, as the cornerstone of pulmonary rehabilitation, is recommended to chronic obstructive pulmonary disease (COPD) patients. The underlying molecular basis and metabolic process were not fully elucidated. Methods: Sprague-Dawley rats were classified into five groups: non-COPD/rest (n = 8), non-COPD/exercise (n = 7), COPD/rest (n = 7), COPD/medium exercise (n = 10), and COPD/intensive exercise (n = 10). COPD animals were exposed to cigarette smoke and lipopolysaccharide instillation for 90 days, while the non-COPD control animals were exposed to room air. Non-COPD/exercise and COPD/medium exercise animals were trained on a treadmill at a decline of 5° and a speed of 15 m/min while animals in the COPD/intensive exercise group were trained at a decline of 5° and a speed of 18 m/min. After eight weeks of exercise/rest, we used ultrasonography, immunohistochemistry, transmission electron microscopy, oxidative capacity of mitochondria, airflow-assisted desorption electrospray ionization-mass spectrometry imaging (AFADESI-MSI), and transcriptomics analyses to assess rectal femoris (RF). Results: At the end of 90 days, COPD rats’ weight gain was smaller than control by 59.48 ± 15.33 g (P = 0.0005). The oxidative muscle fibers proportion was lower (P < 0.0001). At the end of additional eight weeks of exercise/rest, compared to COPD/rest, COPD/medium exercise group showed advantages in weight gain, femoral artery peak flow velocity (Δ58.22 mm/s, 95% CI: 13.85–102.60 mm/s, P = 0.0104), RF diameters (Δ0.16 mm, 95% CI: 0.04–0.28 mm, P = 0.0093), myofibrils diameter (Δ0.06 μm, 95% CI: 0.02–0.10 μm, P = 0.006), oxidative muscle fiber percentage (Δ4.84%, 95% CI: 0.15–9.53%, P = 0.0434), mitochondria oxidative phosphorylate capacity (P < 0.0001). Biomolecules spatial distribution in situ and bioinformatic analyses of transcriptomics suggested COPD-related alteration in metabolites and gene expression, which can be impacted by exercise. Conclusion: COPD rat model had multi-level structure and function impairment, which can be mitigated by exercise.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

General Medicine,General Medicine

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