Pulmonary rehabilitation restores limb muscle mitochondria and improves the intramuscular metabolic profile
10.1097/CM9.0000000000002175
- VernacularTitle:Pulmonary rehabilitation restores limb muscle mitochondria and improves the intramuscular metabolic profile
- Author:
Shiwei QUMU
1
,
2
;
Weiliang SUN
;
Jing GUO
;
Yuting ZHANG
;
Lesi CAI
;
Chaozeng SI
;
Xia XU
;
Lulu YANG
;
Xuanming SITU
;
Tianyi YANG
;
Jiaze HE
;
Minghui SHI
;
Dongyan LIU
;
Xiaoxia REN
;
Ke HUANG
;
Hongtao NIU
;
Hong LI
;
Chang'An YU
;
Yang CHEN
;
Ting YANG
Author Information
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
2. Institute of Respiratory Medicine, Chinese Academy of Medical Science, Beijing 100029, China
- Keywords:
Pulmonary rehabilitation;
Chronic obstructive pulmonary disease;
Airflow-assisted desorption electrospray ionization-mass spectrometry imaging;
Docosapen
- From:
Chinese Medical Journal
2023;136(4):461-472
- CountryChina
- Language:Chinese
-
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.
