Cited by 122Muscle Physiology and DisordersChronic Obstructive Pulmonary Disease (COPD) ResearchExercise and Physiological Responses

Effects of rehabilitative exercise on peripheral muscle TNF , IL-6, IGF-I and MyoD expression in patients with COPD

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Vogiatzis, I., Stratakos, G., Simoes, D. C M, Terzis, G., Georgiadou, O., Roussos, C., Zakynthinos, S.·2007·Thorax

Abstract

BACKGROUND: Skeletal muscle wasting commonly occurs in patients with chronic obstructive pulmonary disease (COPD) and has been associated with the presence of systemic inflammation. This study investigated whether rehabilitative exercise training decreases the levels of systemic or local muscle inflammation or reverses the abnormalities associated with muscle deconditioning. METHODS: Fifteen patients with COPD (mean (SE) forced expiratory volume in 1 s 36 (4)% predicted) undertook high-intensity exercise training 3 days/week for 10 weeks. Before and after the training programme the concentration of tumour necrosis factor alpha (TNFalpha), interleukin-6 (IL-6) and C-reactive protein (CRP) in plasma was determined by ELISA, and vastus lateralis mRNA expression of TNFalpha, IL-6, total insulin-like growth factor-I (IGF-I) and its isoform mechanogrowth factor (MGF) and myogenic differentiation factor D (MyoD) were assessed by real-time PCR. Protein levels of TNFalpha, IGF-I and MyoD were measured by Western blotting. RESULTS: Rehabilitation improved peak exercise work rate by 10 (2%) (p = 0.004) and mean fibre cross-sectional area from 4061 (254) microm(2) to 4581 (241) microm(2) (p = 0.001). Plasma inflammatory mediators and vastus lateralis expression of TNFalpha and IL-6 were not significantly modified by training. In contrast, there was a significant increase in mRNA expression of IGF-I (by 67 (22)%; p = 0.044), MGF (by 67 (15)%; p = 0.002) and MyoD (by 116 (30)%; p = 0.001). The increase observed at the mRNA level was also seen at the protein level for IGF-I (by 72 (36)%; p = 0.046) and MyoD (by 67 (21)%; p = 0.012). CONCLUSIONS: Pulmonary rehabilitation can induce peripheral muscle adaptations and modifications in factors regulating skeletal muscle hypertrophy and regeneration without decreasing the levels of systemic or local muscle inflammation.

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Crossref · 10.1136/thx.2006.069310

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  • Inflammation is not the sole driver of COPD muscle atrophy, as exercise can affect factors regulating muscle hypertrophy and regeneration without affecting levels of systemic or local muscle inflammation.

    “However, inflammation is not the sole driver as exercise can affect factors regulating muscle hypertrophy and regeneration without affecting the levels of systemic or local muscle inflammation [19].”

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Authors
Vogiatzis, I., Stratakos, G., Simoes, D. C. M., Terzis, G., Georgiadou, O., Roussos, C., & Zakynthinos, S.
Affiliations
National and Kapodistrian University of Athens (GR)
Corresponding author
Vogiatzis, I.
Venue
Thorax
Publisher
BMJ
Published
2007-05-25
Volume
62
Issue
11
Pages
950-956
ISSN
0040-6376 (ISSN-L)
OpenAlex
W2023201233
Cited by
122
References
5
Citations by year
2026: 1 · 2025: 5 · 2024: 2 · 2023: 7 · 2022: 5 · 2021: 2 · 2020: 2 · 2019: 5 · 2018: 9 · 2017: 5 · 2016: 7 · 2015: 3 · 2014: 14 · 2013: 8 · 2012: 10
FWCI
3.58
Type
journal article
Language
en
Open access
Locations
  • Thorax (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • Northumbria Research Link (Northumbria University) (submittedVersion)
  • HighWire Press Open Archive (submittedVersion)
Funders
Pfizer
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
  • Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Chronic Obstructive Pulmonary Disease (COPD) Research
  • Health Sciences › Medicine › Rehabilitation › Exercise and Physiological Responses
Keywords
chronic obstructive pulmonary disease, pulmonary rehabilitation, high-intensity training, skeletal muscle atrophy, muscle inflammation, TNF-α, interleukin-6, insulin-like growth factor I, MyoD, vastus lateralis, muscle hypertrophy, muscle regeneration, systemic inflammation, C-reactive protein
MeSH terms
Aged, Exercise Therapy, Female, Forced Expiratory Volume, Humans, Insulin-Like Growth Factor I, Male, RNA, Messenger, Tumor Necrosis Factor-alpha, Vital Capacity, Interleukin-6, MyoD Protein, Muscle, Skeletal, Pulmonary Disease, Chronic Obstructive

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