Cellular protein breakdown and systemic inflammation are unaffected by pulmonary rehabilitation in COPD
- Charlotte E Bolton1,*,
- Roelinka Broekhuizen2,*,
- Alina A Ionescu1,
- Lisette S Nixon1,
- Emiel F M Wouters2,
- Dennis J Shale1,
- Annemie M W J Schols2
- 1Department of Respiratory Medicine, Wales College of Medicine, Cardiff University, Academic Centre, Llandough Hospital, Vale of Glamorgan, Cardiff, UK
- 2Department of Respiratory Medicine, University Hospital Maastricht, Maastricht, The Netherlands
- Correspondence to:
Dr C E Bolton
Department of Respiratory Medicine, School of Medicine, Cardiff University, Academic Centre, Llandough Hospital, Vale of Glamorgan CF64 2XX, UK;
- Received 9 February 2006
- Accepted 5 August 2006
- Published Online First 23 August 2006
Background: Pulmonary rehabilitation can improve the functional capacity, but has a variable effect on the low fat-free mass (FFM) in patients with chronic obstructive pulmonary disease.
Hypothesis: Pulmonary rehabilitation would not affect catabolic drives such as systemic inflammation and also protein breakdown.
Methods: Patients (n = 40) were studied at the start of an 8-week in-patient pulmonary rehabilitation programme, at the end of the programme and 4 weeks later. FFM and functional capacity (quadriceps strength, handgrip strength and peak workload) were assessed. Pseudouridine (PSU) urinary excretion (cellular protein breakdown) and inflammatory status were determined. Healthy participants had a single baseline assessment (n = 18).
Results: PSU, (IL)-6 and soluble tumour necrosis factor (sTNF)α R75 were increased in patients compared with healthy participants, whereas FFM and functional capacity were reduced (all p<0.01). PSU was inversely related to both FFM and skeletal muscle function. FFM and functional parameters increased with rehabilitation, but PSU and inflammatory status were unaffected. The gain in FFM was lost 4 weeks after the completion of rehabilitation (p<0.01).
Conclusion: The anabolic effect of pulmonary rehabilitation improved FFM, but it did not reverse the increased protein breakdown or systemic inflammation. Thus, on cessation of pulmonary rehabilitation the FFM gains were lost owing to a loss of anabolic drive.
- BMI, body mass index
- COPD, chronic obstructive pulmonary disease
- FEV1, forced expiratory volume in 1 s, FFM, fat free mass
- FFMI, Fat-Free Mass Index
- GOLD, Global Initiative for Chronic Obstructive Lung Disease
- HPLC, high-performance liquid chromatography
- PSU, pseudouridine
- sTNF, soluble tumour necrosis factor
↵* These authors contributed equally to this work.
Published Online First 23 August 2006
Funding: This study was supported by the British Lung Foundation (P01/7), GlaxoSmithKline (UK/NL), AstraZeneca (UK), Numico Research (The Netherlands), Capricorn (funded by Welsh Assembly Government) and European Union Grant QLK6-CT-2002-02285.
Competing interests: DJS has received research grants from AstraZeneca and GlaxoSmithKline. AMWJS has received research grants from GlaxoSmithkline and Numico Research. EFMW serves as a consultant to GlaxoSmithKline (GSK) and is a member of the scientific advisory board for GSK. He received lecture fees and research grants between 2001 and 2004 from GSK.
Written informed consent was obtained from all subjects, and the ethical review board of the University Hospital Maastricht approved the study.