Authors

  1. Kalra, Sanjay MD, FRCP
  2. Roitman, Jeffrey L. EdD

Article Content

Bolton CE, Broekhuizen R, Ionescu AA, Nixon LS, Wouters EFM, Shale DJ, Schols AMWJ

 

Thorax. 2007;62:109-114.

 

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) 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.

 

Editor's Comment.

Some extrapulmonary abnormalities in patients with chronic obstructive pulmonary disease, primarily weight loss and reduction in muscle mass, are widely believed to represent systemic inflammation. Changes in the sputum and blood cytokine profile have been described both in animal and human subjects, but the influence of pulmonary rehabilitation on these abnormalities is unknown. This study examines markers of muscle catabolism and systemic inflammation (urinary pseudouridine for the former and blood interleukin-6, tumor necrosis factor-[alpha], and soluble tumor necrosis factor receptor for the latter) in patients with moderate to severe chronic obstructive pulmonary disease before and after a standard 8-week pulmonary rehabilitation program. Although there was a predictable increase in the FFM with rehabilitation, especially in patients with a low FFM to start with, there was no change in any of the catabolism/inflammation measures, and the increase in muscle mass waned 4 weeks after the end of pulmonary rehabilitation. This serves to demonstrate that although some consequences of chronic obstructive pulmonary disease may at least be temporarily ameliorated by an exercise program, the less well-defined systemic catabolic/inflammatory effects are not measurably affected.

 

SK