1. Rochester, Carolyn L. MD

Article Content

Nishiyama O, Taniguchi H, Kondoh Y, Kimura T, Ogawa T, Watanabe F, Arizono S.


Chest. June 2005;127(6):2028-2033.


Study Objective:

In COPD, it has been shown that peripheral muscle dysfunction is a factor determining exercise intolerance. We examined the hypothesis that exercise capacity of patients with idiopathic pulmonary fibrosis (IPF) is, at least in part, determined by peripheral muscle dysfunction.



Maximum oxygen uptake (V2max) was evaluated in 41 consecutive patients with IPF, along with potential determinants of exercise capacity, both in the lungs and in the peripheral muscles.



Patients had reduced V2max (893 +/- 314 mL, 46.0% predicted) and reduced quadriceps force (QF) [65% predicted]. Significant correlates of V2max reduction were vital capacity (VC) (r = 0.79), total lung capacity (r = 0.64), diffusion capacity (r = 0.64), QF (r = 0.62), maximum expiratory pressure (r = 0.48), and Pa2 at rest (r = 0.33). In stepwise multiple regression analysis, VC and QF were independent predictors of V2max. Furthermore, in subgroup analysis, QF was a significant contributing factor for V2max in patients who discontinued exercise because of dyspnea and/or leg fatigue.



We conclude that QF is a predictor of exercise capacity in IPF. Measures that improve muscle function might improve exercise tolerance.



Skeletal muscle dysfunction is a major factor contributing to exercise limitation in patients with COPD. It is well established that this dysfunction is improved by undergoing exercise training/pulmonary rehabilitation. Indeed, the documented improvements in skeletal muscle function following exercise training forms a significant portion of the scientific rationale for pulmonary rehabilitation. Given that many factors thought to cause skeletal muscle dysfunction in COPD such as disuse/deconditioning, nutritional impairment, and systemic inflammation (among others) are present in other forms of chronic respiratory disease, it stands to reason that patients with disorders other than COPD likely also have skeletal muscle dysfunction that may contribute to their exercise limitation. In the present study by Nishiyama et al, the authors have investigated the relationship between quadriceps force and exercise limitation among patients with idiopathic pulmonary fibrosis. Not surprisingly, in this study, the patients had evidence of both impaired exercise capacity (reduced V2max) and reduced quadriceps force (QF). Importantly, both indices of lung function and QF were independent predictors of V2max. This is an important study because it demonstrates for the first time that there is skeletal muscle dysfunction in patients with chronic respiratory disease other than COPD, and that this does correlate (as it does in patients with COPD) with impaired exercise capacity. Although the basis of the impairment of QF in patients with pulmonary fibrosis remains to be elucidated, this study provides the rationale for inclusion of patients with non-COPD disorders such as pulmonary fibrosis routinely in PR programs.