Canadian Health and Care Mall: Discussion of Quadriceps Weakness Is Related to Exercise Capacity in Idiopathic Pulmonary Fibrosis
In the present study, we found that QF is reduced in patients with IPF, and this weakness correlates with exercise limitation as well as lung function impairment in those patients. Among these variables, VC and QF were particularly significant contributing factors according to the stepwise analysis. To our knowledge, this is the first report clarifying the relationship between peripheral muscle performance and exercise capacity in patients with IPF.
Some factors and mechanisms that determine exercise capacity in ILD have been reported, although those in IPF have not been extensively studied. A decrease in exercise capacity has been reported even in ILD patients who have normal resting pulmonary function results. Thus, directly measuring exercise capacity of patients with ILD is important in evaluating impairment. Factors reported to correlate with exercise limitation in patients with ILD include VC, FEV1, TLC, Dlco, and, possibly, Pa02. Mechanism of exercise limitation in patients with ILD has also been explored. Marciniuk et al described expiratory flow limitation in all patients who stopped exercise due to dyspnea. In the remaining patients who discontinued exercise because of leg fatigue, no flow limitation was evi-dent. Harris-Eze et al reported that patients with ild were able to increase both peak ventilation and exercise performance with supplemental oxygen. This finding suggests a hypothesis that arterial hypoxemia, not ventilatory limitation, limits exercise. As another contributing factor, ventilation-perfusion mismatching, may contribute to exercise limita-tion. Diffusion limitation and circulatory limitation can also affect exercise tolerance of patients with ILD. Hansen and Wasserman reported that Dlco was the best correlate of Vo2max in ILD. It is also suggested that higher respiratory drive during exercise can be attributed to increased afferent reflexes originating from the lung or chest wall, which might thereby limit exercise tolerance. To become familiar with ordering procedure online you may go to the page using the link – canadian health care mall publications on wordpress.
Despite these previous studies, the pathophysiology of exercise limitation in ILD has been inadequately elucidated. Moreover, studies that investigated mechanisms of exercise limitation in patients with ILD generally included a variety of diseases, such as idiopathic interstitial pneumonia, sarcoidosis, and collagen vascular diseases. It seems likely that the factors that determine exercise limitation depend on the etiologies of ILD. Thus, our evaluation of exercise capacity in one disease, IPF, seems valuable. Furthermore, the fact that the QF is decreased and is a significant correlate of exercise capacity in IPF seems to be important in elucidating the mechanism of exercise limitation in the disease.
In the present study, a marked decrease in V02max was observed in patients with IPF, even if impairment in lung function was not so severe as has been reported in some previous studies. Moreover, lung function including VC, TLC, and Dlco significantly correlated with Vo2max. Pao2 and VE/VC02 at the end of exercise significantly correlated with V02max in patients who terminated the exercise due to dyspnea, but not in those who stopped due to leg fatigue. This is consistent with the concept that respiratory limitation contributes to limitation of exercise capacity in patients who stopped the test because of dyspnea. Even in those patients, QF was a strong correlate of V02max. If exercise capacity is assessed by AT, similar results were obtained. This supports the importance of QF as a determinant of exercise capacity in IPF. Moreover, a significant correlation between dyspnea at end-exercise and QF indicates that the quadriceps limitation is less than that in those patients who are more tolerant of the discomfort of dyspnea. The decreased compliance of the lungs in IPF imposes a chronic load on the muscles of inspiration. As a result, these muscles are likely to be quite “fit,” possibly explaining the normal Plmax values. In contrast, expiration is likely to be passive under almost all conditions, resulting of relative deconditioning of the expiratory muscles, possibly explaining the low PEmax values observed.
The pathophysiology underlying quadriceps weakness that was observed in the present study is not yet known. One possible mechanism is deconditioning due to limitation in activities of daily living. The normal HF observed in the study may be explained in that hand strength may not respond to decreased activity to the same degree as the quadriceps. Another possible mechanism of quadriceps weakness is related to the inflammatory disease process of IPF. Other possible mechanisms include decreased levels of anabolic hormones and myopathy specific to IPF, similar to that reported in COPD. Clearly, additional research will be necessary to elucidate the pathophysiology of the muscles of ambulation in IPF.
The ATS/ERS consensus statement recommends therapeutic trial of corticosteroid therapy in patients with IPF. Myopathy induced by corticosteroids has been reported to enhance peripheral muscle weakness in these patients. Myopathy of respiratory muscle reportedly can occur from the use of corti-costeroids, which can potentially affect the exercise tolerance of patients. However, these factors were not present in this study because subjects had not been treated with corticosteroids.
In our study, exercise-induced desaturation did not correlate with V02max, possibly because only patients with mild-to-moderate impairment in lung function were enrolled, and desaturation was only mild.
The results of the present study imply that the training of peripheral muscles, especially in the lower extremities, might increase exercise capacity of patients with IPF. In COPD, training of the lower extremities is the most important factor in pulmonary rehabilitation., Although Foster and Thomas demonstrated the efficacy of pulmonary rehabilitation for non-COPD patients, there are few reports about pulmonary rehabilitation for patients with ILD including IPF. Although pulmonary rehabilitation has not yet been shown to be effective for patients with ILD, our results suggest the possibility of the efficacy of pulmonary rehabilitation for IPF.
Hence, the role of pulmonary rehabilitation for patients with IPF should be evaluated in additional studies, including the training of peripheral muscles.
There are some limitations in this study. First, we included only patients with mild-to-moderate lung impairment (VC, 76.6 ± 16.8%). This was because patients with a new diagnosis were studied because we wished to avoid the confounding effects of pharmacotherapy for IPF on the muscles. So, it is unclear whether our results can be applied to more severe cases. Secondly, not all patients received a diagnosis pathologically. Some reports,’ however, have demonstrated that the accuracy of thin-section CT in identifying IPF is quite high. The patients receiving a diagnosis of IPF clinically and included in the study are unlikely to have other ILD.
In conclusion, both measures of pulmonary function and of QF significantly correlate with exercise capacity in patients with IPF. VC, QF, and VE/VC02 at peak exercise are independent predictors of exercise capacity in patients with IPF.