Background: Physical capacity (PC) and physical activity (PA) represent associated but separate domains of physical function. It remains unknown whether this framework may support a better understanding of the impaired physical function in patients with chronic obstructive pulmonary disease (COPD). The current study had two aims: (1) to determine the distribution of patients with COPD over the PC-PA quadrants, and (2) to explore whether differences exist in clinical characteristics between these quadrants. Methods: In this retrospective study, PC was measured using the six-minute walk distance (6MWD), and PA was assessed with an accelerometer. Moreover, patients’ clinical characteristics were obtained. Patients were divided into the following quadrants: (I) low PC (6MWD <70% predicted), low PA, using a step-defined inactivity index (<5000 steps/day, ”can’t do, don’t do” quadrant); (II) preserved PC, low PA (“can do, don’t do” quadrant); (III) low PC, preserved PA (“can’t do, do do” quadrant); and (IV) preserved PC, preserved PA (“can do, do do” quadrant). Results: The distribution of the 662 COPD patients over the quadrants was as follows: “can’t do, don’t do”: 34%; “can do, don’t do”: 14%; “can’t do, do do”: 21%; and “can do, do do”: 31%. Statistically significant differences between quadrants were found for all clinical characteristics, except for educational levels. Conclusions: This study proves the applicability of the PC-PA quadrant concept in COPD. This concept serves as a pragmatic clinical tool, that may be useful in the understanding of the impaired physical functioning in COPD patients and therefore, may improve the selection of appropriate interventions to improve physical function.

Postoperative pulmonary complications are significant contributors to morbidity in patients who have undergone upper abdominal, thoracic, or cardiac surgery. The pathophysiology of these complications might involve postoperative inspiratory muscle weakness. The nature of postoperative inspiratory muscle weakness is unknown. Objective To investigate the effect of surgery on the functioning of the diaphragm, the main muscle of inspiration. Methods Serial biopsies from the diaphragm and the latissimus dorsi muscle were obtained from 6 patients during thoracotomy for resection of a tumor in the right lung. Biopsies were taken as soon as the diaphragm had been exposed (t(0)) and again after 2 hours (t(2)). The contractile performance of demembranated muscle fibers, as well as fiber morphology and markers for proteolysis, was determined. Results In all patients, the force-generating capacity of diaphragm muscle fibers at t(2) was significantly reduced (~35%) compared with that at t(0), with a more pronounced force loss in type 2 fibers compared with type 1 fibers. Diaphragm weakness was not part of a generalized muscle weakness as contractile performance of latissimus dorsi fibers was preserved at t(2). Diaphragm fiber size and myofibrillar structure were not different at t(2) compared with t0, but myosin heavy chain type 2 was significantly reduced at t(2) and MuRF-1 mRNA and protein levels were elevated at t(2). Conclusions Only 2 hours of thoracic surgery causes marked, and selective, diaphragm muscle fiber weakness.

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Atrophy and fatty infiltration are important causes of muscle weakness in inclusion body myositis (IBM). Muscle weakness can also be caused by reduced specific force; i.e. the amount of force generated per unit of residual muscle tissue. This study investigates in vivo specific force of the quadriceps and ex vivo specific force of single muscle fibers in patients with IBM. We included 8 participants with IBM and 12 healthy controls, who all underwent quantitative muscle testing, quantitative MRI of the quadriceps and paired muscle biopsies of the quadriceps and tibialis anterior. Single muscle fibers were isolated to measure muscle fiber specific force and contractile properties. Both in vivo quadriceps specific force and ex vivo muscle fiber specific force were reduced. Muscle fiber dysfunction was accompanied by reduced active stiffness, which reflects a decrease in the number of attached actin-myosin cross-bridges during activation. Myosin concentration was reduced in IBM fibers. Because reduced specific force contributes to muscle weakness in patients with IBM, therapeutic strategies that augment muscle fiber strength may provide benefit to patients with IBM.