Abstract
Chronic obstructive pulmonary disease (COPD) produces skeletal muscle atrophy and weakness, leading to impairments of exercise performance. The mechanical work needed for movement execution is also provided by the passive tension developed by musculoarticular connective tissue. To verify whether COPD affects this component, the passive viscoelastic properties of the knee joint were evaluated in 11 patients with COPD and in 11 healthy individuals. The levels of stiffness and viscosity were assessed by means of the pendulum test, consisting in a series of passive leg oscillations. In addition, to explore the contribution of passive tension in the mechanical output of a simple motor task, voluntary leg flexion–extension movements were performed. Patients with COPD showed a statistically significant reduction in stiffness and viscosity compared to controls. Voluntary execution of flexion–extension movements revealed that the electromyographic activity of the Rectus Femoris and Biceps Femoris was lower in patients than in controls, and the low viscoelastic tension in the patients conditioned the performance of active movements. These results provide novel insights on the mechanism responsible for the movement impairments associated with COPD.
Highlights
Chronic obstructive pulmonary disease (COPD) produces skeletal muscle atrophy and weakness, leading to impairments of exercise performance
Passive tensions can be produced by the connective tissue integrated into the muscle structure, tendons, noncontractile sarcomere proteins and tissues associated with the joints, such as ligaments or capsules
Comparing the two samples of participants, we found that COPD and control groups differed significantly for all kinematic parameters measured during the first knee flexion–extension movement (Fig. 3A–D)
Summary
Chronic obstructive pulmonary disease (COPD) produces skeletal muscle atrophy and weakness, leading to impairments of exercise performance. Voluntary execution of flexion–extension movements revealed that the electromyographic activity of the Rectus Femoris and Biceps Femoris was lower in patients than in controls, and the low viscoelastic tension in the patients conditioned the performance of active movements These results provide novel insights on the mechanism responsible for the movement impairments associated with COPD. Symptoms and rate of clinical progression of the disease may vary widely among individuals, but all patients with stable COPD exhibit reduced peripheral muscle endurance and great fatigability[1,2,3] This uncomfortable condition leads to limitation of physical activity, with the consequence of further alterations in muscle function and a progressive decline in their ability to perform exercise. These structures develop a passive viscoelastic tension that can counterbalance or assist muscle active tension and contribute to the level of joint stability and m
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