Exercise limitations

Pulmonary hypertension develops late in the course of COPD, usually after the development of severe hypoxemia. It is the most common cardiovascular complication of COPD and can result in cor pulmonale, or right-sided heart failure. Hypoxemia plays the primary role in the development of pulmonary hypertension by causing vasoconstriction of the pulmonary arteries and by promoting vessel wall remodeling. Destruction of the pulmonary capillary bed by emphysema further contributes by increasing the pressure required to perfuse the pulmonary vascular bed. Cor pulmonale is associated with venous stasis and thrombosis that may result in pulmonary embolism. Another important systemic effect is the progressive loss of skeletal muscle mass, which contributes to exercise limitations and declining health status. 

OSC handles procurement for PMCD, but PMCD exercises limited delegated authority through a contracting officer representative. 

Tirdel et al. [118] researched metabolic myopathy as a cause of the exercise limitation in lung transplant recipients, while Noriyuki et al. [119] evaluated lung tissue oxygenation using NIR spectroscopy. 

G. B. Tirdel, R. Girgis, R. S. Fishman, and J. Theodore, Metabolic Myopathy as a Cause of the Exercise Limitation in Lung Transplant Recipients, J. Heart Lung Transpl., 17(12), 1231-1237 (1998). 

Airway resistance may increase because of toxic inhalational injury, resulting in increased work of respiration. Air trapping secondary to increased airway resistance increases intrathoracic pressure. Increased work of respiration and decreased venous return result in exercise limitation. Ventilation-perfusion abnormalities of disordered airway function limit oxygen delivery and carbon dioxide clearance, which also compromises exercise tolerance. 

Dyspnea may be present long after the chest radiograph, physical examination, and resting values for ABG return to normal. Exercise evaluation of these individuals (with ABG readings as a necessary part of that evaluation) must be undertaken to understand the exposed individual s complaints. Failure to make these measurements in a soldier complaining of exercise limitation displays a lack of understanding of both toxic inhalant exposures and basic exercise physiology. 

Exercise limitation and functional disability in COPD have a complex, multifactorial basis. Ventilatory limitation is caused by increased airways resistance, static and dynamic hyperinflation, increased elastic load to breathing, gas exchange disturbances, and mechanical disadvantage and/or weakness of the respiratory muscles (4-6). Car-diocirculatory disturbances (7,8), nutritional factors (9), and psychological factors, such as anxiety and fear, also contribute commonly to exercise intolerance. Skeletal muscle dysfunction is characterized by reductions in muscle mass (10,11), atrophy of type I (slow twitch, oxidative, endurance) (12,13) and type Ila (fast twitch) muscle fibers (14), altered myosin heavy chain expression (15), as well as reductions in fiber capillarization (16) and oxidative enzyme capacity (17,18). Such a dysfunction is another key factor that contributes... 

Gallagher CG. Exercise limitation and clinical exercise testing in chronic obstructive pulmonary disease. Clin Chest Med 1994 15 305-326. 

Gosselink R, Troosters T, Decramer M. Peripheral muscle weakness contributes to exercise limitation in COPD. Am J Respir Crit Care Med 1996 153 976-980. 

Plankeel JE, McMullen B, MacIntyre NR. Exercise outcomes after pulmonary rehabilitation depend on the initial mechanism of exercise limitation among non-oxygen-dependent COPD patients. Chest 2005 127 110-116. 

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