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Pathologic alterations induced by corticosteroid administration were evaluated in the respiratory muscles and compared to those in the peripheral skeletal muscles of the rabbit. Alterations in gross and microscopic pathology as well as histochemistry were determined in the diaphragm, intercostal, sternocleidomastoid, extensor digitorum longus, and soleus muscles following 3 wk of intramuscular cortisone injections. Corticosteroid administration induced significant pathologic changes in all the muscles except the soleus. Although gross pathologic changes were greatest in the extensor digitorum longus, microscopic changes were greatest in the diaphragm. Reductions in total muscle fiber volume were similar in the diaphragm, sternocleidomastoid, and extensor digitorum longus muscles. The composition of muscle fiber types and the number of fibers in a muscle were not altered in any of the muscles studied following corticosteroids. There was significant atrophy of individual muscle fibers in all the muscles except the soleus. In the diaphragm, corticosteroids induced atrophy of all fiber types, including type I fibers. Atrophy of type I fibers was not present in the peripheral skeletal muscles or the other respiratory muscles. On the other hand, corticosteroids induced selective atrophy of type IIb muscle fibers in the intercostal and sternocleidomastoid muscles similar to that in the peripheral skeletal muscles. These findings suggest that the effect of corticosteroids on the diaphragm is unique, and one cannot extrapolate form the effect of corticosteroids on peripheral skeletal muscles to that in the diaphragm. In addition, these pathologic changes may have functional relevance, since atrophy of type I fibers may result in a reduction in muscle endurance.

Twenty-two patients undergoing thoracotomy for the diagnosis or treatment of a suspected pulmonary neoplasm had separate biopsies taken from their external and internal intercostal muscles at the time of surgery. Pulmonary function abnormalities ranged from none to moderate airway obstruction. Seventeen of the twenty-two patients had morphologic changes (targeting, variation in fiber size, splitting, and atrophy) in both respiratory muscles, but not in the control latissimus dorsi. Fiber atrophy was more marked in the internal intercostal muscle and was significantly related to the degree of airway obstruction, but not to age, malignancy, or weight loss. Biochemical analyses revealed decreased adenosine triphosphate (ATP) and phosphocreatine (PC) in 47 of 52 muscles, including the latissimus dorsi. The data suggested a relation between increasing airway obstruction and decreasing amounts of phosphocreatine in both intercostal muscles. This relationship may have been enhanced by the presence of malignancy or weight loss. There was a selective decrease in muscle glycogen found only in the external intercostal muscle that was not affected by airway obstruction, malignancy, or weight loss. Intercostal muscle abnormalities are common in patients with obstructive lung disease who undergo thoracotomy, and are probably multifactorial in origin. It is possible that these abnormalities affect the natural history of lung disease in some patients.