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American Journal of Respiratory and Critical Care Medicine Vol 166. pp. 479-484, (2002)
© 2002 American Thoracic Society

Original Article

Respiratory and Limb Muscle Weakness Induced by Tumor Necrosis Factor-{alpha}

Involvement of Muscle Myofilaments

Michael B. Reid, Jan Lännergren and Håkan Westerblad

Baylor College of Medicine, Houston, Texas; and Karolinska Institutet, Stockholm, Sweden

Correspondence and requests for reprints should be addressed to Michael B. Reid, Ph.D., Pulmonary Medicine, Suite 520B, Baylor College of Medicine, Houston, TX 77030. E-mail: reid{at}bcm.tmc.edu

The respiratory and limb skeletal muscles become weakened in sepsis, congestive heart failure, and other inflammatory diseases. A potential mediator of muscle weakness is tumor necrosis factor (TNF)-{alpha}, a cytokine that can stimulate muscle wasting and also can induce contractile dysfunction without overt catabolism. This study addressed the latter process. Murine diaphragm and limb muscle (flexor digitorum brevis [FDB]) preparations were used to determine the relative sensitivities of these muscles to TNF-{alpha}. Intact muscle fibers were isolated from FDB and microinjected with indo-1 to measure changes in sarcoplasmic calcium regulation. We found that TNF-{alpha} depressed tetanic force of the diaphragm and FDB to comparable degrees across a range of stimulus frequencies. In isolated muscle fibers, TNF-{alpha} decreased tetanic force without altering tetanic calcium transients or resting calcium levels. We conclude that (1) TNF-{alpha} compromises contractile function of diaphragm and limb muscle similarly, and (2) TNF-{alpha} decreases force by blunting the response of muscle myofilaments to calcium activation.

Key Words: respiratory muscles • muscle, skeletal • cytokines • tumor necrosis factor • muscle contraction




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