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J Appl Physiol 102: 1850-1855, 2007. First published February 15, 2007; doi:10.1152/japplphysiol.01177.2006
8750-7587/07 $8.00
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Myofibrillar protein oxidation and contractile dysfunction in hyperthyroid rat diaphragm

Takashi Yamada,1 Takaaki Mishima,2 Makoto Sakamoto,2 Minako Sugiyama,2 Satoshi Matsunaga,3 and Masanobu Wada1

1Graduate School of Integrated Arts and Sciences and 2Graduate School of Biosphere Science, Hiroshima University, Hiroshima; and 3Research Center for Urban Health and Sports, Osaka City University, Sugimoto, Osaka, Japan

Submitted 18 October 2006 ; accepted in final form 29 January 2007

The purpose of the present study was to test the hypothesis that administration of thyroid hormone [3,5,3'-triiodo-L-thyronine (T3)] could result in oxidation of myofibrillar proteins and, in turn, induce alterations in respiratory muscle function. Daily injection of T3 for 21 days depressed isometric forces of diaphragm fiber bundles across a range of stimulus frequencies (1, 10, 20, 40, 75, and 100 Hz) (P < 0.05). These reductions in force production were accompanied by a remarkable increment (104%; P < 0.05) in carbonyl groups of myofibrillar proteins. In contrast, T3 treatment has no effects on the carbonyl content in myosin heavy chain. In additional experiments, we have also tested the efficacy of carvedilol, a nonselective β1- β2-blocker that possesses antioxidative properties. Treatment with carvedilol dramatically improved isometric tetanic force production at stimulus frequencies from 40 to 100 Hz (P < 0.05). Carvedilol also prevented T3-induced contractile protein oxidation (P < 0.05). These data suggest that the oxidative modification of myofibrillar proteins may account, at least in part, for an impairment of diaphragm in hyperthyroidism.

reactive oxygen species; hyperthyroidism; specific force reduction; myosin heavy chain


Address for reprint requests and other correspondence: M. Wada, Graduate School of Integrated Arts and Sciences, Hiroshima Univ., 1-7-1, Higashihiroshima-shi, Hiroshima, Japan 739-8521 (e-mail: wada{at}hiroshima-u.ac.jp)




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