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J Appl Physiol 80: 1934-1939, 1996;
8750-7587/96 $5.00
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Journal of Applied Physiology, Vol 80, Issue 6 1934-1939, Copyright © 1996 by American Physiological Society


ARTICLES

Hypothyroid-mediated changes in adult rat diaphragm muscle contractile properties and MHC isoform expression

L. E. Gosselin, W. Z. Zhan and G. C. Sieck
Department of Physical Therapy and Exercise Science, State University of New York at Buffalo 14214, USA.

The purpose of the present study was to examine the effect of acute hypothyroidism on myosin heavy chain (MHC) isoform composition and contractile properties in the adult rat diaphragm muscle. Hypothyroidism was induced by the addition of propylthiouracil (0.05%) in the drinking water for a period of 3 wk. MHC isoform composition of control and hypothyroid diaphragm muscles was assessed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. In vitro isometric contractile properties of midcostal diaphragm muscle segements were measured at 26 degrees C, whereas the maximal unloaded shortening velocity was measured at 15 degrees C with the "slack test" method. Serum triiodothyronine and thyroxine values were significantly lower in the hypothyroid compared with the control group. A small but significant increase in the percentage of slow MHC isoform in the diaphragm was observed with acute hypothyroidism, whereas the percentage of the fast MHC isoforms (2A, 2X, and 2B) did not significantly differ between groups. Peak twitch force did not differ between groups. However, twitch contraction and half-relaxation times were significantly prolonged in the hypothyroid group compared with control. Maximal specific force was reduced in the hypothyroid compared with the control group, averaging 15.7 and 19.8 N/cm2, respectively (P < 0.05). The maximal unloaded shortening velocity averaged 4.3 and 8.2 muscle lengths/s in the hypothyroid and control groups, respectively (P < 0.05). We conclude that acute hypothyroidism results in alterations in adult diaphragm muscle contractile properties that cannot be attributed solely to changes in MHC isoform composition.


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