Journal of Applied Physiology, Vol 49, Issue 1 102-106, Copyright © 1980 by American Physiological Society
Respiratory capacity and glycogen depletion in thyroid-deficient muscle
K. M. Baldwin, A. M. Hooker, R. E. Herrick and L. F. Schrader
This study was undertaken to determine the effects of
propylthiouracil-induced thyroid deficiency on a) the capacity of muscle
homogenates to oxidize [2-14C]pyruvate and [U-14C]palmitate and b) glycogen
depletion during exercise in liver and in fast-oxidative-glycogenolytic
(FOG), fast-glycogenolytic (FG), and slow-oxidative (SO) muscle. Relative
to the rates for normal rats, oxidation with pyruvate was reduced by 53,
68, and 58%, and palmitate by 40, 50, and 48% in FOG, FG, and SO muscle,
respectively (P less than 0.05). Normal rats ran longer than
thyroid-deficient rats at 26.7 m/min (87 +/- 8 vs. 37 +/- 5 min). After 40
min of running (22 m/min), the amount of glycogen consumed in normal FOG,
FG, and SO muscle and in liver amounted to only 23, 12, 66, and 52%,
respectively, of that for their thyroid-deficient counterparts. Also,
normal rats maintained higher plasma free fatty acid levels than
thyroid-deficient rats during both rest and exercise (P less than 0.05).
These findings suggest that thyroid deficiency causes a reduced potential
for FFA utilization in skeletal muscle that enhances its consumption of
glycogen, thereby limiting endurance capacity.
