Respiratory capacity and glycogen depletion in thyroid-deficient muscle.
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.
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D002950:Citrate (si)-Synthase / Q000378:metabolism; D005230:Fatty Acids, Nonesterified / Q000378:metabolism; D005260:Female; D006003:Glycogen / Q000378:metabolism*; D006593:Hexokinase / Q000378:metabolism; D007037:Hypothyroidism / Q000139:chemically induced*; D008291:Malate Dehydrogenase / Q000378:metabolism; D009132:Muscles / Q000187:drug effects* / Q000201:enzymology; D005082:Physical Exertion; D011441:Propylthiouracil / Q000494:pharmacology*; D051381:Rats; D012119:Respiration / Q000187:drug effects*
D001786:Blood Glucose; D005230:Fatty Acids, Nonesterified; D011441:Propylthiouracil; D006003:Glycogen; D008291:Malate Dehydrogenase; D002950:Citrate (si)-Synthase; D006593:Hexokinase