McAllister R M, Sansone J C, Laughlin M H
Department of Veterinary Biomedical Sciences, College of Veterinary Medicine, University of Missouri, Columbia 65211.
Am J Physiol. 1995 Jan;268(1 Pt 2):H330-5. doi: 10.1152/ajpheart.1995.268.1.H330.
Hyperthyroidism is associated with exercise intolerance. Previous research, however, has shown that cardiac output is either normal or enhanced during exercise in the hyperthyroid state. We therefore hypothesized that blood flow to working skeletal muscle is augmented in hyperthyroid animals during in vivo submaximal exercise and, consequently, that noncardiovascular factors are responsible for intolerance to exercise. To test this hypothesis, rats were made hyperthyroid (Hyper) over 6-12 wk with injections of triiodothyronine (300 micrograms/kg). Hyperthyroidism was evidenced by left ventricular hypertrophy [euthyroid (Eut), 2.12 +/- 0.05 mg/g body wt; Hyper, 2.78 +/- 0.06; P < 0.005], 25-60% increases in citrate synthase activities in Hyper hindlimb muscles over those of Eut rats, and higher preexercise heart rates (Eut, 415 +/- 18 beats/min; Hyper, 479 +/- 19; P < 0.025). Regional blood flows were determined by the radiolabeled microsphere method, preexercise, and at 1-2 min of treadmill running at 15 m/min (0% grade). Total hindlimb muscle blood flow preexercise was unaffected (Eut, 31 +/- 4 ml.min-1.(100) g-1, n = 11; Hyper, 40 +/- 6, n = 9; not significant) but was higher (P < 0.025) in Hyper (127 +/- 17, n = 9) compared with Eut (72 +/- 11, n = 9) during treadmill running. During exercise, flows to individual muscles and muscle sections were approximately 50-150% higher in Hyper compared with Eut rats. Visceral blood flows were largely similar between groups. These findings indicate that hyperthyroidism is associated with augmented blood flow to skeletal muscle during submaximal exercise. Thus hypoperfusion of skeletal muscle does not account for the poor exercise tolerance characteristic of hyperthyroidism.
甲状腺功能亢进与运动不耐受有关。然而，先前的研究表明，在甲状腺功能亢进状态下运动时心输出量正常或增加。因此，我们推测，在体内次最大运动期间，甲状腺功能亢进动物流向工作骨骼肌的血流量会增加，因此，非心血管因素是运动不耐受的原因。为了验证这一假设，通过注射三碘甲状腺原氨酸（300微克/千克）使大鼠在6 - 12周内甲状腺功能亢进（Hyper）。甲状腺功能亢进的证据包括左心室肥厚[正常甲状腺（Eut），2.12±0.05毫克/克体重；Hyper，2.78±0.06；P<0.005]，Hyper后肢肌肉中的柠檬酸合酶活性比Eut大鼠高25 - 60%，以及运动前心率更高（Eut，415±18次/分钟；Hyper，479±19；P<0.025）。通过放射性微球法在运动前以及在跑步机上以15米/分钟（0%坡度）跑步1 - 2分钟时测定局部血流量。运动前总后肢肌肉血流量未受影响（Eut，31±4毫升·分钟-1·（100）克-1，n = 11；Hyper，40±6，n = 9；无显著差异），但在跑步机跑步期间，Hyper组（127±17，n = 9）比Eut组（72±11，n = 9）更高（P<0.025）。在运动期间，与Eut大鼠相比，Hyper大鼠流向各个肌肉和肌肉部分的血流量大约高50 - 150%。各组间内脏血流量基本相似。这些发现表明，甲状腺功能亢进与次最大运动期间骨骼肌血流量增加有关。因此，骨骼肌灌注不足并不能解释甲状腺功能亢进所特有的运动耐力差的问题。
