Exercise capacity and cardiac function in trained and untrained thyroid-deficient rats.
This study was undertaken to ascertain the extent that impairments in a) the oxidative capacity of skeletal muscle, b) cardiac functional and biochemical correlates of contractile capacity, and c) maximal oxygen consumption (VO2 max) can be reversed in thyroid-deficient (TD) female rats subjected to an 8-wk physical training (running) program. Compared with a normal control (NC) group, thyroid deficiency caused reductions in the following: VO2 max (-32%), skeletal muscle homogenate respiratory capacity (-50%), cardiac myosin ATPase (-58%), and in situ-derived ventricular dP/dt max (-58%) (P < 0.001). The training program restored to within normal limits skeletal muscle oxidative capacity and VO2 max, but it did not improve cardiac myosin ATPase, Ca2+ regulation of myofibril ATPase, and dP/dt max relative to TD sedentary rats. However, the heart weight-to-body weight ratio was highest among the three groups in the TD trained group. These findings suggest that maximal oxygen utilization capacity of TD rats can be normalized by physical training, even though intrinsic contractile capacity of the heart could not.
D000251:Adenosine Triphosphatases / Q000378:metabolism; D000818:Animals; D005260:Female; D006321:Heart / Q000503:physiopathology*; D007037:Hypothyroidism / Q000503:physiopathology*; D009200:Myocardial Contraction; D009206:Myocardium / Q000378:metabolism; D009929:Organ Size; D010084:Oxidation-Reduction; D010101:Oxygen Consumption; D010806:Physical Education and Training; D005082:Physical Exertion; D051381:Rats
D000251:Adenosine Triphosphatases