Abstract
Hyperthyroidism induces marked changes in hemodynamics. Although considerable research has been done to study the effect of hyperthyroidism on the cardiovascular system, few studies have isolated the short-term, nongenomic effects of thyroid hormone on cardiovascular responses to exercise. We used near-infrared spectroscopy to measure muscle oxygenation, Doppler ultrasound to measure skeletal muscle blood flow, and microneurography to measure muscle sympathetic nerve activity (MSNA) during fatiguing dynamic handgrip in twelve healthy males (26 ± 1 years). Subjects were measured separately in both the euthyroid state, and acute hyperthyroid state (approximately ten times the normal levels of T3), induced by oral dosage of 300 μg of triiodothyronine (T3). Forearm blood flow was increased as a function of exercise time in the euthyroid and hyperthyroid state (Δ161.8 ± 45.0 mL/min and Δ140.7 ± 16.3 mL/min, respectively) but there was no significant difference between trials. Forearm vascular conductance (FVC) also increased as a function of exercise time with no significant difference between treatments at submaximal exercise but was significantly less with T3 treatment. MSNA was not different at rest or during submaximal exercise; however, MSNA was significantly greater at fatigue during the hyperthyroid state. Muscle oxyhemoglobin concentration was decreased during exercise in both euthyroid and hyperthyroid states (Δ19.7 ± 10.8% and Δ14.8 ± 9.6%, respectively); whereas deoxyhemoglobin concentration was increased (Δ50.0 ± 4.1% and Δ50.0 ± 6.2%, respectively). These results indicate that T3 had no direct effect on skeletal muscle oxygenation or blood flow during dynamic exercise, but elicited greater MSNA and lower FVC during fatiguing exercise.