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SUMMARY Studies in man produce conflicting evidence of the role of the Frank-Starling mechanism in in-creasing cardiac output during exercise, though animal studies indicate that it may help to improve cardiac performance during severe exertion. Twelve healthy volunteers (mean age 35.8 i 2.8 years) performed graded exercise to exhaustion on a bicycle ergometer in the semisupine position for 8.9 i 0.9 minutes (maximum work load 900 kg-m/min). Echocardiographic recordings of left ventricular dimensions were obtained con-tinuously and end-expiratory tracings digitized. Heart rate increased from 64 ± 3 to 152 ± 4 beats/min. At peak exercise, end-diastolic diameter increased from 4.52 ± 0.20 to 5.24 ± 0.17 cm (p 0.001), but was un-changed at lower heart rates of 90 and 110 beats/min. End-systolic diameter did not change at any heart rate. Stroke dimension (end-diastolic minus end-systolic diameter) increased from 1.77 ± 0.14 to 2.50 ± 0.11 cm (p 0.005), but was unchanged at lower levels of exercise. Percent shortening in diameter rose from 38.8 + 1.7 at rest to 48.0 2.1 % at peak exercise (p 0.01), having increased to 43.0 ± 2.5 % at 110 beats/min (p 0.05). Mean velocity of circumferential shortening increased with progressively higher heart rates from its resting value of 5.05 ± 0.49 cm/sec to 9.37 ± 0.77 cm/sec at peak exercise (p 0.0005). Similarly, velocity of circumferential shortening normalized for end-diastolic diameter increased progressively, from 1.10 0.09 sec-1 at rest to 1.87 ± 0.17 sec-1 at peak exercise (p 0.0005). Maximum
Weiss et al. (Sun,) studied this question.