Cardiopulmonary receptor reflexes in normotensive athletes with cardiac hypertrophy.

Abstract

Cardiopulmonary receptor control of the circulation is impaired in a variety of diseases having cardiac hypertrophy as a common feature. Whether this also occurs in the so-called "physiological" cardiac hypertrophy of the athlete, however, is unknown. We studied nine sedentary healthy subjects and 19 age-matched professional runners or hammer throwers who had trained at least 2 hours per day, 5 days per week for 7 years. The left ventricular mass index (echocardiography) was 99 +/- 7.4 and 135 +/- 5.9 g/m2 in the two groups, respectively. Cardiopulmonary receptor stimulation and deactivation were obtained by increasing and reducing left ventricular end-diastolic diameter for 5 minutes by leg raising and lower body negative pressure, keeping both stimuli at a level not affecting blood pressure and heart rate. In the sedentary healthy subjects, forearm vascular resistance (the ratio between mean arterial pressure and forearm blood flow) and plasma norepinephrine fell during leg raising (forearm vascular resistance, -7 +/- 1.7 units; norepinephrine, -57.4 +/- 1.4 pg/ml) and increased during lower, body negative pressure (forearm vascular resistance, 20 +/- 5.3 units; norepinephrine, 97.7 +/- 21.5 pg/ml). For similar or greater alterations in left ventricular end-diastolic diameter, the correspondent changes observed in the professional runners or hammer throwers were -5.3 +/- 1.3 units (forearm vascular resistance), -35.4 +/- 9.6 pg/ml (norepinephrine), 9.1 +/- 1.4 units (forearm vascular resistance), and 30.9 +/- 6.9 pg/ml (norepinephrine). This represented an attenuation of 25%, 38%, 55%, and 68%, respectively (p less than 0.01), of the control response.(ABSTRACT TRUNCATED AT 250 WORDS)