β-Adrenergic receptor density and responsiveness may be increased in experimental animals by physical conditioning, and the opposite effects have been observed after a single bout of exercise. To determine whether the chronic and acute effects of exercise include similar alterations in cardiovascular function in humans, we characterized heart rate, blood pressure, and distal lower extremity blood flow responses to graded-dose isoproterenol infusion in 15 young healthy subjects before and after exercise training and with and without a single preceding bout of prolonged exercise of either low or high intensity (61 ± 1 or 82 ± 1% maximal heart rate). V̇O(2 max) was increased 18% after exercise training (43.2 ± 2.7 to 51.1 ± 3.3 ml · kg-1 · min-1; P < 0.001). Despite a concomitant fall in resting heart rate (59 ± 3 to 50 ± 2 beats/min; P < 0.001), chronotropic and lower extremity blood flow responses to isoproterenol remained unchanged. Similarly, 1 h of acute high-intensity treadmill exercise altered baseline heart rate (58 ± 4 to 74 ± 5 beats/min; P < 0.02), but neither low- nor high-intensity acute exercise influenced heart rate or lower extremity blood flow responses to isoproterenol. In contrast, the systolic pressure response to isoproterenol was blunted after high- but not low-intensity prolonged exercise (P < 0.02). These data indicate that cardiac chronotropic (primarily β1) and vascular (β2) adrenergic agonist responses are not altered in humans by training or acute exercise. The systolic blood pressure response to β-adrenergic stimulation is decreased by a single bout of high-intensity prolonged exercise by mechanisms that remain to be defined.
|Number of pages||6|
|Journal||Journal of Applied Physiology|
|State||Published - Jan 1 1991|
- blood pressure
- exercise training
- heart rate
- vascular conductance