 The purpose of this study is to prove: 1 Myocardial ischemia, cardiac arrhythmias and hypertensive response at rest and provoked by stress are decreased by EA; 2 The mechanism of the ischemic response is an imbalance between myocardial oxygen supply and demand originating as an increase in autonomic nervous system sympathetic activity causing increased oxygen demand. EA inhibits the sympathetic nervous system, decreases blood pressure and reduces the oxygen demand. Our prior data in animals shows that improvements in cardiovascular function during myocardial ischemia are mediated by an EA-induced sensory neural reflex originating in somatic nerves to reduce sympathetic nerve activity. The specific aims of the present study will allow us to better understand and modulate the sympathetic nervous discharge activity that can precipitate coronary ischemia, arrhythmias and hypertension in exercise stress in humans. Potential clinical application is the therapeutic value of EA in patients with hypertension. 