jalal j replied: "Although after acute caffeine ingestion, an increase in heart rate, or no change has been reported, the commoner response may be slight decrease in heart rate, in laboratory settings lasting approximately 75 min after caffeine ingestion in borderline hypertensives, and also on ambulatory monitoring, presumably due to direct vagal stimulation, baroreceptor reflex, or effect on the sinoatrial node. Not surprisingly, inconsistent effect has been reported in patients with autonomic failure, who have diminished baroreflexes, in response to caffeine. It has been suggested that Caffeine probably has a direct cardioacceleratory effect and elicits a vagally mediated bradycardia by baroreflex activation consequent to it's pressor effect . Heart rate was slowed in a dose related manner, started at 30 min and lasted till 3 hours. The mean decrease was 10 bpm in group receiving 8.8 mg/kg at 30 min. Bradycardia was the only parameter that correlated with time course of plasma caffeine levels. There was no consistent correlation between heart rate and BP, thus bradycardia is not due to baroreflex, but possibly due to direct central vagal stimulation. Thus the administration of 250 to 350 mg of caffeine may produce small decreases in heart rate and modest increases in both systolic and diastolic blood pres­sure. Such doses may have no effect on these parameters in those who consume caffeine regularly. ARRHYTHMIAS At higher concentrations (>10 mg/kg/day) caffeine produces definite tachycardia54; sensitive individuals may experience other arrhythmias55,56, such as premature ventricular contractions. Ar­rhythmias may also be encountered in persons who use caffeine-containing beverages to excess. However, it appears that the risk of inducing cardiac arrhythmias in normal subjects is quite low, and that patients with ischaemic heart disease or pre-existing ventricular ectopy can usually tolerate moderate amounts of caffeine without provoking an appre­ciable increase in the frequency of arrhythmias. No significant arrhythmias were observed during maximal exercise stress test in old individuals with stable angina on medical therapy. MYOCARDIUM Substantial increases in circulating epinephrine (+207%), NE (+75%), and plasma renin activity (+57%) have been documented after a 250 mg dose in normal subjects. Thus it might be expected that caffeine would potentiate exercise induced increases in myocardial oxygen consumption by a net increase in peak systolic pressure or peak heart rate, or both. An increase in myocardial oxygen demand at any given workload would be expected to reduce exercise duration in patients with coronary artery disease. Both angina and marked elevation in left heart filling pressure, with secondary pulmonary congestion, would be potential consequences. Caffeine might also be expected to produce abnormal diastolic relaxation. In study by Paulus the observed increases in left ventricular end diastolic pressure during pacing induced ischemia persisted more than three times as long after caffeine pretreatment than with myocardial ischaemia alone. Tolerance to caffeine has been documented in some studies, an individual's previous use of caffeine may be a determinant of the pharmacodynamics of caffeine. In dogs with coronary stenoses, large doses of intravenous caffeine potentiate impaired left ventricular diastolic relaxation, resulting in marked elevation of left ventricular diastolic pressure. In isolated heart muscle, caffeine and other methylxanthines prolong the time course of ventricular relaxation by reducing the rate of intracellular calcium sequestration during diastole by sarcoplasmic reticulum. There is controversy as to whether circu­lating catecholamines or plasma renin activity is increased significantly in caffeine-naive subjects; however, it is generally agreed that little change occurs in chronic users. While some studies have shown elevated cardiac output and stroke volume, in other studies caffeine has not been shown to have significant effects on LV ejection fraction and cardiac index, in young healthy men, at rest, or during exercise. Selected patients with history of stable angina pectoris had no significant change in total exercise duration, time to onset of angina and time to onset of 0.1 mV of ST depression. Rate pressure product at onset of angina and onset of 0.1 mV of ST depression were not significantly different after caffeine ingestion. In response to exercise, echocardiographic measures of LVSF and LVDF were similar in both groups, in all but two patients who showed worsening of diastolic function at rest and further worsening with exercise after caffeine. There was no significant increase in frequency or severity of atrial or ventricular arrhythmias. A similar lack of effect of caffeine on exercise duration, time to 0.1 mV ST depression , and heart rate blood pressure product was demonstrated by Piters in patients in whom medications were withheld on the day of the testing. However a significant increase in exercise duration before the onset of angina was noted. Caffeine has been shown to increase circulating free fatty acids and glycerol during exercise in normal subjects, with associated improvements in exercise duration, maximum oxygen consumption, resting metabolic rate, or perceived exertion. Some authors have not observed these changes. Enhanced peripheral lipolysis may not be noted at lower workloads achieved in patients with ischaemic heart disease, especially in presence of B-blockers."

Peter S replied: "Increases the heart beat."

im replied: "http://en.wikipedia.org/wiki/Caffeine#Mechanism_of_action Please provide 10 points."

The Truth Seeker replied: "Yes - see academic journals dealing with the issue."

cnjard replied: "An accelerated heart rate is often associated with a decreased ejection fraction. The faster the heart beats, the less time the left ventricle has to fill, thus the lower EF."