Sudden cardiac and cerebral events are most common in the morning. A fundamental question is whether these events are triggered by the increase in physical activity after waking, and/or a result of circadian variation in the responses of circulatory function to exercise. Although signaling pathways from the master circadian clock in the suprachiasmatic nuclei to sites of circulatory control are not yet understood, it is known that cerebral blood flow, autoregulation and cerebrovascular reactivity to changes in CO(2) are impaired in the morning and, therefore, could explain the increased risk of cerebrovascular events. Blood pressure (BP) and the rate pressure product (RPP) show marked 'morning surges' when people are studied in free-living conditions, making the rupture of a fragile atherosclerotic plaque and sudden cardiac event more likely. Since cerebral autoregulation is reduced in the morning, this surge in BP may also exacerbate the risk of hemorrhagic and ischemic strokes in the presence of other acute and chronic risk factors. Increased sympathetic activity, decreased endothelial function, and increased platelet aggregability could also be important in explaining the morning peak in cardiac and cerebral events but how these factors respond to exercise at different times of day is unclear. Evidence is emerging that the exercise-related responses of BP and RPP are increased in the morning when prior sleep is controlled. We recommend that such 'semi-constant routine' protocols are employed to examine the relative influence of the body clock and exogenous factors on the 24-h variation in other circulatory factors.