Tilt and exercise, but not mental stress, caused an increase in platelet count simultaneously with large increases in epinephrine. The increase in catecholamines may explain—at least in part—the observed changes in platelet count, because catecholamines can stimulate immediate release of platelets from the spleen. The increase in platelet count may subsequently help explain the simultaneous increase in platelet aggregability in response to these behavioral stressors. On the other hand, the platelet surface makers did not consistently increase specifically during the tilt and exercise tests, nor decrease during the recovery phases following these stressors. The absence of a clear effect of postural stress on platelet surface markers of platelet activation and the presence of a clear increase in WBA, platelet count, and epinephrine in response to the head-up tilt is consistent with a previous study that examined the effect on platelets of the transition from lying to standing. Also the absence of a clear effect of exercise on surface markers of platelet activation is consistent with a previous study by our group in which exercise failed to cause consistent changes in platelet activation in physically active subjects. Interestingly, in that same study, we showed that exercise by sedentary subjects did result in significant platelet activation. There is clear evidence that the presently measured markers of platelet activation are clinically relevant. FDA-approved drugs that block GPIIb-IIIa are of benefit as antithrombotic therapy in acute coronary syndromes. In animal models, antagonism of platelet surface P-selectin and platelet surface GPIb has antithrombotic benefit. A better understanding of the relative importance of circadian rhythms and behaviors on platelet function may help reveal new therapeutic targets for cardiac patients. Ultimately, chronotherapy could be designed to specifically target pharmacological or behavioral interventions to those time windows of greatest risk for cardiovascular events. Rather than the current clinical practice of attempting to maintain therapeutic levels of antiplatelet drugs throughout each day and night or base medication timing on presumed patient convenience, it may be therapeutically beneficial for antiplatelet agents to specifically target the circadian phases of greatest platelet aggregability to reduce thrombotic complications, while minimizing hemorrhagic complications during periods of reduced platelet aggregation. Hypoxia in environment can be the result of multiple factors but pollution and eutrophication are most concerned. Hypoxic stress causes different metabolic changes in aerobic organisms, in which metabolic suppression is crucial for GSI-IX organisms to adapt to hypoxia. Evidence has shown that the key to adaptation to chronic hypoxia is a simultaneous reduction in metabolic rate and metabolic demands, i.e., by reducing or suspending many bioenergetic processes. Thus, the importance of understanding the effects of hypoxia is not limited to environmental studies but is extended to cell biology, physiology and developmental biology.