Norepinephrine, but not epinephrine, enhances platelet reactivity and coagulation after exercise in humans

Abstract

The effects of exercise and catecholamines on platelet reactivity or coagulation and fibrinolysis appear to be inconsistent. This may be partly due to the methods employed in previous studies. In the present study, we investigated the effects of acute aerobic exercise and catecholamines on the thrombotic status by a novel in vitro method, shear-induced hemostatic plug formation (hemostatometry), using nonanticoagulated (native) blood. Aerobic exercise (60% maximal O2 consumption) was performed by healthy male volunteers for 20 min, and the effect on platelet reactivity and coagulation was assessed by performing hemostatometry before and immediately after exercise. Exercise significantly increased shear-induced platelet reactivity, coagulation, and catecholamine levels. The effect of catecholamines on platelet reactivity and coagulation was assessed in vitro by adding catecholamines to blood collected in the resting state. The main findings of the present study are that elevation of circulating norepinephrine at levels that are attained during exercise causes platelet hyperreactivity and a platelet-mediated enhanced coagulation. This may be a mechanism of an association of aerobic exercise with thrombotic risk.

Strenuous but not moderate exercise increases the thrombotic tendency in healthy sedentary male volunteers

“…Exercise induces the release of cathecholamines (12,14,23,28). At high concentrations, epinephrine promotes platelet aggregation, and at low concentrations, it potentiates platelet aggregation induced by other platelet agonists such as ADP or collagen (11).…”

Effects of the Duration of Highly Intensive Exercise on Lymphocyte Cell Death in Rats

“…그 원인으로서 고강도운동에 따른 혈류속도 증가에 의해 혈관 내에 물리적인 손상이 일어나 [20] 적혈구의 용혈과 혈관내피 세포의 손상 [33] 등이 야기되기도 한다. 이 외에도 운동 스트레 스에 따른 카테콜아민 분비증가 [11] leukocyte. Data were expressed as the mean±SE.…”

Controversial Issues Concerning Norepinephrine and Intensive Care Following Severe Traumatic Brain Injury

“…a 2 -adrenergic stimulation activates intracellular cascades and dose-dependently promotes thrombocyte activation [94,95] which is inhibited pharmacologically [94,96,97]. Sustained norepinephrine-stimulated activation with subsequent consumption and peripheral sequestration of thrombocyte-bound leukocytes can decrease circulating thrombocytes and contribute to multiorgan failure [85,98,99] (Figure 4c).…”

“…In this context, prolonged endogenous as well as exogenous catecholamine administration reduces a 2 receptor affinity in human thrombocytes [95] and rat brain [213], and decreases b 2 receptors in human mononuclear leukocytes [214] which might be influenced by certain genetic predisposition to differential b 2 adrenergic receptor regulation as seen in human lymphocytes [215] and human neutrophils [216]. In critically ill patients, b-adrenergic receptors of circulating lymphocytes are reduced [217] and inflammatory cytokines might impair b-adrenergic receptor-dependent production of the regulatory cAMP [217].…”