Tsatsoulis Agathocles, Fountoulakis Stelios
Department of Endocrinology, University of Ioannina, Ioannina 45110, Greece.
Ann N Y Acad Sci. 2006 Nov;1083:196-213. doi: 10.1196/annals.1367.020.
The human body, when under threat, elicits a set of neuroendocrine responses, including an increased secretion of glucocorticoids (GCs) and catecholamines from the adrenal gland and the activation of the sympathetic nervous system. These hormonal secretions allow a "fight or flight" response by mobilizing endogenous substrate and inducing a state of insulin resistance in the liver and skeletal muscles. Although the stress response was essential in ancient times to survive physical aggression, this threat has disappeared in our industrialized societies. However, in today's environment, the same stress responses can be elicited by emotional stimuli or professional and social stress. Such psychological stress may be protracted and unrelated to an increased metabolic demand. Thus, the energy mobilized is not used but is stored in visceral fat depots by the combined action of hypercortisolism and hyperinsulinemia. In addition, chronic activation of the stress system causes suppression of the gonadal, growth hormone (GH), and thyroid axes. These metabolic disturbances, in concert, lead to the clinical expression of a number of comorbidities including central obesity, hypertension, dyslipidemia, and endothelial dysfunction, all components of the metabolic syndrome and cardiometabolic risk factors. Moreover, chronic stress has deleterious effects on the brain and, in particular, affects hippocampal structure and function leading to cognitive and mood disturbances. Importantly, this stress-induced clinical phenotype is likely to be exaggerated in the presence of physical inactivity, resulting in a "stress-induced/exercise deficient" phenotype. Assuming that the stress response is a neuroendocrine mechanism that occurs in anticipation of physical action, then physical activity should be the natural means to prevent the consequences of stress. Indeed, accumulating evidence documents the beneficial effects of regular exercise in preventing or ameliorating the metabolic and psychological comorbidities induced by chronic stress. These benefits are thought to derive from a central effect of exercise to reduce the sensitivity to stress and also peripheral actions influencing metabolic functions and, in particular, insulin sensitivity and the partitioning of fuels toward oxidation rather than storage. It is concluded that chronic psychosocial stress, in the presence of physical inactivity, is likely to contribute to the epidemic of cardiometabolic and emotional disease of our current society. The way to prevent and combat this burden is by regular exercise.
人体在受到威胁时会引发一系列神经内分泌反应，包括肾上腺糖皮质激素（GCs）和儿茶酚胺分泌增加以及交感神经系统激活。这些激素分泌通过动员内源性底物并在肝脏和骨骼肌中诱导胰岛素抵抗状态，从而引发“战斗或逃跑”反应。虽然应激反应在古代对于在身体攻击中生存至关重要，但在我们的工业化社会中这种威胁已不复存在。然而，在当今环境中，情绪刺激或职业及社会压力也可引发相同的应激反应。这种心理压力可能持续存在且与代谢需求增加无关。因此，动员的能量未被利用，而是通过高皮质醇血症和高胰岛素血症的共同作用储存在内脏脂肪库中。此外，应激系统的慢性激活会导致性腺轴、生长激素（GH）轴和甲状腺轴受到抑制。这些代谢紊乱共同导致了多种合并症的临床表现，包括中心性肥胖、高血压、血脂异常和内皮功能障碍，这些都是代谢综合征和心血管代谢危险因素的组成部分。此外，慢性应激对大脑有有害影响，尤其会影响海马结构和功能，导致认知和情绪障碍。重要的是，在缺乏身体活动的情况下，这种应激诱导的临床表型可能会加剧，从而导致“应激诱导/运动不足”表型。假设应激反应是一种预期身体行动而发生的神经内分泌机制，那么身体活动应该是预防应激后果的自然方式。事实上，越来越多的证据证明定期运动在预防或改善慢性应激诱导的代谢和心理合并症方面具有有益作用。这些益处被认为源于运动的核心作用，即降低对应激的敏感性，以及外周作用，影响代谢功能，特别是胰岛素敏感性和燃料分配向氧化而非储存的方向。结论是，在缺乏身体活动的情况下，慢性心理社会应激可能会导致我们当前社会中心血管代谢和情绪疾病的流行。预防和对抗这种负担的方法是定期运动。
