Melancon M O, Lorrain D, Dionne I J
Research center on aging, Sherbrooke geriatric university institute-health and social services center, 1036, Belvedere South, J1H 4C4 Sherbrooke, QC, Canada; Department of kinanthropology, faculty of physical and sport education, university of Sherbrooke, 2500, boulevard de l'Université, J1K 2R1 Sherbrooke, QC, Canada.
Research center on aging, Sherbrooke geriatric university institute-health and social services center, 1036, Belvedere South, J1H 4C4 Sherbrooke, QC, Canada; Department of psychology, faculty of human sciences, university of Sherbrooke, 2500, boulevard de l'Université, J1K 2R1 Sherbrooke, QC, Canada.
Pathol Biol (Paris). 2014 Oct;62(5):276-83. doi: 10.1016/j.patbio.2014.07.004. Epub 2014 Aug 4.
Reductions in central serotonin activity with aging might be involved in sleep-related disorders in later life. Although the beneficial effects of aerobic exercise on sleep are not new, sleep represents a complex recurring state of unconsciousness involving many lines of transmitters which remains only partly clear despite intense ongoing research. It is known that serotonin released into diencephalon and cerebrum might play a key inhibitory role to help promote sleep, likely through an active inhibition of supraspinal neural networks. Several lines of evidence support the stimulatory effects of exercise on higher serotonergic pathways. Hence, exercise has proved to elicit acute elevations in forebrain serotonin concentrations, an effect that waned upon cessation of exercise. While adequate exercise training might lead to adaptations in higher serotonergic networks (desensitization of forebrain receptors), excessive training has been linked to serious brain serotonergic maladaptations accompanied by insomnia. Dietary supplementation of tryptophan (the only serotonin precursor) is known to stimulate serotonergic activity and promote sleep, whereas acute tryptophan depletion causes deleterious effects on sleep. Regarding sleep-wake regulation, exercise has proved to accelerate resynchronization of the biological clock to new light-dark cycles following imposition of phase shifts in laboratory animals. Noteworthy, the effect of increased serotonergic transmission on wake state appears to be biphasic, i.e. promote wake and thereafter drowsiness. Therefore, it might be possible that acute aerobic exercise would act on sleep by increasing activity of ascending brain serotonergic projections, though additional work is warranted to better understand the implication of serotonin in the exercise-sleep axis.
随着年龄增长，中枢5-羟色胺活性降低可能与晚年睡眠相关障碍有关。尽管有氧运动对睡眠的有益影响并非新鲜事，但睡眠是一种复杂的反复出现的无意识状态，涉及多种神经递质，尽管目前正在进行深入研究，但仍只有部分是清楚的。已知释放到间脑和大脑中的5-羟色胺可能发挥关键的抑制作用，以帮助促进睡眠，可能是通过对脊髓上神经网络的主动抑制。有几条证据支持运动对更高5-羟色胺能通路的刺激作用。因此，运动已被证明会引起前脑5-羟色胺浓度的急性升高，这种作用在运动停止后会减弱。虽然适当的运动训练可能会导致更高5-羟色胺能网络的适应性变化（前脑受体脱敏），但过度训练与严重的脑5-羟色胺能适应不良及失眠有关。已知膳食补充色氨酸（唯一的5-羟色胺前体）可刺激5-羟色胺能活性并促进睡眠，而急性色氨酸耗竭会对睡眠产生有害影响。关于睡眠-觉醒调节，在实验室动物中施加相位变化后，运动已被证明能加速生物钟与新的明暗周期重新同步。值得注意的是，5-羟色胺能传递增加对觉醒状态的影响似乎是双相的，即促进觉醒，然后导致嗜睡。因此，急性有氧运动可能通过增加上行脑5-羟色胺投射的活性来作用于睡眠，不过需要更多的研究来更好地理解5-羟色胺在运动-睡眠轴中的作用。
