Johnson J M
Exerc Sport Sci Rev. 1992;20:59-97.
Our understanding of the control of the cutaneous circulation has increased over the past decade, but is still far from complete. There is a cutaneous vasoconstriction at the beginning of exercise that usually effectively competes with concurrent thermoregulatory drives for vasodilation. This cutaneous vasoconstrictor response, however, requires dynamic activity by a significant muscle mass as small muscle groups or isometric exercise are ineffective or nearly so. Also, exercise causes the threshold internal temperature relative to rest such that SKBF is lower during exercise than in resting conditions for a given thermal stimulus. A further influence by exercise on the cutaneous circulation is to limit the degree of cutaneous vasodilation when heat stress and exercise are combined. These three roles for exercise compete with the thermogenic role that promotes vasodilation. The previously described effects act through the adrenergic vasoconstrictor system and the separate active vasodilator system. The increase in SKBF with heat stress represents the combination of withdrawal of vasoconstrictor activity and elevation of active vasodilator activity. The vasoconstrictor effect of the initiation of exercise is accomplished strictly through enhanced vasoconstrictor activity; vasodilator withdrawal does not participate [72]. However, both the exercise-induced elevation in thermoregulatory threshold for raising SKBF and the limitation to cutaneous vasodilation during exercise are strictly functions of the active vasodilator system [69, 73, 78]. In the first case, active vasodilation is delayed until a higher (relative to rest) level of internal temperature is reached. In the second case, the plateau in SKBF during exercise in the heat is due to a similar plateau in active vasodilator activity. Exercise has also served as a tool for the study of other influences on the cutaneous circulation. The influences of alterations in body fluid volumes, osmolarity, acclimatization, hypertension, time of day, menstrual phase, and others on the control of SKBF have been assessed by using exercise as a calorigenic source. The question as to whether the nonthermoregulatory influences of exercise interact with these other influences to give a modification of the pattern of control different from what might be observed at rest is largely unanswered. Future directions for research are numerous, but several fundamental questions are outstanding. The mechanism of active cutaneous vasodilation has been elusive since its discovery and remains an exceptionally important question. Second, the sensory elements associated with exercise giving rise to the alterations in the pattern of control are unclear. This problem is made challenging by the fact that the efferent control by exercise differs between its initiation and events later in exercise.(ABSTRACT TRUNCATED AT 400 WORDS)
在过去十年中,我们对皮肤循环控制的理解有所增加,但仍远未完善。运动开始时会出现皮肤血管收缩,这通常会有效地与同时发生的血管舒张的体温调节驱动力相竞争。然而,这种皮肤血管收缩反应需要大量肌肉进行动态活动,因为小肌肉群或等长运动无效或几乎无效。此外,运动导致相对于休息时的阈值内部温度升高,以至于在给定的热刺激下,运动期间的皮肤血流量(SKBF)低于休息状态。运动对皮肤循环的另一个影响是,当热应激和运动同时存在时,会限制皮肤血管舒张的程度。运动的这三个作用与促进血管舒张的产热作用相互竞争。上述影响是通过肾上腺素能血管收缩系统和独立的活性血管舒张系统起作用的。热应激导致的SKBF增加代表了血管收缩活动的减弱和活性血管舒张活动的增强的综合结果。运动开始时的血管收缩作用完全是通过增强血管收缩活动实现的;血管舒张的减弱并未参与其中[72]。然而,运动引起的提高SKBF的体温调节阈值的升高以及运动期间对皮肤血管舒张的限制,严格来说都是活性血管舒张系统的功能[69, 73, 78]。在第一种情况下,活性血管舒张会延迟,直到达到更高(相对于休息)的内部温度水平。在第二种情况下,热环境中运动期间SKBF的平稳状态是由于活性血管舒张活动出现类似的平稳状态。运动也一直是研究对皮肤循环的其他影响的工具。通过将运动作为产热源,已经评估了体液量、渗透压、适应、高血压、一天中的时间、月经周期等变化对SKBF控制的影响。关于运动的非体温调节影响是否与这些其他影响相互作用,从而导致控制模式的改变不同于在休息时可能观察到的情况,这个问题在很大程度上尚未得到解答。未来的研究方向众多,但有几个基本问题仍未解决。自发现以来,活性皮肤血管舒张的机制一直难以捉摸,仍然是一个极其重要的问题。其次,与运动相关的导致控制模式改变的感觉因素尚不清楚。由于运动的传出控制在开始时和运动后期有所不同,这个问题变得具有挑战性。(摘要截于400字)