Macefield Vaughan G, Henderson Luke A
School of Medicine, University of Western Sydney, NSW, Australia; Neuroscience Research Australia, Sydney, NSW, Australia.
Department of Anatomy and Histology, University of Sydney, Sydney, NSW, Australia.
Auton Neurosci. 2015 Mar;188:10-8. doi: 10.1016/j.autneu.2014.10.021. Epub 2014 Oct 23.
Sustained isometric contraction of skeletal muscle causes an increase in blood pressure, due to an increase in cardiac output and an increase in total peripheral resistance-brought about by an increase in sympathetically-mediated vasoconstriction. Both central command and reflex inputs from metaboreceptors in the contracting muscles have been shown to contribute to this sympathetically mediated increase in blood pressure. Occluding the blood supply and trapping the metabolites in the contracted muscle (post-exercise ischaemia) has shown that, while heart rate returns to baseline following exercise, the increase in MSNA and blood pressure persists in the absence of central command-sustained by peripheral inputs. Post-exercise ischaemia activates group III and IV muscle afferents, which are also activated during noxious stimulation. Indeed, post-exercise ischaemia is painful, so what is the role of pain in the increase in blood pressure? Intramuscular injection of hypertonic saline causes a deep dull ache, not unlike that produced by post-exercise ischaemia, and we have shown that this can cause a sustained increase in MSNA and blood pressure. We have used functional Magnetic Resonance Imaging (fMRI) of the brain to identify the cortical and subcortical sites involved in the sensory processing of muscle pain, and in the generation of the autonomic responses to muscle pain, produced either by post-exercise ischaemia or intramuscular injection of hypertonic saline. During static hand-grip exercise there were parallel increases in signal intensity in the contralateral primary motor cortex, deep cerebellar nuclei and cerebellar cortex that ceased at the end of the exercise, reflecting the start and end of central command. Progressive increases during the contraction phase occurred in the contralateral insula, as well as the contralateral primary somatosensory cortex, and continued during the period of post-exercise ischaemia. Decreases in signal intensity occurred in the perigenual anterior cingulate cortex during the contraction phase; these too were sustained during post-exercise ischaemia. That similar changes occurred with intramuscular injection of hypertonic saline suggests that much of the cortical and subcortical changes seen during post-exercise ischaemia reflect the sensory and affective attributes of the muscle pain, rather than in furnishing the cardiovascular responses per se.
骨骼肌的持续等长收缩会导致血压升高，这是由于心输出量增加以及交感神经介导的血管收缩增强所引起的总外周阻力增加。中枢指令和来自收缩肌肉中代谢感受器的反射性输入均已被证明会导致这种交感神经介导的血压升高。阻断血液供应并使代谢产物滞留在收缩的肌肉中（运动后缺血）已表明，虽然运动后心率恢复到基线水平，但在没有中枢指令的情况下，肌肉交感神经活动（MSNA）和血压的升高会在外周输入的维持下持续存在。运动后缺血会激活Ⅲ类和Ⅳ类肌肉传入神经，这些神经在有害刺激期间也会被激活。事实上，运动后缺血是疼痛的，那么疼痛在血压升高中起什么作用呢？肌肉内注射高渗盐水会引起一种深部钝痛，与运动后缺血产生的疼痛并无不同，并且我们已经表明这会导致MSNA和血压持续升高。我们利用大脑功能磁共振成像（fMRI）来确定参与肌肉疼痛感觉处理以及对运动后缺血或肌肉内注射高渗盐水所产生的肌肉疼痛自主反应生成的皮质和皮质下部位。在静态握力运动期间，对侧初级运动皮层、小脑深部核团和小脑皮层的信号强度平行增加，运动结束时停止，这反映了中枢指令的开始和结束。在收缩期，对侧脑岛以及对侧初级躯体感觉皮层的信号强度逐渐增加，并在运动后缺血期间持续。在收缩期，膝周前扣带回皮层的信号强度降低；这些在运动后缺血期间也持续存在。肌肉内注射高渗盐水时出现类似变化表明，运动后缺血期间所见的许多皮质和皮质下变化反映了肌肉疼痛的感觉和情感属性，而不是心血管反应本身。
