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首页> 外文期刊>American Journal of Physiology >Muscle metaboreflex activation during dynamic exercise vasoconstricts ischemic active skeletal muscle
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Muscle metaboreflex activation during dynamic exercise vasoconstricts ischemic active skeletal muscle

机译:动态运动过程中肌肉肌瘤激活激活血管电机缺血活性骨骼肌

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摘要

Metabolite accumulation due to ischemia of active skeletal muscle stimulates group III/IV chemosen-sitive afferents eliciting reflex increases in arterial blood pressure and sympathetic activity, termed the muscle metaboreflex. We and others have previously demonstrated sympathetically mediated vasoconstric-tion of coronary, renal, and forelimb vasculatures with muscle metaboreflex activation (MMA). Whether MMA elicits vasoconstric-tion of the ischemic muscle from which it originates is unknown. We hypothesized that the vasodilation in active skeletal muscle with imposed ischemia becomes progressively restrained by the increasing sympathetic vasoconstriction during MMA. We activated the metaboreflex during mild dynamic exercise in chronically instrumented canines via graded reductions in hindlimb blood flow (HLBF) before and after alpha_1-adrenergic blockade [prazosin (50 mug/kg)], beta-ad-renergic blockade [propranolol (2 mg/kg)], and alpha_1 + beta-blockade. Hindlimb resistance was calculated as femoral arterial pressure/ HLBF. During mild exercise, HLBF must be reduced below a threshold level before the reflex is activated. With initial reductions in HLBF, vasodilation occurred with the imposed ischemia. Once the muscle metaboreflex was elicited, hindlimb resistance increased. This increase in hindlimb resistance was abolished by alpha_1-adrenergic blockade and exacerbated after beta-adrenergic blockade. We conclude that metaboreflex activation during submaximal dynamic exercise causes sympathetically mediated alpha-adrenergic vasoconstriction in ischemic skeletal muscle. This limits the ability of the reflex to improve blood flow to the muscle.
机译:由于活性骨骼肌缺血导致的代谢物积累刺激III / IV化学物质局部传入诱导反射的动脉血压和交感神经活动,称为肌肉元射流。我们和其他人以前表现出同情介导的冠状动脉,肾和前肢血管与肌肉元射流激活(MMA)。 MMA是否引发了缺血性肌肉的血管型肌肉,它来自它起源的缺血性肌肉是未知的。我们假设具有施加缺血的活性骨骼肌中的血管沉积因MMA期间的同情血管收缩而变得逐渐抑制。在α_1-肾上腺素能阻滞之前和之后,在长期仪器血流(HLBF)中,在慢性仪器血液流动(HLBF)中,在温和的动态运动期间激活了Metaboreflex。α_1-肾上腺素能阻断[Prazosin(50 mug / kg)],β-ad-genericsα,β-ad-genericα,β-肾上腺素(2毫克) / kg)],和alpha_1 + beta-elclosadade。将后肢抗性计算为股动脉压/ HLBF。在轻度运动期间,在反射被激活之前,HLBF必须低于阈值水平。通过初始减少HLBF,血管舒张发生施加的缺血。一旦肌肉肌及比塞被引发,后肢阻力就会增加。通过α-1-肾上腺素能阻断,在β-肾上腺素能阻滞后加剧了后肢抗性的这种增加。我们得出结论,在血管动态锻炼期间的Metaboreflex活化会导致血糖骨骼肌中的令人恐惧介导的α-肾上腺素能血管收缩。这限制了反射能力改善血液流向肌肉的能力。

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