Jacobs T L, Segal S S
The John B. Pierce Laboratory and Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, CT 06519, USA.
J Physiol. 2000 May 1;524 Pt 3(Pt 3):929-41. doi: 10.1111/j.1469-7793.2000.00929.x.
We tested the hypothesis that muscle fatigue would attenuate vasodilatory responsiveness throughout the resistance network. The retractor muscle of anaesthetized hamsters was contracted (once per 2 s for 1 min) at duty cycles of 2.5, 10 and 20 % before and after fatiguing contractions that diminished peak tension and muscle glycogen by >50 %. Arterioles and feed arteries (FA) dilated maximally during fatiguing contractions. Resting vasomotor tone consistently recovered following contractions. Peak blood flow was proportional to integrated tension (tension x time, expressed in mN mm-2 s); both increased with duty cycle and decreased with fatigue. Total integrated vasodilatory responses (diameter x time, expressed in microm s) increased with duty cycle and decreased with fatigue. Vasodilatation during contractions plateaued at approximately 50 % of peak integrated tension. Post-contraction vasodilatation increased with integrated tension and both were attenuated with fatigue. As integrated tension increased, distal arterioles dilated first and to the greatest extent relative to proximal arterioles and FA. Fatigue had little effect on dilatation of distal arterioles whereas dilatation of proximal arterioles and FA was suppressed. Latency of onset for vasodilatation decreased as duty cycle increased and was unaffected by fatigue. Vasodilatation and blood flow increase in proportion to integrated tension, with an ascending locus of vasomotor control and prolongation of post-contraction vasodilatation. With muscle fatigue, the locus of flow control resides in distal arterioles; both ascending and post-contraction vasodilatations are attenuated despite normal vasomotor tone.
肌肉疲劳会减弱整个阻力网络的血管舒张反应性。在使峰值张力和肌肉糖原减少超过50%的疲劳收缩前后，对麻醉仓鼠的牵张肌以2.5%、10%和20%的工作周期进行收缩（每2秒收缩1次，持续1分钟）。在疲劳收缩期间，小动脉和供血动脉（FA）会最大限度地扩张。收缩后静息血管运动张力持续恢复。峰值血流与积分张力（张力×时间，以mN mm-2 s表示）成正比；二者均随工作周期增加而增加，随疲劳而降低。总的血管舒张反应积分（直径×时间，以μm s表示）随工作周期增加而增加，随疲劳而降低。收缩期间的血管舒张在约50%的峰值积分张力时达到平台期。收缩后血管舒张随积分张力增加，且二者均随疲劳而减弱。随着积分张力增加，相对于近端小动脉和FA，远端小动脉首先扩张且扩张程度最大。疲劳对远端小动脉的扩张影响较小，而近端小动脉和FA的扩张受到抑制。血管舒张的起始潜伏期随工作周期增加而缩短，且不受疲劳影响。血管舒张和血流增加与积分张力成正比，血管运动控制位点上升，收缩后血管舒张延长。随着肌肉疲劳，血流控制位点位于远端小动脉；尽管血管运动张力正常，但上升性和收缩后血管舒张均减弱。
