Dept. of Applied Physiology and Kinesiology, Center for Exercise Science, 124 FLG, PO Box 118205, Univ. of Florida, Gainesville, FL 32611, USA.
J Appl Physiol (1985). 2010 Jan;108(1):14-20. doi: 10.1152/japplphysiol.00970.2009. Epub 2009 Oct 1.
Aging is associated with an altered ability to match oxygen delivery (QO2) to consumption ((.)VO2) in skeletal muscle and differences in the temporal profile of vasodilation may provide a mechanistic basis for the QO2-to-(.)VO2 mismatching during the rest-to-exercise transition. Therefore, we tested the hypothesis that the speed of vasodilation will be blunted in skeletal muscle first-order arterioles from old vs. young rats. Arterioles from the soleus and the red portion of the gastrocnemius (Gast(Red)) muscles were isolated from young (Y, 6 mo; n = 9) and old (O, 24 mo; n = 9) Fischer 344 rats and studied in vitro. Vessels were exposed to acetylcholine (ACh; 10(-6) M), sodium nitroprusside (SNP; 10(-4) M), and increased intraluminal flow, and the subsequent vasodilation was recorded at 30 frames/s. The data were fit to a monoexponential model and the dynamics of vasodilation [i.e., time delay, time constant (tau), and rate of change (delta/tau)] were calculated. With old age, the rate of vasodilation was significantly blunted in resistance vessels from the soleus to ACh (Y, 27.9 +/- 3.6; O, 8.8 +/- 2.6 microm/s) and flow (Y, 12.8 +/- 2.1; O, 3.1 +/- 0.9 microm/s). In the Gast(Red) the old age-associated impairment of endothelium-dependent vasodilator dynamics was even greater than that of the soleus. With SNP neither the magnitude nor time constant of vasodilation was affected by age in either muscle. The results indicate that aging impairs the dynamics of vasodilation in resistance vessels from the soleus and Gast(Red) muscles mediated, in part, through the endothelium. Thus the old age-associated slower rate and magnitude of vasodilation could inhibit the delivery of O2 during the critical transition from rest to exercise in moderate to highly oxidative skeletal muscle.
衰老与骨骼肌氧输送(QO2)与消耗((.)VO2)匹配能力的改变以及血管舒张时程的差异有关,这可能为休息到运动过渡期间 QO2 与(.)VO2 不匹配提供了机制基础。因此,我们假设衰老会使来自老年大鼠的比目鱼肌和比目鱼肌红色部分(Gast(Red))第一级动脉的血管舒张速度变钝。从年轻(Y,6 个月;n = 9)和老年(O,24 个月;n = 9)Fischer 344 大鼠中分离出比目鱼肌和比目鱼肌红色部分(Gast(Red))的动脉,并在体外进行研究。血管暴露于乙酰胆碱(ACh;10(-6)M)、硝普钠(SNP;10(-4)M)和增加的管腔内流动,随后以 30 帧/秒记录随后的血管舒张。数据拟合单指数模型,并计算血管舒张动力学[即时间延迟、时间常数(tau)和变化率(delta/tau)]。随着年龄的增长,来自比目鱼肌的血管对 ACh(Y,27.9 +/- 3.6;O,8.8 +/- 2.6 μm/s)和流动(Y,12.8 +/- 2.1;O,3.1 +/- 0.9 μm/s)的血管舒张速度明显变钝。在 Gast(Red)中,与比目鱼肌相比,老年相关的内皮依赖性血管舒张动力学损伤更大。对于 SNP,两种肌肉的血管舒张幅度和时间常数均不受年龄影响。结果表明,衰老会损害比目鱼肌和 Gast(Red)肌肉的阻力血管的血管舒张动力学,部分通过内皮介导。因此,衰老相关的血管舒张速度和幅度较慢可能会在从中度到高度氧化的骨骼肌从休息到运动的关键过渡期间抑制 O2 的输送。