Aging and exercise training reduce testes microvascular PO2 and alter vasoconstrictor responsiveness in testicular arterioles
Aging and exercise training reduce testes microvascular PO2 and alter vasoconstrictor responsiveness in testicular arterioles
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DOI：
10.1152/ajpregu.00203.2011
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发表时间：
2011-09-01
影响因子：
2.8
通讯作者：
Behnke, Bradley J.
中科院分区：
文献类型：
--
作者：
Dominguez, James M., II;Davis, Robert T., III;Behnke, Bradley J.
多明格斯JM第二，戴维斯RT第三，麦卡洛DJ，Stabley JN，Behnke BJ。衰老和运动训练降低睾丸微血管PO 2，改变睾丸小动脉血管收缩反应性。Am J Physiol Regul Integr Comp Physiol 301：R801-R810，2011年。首次发表于2011年6月15日; doi：10.1152/ajpregu.00203.2011。睾丸功能和相关的睾酮浓度随着年龄的增长而下降，受损的O-2供应可能部分导致这种下降。我们假设，将有一个减少的微血管PO 2（PO 2 m）在老年大鼠的睾丸，这减少PO 2 m将与受损的血管控制在孤立的阻力小动脉。此外，考虑到运动对微血管PO 2和小动脉功能的积极影响，我们进一步假设有氧运动训练后老年动物睾丸中的PO 2 m会增强。睾丸PO 2 m通过磷光淬灭在体内测定年轻和老年久坐（SED）和运动训练（ET; 15 m/min的跑步机行走，15度倾斜，5天/周，持续10周）的雄性Fischer-344大鼠。在体外评估睾丸小动脉对α-肾上腺素能[去甲肾上腺素（NE）和苯肾上腺素（PE）]和肌源性刺激的血管收缩。在SED动物中，睾丸PO 2 m随着年龄的增长降低了50%（老年SED 11.8 +/- 1.9 vs年轻SED 22.1 +/- 1.1 mmHg; P = 0.0001）。与我们的假设相反，运动训练没有改变老年组的PO 2 m，并降低了年轻动物的睾丸PO 2 m，消除了年龄相关的差异（年轻ET，10.0 +/- 0.8与老年ET，10.7 +/- 0.9 mmHg; P = 0.37）。与年轻人相比，老年人对NE和PE的血管收缩反应性降低（NE：年轻SED，58 +/- 2 vs.老年SED，47 +/- 2%; P = 0.001）（PE：年轻SED，51 +/- 3 vs.老年SED，36 +/- 5%; P = 0.008）。运动训练并没有改变最大血管收缩去甲肾上腺素在年轻或老年组。总之，年龄增长与睾丸PO 2 m降低和肾上腺素能血管收缩受损相关。减少睾丸微血管驱动压力的O-2和相关的血管功能障碍提供了机械洞察老年相关的睾丸功能下降，和减少PO 2 m可能有助于，部分，减少运动训练后的生育标志物。
Dominguez JM 2nd, Davis RT 3rd, McCullough DJ, Stabley JN, Behnke BJ. Aging and exercise training reduce testes microvascular PO2 and alter vasoconstrictor responsiveness in testicular arterioles. Am J Physiol Regul Integr Comp Physiol 301: R801-R810, 2011. First published June 15, 2011; doi:10.1152/ajpregu.00203.2011.-Testicularfunction and associated testosterone concentration decline with advancing age, and an impaired O-2 supply may contribute, in part, to this reduction. We hypothesized that there would be a reduced microvascular PO2 (PO2m) in the testes from aged rats, and this reduced PO2m would be associated with impaired vasomotor control in isolated resistance arterioles. In addition, given the positive effect of exercise on microvascular PO2 and arteriolar function, we further hypothesized that there would be an enhanced PO2m in the testes from aged animals after aerobic exercise training. Testicular PO2m was measured in vivo via phosphorescence quenching in young and aged sedentary (SED) and exercise-trained (ET; 15 m/min treadmill walking, 15-degree incline, 5 days/wk for 10 wk) male Fischer-344 rats. Vasoconstriction to alpha-adrenergic [norepinephrine (NE) and phenylephrine (PE)] and myogenic stimuli in testicular arterioles was assessed in vitro. In the SED animals, testicular PO2m was reduced by similar to 50% with old age (aged SED 11.8 +/- 1.9 vs. young SED 22.1 +/- 1.1 mmHg; P = 0.0001). Contrary to our hypothesis, exercise training did not alter PO2m in the aged group and reduced testicular PO2m in the young animals, abolishing age-related differences (young ET, 10.0 +/- 0.8 vs. aged ET, 10.7 +/- 0.9 mmHg; P = 0.37). Vasoconstrictor responsiveness to NE and PE was diminished in aged compared with young (NE: young SED, 58 +/- 2 vs. aged SED, 47 +/- 2%; P = 0.001) (PE: young SED, 51 +/- 3 vs. aged SED, 36 +/- 5%; P = 0.008). Exercise training did not alter maximal vasoconstriction to NE in young or aged groups. In summary, advancing age is associated with a reduced testis PO2m and impaired adrenergic vasoconstriction. The diminished testicular microvascular driving pressure of O-2 and associated vascular dysfunction provides mechanistic insight into the old age-related decrease in testicular function, and a reduced PO2m may contribute, in part, to reduced fertility markers after exercise training.