Department of Applied Physiology and Kinesiology, Center for Exercise Science, University of Florida, Gainesville, Florida, USA.
Am J Physiol Regul Integr Comp Physiol. 2011 Sep;301(3):R801-10. doi: 10.1152/ajpregu.00203.2011. Epub 2011 Jun 15.
Testicular function and associated testosterone concentration decline with advancing age, and an impaired O₂ supply may contribute, in part, to this reduction. We hypothesized that there would be a reduced microvascular Po₂ (Po₂(m)) in the testes from aged rats, and this reduced Po₂(m) 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 Po₂(m) in the testes from aged animals after aerobic exercise training. Testicular Po₂(m) 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 α-adrenergic [norepinephrine (NE) and phenylephrine (PE)] and myogenic stimuli in testicular arterioles was assessed in vitro. In the SED animals, testicular Po₂(m) was reduced by ∼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 Po₂(m) in the aged group and reduced testicular Po₂(m) 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 Po₂(m) and impaired adrenergic vasoconstriction. The diminished testicular microvascular driving pressure of O₂ and associated vascular dysfunction provides mechanistic insight into the old age-related decrease in testicular function, and a reduced Po₂(m) may contribute, in part, to reduced fertility markers after exercise training.
睾丸功能和相关的睾酮浓度随着年龄的增长而下降,而供氧受损可能部分导致这种减少。我们假设老年大鼠的睾丸内会出现微血管氧分压(Po₂(m))降低,而这种降低的 Po₂(m)与分离的阻力小动脉的血管舒缩控制受损有关。此外,鉴于运动对微血管 Po₂和小动脉功能有积极影响,我们进一步假设,经过有氧训练后,老年动物的睾丸内会出现增强的 Po₂(m)。通过在年轻和老年久坐(SED)和运动训练(ET;15 m/min 跑步机步行,15 度倾斜,每周 5 天,共 10 周)雄性 Fischer-344 大鼠体内通过磷光猝灭来测量睾丸内 Po₂(m)。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 Po₂(m)随年龄增长降低了约 50%(老年 SED 为 11.8 ± 1.9 与年轻 SED 22.1 ± 1.1 mmHg;P = 0.0001)。与我们的假设相反,运动训练并没有改变老年组的 Po₂(m),反而降低了年轻动物的睾丸 Po₂(m),消除了与年龄相关的差异(年轻 ET 为 10.0 ± 0.8 与老年 ET 为 10.7 ± 0.9 mmHg;P = 0.37)。与年轻相比,老年时对 NE 和 PE 的血管收缩反应减弱(NE:年轻 SED 为 58 ± 2%与老年 SED 为 47 ± 2%;P = 0.001)(PE:年轻 SED 为 51 ± 3%与老年 SED 为 36 ± 5%;P = 0.008)。运动训练并没有改变年轻或老年组对 NE 的最大血管收缩。总之,随着年龄的增长,睾丸的 Po₂(m)降低,肾上腺素能血管收缩受损。O₂的降低的睾丸微血管驱动压和相关的血管功能障碍为与年龄相关的睾丸功能下降提供了机制上的见解,而运动训练后生育力标志物的降低可能部分与 Po₂(m)降低有关。