title: Aging and exercise training reduce testes microvascular PO2 and alter vasoconstrictor responsiveness in testicular arterioles.
abstract: 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.
authors.affiliation: Department of Applied Physiology and Kinesiology, Center for Exercise Science, University of Florida, Gainesville, Florida, USA.
authors.forename: James M
authors.initials: JM
authors.lastname: Dominguez
authors.forename: Robert T
authors.initials: RT
authors.lastname: Davis
authors.forename: Danielle J
authors.initials: DJ
authors.lastname: McCullough
authors.forename: John N
authors.initials: JN
authors.lastname: Stabley
authors.forename: Bradley J
authors.initials: BJ
authors.lastname: Behnke
mesh_terms: D000322:Adrenergic Agonists / Q000494:pharmacology; D000367:Age Factors; D000375:Aging; D000704:Analysis of Variance; D000818:Animals; D001160:Arterioles / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D005298:Fertility; D008297:Male; D008833:Microcirculation / Q000187:drug effects; D010100:Oxygen / Q000097:blood*; D010807:Physical Endurance; D051381:Rats; D011916:Rats, Inbred F344; D013737:Testis / Q000098:blood supply*; D014661:Vasoconstriction / Q000187:drug effects; D014662:Vasoconstrictor Agents / Q000494:pharmacology
chemical_list: D000322:Adrenergic Agonists; D014662:Vasoconstrictor Agents; D010100:Oxygen