Now we have even more reason to excercise on a consistent basis.
Run training ameliorates the established erectile dysfunction in rats under long-term nitric oxide (NO) blockade
FULL STUDY with graph: http://www.biomedcentral.com/1471-2210/7/S1/P11
Stimulation of nitrergic neurons and endothelial cells in the erectile tissue results in release of NO
that diffuse to surrounding smooth muscle cells where it activates the soluble guanylate cyclase (sGC), facilitating the conversion of GTP to cGMP. This second messenger diminishes the intracellular levels of calcium thereby causing penile smooth muscle relaxation and penile erection .
Epidemiological studies have shown a strong association between erectile dysfunction (ED) and arterial hypertension , where the deficiency of the NO-cGMP pathway seems to greatly contribute to such association
Regular physical exercise has been shown to increase the NO production thus ameliorating cardiovascular diseases
[2,4]. Recently, we have shown that prior physical conditioning improves the erectile function in normotensive rats  and prevents the impaired corpus cavernosum relaxation secondary to chronic NO blockade in rats
Our findings show that run training significantly reverses the established erectile dysfunction due to impairment of the NO-GMPc signalling pathway in rats.
Chronic Exercise Increases Both Inducible and Endothelial Nitric Oxide Synthase Gene Expression in Endothelial Cells of Rat Aorta
http://content.karger.com/ProdukteDB/pr ... elNr=48211
Chronic exercise upregulates endothelial nitric oxide synthase (eNOS) gene expression
. Whether the expression of inducible nitric oxide synthase (iNOS) is affected by exercise is unknown.
We therefore investigated the effects of chronic exercise on iNOS and eNOS expression in isolated rat aortic endothelial and smooth muscle cells separately. Five-week-old male Wistar rats were randomly divided into control and exercise groups.
After 10 weeks of running training, animals were sacrificed under ether anesthesia. The standard curve quantitative competitive reverse transcriptase-polymerase chain reaction method was used to quantify NOS mRNA expression in isolated endothelial/smooth muscle cells.
To evaluate the functional role of iNOS, we examined phenylephrine-induced vascular responses with or without pretreatment with aminoguanidine.
We found that (1) expression of iNOS and eNOS mRNA in endothelial cells was increased by chronic exercise and (2) chronic exercise blunted phenylephrine-induced vascular responses, probably by increasing NO release via iNOS.
Our results show that chronic exercise increases both iNOS and eNOS gene expression in endothelium.
These alterations may be partially responsible for the change in vascular response after exercise.
Both physical fitness and acute exercise regulate nitric oxide formation in healthy humans
Both physical fitness and acute exercise regulate nitric oxide formation in healthy humans.
We analyzed nitrate, a major stable end product of nitric oxide (NO) metabolism in vivo in plasma and urine from groups of healthy subjects with different working capacities
Resting plasma nitrate was higher in athletic subjects than in nonathletic controls [45 ± 2 vs. 34 ± 2 (SE) µM; P < 0.01]. In other subjects, both the resting plasma nitrate level (r = 0.53; P < 0.01) and the urinary excretion of nitrate at rest (r = 0.46; P < 0.01) correlated to the subjects' peak work rates, as determined by bicycle ergometry. Two hours of physical exercise elevated plasma nitrate by 18 ± 4 (P < 0.01) and 16 ± 6% (P < 0.01), respectively, in athletes and nonathletes, compared with resting nitrate before exercise.
We conclude that physical fitness and formation of NO at rest are positively linked to each other. Furthermore, a single session of exercise elicits an acute elevation of NO formation
The observed positive relation between physical exercise and NO formation may help to explain the beneficial effects of physical exercise on cardiovascular health.
Effect of exercise training on endothelium-derived nitric oxide function in humans
http://www3.interscience.wiley.com/jour ... 1&SRETRY=0
"... Exercise training has been shown, in many animal and human studies, to augment endothelial, NO-dependent vasodilatation in both large and small vessels
. The extent of the improvement in humans depends upon the muscle mass subjected to training; with forearm exercise, changes are restricted to the forearm vessels while lower body training can induce generalized benefit
Increased NO bioactivity with exercise training has been readily and consistently demonstrated
in subjects with cardiovascular disease and risk factors, in whom antecedent endothelial dysfunction exists."
"... Recent human studies also indicate that exercise training may improve endothelial function by up-regulating eNOS protein expression and phosphorylation
. While improvement in NO vasodilator function has been less frequently found in healthy subjects, a higher level of training may lead to improvement.
Regarding time course, studies indicate that short-term training increases NO bioactivity
, which acts to homeostatically regulate the shear stress associated with exercise. Whilst the increase in NO bioactivity dissipates within weeks of training cessation, studies also indicate that if exercise is maintained, the short-term functional adaptation is succeeded by NO-dependent structural changes, leading to arterial remodelling and structural normalization
of shear. "
Exercise increases systemic nitric oxide production in men
FULL PDF: http://www.med.uni-magdeburg.de/fme/ins ... isk173.pdf