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Exercise Induced Endothelial Dysfunction?
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<blockquote data-quote="JakeH" data-source="post: 87949" data-attributes="member: 14326"><p>Guys,</p><p></p><p>I am obsessed with endothelial health and maintaining its health (because penis health), which includes not damaging it. The below study seems to suggest that certain exercise selections can hinder endothelial health due to desensitization of cells. Am I reading this correctly? </p><p></p><p><span style="color: #333333">A large body of evidence suggests that endothelial dysfunction can be improved by physical activity (</span><a href="http://www.onlinejacc.org/content/48/4/790#ref-7" target="_blank">7–11,35</a><span style="color: #333333">), whereas the training effects on endothelial function in subjects with normal baseline endothelial function are inconsistent (</span><a href="http://www.onlinejacc.org/content/48/4/790#ref-12" target="_blank">12,16–19</a><span style="color: #333333">). Possible explanations for disparities among these studies include differences in types of sport (endurance- versus strength-training, lower versus upper versus whole body exercise) and in training intensity and duration. Furthermore, 2 studies even revealed adverse training effects on vascular function in volunteers with high-intensity exercise (</span><a href="http://www.onlinejacc.org/content/48/4/790#ref-36" target="_blank">36,37</a><span style="color: #333333">). Our findings now add significant new insights into the effects of exercise on the healthy human vasculature by demonstrating that exercise increases shear-stress induced NO release. <strong>The reduced endothelial-independent dilatation</strong> observed in rowers might be explained by 1 of 2 mechanisms. <strong>Chronic increases in NO production might lead to desensitization of smooth muscle relaxation (biochemical problem). Alternatively, the smooth muscle cell layer in rowers could potentially be thicker compared with sedentary control subjects, which could lead to a reduced response to exogenous NO owing to a longer diffusion distance (biomechanical problem). </strong>Accordingly, net flow-mediated dilatation responses in trained subjects appear no different than those of control subjects. Our findings suggest, for the first time, that the phenomenon of “tolerance” to NO might occur in healthy humans as a physiological mechanism</span></p><p></p><p>Source: <a href="http://www.onlinejacc.org/content/48/4/790" target="_blank">http://www.onlinejacc.org/content/48/4/790</a></p></blockquote><p></p>
[QUOTE="JakeH, post: 87949, member: 14326"] Guys, I am obsessed with endothelial health and maintaining its health (because penis health), which includes not damaging it. The below study seems to suggest that certain exercise selections can hinder endothelial health due to desensitization of cells. Am I reading this correctly? [COLOR=#333333][FONT=Roboto]A large body of evidence suggests that endothelial dysfunction can be improved by physical activity ([/FONT][/COLOR][URL="http://www.onlinejacc.org/content/48/4/790#ref-7"]7–11,35[/URL][COLOR=#333333][FONT=Roboto]), whereas the training effects on endothelial function in subjects with normal baseline endothelial function are inconsistent ([/FONT][/COLOR][URL="http://www.onlinejacc.org/content/48/4/790#ref-12"]12,16–19[/URL][COLOR=#333333][FONT=Roboto]). Possible explanations for disparities among these studies include differences in types of sport (endurance- versus strength-training, lower versus upper versus whole body exercise) and in training intensity and duration. Furthermore, 2 studies even revealed adverse training effects on vascular function in volunteers with high-intensity exercise ([/FONT][/COLOR][URL="http://www.onlinejacc.org/content/48/4/790#ref-36"]36,37[/URL][COLOR=#333333][FONT=Roboto]). Our findings now add significant new insights into the effects of exercise on the healthy human vasculature by demonstrating that exercise increases shear-stress induced NO release. [B]The reduced endothelial-independent dilatation[/B] observed in rowers might be explained by 1 of 2 mechanisms. [B]Chronic increases in NO production might lead to desensitization of smooth muscle relaxation (biochemical problem). Alternatively, the smooth muscle cell layer in rowers could potentially be thicker compared with sedentary control subjects, which could lead to a reduced response to exogenous NO owing to a longer diffusion distance (biomechanical problem). [/B]Accordingly, net flow-mediated dilatation responses in trained subjects appear no different than those of control subjects. Our findings suggest, for the first time, that the phenomenon of “tolerance” to NO might occur in healthy humans as a physiological mechanism[/FONT][/COLOR] Source: [URL]http://www.onlinejacc.org/content/48/4/790[/URL] [/QUOTE]
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