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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone Side Effect Management
Hematocrit drives Blood Viscosity- Does that Matter in Men on TRT? Effect of Altitude?
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<blockquote data-quote="tareload" data-source="post: 183042"><p>You mean "None of this matters to YOU." Unless your experience accurately represents all humans on this planet, your statement seems irresponsible. Especially after I have painstakingly shown that not all Hct values are created equal.</p><p></p><p>My response to an Hct of 52 is different that yours. Take a look:</p><p></p><p><a href="http://Acute%20reductions%20in%20hematocrit%20increase%20flow%E2%80%90mediated%20dilation%20independent%20of%20resting%20nitric%20oxide%20bioavailability%20in%20humans" target="_blank">https://physoc.onlinelibrary.wiley.com/doi/abs/10.1113/JP280141</a></p><p></p><p>[ATTACH=full]10193[/ATTACH]</p><p></p><p><span style="font-size: 18px"><strong>Abstract</strong></span></p><p> </p><p> <span style="font-size: 18px"><strong> Key points</strong></span></p><p></p><ul> <li data-xf-list-type="ul">Changes in hematocrit influence nitric oxide signalling through alterations in shear stress stimuli and hemoglobin scavenging of nitric oxide; these two regulatory factors have not been assessed simultaneously</li> <li data-xf-list-type="ul">Isovolumic hemodilution led to a marked increase in brachial artery flow‐mediated dilation in humans</li> <li data-xf-list-type="ul">The increase in flow‐mediated dilation occurred in the face of an unaltered shear stress stimulus for vasodilation and reduced resting steady‐state nitric oxide levels in the blood</li> <li data-xf-list-type="ul">Collectively, our data point towards hemoglobin scavenging of nitric oxide as a key regulatory factor of brachial flow‐mediated dilation and highlight the importance of simultaneous consideration of nitric oxide production and inactivation when investigating vascular function in humans</li> </ul><p> </p><p></p><p> <span style="font-size: 18px"><strong> Abstract</strong></span></p><p>Hemoglobin (Hb) may impact the transduction of endothelium‐dependent and nitric oxide (NO) mediated vasodilator activity, given its contribution to shear stress stimuli and diverse biochemical reactions with NO. We hypothesized that an acute reduction in [Hb] and hematocrit (Hct) would increase brachial artery flow‐mediated dilation (FMD). In eleven healthy males (28 ± 7 years; 23 ± 2 kg m−2), FMD (Duplex ultrasound), arterial blood gases, Hct and [Hb], blood viscosity, and NO metabolites (ozone‐based chemiluminescence) were measured before and after isovolumic hemodilution, where ∼20% of whole blood was removed and replaced with 5% human serum albumin. Hemodilution reduced Hct by 18 ± 2% (<em>P </em> < 0.001) and whole blood viscosity by 22 ± 5% (<em>P </em> < 0.001). Plasma nitrite (P = 0.01), <em>S</em>‐nitrosothiols (P = 0.03), and total red blood cell NO (P = 0.001) were collectively reduced by ∼15–40%. Brachial artery FMD increased by ∼160% from 3.8 ± 2.1 to 9.7 ± 4.5% (P = 0.004). Statistical covariation for the shear stress stimulus did not alter FMD, indicating that the increase in FMD was not directly related to alterations in whole blood viscosity and the shear stimulus. Collectively, these findings indicate that hemoglobin scavenging of NO appears to be an important factor in the regulation of FMD under normal conditions through constraint of endothelium‐dependent NO‐mediated vasodilation in healthy humans.</p><p></p><p></p><p>Hot off the press. Evidently, these researchers didn't get your memo. I am glad you don't suffer elevated BP and reduced FMD with increased Hct.</p></blockquote><p></p>
[QUOTE="tareload, post: 183042"] You mean "None of this matters to YOU." Unless your experience accurately represents all humans on this planet, your statement seems irresponsible. Especially after I have painstakingly shown that not all Hct values are created equal. My response to an Hct of 52 is different that yours. Take a look: [URL='http://Acute%20reductions%20in%20hematocrit%20increase%20flow%E2%80%90mediated%20dilation%20independent%20of%20resting%20nitric%20oxide%20bioavailability%20in%20humans']https://physoc.onlinelibrary.wiley.com/doi/abs/10.1113/JP280141[/URL] [ATTACH type="full"]10193[/ATTACH] [SIZE=18px][B]Abstract[/B][/SIZE] [SIZE=18px][B] Key points[/B][/SIZE] [LIST] [*]Changes in hematocrit influence nitric oxide signalling through alterations in shear stress stimuli and hemoglobin scavenging of nitric oxide; these two regulatory factors have not been assessed simultaneously [*]Isovolumic hemodilution led to a marked increase in brachial artery flow‐mediated dilation in humans [*]The increase in flow‐mediated dilation occurred in the face of an unaltered shear stress stimulus for vasodilation and reduced resting steady‐state nitric oxide levels in the blood [*]Collectively, our data point towards hemoglobin scavenging of nitric oxide as a key regulatory factor of brachial flow‐mediated dilation and highlight the importance of simultaneous consideration of nitric oxide production and inactivation when investigating vascular function in humans [/LIST] [SIZE=18px][B] Abstract[/B][/SIZE] Hemoglobin (Hb) may impact the transduction of endothelium‐dependent and nitric oxide (NO) mediated vasodilator activity, given its contribution to shear stress stimuli and diverse biochemical reactions with NO. We hypothesized that an acute reduction in [Hb] and hematocrit (Hct) would increase brachial artery flow‐mediated dilation (FMD). In eleven healthy males (28 ± 7 years; 23 ± 2 kg m−2), FMD (Duplex ultrasound), arterial blood gases, Hct and [Hb], blood viscosity, and NO metabolites (ozone‐based chemiluminescence) were measured before and after isovolumic hemodilution, where ∼20% of whole blood was removed and replaced with 5% human serum albumin. Hemodilution reduced Hct by 18 ± 2% ([I]P [/I] < 0.001) and whole blood viscosity by 22 ± 5% ([I]P [/I] < 0.001). Plasma nitrite (P = 0.01), [I]S[/I]‐nitrosothiols (P = 0.03), and total red blood cell NO (P = 0.001) were collectively reduced by ∼15–40%. Brachial artery FMD increased by ∼160% from 3.8 ± 2.1 to 9.7 ± 4.5% (P = 0.004). Statistical covariation for the shear stress stimulus did not alter FMD, indicating that the increase in FMD was not directly related to alterations in whole blood viscosity and the shear stimulus. Collectively, these findings indicate that hemoglobin scavenging of NO appears to be an important factor in the regulation of FMD under normal conditions through constraint of endothelium‐dependent NO‐mediated vasodilation in healthy humans. Hot off the press. Evidently, these researchers didn't get your memo. I am glad you don't suffer elevated BP and reduced FMD with increased Hct. [/QUOTE]
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Testosterone Replacement, Low T, HCG, & Beyond
Testosterone Side Effect Management
Hematocrit drives Blood Viscosity- Does that Matter in Men on TRT? Effect of Altitude?
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