Ökar kreatin/ALA/AAKG/NOX osv vaskuläriteten på sikt? - Kolozzeum Forum

tejpis · 2004-09-09, 11:07

Se topic. Om man använder liknande ovanstående medel, såna som höjer pumpen, ger detta en högre vaskularitet på sikt också? Dvs "kroniskt"?

Vaskulariteten ökar också "kroniskt" ju mer muskler man har?

edit: Vaskularitet stavas det ju!

tejpis · 2004-09-09, 23:45

buuuump, hjälp!

Upplever ni bättre vaskuläritet (synligare/större ådror) av att käka pumphöjande tillskott? Vaskularitet som även håller i sig efter "kuren"?

edit: stavade vaskularitet fel !

Beast · 2004-09-10, 02:06

Kreatin och ala är inga "pump" grejer.. Nox däremot får man bra pumpar utav samtidigt som ådrorna syns lite mer.

Grahn · 2004-09-10, 05:14

Pm NOX märkbart påverkar vaskulariteten på det viset torde preparatet vara livsfarligt för blodtrycket.

snakeplisken · 2004-09-10, 11:03

Hur länge tar det innan man märker effekten av NOX? Har börjat käka nyligen, andra dagen idag men har inte märkt av någon effekt ännu!!

Trytter · 2004-09-10, 23:37

Dum fråga kanske, men vad är AAKG?

Styx · 2004-09-11, 00:12

Arginin alfa-ketoglutarat,
Det aktiva substansen i dom flesta "NO produkterna". Arginin kan i cellerna omvandlas till NO.

LunaSpice · 2004-09-11, 01:09

Vaskularisationen ökar (och i vissa fall även kolaterala kärl) och kan kvarstå till viss grad efter kraftig muskeltillväxt. Det har dock med fyllnadstryck och blodtryck att göra också.

Grahn, NO _är_ inte bra för blodtrycket när det tas som tillskott.

Endothelial dysfunction and alteration of nitric oxide/ cyclic GMP pathway in patients with exercise-induced hypertension.

Chang HJ, Chung JH, Choi BJ, Choi TY, Choi SY, Yoon MH, Hwang GS, Shin JH, Tahk SJ, Choi BI.

Yonsei Med J. 2003 Dec 30;44(6):1014-20.

The diagnostic and prognostic implication of exaggerated blood pressure response to exercise have been controversial, with opinions ranging from a benign process to a harbinger of potential cardiovascular morbidity. Endothelial dysfunction has been demonstrated in patients with atherosclerosis and as a risk factor for coronary artery disease. However, whether the cause of exercise-induced hypertension might be related to endothelial dysfunction has not been well elucidated. We evaluated endothelial function in patients who showed a systolic blood pressure > or = 210 mmHg in males and > or = 190 mmHg in females during treadmill exercise test. We measured the endothelial function of the brachial artery in 35 patients with exercise-induced hypertension, and in 35 age- and gender-matched normal control subjects, by a high resolution ultrasound technique, and the concentration of NO2-/NO3- and cyclic guanosine monophosphate (GMP). Endothelial-dependent vasodilation was impaired in patients with hypertension compared to normal controls (3.14 +/- 0.61 vs. 6.5 +/- 0.76%, p < 0.05). The extent of vasodilation was significantly correlated with age (r=-0.28, p < 0.05) and systolic blood pressure difference (r=-0.36, p < 0.05). The levels of NO2-/NO3- and cyclic GMP at maximal exercise were significantly higher than those at rest and recovery in both controls and the hypertensive group (p < 0.05). Although there was no significant difference in the increment of NO2-/NO3- during maximal exercise between the controls and hypertensive group (55 +/- 17 vs. 56 +/- 12 micro mol/L, p=NS), cyclic GMP level during maximal exercise was significantly higher in the control group than the hypertensive group (10 +/- 1.8 vs. 8.3 +/- 2.5 pmol/ml, p 0.05). Patients with exercise-induced hypertension have poor endothelium-dependent vasodilation due to an impaired nitric oxide/cyclic GMP pathway, which may play a significant role in increasing blood pressure during exercise with inadequate peripheral adjustment to changing cardiac output.