CClaude wrote: Luciano136 wrote:
sjarelkwint wrote:EDIT: The more I think about the IQ test the more interesting it gets .. The days you are at altitude you can test people ... You can try to arrange with the people to test them when they get back and aren't wasted (altitude + tired + ...) anymore in mendoza ...
I'm 100% positive it will lower IQ significantly but it would be interesting to see by how much.
Try to do some math when you get to 14k. Boy, is it ever tough. I remember on a few occasions trying to count how many hours and minutes it took me to get to the top and I have to seriously concentrate LOL
That has actually been studied.
Actually, I was only serious because I've been wondering about the affect of l-arginine for about 4 yrs.
Now if you want, you could also have as a secondary endpoint the affect of l-arginine on male/female (sheep, goat, llama,.....) relationships at altitude (which in theory should also be affected by vascular tone
Am. J. Respir. Crit. Care Med., Volume 162, Number 1, July 2000, 221-224
Exhaled Nitric Oxide in High-Altitude Pulmonary Edema
Role in the Regulation of Pulmonary Vascular Tone and Evidence for a Role against Inflammation
HERVÉ DUPLAIN, CLAUDIO SARTORI, MATTIA LEPORI, MARC EGLI, YVES ALLEMANN, PASCAL NICOD, and URS SCHERRER
Department of Internal Medicine and the Botnar Center for Clinical Research, Centre Hospitalier Universitaire Vaudois, Lausanne; and Department of Cardiology, Inselspital, Bern, Switzerland
High-altitude pulmonary edema (HAPE) is a life-threatening condition occurring in predisposed subjects at altitudes above 2,500 m. It is not clear whether, in addition to hemodynamic factors and defective alveolar fluid clearance, inflammation plays a pathogenic role in HAPE. We therefore made serial measurements of exhaled pulmonary nitric oxide (NO), a marker of airway inflammation, in 28 HAPE-prone and 24 control subjects during high-altitude exposure (4,559 m). To examine the relationship between pulmonary NO synthesis and pulmonary vascular tone, we also measured systolic pulmonary artery pressure (Ppa). In the 13 subjects who developed HAPE, exhaled NO did not show any tendency to increase during the development of lung edema. Throughout the entire sojourn at high altitude, pulmonary exhaled NO was roughly 30% lower in HAPE-prone than in control subjects, and there existed an inverse relationship between Ppa and exhaled NO (r = 0.51, p < 0.001). These findings suggest that HAPE is not preceded by airway inflammation. Reduced exhaled NO may be related to altered pulmonary NO synthesis and/or transport and clearance, and the data in our study could be consistent with the novel concept that in HAPE-prone subjects, a defect in pulmonary epithelial NO synthesis may contribute to exaggerated hypoxic pulmonary vasoconstriction and in turn to pulmonary edema
© 2002 American Heart Association, Inc.
Clinical Investigation and Reports
Positive Association of the Endothelial Nitric Oxide Synthase Gene Polymorphisms With High-Altitude Pulmonary Edema
Yunden Droma, MD; Masayuki Hanaoka, MD; Masao Ota, PhD; Yoshihiko Katsuyama, PhD; Tomonobu Koizumi, MD; Keisaku Fujimoto, MD; Toshio Kobayashi, MD; Keishi Kubo, MD
From the Departments of Medicine (Y.D., M.H., T. Koizumi, K.F., T. Kobayashi, K.K.), Legal Medicine (M.O.), and Pharmacy (Y.K.), Shinshu University School of Medicine, Matsumoto, Japan.
Correspondence to Masayuki Hanaoka, MD, First Department of Medicine, Shinshu University School of Medicine, 3-1-1 Asahi, Matsumoto 390-8621, Japan. E-mail [email protected]
Background— A defect of nitric oxide (NO) synthesis in the lung of high-altitude pulmonary edema (HAPE) has been suggested to contribute to its exaggerated pulmonary hypertension. Several polymorphisms have been identified in the gene encoding endothelial nitric oxide synthase (eNOS), which is a key enzyme responsible for NO synthesis, some of which were reported to be associated with vascular disorders.
Methods and Results— We studied 41 HAPE-susceptible subjects (HAPE-s) and 51 healthy climbers (control group) in a Japanese population. We examined 2 polymorphisms of the eNOS gene, including the Glu298Asp variant and 27-base pair (bp) variable numbers of tandem repeats using polymerase chain reaction followed by restriction fragment length polymorphism. The Asp allelic frequency of the Glu298Asp variant was 25.6% in the HAPE-s and 9.8% in the controls, which was significantly different between the two groups (P=0.0044). The eNOS4a allelic frequency of 27-bp variable numbers of tandem repeats was 23.2% in the HAPE-s, significantly higher than that of 6.9% in the controls (P=0.0016). In HAPE-s group, 11 of 41 (26.8%) subjects possessed simultaneously both of the two significant alleles, but among the controls, none did, which showed a high statistical difference between the two groups (P=0.000059).
Conclusions— Both polymorphisms of the eNOS gene were significantly associated with HAPE. A genetic background may underlie the impaired NO synthesis in the pulmonary circulation of HAPE-s. These polymorphisms could be genetic markers for predicting the susceptibility to HAPE.
And the association of l-arginine and No synthase is from Prof John Cooke (Stanford University)
Cooke JP, Tsao PS. Arginine: a new therapy for atherosclerosis? Circulation
There was also a clinical trial in 2002 that pre-dates the VINTAGE MI trial showing an affect of arginine/NO and /AMI's published in Circulation which I'll get the reference for
J Am Coll Cardiol,
© 1998 by the American College of Cardiology Foundation
Restoring vascular nitric oxide formation by L-arginine improves the symptoms of intermittent claudication in patients with peripheral arterial occlusive disease
Rainer H. Böger, MD*, Stefanie M. Bode-Böger, MD*, Wolfgang Thiele*, Andreas Creutzig, MD, Klaus Alexander, MD and J.ürgen C. Frölich, MD*
Whereas the contraindication for AMI patient populations is based on the VINTAGE MI clinical trial (2007)
and if you peruse the literature you'll also see the affect of NO/arginine on VEGF regulation