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anyone has any experience with myo-inositol trispyrophosphate (itpp) ?
they give it to race horses and greyhounds.
wonder if anyone who compete in MMA, Boxing, marathons etc..
have any experience or recent news on this stuff
they give it to race horses and greyhounds.
wonder if anyone who compete in MMA, Boxing, marathons etc..
have any experience or recent news on this stuff
Enhanced exercise capacity in mice with severe heart failure treated with an allosteric effector of hemoglobin, myo-inositol trispyrophosphate
Andreia Bioloa, Ruth Greferathb,c, Deborah A. Siwika, Fuzhong Qina, Eugene Valskya, Konstantina C. Fylaktakidouc,1, Srinivasu Pothukanuric, Carolina D. Duartec, Richard P. Schwarzb, Jean-Marie Lehnc,2, Claude Nicolaub,c,d,2 and Wilson S. Coluccia,2
+Author Affiliations
aCardiovascular Section, Department of Medicine, Boston University Medical Center, and Myocardial Biology Unit, Boston University School of Medicine, Boston, MA 02115;
bNormOxys, Inc., 200 Boston Avenue, Medford, MA 02155;
cInstitut de Science et d'Ing?nierie Supramol?culaires, Universit? Louis Pasteur, 8 All?e Gaspard Monge, 67000 Strasbourg, France; and
dFriedman School of Nutrition Science and Policy, Tufts University, Boston, MA 02115
Contributed by Jean-Marie Lehn, December 31, 2008 (received for review December 1, 2008)
Abstract
A major determinant of maximal exercise capacity is the delivery of oxygen to exercising muscles. myo-Inositol trispyrophosphate (ITPP) is a recently identified membrane-permeant molecule that causes allosteric regulation of Hb oxygen binding affinity. In normal mice, i.p. administration of ITPP (0.5?3 g/kg) caused a dose-related increase in the oxygen tension at which Hb is 50% saturated (p50), with a maximal increase of 31%. In parallel experiments, ITPP caused a dose-related increase in maximal exercise capacity, with a maximal increase of 57 ? 13% (P = 0.002). In transgenic mice with severe heart failure caused by cardiac-specific overexpression of Gαq, i.p. ITPP increased exercise capacity, with a maximal increase of 63 ? 7% (P = 0.005). Oral administration of ITPP in drinking water increased Hb p50 and maximal exercise capacity (+34 ? 10%; P < 0.002) in normal and failing mice. Consistent with increased tissue oxygen availability, ITPP decreased hypoxia inducible factor-1α mRNA expression in myocardium. It had no effect on myocardial contractility in isolated mouse cardiac myocytes and did not affect arterial blood pressure in vivo in mice. Thus, ITPP decreases the oxygen binding affinity of Hb, increases tissue oxygen delivery, and increases maximal exercise capacity in normal mice and mice with severe heart failure. ITPP is thus an attractive candidate for the therapy of patients with reduced exercise capacity caused by heart failure.