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It's been widely disussed of Trens fat burning properties through rises in IGF and Prostaglandins. While IGF is a fairly well known substance in the bodybuilding world today, prostaglandins are fairly unknown in terms of formation and roles in the body.
So below, a brief dicription of prostoglandins and their role in fat burning, "fina cough", and why a person going through Tren administration can experience it's fat burning effects without the dreaded "Cough"
The term prostaglandin comes from the word-Prostate. The first prostoglandins were first dicovered in semen about the mid 1930's and it was thought that prostaglandins were made from the prostate. Since this time, it has been dicovered that most prostaglandins are not even constructed in the prostate.
Prostaglandins are made by two different pathways(Cyclooxygenase and Lipoxygenase), and considering prostaglandins are a group of about 20 lipid cells, they have contrary function; responsible for stimulating as well as alleviating inflammation(Inflammation stimulation is the rapid metabolism of them expelled through the bronchials), regulate blood flow to particular organs, control ion transport across membranes, modulate synaptic transmission, induce sleep, mediate lipid release, and regulate metabolism is various tissue.
Prostaglandins are synthesized from arachidonate(Lipoxygenase which catalyze the dioxygenation of polyunsaturated fatty acids) in the cell membrane by the action of phospholipase A2. Cyclooxygenase and lipoxygenase pathways, compete with one another to form prostaglandins(as well as thromboxane or leukotriene-leukotriene being a bronchial stimulator),
In the cyclooxygenase pathway, the prostaglandins D, E and F plus thromboxane and prostacyclin are made. Thromboxanes are made in platelets and cause constriction of vascular smooth muscle and platelet aggregation
Leukotrienes are made in leukocytes and macrophages via the lipoxygenase pathway. They are potent constrictors of the bronchial airways. They are also important in inflammation and hypersensitivity reactions as they increase vascular permeability.
Being that prostaglandins from either pathway, are still fatty acids of a group, they mediate lipid release and controll tissue metabolization, so fat burning is a luxerry of either pathway of formation. It's the pathway from which they are constructed that dictates "fina cough". As prostaglandins made from the Cyclooxygenase pathway dictate muscle constriction and platlet aggregation, and the Lipoxygenase pathway dictates bronchial constriction(the main form of expulsion)
Refs:
Cackatoo Press
Columbia Encyclopedia 6th Edition
Science Daily Magazine
--------------------------------------------------------
Therefore,
Trenbolone causes the rate of production of prostaglandins to rise.
Leukotrienes are synthesized in the cell from arachidonic acid by 5-lipoxygenase. The catalytic mechanism involves the insertion of an oxygen moiety at a specific position in the arachidonic acid backbone.
The lipoxygenase pathway is active in leukocytes, including mast cells, eosinophils, neutrophils, monocytes, and basophils. When such cells are activated, arachidonic acid is liberated from cell membrane phospholipids by phospholipase A2, and donated by the 5-lipoxygenase-activating protein (FLAP) to 5-lipoxygenase.
5-Lipoxygenase (5-LO) uses FLAP to convert arachidonic acid into 5-hydroperoxyeicosatetraenoic acid (5-HPETE), which spontaneously reduces to 5-hydroxyeicosatetraenoic acid (5-HETE). The enzyme 5-LO acts again on 5-HETE to convert it into leukotriene A4 (LTA4), an unstable epoxide.
Leukotrienes cause allergy sympto in the lungs such as wheezing and shortness of breath.
Singulair (Montelukast), a common allergy medication, is a Leukotriene Modifier. It blocks the Leukotriene receptors in your lungs, eliminating trenbolone sides such as wheezing and shortness of breath.
Put simply, taking Singulair, or certain other Leukotriene modifiers will block the "tren cough", and cardio problems.
by,
kyle486
So below, a brief dicription of prostoglandins and their role in fat burning, "fina cough", and why a person going through Tren administration can experience it's fat burning effects without the dreaded "Cough"
The term prostaglandin comes from the word-Prostate. The first prostoglandins were first dicovered in semen about the mid 1930's and it was thought that prostaglandins were made from the prostate. Since this time, it has been dicovered that most prostaglandins are not even constructed in the prostate.
Prostaglandins are made by two different pathways(Cyclooxygenase and Lipoxygenase), and considering prostaglandins are a group of about 20 lipid cells, they have contrary function; responsible for stimulating as well as alleviating inflammation(Inflammation stimulation is the rapid metabolism of them expelled through the bronchials), regulate blood flow to particular organs, control ion transport across membranes, modulate synaptic transmission, induce sleep, mediate lipid release, and regulate metabolism is various tissue.
Prostaglandins are synthesized from arachidonate(Lipoxygenase which catalyze the dioxygenation of polyunsaturated fatty acids) in the cell membrane by the action of phospholipase A2. Cyclooxygenase and lipoxygenase pathways, compete with one another to form prostaglandins(as well as thromboxane or leukotriene-leukotriene being a bronchial stimulator),
In the cyclooxygenase pathway, the prostaglandins D, E and F plus thromboxane and prostacyclin are made. Thromboxanes are made in platelets and cause constriction of vascular smooth muscle and platelet aggregation
Leukotrienes are made in leukocytes and macrophages via the lipoxygenase pathway. They are potent constrictors of the bronchial airways. They are also important in inflammation and hypersensitivity reactions as they increase vascular permeability.
Being that prostaglandins from either pathway, are still fatty acids of a group, they mediate lipid release and controll tissue metabolization, so fat burning is a luxerry of either pathway of formation. It's the pathway from which they are constructed that dictates "fina cough". As prostaglandins made from the Cyclooxygenase pathway dictate muscle constriction and platlet aggregation, and the Lipoxygenase pathway dictates bronchial constriction(the main form of expulsion)
Refs:
Cackatoo Press
Columbia Encyclopedia 6th Edition
Science Daily Magazine
--------------------------------------------------------
Therefore,
Trenbolone causes the rate of production of prostaglandins to rise.
Leukotrienes are synthesized in the cell from arachidonic acid by 5-lipoxygenase. The catalytic mechanism involves the insertion of an oxygen moiety at a specific position in the arachidonic acid backbone.
The lipoxygenase pathway is active in leukocytes, including mast cells, eosinophils, neutrophils, monocytes, and basophils. When such cells are activated, arachidonic acid is liberated from cell membrane phospholipids by phospholipase A2, and donated by the 5-lipoxygenase-activating protein (FLAP) to 5-lipoxygenase.
5-Lipoxygenase (5-LO) uses FLAP to convert arachidonic acid into 5-hydroperoxyeicosatetraenoic acid (5-HPETE), which spontaneously reduces to 5-hydroxyeicosatetraenoic acid (5-HETE). The enzyme 5-LO acts again on 5-HETE to convert it into leukotriene A4 (LTA4), an unstable epoxide.
Leukotrienes cause allergy sympto in the lungs such as wheezing and shortness of breath.
Singulair (Montelukast), a common allergy medication, is a Leukotriene Modifier. It blocks the Leukotriene receptors in your lungs, eliminating trenbolone sides such as wheezing and shortness of breath.
Put simply, taking Singulair, or certain other Leukotriene modifiers will block the "tren cough", and cardio problems.
by,
kyle486
