I was recently asked "What do you think is the contributing issue with Tren cough immediately after injection? What do you think are some ways to help avoid the issue from surfacing in the first place?"
Over the years I have read various theories from prostaglandin metabolization to pulmonary oil microembolism. I imagine that the causes of "Tren Cough" are varied and it's not always just because of one thing.
I personally have experienced "Tren Cough" on numerous occasions. The symptoms immediately followed a deep IM injection of Trenbolone Acetate. Within seconds after the injection I began having trouble breathing. My airways felt restricted and my eyes began to water from violent coughing that would not relieve the effect. I felt pressure on my chest and had to mentally calm myself during the episode. This violent fit of coughing lasted roughly 2-3 minutes. Towards the end of the episode I felt a bit dizzy or faint. My airways then began to clear and I began to feel relief. It was a scary experience even though I knew about this reaction from reading about it previously. This experience felt life threatening so those who experience it without any prior knowledge must feel very alarmed.
I have noticed that "Tren Cough" seems to happen mostly with the acetate ester and for me personally with higher mg/ml concentrations. I have also noted that "Tren Cough" seems to happen with more frequency when the final product has been converted from Finaplix cattle implants. This may lend support to theories that impurities are a partial cause.
Interestingly, one day I was injecting prescription Testosterone Cypionate into my gluteal muscle IM and I experienced the exact same symptoms as "Tren Cough". The reaction was violent and severe. It was an identical reaction as before. This lends support to the pulmonary oil microembolism theory. I have since had several more minor episodes that were similar but shorter in duration after Testosterone injections.
In 2009 I began experimenting with Subcutaneous (SC) testosterone injections. After I administered a several week course of Testosterone SC I then tried administering Trenbolone acetate subcutaneously. During this next several weeks experiment I had absolutely no "Tren Cough" This may be a suitable method for avoiding "Tren Cough".
SC injections have a slower onset of action in comparison to IM. This slowing of absorption into the blood stream is likely one of the factors that mitigates "Tren Cough" when using this type of injection.
The following abstract offers the pulmonary oil microembolism theory.
Hum Reprod. 1995 Apr;10(4):862-5.
Tolerability of intramuscular injections of testosterone ester in oil vehicle.
Mackey MA, Conway AJ, Handelsman DJ.
Andrology Unit, Royal Prince Alfred Hospital, Sydney NSW, Australia.
We undertook a prospective survey of the tolerability of deep i.m. injections of testosterone enanthate in a castor oil vehicle, the most widely used form of androgen replacement therapy. Over a period of 8 months, 26 men received 551 weekly injections into the gluteal, deltoid or thigh muscle and side-effects were recorded immediately and 1 week after each injection by the same nurse using a standardized questionnaire. Most injections caused no complaints [389/551, 70.6% (95% confidence interval 66.6-74.4%)] but minor local side-effects, mostly pain and bleeding, were common [162/551, 29.4% (25.6-33.4%)]; no serious side-effects were observed. Considering all side-effects, the gluteal site had fewer complaints and was less prone to bleeding but was painful more often than deltoid or thigh injection sites. The laterality of injection at any site had no significant effect on side-effects. The only systemic side-effect was episodes of sudden-onset, non-productive cough associated with faintness following eight injections [1.5% (0.6-2.9%)] which we speculate may have been due to pulmonary oil microembolism. We conclude that, when administered by an experienced nurse, deep i.m. injection of testosterone enanthate in a castor oil vehicle is generally safe and well tolerated but causes relatively frequent minor side-effects, including pain and bleeding. An improved depot form of testosterone would be highly desirable for androgen replacement therapy and hormonal male contraception.
PMID: 7650133 [PubMed - indexed for MEDLINE]
The following explaination below appears at http://www.basskilleronline.com/tren_cough.shtml
Tren Fat burning and fina cough both from prostaglandin metabolization
"-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)"