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needsize said:
Well that's good news!!
Thanks for all the input bros.
Heart problems from roid use?
- Thread starter Muscle Mafia
- Start date
Well that's good news!!
Thanks for all the input bros.
got2getripped
New member
meatneck said:
Loving everything you see!
Yes, its possible.
Androgen Receptors Mediate Hypertrophy in Cardiac Myocytes
James D. Marsh, MD; Michael H. Lehmann, MD; Rebecca H. Ritchie, PhD; Judith K. Gwathmey, VMD, PhD; Glenn E. Green, MD; ; Rick J. Schiebinger, MD
From the Program in Molecular and Cellular Cardiology, Departments of Medicine and Otolaryngology, Harper Hospital, Detroit, Mich; the VA Medical Center, Boston University Medical Center, Boston, Mass (J.K.G.); and the Arrhythmia Center/Sinai Hospital (M.H.L.) and Wayne State University School of Medicine, Detroit, Mich (J.D.M.).
Correspondence to James D. Marsh, MD, Wayne State University School of Medicine, 421 E Canfield Ave, Detroit, MI 48201. E-mail [email protected]
Abstract
Top
Abstract
Introduction
Methods
Results
Discussion
References
Background—The role of androgens in producing cardiac hypertrophy by direct action on cardiac myocytes is uncertain. Accordingly, we tested the hypothesis that cardiac myocytes in adult men and women express an androgen receptor gene and that myocytes respond to androgens by a hypertrophic response.
Methods and Results—We used reverse transcription–polymerase chain reaction methods to demonstrate androgen receptor transcripts in multiple tissues and [3H]phenylalanine incorporation and atrial natriuretic peptide secretion as markers of hypertrophy in cultured rat myocytes. Messenger RNA encoding androgen receptors was detected in myocytes of male and female adult rats, neonatal rat myocytes, rat heart, dog heart, and infant and adult human heart. Both testosterone and dihydrotestosterone produced a robust receptor-specific hypertrophic response in myocytes, determined by indices of protein synthesis and atrial natriuretic peptide secretion.
Conclusions—Androgen receptors are present in cardiac myocytes from multiple species, including normal men and women, in a context that permits androgens to modulate the cardiac phenotype and produce hypertrophy by direct, receptor-specific mechanisms. There are clinical implications for therapeutic or illicit use of androgens in humans.
Androgen Receptors Mediate Hypertrophy in Cardiac Myocytes
James D. Marsh, MD; Michael H. Lehmann, MD; Rebecca H. Ritchie, PhD; Judith K. Gwathmey, VMD, PhD; Glenn E. Green, MD; ; Rick J. Schiebinger, MD
From the Program in Molecular and Cellular Cardiology, Departments of Medicine and Otolaryngology, Harper Hospital, Detroit, Mich; the VA Medical Center, Boston University Medical Center, Boston, Mass (J.K.G.); and the Arrhythmia Center/Sinai Hospital (M.H.L.) and Wayne State University School of Medicine, Detroit, Mich (J.D.M.).
Correspondence to James D. Marsh, MD, Wayne State University School of Medicine, 421 E Canfield Ave, Detroit, MI 48201. E-mail [email protected]
Abstract
Top
Abstract
Introduction
Methods
Results
Discussion
References
Background—The role of androgens in producing cardiac hypertrophy by direct action on cardiac myocytes is uncertain. Accordingly, we tested the hypothesis that cardiac myocytes in adult men and women express an androgen receptor gene and that myocytes respond to androgens by a hypertrophic response.
Methods and Results—We used reverse transcription–polymerase chain reaction methods to demonstrate androgen receptor transcripts in multiple tissues and [3H]phenylalanine incorporation and atrial natriuretic peptide secretion as markers of hypertrophy in cultured rat myocytes. Messenger RNA encoding androgen receptors was detected in myocytes of male and female adult rats, neonatal rat myocytes, rat heart, dog heart, and infant and adult human heart. Both testosterone and dihydrotestosterone produced a robust receptor-specific hypertrophic response in myocytes, determined by indices of protein synthesis and atrial natriuretic peptide secretion.
Conclusions—Androgen receptors are present in cardiac myocytes from multiple species, including normal men and women, in a context that permits androgens to modulate the cardiac phenotype and produce hypertrophy by direct, receptor-specific mechanisms. There are clinical implications for therapeutic or illicit use of androgens in humans.
I am no doctor, but this question keeps coming up and this is what I know. Steroids or not, the left ventricle can enlarge just from BB. This is not uncommon and is called 'hypertrophy' . The heart muscle enlarges like other muscles. So, steroids will potentiate the enlargement. I have not seen studies that show this to be of significant concern. I have this condition and I have not used AAS, just a natural BB. There is also cardiomyopathy, which is the stretching of the ventricle. This is bad as it reduces the elasticity and the pumping ability and may be that this is what the poster is referring to. I have not seen studies that show steroids cause this condition. With all that said, I am sure there is more research out there that can shed light on this. And of course, constant elevated lipids over the long term would not be good for the cardiovascular system. Hope I am not too far off from what is being asked as it has been a long day.
Oh, I guess the other hormone is GH, which has the reputation for potentially enlarging organs. That one I do not have enough knowledge to comment on.
Oh, I guess the other hormone is GH, which has the reputation for potentially enlarging organs. That one I do not have enough knowledge to comment on.
instant.muscle
New member
dont wanna sound like an idiot but can someone giv me a mature response, what is AAS? thx
