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Warlobo Or W6!!
- Thread starter hardbdygrl
- Start date
hardbdygrl
New member
ok NYM i have not said "10 x''s dont call me crazy"
I want to know how this can work to make you leaner!
That was my original question. I know i dont need it,, but theres a lot of things none of us need but we take it,
So now tell me about that stack you are talking about!!! hahaha
I want to know how this can work to make you leaner!
That was my original question. I know i dont need it,, but theres a lot of things none of us need but we take it,
So now tell me about that stack you are talking about!!! hahaha
Food for thought.
ACE inhibitors inhibit angiotensin converting enzyme blocking the conversion of ANG I to ANG II thus blocking the pressor effects of ANG II and release of aldosterone.
In addition, there are direct effects. It appears that ANG II is required for skeletal muscle hypertrophy in response to overload (i.e., lifting weights). See below abstract. Look up the paper for more specifics and mechanisms if you want.
My suggestion is leave the ACE inhibitors for the overweight, hypertensive folks. Don't f**k with it, you're asking for trouble.
W6
ANG II is required for optimal overload-induced skeletal muscle hypertrophy
Scott E. Gordon1,2, Bradley S. Davis1,2, Christian J. Carlson1,2, and Frank W. Booth1,2
1 Department of Integrative Biology and Pharmacology, University of Texas - Houston Health Science Center, Houston, Texas 77030; and 2 Department of Veterinary Biomedical Sciences, University of Missouri, Columbia, Missouri 65211
ANG II mediates the hypertrophic response of overloaded cardiac muscle, likely via the ANG II type 1 (AT1) receptor. To examine the potential role of ANG II in overload-induced skeletal muscle hypertrophy, plantaris and/or soleus muscle overload was produced in female Sprague-Dawley rats (225-250 g) by the bilateral surgical ablation of either the synergistic gastrocnemius muscle (experiment 1) or both the gastrocnemius and plantaris muscles (experiment 2). In experiment 1 (n = 10/ group), inhibiting endogenous ANG II production by oral administration of an angiotensin-converting enzyme (ACE) inhibitor during a 28-day overloading protocol attenuated plantaris and soleus muscle hypertrophy by 57 and 96%, respectively (as measured by total muscle protein content). ACE inhibition had no effect on nonoverloaded (sham-operated) muscles. With the use of new animals (experiment 2; n = 8/group), locally perfusing overloaded soleus muscles with exogenous ANG II (via osmotic pump) rescued the lost hypertrophic response in ACE-inhibited animals by 71%. Furthermore, orally administering an AT1 receptor antagonist instead of an ACE inhibitor produced a 48% attenuation of overload-induced hypertrophy that could not be rescued by ANG II perfusion. Thus ANG II may be necessary for optimal overload-induced skeletal muscle hypertrophy, acting at least in part via an AT1 receptor-dependent pathway.
ACE inhibitors inhibit angiotensin converting enzyme blocking the conversion of ANG I to ANG II thus blocking the pressor effects of ANG II and release of aldosterone.
In addition, there are direct effects. It appears that ANG II is required for skeletal muscle hypertrophy in response to overload (i.e., lifting weights). See below abstract. Look up the paper for more specifics and mechanisms if you want.
My suggestion is leave the ACE inhibitors for the overweight, hypertensive folks. Don't f**k with it, you're asking for trouble.
W6
ANG II is required for optimal overload-induced skeletal muscle hypertrophy
Scott E. Gordon1,2, Bradley S. Davis1,2, Christian J. Carlson1,2, and Frank W. Booth1,2
1 Department of Integrative Biology and Pharmacology, University of Texas - Houston Health Science Center, Houston, Texas 77030; and 2 Department of Veterinary Biomedical Sciences, University of Missouri, Columbia, Missouri 65211
ANG II mediates the hypertrophic response of overloaded cardiac muscle, likely via the ANG II type 1 (AT1) receptor. To examine the potential role of ANG II in overload-induced skeletal muscle hypertrophy, plantaris and/or soleus muscle overload was produced in female Sprague-Dawley rats (225-250 g) by the bilateral surgical ablation of either the synergistic gastrocnemius muscle (experiment 1) or both the gastrocnemius and plantaris muscles (experiment 2). In experiment 1 (n = 10/ group), inhibiting endogenous ANG II production by oral administration of an angiotensin-converting enzyme (ACE) inhibitor during a 28-day overloading protocol attenuated plantaris and soleus muscle hypertrophy by 57 and 96%, respectively (as measured by total muscle protein content). ACE inhibition had no effect on nonoverloaded (sham-operated) muscles. With the use of new animals (experiment 2; n = 8/group), locally perfusing overloaded soleus muscles with exogenous ANG II (via osmotic pump) rescued the lost hypertrophic response in ACE-inhibited animals by 71%. Furthermore, orally administering an AT1 receptor antagonist instead of an ACE inhibitor produced a 48% attenuation of overload-induced hypertrophy that could not be rescued by ANG II perfusion. Thus ANG II may be necessary for optimal overload-induced skeletal muscle hypertrophy, acting at least in part via an AT1 receptor-dependent pathway.
hardbdygrl
New member
Thank you wilson6
and yes dont u just love how i get treated around here?? lol
NYM you are just sooo kind!
and yes dont u just love how i get treated around here?? lol
NYM you are just sooo kind!
N
new@gettinbig
Guest
Bodyfat in the legs are usually the last to go on most women...I would not mess w/ the stuff...keep clean diet...hard training..an eca stack, some HIIT training and they dial in usually the last 4 weeks before a show etc...most women experience this so you are not alone trust me
monstertruck
New member
I have high blood pressure and was treated with captopril for about 6 yrs. Only started weight training seriously 3 years ago, and went off the captopril about 6 months ago (after a sudden allergic reaction - my tongue swelled to twice the size of my head and that's all the docs could blame it on). In the six months since I've been off (now on a beta blocker) I've seen no difference, and I'm dieting pretty strictly. I say stay away from it too
Captopril work by the same mechanism as yohimbine with one big difference yohimbine blocks the A2 receptor while ace inhibitors causes rceptor suicide and no replacement so overtime you have fewer a2s fighting your Beta2 recetors.
As for your lower bodyfat you might try nolvodex, yohimburn or if you want to go really not injectable yohimbine.
Hope this helps Late......
As for your lower bodyfat you might try nolvodex, yohimburn or if you want to go really not injectable yohimbine.
Hope this helps Late......
Captopril work by the same mechanism as yohimbine with one big difference yohimbine blocks the A2 receptor while ace inhibitors causes rceptor suicide and no replacement so overtime you have fewer a2s fighting your Beta2 recetors.
As for your lower bodyfat you might try nolvodex, yohimburn or if you want to go really not injectable yohimbine.
Hope this helps Late......
As for your lower bodyfat you might try nolvodex, yohimburn or if you want to go really not injectable yohimbine.
Hope this helps Late......
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