Pharmacological Fat Burners always come ‘ after” Caloric Restriction.. after not before and not in place of !
and don’t “over use them” that is where the problems lie..
a small amount of a number of different synergistic compounds, ones that work on different Metabolic Pathways will always be far more effective than the overuse of ” just one pathway” to our goals…
Downside to this model ?
Well there is going to be more moving parts and more to learn ?
Yes the Chronic administration of Clenbuterol significantly downregulated the density of B2 AR in skeletal muscle… but…
Another proof point that just because the chronic administration of Clenbuterol significantly downregulated the density of B2 AR in skeletal muscle.. like by about 50 percent after 18 days…
That does not mean its effect on fat loss are also degraded… they might even be upregulated.
If you can only provide a single proof point for your case… its probably not that strong a case… I have more here than I am going to bore you with..
There is nothing new here .. this is hardly cutting edge stuff.
I just dont read the steroid website for my education of how things work.. so I am not blinded by dogma and Bro Science
“ Thus, it would appear that muscle protein perfusion in both the unstimulated and clenbuterol-stimulated condition is reduced by chronic treatment with the B2-agonist, and this appears to be reflected in the changes in B2-adrenoceptor density.
The methods used to estimate B-adrenoceptor density and subtype in this study have been described in detail and validated previously by ourselves (Rothwell et al., 1985) and others (e.g. Minneman & Molinoff, 1980). The B-receptor density of the microsomal fraction was relatively low in muscle from untreated rats (B,. = 20 fmol mg-‘ protein) compared to heart (154 fmol mg-‘ protein), and density was markedly reduced in both tissues by chronic clenbuterol treatment.
A similar decrease in muscle B-receptor density has been observed in rats treated chronically with isoprenaline (Vallieres et al., 1979). This reduction is consistent with the concept of ‘down-regulation’ of receptors in response to repetitive stimulation (for review see Hertel & Perkins, 1984), and suggests that clenbuterol can influence muscle metabolism and/or blood flow through direct effects on B-adrenoceptors.
It would appear, therefore, that ‘up-regulation’ of receptors accompanies motoneurone activation of muscle metabolism, while ‘down-regulation’ results from humoral activation of metabolism by exogenous adrenoceptor agonists.
So yes I 100 percent agree after the Chronic Administration of Clenbuterol we see a marked downregulation in B2–receptor denisity.. and consequentially in its Anabolic Effect.
However when we use Clenbuterol as a Fat Loss Agent ?
The elevated blood flow to white and brown adipose tissue seen after CHRONIC clenbuterol treatment probably reflects the lipolytic and thermogenic actions of this B2-agonist.
Clenbuterol has been shown to be a potent agonist for brown fat thermogenesis (Winter, 1983) and the tissue has a high density of B2-adrenoceptors (Rothwell et al., 1985).
As well as the chronic increase in brown fat blood flow seen here, there was also a very large response to a single, acute injection of clenbuterol after chronic treatment, with flows reaching values as high as 20 ml g1’min-‘. This suggests that the thermogenic (and perhaps lipolytic) effects of clenbuterol are potentiated by chronic treatment, and would help explain the re-partitioning effects of the agonist on body composition.
Let me repeat that
This suggests that the thermogenic (and perhaps lipolytic) effects of clenbuterol are potentiated by chronic treatment, and would help explain the re-partitioning effects of the agonist on body composition.
The re-partitioning effects are seen as an increase in the lean: fat ratio of the carcass (see Stock & Rothwell, 1986 for review), and could result from decreases in fat deposition independently of any effects of clenbuterol on protein synthesis and deposition.
In conclusion, any effect of clenbuterol on muscle growth which is mediated by increases in blood flow can only be transient, and is not sustained during chronic treatment.
Stop breath and read this line..
Conversely, effects on blood flow to white and brown adipose tissue are sustained and would continue to influence fat and energy metabolism.
” But Bruh you gotta cycle it.. it looses it effect after a couple of weeks. “
Again
Do you mean for its Anabolic Hypertrophic Effect ?
Its effect as a Bronchodilator ?
Or its effect as a Fat Loss Agent ?
Takeway ?
Stop reading Steroid Websites for your Education..
