During the two 'off' weeks, an ECA stack can be used as required. ECA will not cause such a pronounced down regulation and desensitization of the receptors, certainly not to the extent of clen. Ephedrine has a short half life in contrast to clen which results in times throughout the day where the betas will partially recover from stimulation by adrenaline and nor-adrenaline. Potency is also much weaker that that of clen, as it is not a specific agonist. Ephedrine is also thought to increase the conversion of endogenous/exogenous T4 to T3 through the activation of deiodinase enzymes responsible for this process. This is important as clen is known to slow the rate of T4 to T3 conversion. As a side note, some bodybuilders will use T3 concurrently with the Clenbuterol/ECA cutting cycle (together with certain anabolic/androgenic steroids no doubt!) in an attempt to at least maintain plasma T3 levels.
This process is illustrated by the insulin receptor sites on target cells in a person with type 2 diabetes .  Due to the elevated levels of blood glucose in an overweight individual, the β-cells ( islets of Langerhans ) in the pancreas must release more insulin than normal to meet the demand and return the blood to homeostatic levels.  The near-constant increase in blood insulin levels results from an effort to match the increase in blood glucose, which will cause receptor sites on the liver cells to downregulate and decrease the number of receptors for insulin, increasing the subject’s resistance by decreasing sensitivity to this hormone. [ citation needed ] There is also a hepatic decrease in sensitivity to insulin . This can be seen in the continuing gluconeogenesis in the liver even when blood glucose levels are elevated. This is the more common process of insulin resistance , which leads to adult-onset diabetes.