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.
Clenbuterol can induce fat burning via beta-2-adrenergic agonism; it is a highly selective B2 agonist. Via this mechanism, it induces fat burning by increases intra-cellular levels of cyclic AMP which has downstream effects on inducing protein kinase A (PKA) activity  which then acts on hormone sensitive lipase (HSL) and perilipin to mediate lipolysis;  insulin is a negative mediator of this pathway.  PKA may also induce CREB phosphorylation, which is then able to induce JHDM2a (a histone demethylase) promoter activity  and may have downstream influences on PPARα and UCP1, two proteins involved in fatty acid oxidation and uncoupling (respectively).