Clenbuterol HCl belongs to a class of drugs known as beta-2 adrenergic agonists. Its primary known mechanism of action is on the beta-2 adrenergic receptor, also known as ADRB2.  Beta-2 adrenergic agonists are primarily used to treat asthma and other pulmonary/respiratory disorders. Other long-acting beta-2 adrenergic agonists include salmeterol, formoterol, and bambuterol. Clenbuterol has been popularized in the public mind recently by media portrayals of off-label use for fat loss, as well as some professional athlete doping scandals involving the drug.
Clenbuterol has diverse effects, some of them through unknown mechanisms. In a study on mice with no beta-2 adrenergic receptor gene, various doses of clenbuterol stimulated glucose uptake as measured in the soleus muscle independent of any beta-2 adrenergic agonist activity. Clenbuterol not only increases skeletal muscle hypertrophy, it also attenuates muscle-wasting from disuse; this effect is apparently not mediated by locally produced
Although clenbuterol is not a steroid hormone, it possesses anabolic properties that increase muscle mass. Its longer duration of action compared to other beta2-agonists (such as albuterol) make it a desired agent for body-building because of its high and prolonged serum level. The mechanism for the short and long-term cardiovascular complications of clenbuterol is complex. The anabolic effects of clenbuterol are associated with its beta2-adrenoreceptor agonist activity on striated skeletal muscles. In addition, clenbuterol promotes lipolysis through adipocyte beta3-adrenoreceptors.  This conclusion from a study on convalescing heart patients gives a glimpse into clenbuterol’s temptation as a performance-enhancing drug for professional athletes:
Clenbuterol, a beta(2)-agonist with potent anabolic properties, has been shown to improve skeletal muscle function in healthy subjects, and in high doses, promotes cardiac recovery in patients with left ventricular assist devices. In a small, randomized controlled study, we investigated the effect of clenbuterol on skeletal muscle function, cardiac function, and exercise capacity in patients with chronic heart failure. Clenbuterol was well tolerated and led to a significant increase in both lean mass and the lean/fat ratio. Maximal strength increased significantly with both clenbuterol (27%) and placebo (14%); however, endurance and exercise duration decreased after clenbuterol. Prior data support combining exercise training with clenbuterol to maximize performance, and on-going studies will evaluate this approach. 
…however, any off-label use, particularly without the supervision of a medical professional, carries with it a significant risk of misapplication, overdose, or inability to manage or mitigate undesirable effects. Partly because clenbuterol is dosed in micrograms, emergency room reports of the aforementioned problems abound; this, and the doping potential, have resulted in numerous FDA reports on the drug. The following is excerpted from a report by Daubert et al on a bodybuilder who checked himself into the emergency room after a “ten-fold dosing error” of Ventipulmin, a veterinary brand of clenbuterol syrup:
The patient’s urine was negative for any drugs of abuse. Clenbuterol levels were not obtained. A second ECG, 16 hours post ingestion, reflected atrial fibrillation with a ventricular rate of 125 to 147 bpm. On hospital day 3, he was electively cardioverted to sinus rhythm; heart rate and rhythm returned to normal, and he was discharged with oral metoprolol. 
The long duration of these effects is, of course, due to clenbuterol’s 39-hour half-life in the body, another aspect likely to be overlooked by those casually using or abusing the drug without proper medical knowledge or support from a professional.
Because long-term administration of clenbuterol and some other beta-agonists results in various detrimental effects, these drugs offer a potent approach for shorter-term treatment as long as the side-effects are managed and taken into account. Ironically, they are probably not suitable for asthma treatment in most patients, at least not as a stand-alone option, a first choice or, preferably for long-term use. Prather et al write that “If this category of drugs does preserve lean mass in humans, there are legitimate medical applications. Trials of efficacy and safety are needed,” but also that “[t]he rate of extrapolation from animal studies to unsupervised human usage is alarming.
On management of skeletal muscle-wasting, the most compelling but least-studied (in actual human subjects), Ryall and Lynch write:
Stimulation of the pathway with beta-adrenoceptor agonists (beta-agonists) has therapeutic potential for muscle wasting disorders including: sarcopenia, cancer cachexia, disuse and inactivity, unloading or microgravity, sepsis and other metabolic disorders, denervation, burns, HIV-AIDS, chronic kidney or heart failure, and neuromuscular diseases. However, there are also pitfalls associated with beta-agonist administration and clinical applications have so far been limited, largely because of cardiovascular side effects. In rats and mice, newer generation beta-agonists (such as formoterol) can elicit an anabolic response in skeletal muscle even at very low doses, with reduced effects on the heart and cardiovascular system compared with older generation beta-agonists (such as fenoterol and clenbuterol). However, the potentially deleterious cardiovascular side effects of beta-agonists have not been obviated completely and so it is important to refine their development and therapeutic approach in order to overcome these obstacles.