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 undertaken by Ngala, et al, on knockout 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.  Yimlamai et al write that clenbuterol not only increases skeletal muscle hypertrophy, it also attenuates muscle-wasting from disuse; this effect is apparently not mediated by locally produced IGF1. 
According to Spurlock et al, "Beta-adrenergic receptor agonists (BA) induce skeletal muscle hypertrophy, yet specific mechanisms that lead to this effect are not well understood."  Research into the matter by Spurlock et al concluded that the documented BA-induced skeletal muscle hypertrophy occurs through a complex and diverse array of pathways:
Global evaluation of gene expression after administration of clenbuterol identified changes in gene expression and overrepresented functional categories of genes that may regulate BA-induced muscle hypertrophy. Changes in mRNA abundance of multiple genes associated with myogenic differentiation may indicate an important effect of BA on proliferation, differentiation, and/or recruitment of satellite cells into muscle fibers to promote muscle hypertrophy. Increased mRNA abundance of genes involved in the initiation of translation suggests that increased levels of protein synthesis often associated with BA administration may result from a general up-regulation of translational initiators. Additionally, numerous other genes and physiological pathways were identified that will be important targets for further investigations of the hypertrophic effect of BA on skeletal muscle. 
Daubert et al write on the anabolic and lipolytic properties of clenbuterol:
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 performed by Kammalakkannan et al 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:
His electrocardiogram (ECG) demonstrated supraventricular tachycardia with a ventricular rate of 254 bpm. Esmolol was recommended for rate control after the unsuccessful use of adenosine and diltiazem. ...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. 
 NCBI Entrez Gene: ADRB2. Adrb2 adrenergic receptor, beta 2 ( Musmusculus ). http://www.ncbi.nlm.nih.gov/gene/11555
 Ngala RA, O'Dowd J, Wang SJ, Stocker C, Cawthorne MA, Arch JR. Br J Pharmacol. Beta2-adrenoceptors and non-beta-adrenoceptors mediate effects of BRL37344 and clenbuterol on glucose uptake in soleus muscle: studies using knockout mice. 2009 Dec;158(7):1676-82.
 Spurlock DM, McDaneld TG, McIntyre LM. Changes in skeletal muscle gene expression following clenbuterol administration. Department of Animal Sciences, Iowa State University, Ames, IA, USA. firstname.lastname@example.org
 Kamalakkannan G, Petrilli CM, George I, LaManca J, McLaughlin BT, Shane E, Mancini DM, Maybaum S. Clenbuterol increases lean muscle mass but not endurance in patients with chronic heart failure. J Heart Lung Transplant. 2008 Apr;27(4):457-61.
 Daubert GP, Mabasa VH, Leung VW, Aaron C. Acute clenbuterol overdose resulting in supraventricular tachycardia and atrial fibrillation. J Med Toxicol. 2007 Jun;3(2):56-60.
 Yimlamai T, Dodd SL, Borst SE, Park S. Clenbuterol induces muscle-specific attenuation of atrophy through effects on the ubiquitin-proteasome pathway. J Appl Physiol. 2005 Jul;99(1):71-80. Epub 2005 Mar 17.
 Prather ID, Brown DE, North P, Wilson JR. Clenbuterol: a substitute for anabolic steroids? Med Sci Sports Exerc. 1995 Aug;27(8):1118-21.
 Ryall JG, Lynch GS. The potential and the pitfalls of beta-adrenoceptor agonists for the management of skeletal muscle wasting. Pharmacol Ther. 2008 Dec;120(3):219-32. Epub 2008 Sep 16.
*The latter article is intended for educational / informational purposes only. THIS PRODUCT IS INTENDED AS A RESEARCH CHEMICAL ONLY. This designation allows the use of research chemicals strictly for in vitro testing and laboratory experimentation only. Bodily introduction of any kind into humans or animals is strictly forbidden by law.