i did some research on this and found a very interesting study that I think you will find to be quite informative and helpful!
Studies have shown that GW1516, an agonist of peroxisome-proliferator-activated receptor δ (PPAR- δ) and
amp-activated
protein kinase can mimic some of the beneficial effects of exercise in skeletal muscle without really exerting an effort to exercise (Narkar et al. 2008). Studies reported that the signaling of AMPK and that of PPAR are interacting which then results to many adaptations in skeletal muscle. This has been shown in treadmill running tests in mice where pathway-specific drugs endurance capacities were targeted. The investigators found out that the PPAR-delta agonist and training synergistically increase the oxidative myofibers and running endurance in adult mice (Narkar et al. 2008). This is the same with the arguments of Wade (2008) who reported that mouse was supercharged to 75% increase endurance when coupled with exercise.
This has been supported by another investigation conducted by Oliveret al. (2001) where they reported that GW1516 increased expression of the reverse cholesterol transporter ATP-binding cassette A1 as observed in cells of the intestine, fibroblasts and macrophages. Furthermore, they reported that the agonist hormone the apolipoprotein A1-specific efflux of cholesterol. When they administered the drug to the middle-aged rhesus monkeys which develops spontaneous adult-onset obesity, they found out that the drug increased the serum high-density lipoprotein cholesterol (79%), which is the good cholesterol. The ratio was between HDLC and total cholesterol was also improved among all doses used. The administration of which is dose-dependent accompanied with decrease in the concentration of low-density lipoproteins. Decrease in the fasting triglycerides was also observed with the rate of 56%. This decrease if further complemented with the decrease in VLDL (50% decrease) when plasma of the monkeys were analyzed. The study then has clearly demonstrated that administration of the GW1516 allowed the rhesus monkeys to maintain glucose concentrations in the normal range despite the fact that they are hyperinsulinemic, suggesting potential clinical applications in treating and managing diabetes (Oliver et al. 2001).
Another hormone or synthetically produce peptide, AICAR, has been shown to cause mice to experience the benefits of exercise without actually doing it. In addition, other studies demonstrated that 44% increase in resistance and endurance was observed in stagnant mouse, and could be tripled when coupled with GW1516 (Goodyear, 2008).
Acadesine (5-amino-1-[ß-D-ribofuranosyl]imidazole-4-carboxamide), also known as AICAR, is a
protein that is an
amp-activated
protein kinase activator (Menasche et al. 1995). It is a prototype hormone which belongs to a newly recognized classification of therapeutic compounds/agents called adenosine-regulating agents because they primarily induce the increase in the local availability of adenosine, especially for the adenosine triphosphate depleted regions or tissues (Gruber et al. 1989). Its structural conformation is shown as the following:
Chemical properties:
Molecular Formula: C9H14N4O5
Molecular Weight: 258.23
Melting Point: 214-2150C
An important characteristic of Aicar is its ability to elicit inhibition for the production of lipids or lipogenesis through increased phosphorylation of acetyl-coA carboxylase (ACC). This has been shown in mice adipocytes when AICAR was administered and an increased activation of the cellular
amp-activated
protein kinase was observed (Sullivan et al. 1994). The same effects have been observed in sedentary mice that have been treated with AICAR for 4 weeks. They observed that there still induced metabolic genes and even enhanced running endurance by 44% (Narkar et al. 2009). This suggests that Aicar can be used to target the PPAR receptors to elicit exercise-like effects and benefits.
Other studies also demonstrated that the effects of Aicar are enhanced when combined with GW1516. This has been demonstrated in the sedentary mice which produced a transcriptional profile that is unique (189 genes). The interesting thing on this is that, most of the genes (52) out of the 189 genes actually overlapped with many of the genes that have been shown to be regulated by exercise. However, the cultures of muscles from mice have also shown that there is a need for the PPAR-delta for the two hormones (AICAR and GW1516) to take effect (Gough et al. 2008).
The chemical reactivity of acadesine was reported to be silent in normal conditions, meaning when ATP concentrations are in the normal levels, but becomes functional when the said phosphate form is decreased (Mullane 1993). Because of its ability to harvest the positive effects of the protective autocoid without the limiting effects associated with using adenosine as the substrate or a congineer of adenosine, it has been exploited and applied in different medical medications to treat illnesses and abnormalities such ischamia and its sequelae. Acadesine was found to protect the organ from injury during the onset of ischemia (Galinanes et al. 1992). This has been shown in preliminary studies in rats suffering from ischemia, Aicar was applied through perfusion; functional recovery from the illness was immediately observed (2.5 hours). It has also been shown that acadesine reacts immediately and hastily with hypochlorous acid (HOCl) which then provides protection over a number of critical biological targets (Bullough et al. 1993). This has been supported by a number of other studies which also concluded that acadesine indeed offers a cardioprotective effects. Such treatments have also been supplemented to human patients who are suffering from ischemia and/or coronary artery bypass grafting (CABG). Furthermore, acadesine has been proven in clinical studies to prevent aggregation of clotting of blood platelets. Also, it improves contractile functioning of the ventricles in postischemic events, decreases the level of free-radical and oxidant-induced cardiac damages (Matthew et al. 1995); however, it was also demonstrated to have no effect in superoxide anions that were generated by xanthine-xanthine oxidase or hydrogen peroxide induced peroxidation (Bullough et al. 1993). In addition, it also allows adherence of the inhibitneutrophil (PMN) to endothelium and inhibits the accumulation of the PMN in the myocardium experiencing ischemia (Levin et al. 1990).
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