Luteineizing Hormone Boosting Fungus Cordyceps Sinensis is A Powerful Ergogenic: 1.79-fold Increase in Exercise Endurance in Rodents

Figure 1: Cordyceps sinensis
(photo NW Botanicals)

Would you have suspected that the parasitic relationship between the fungus and the larva of the ghost moth would turn out to be a powerful ergogenic? No? Well, what if I told you that this very "relationship" is the resource of which the commonly known fungus Cordyceps sinensis is derived? Ok, I see you know this one... A very recent study (Kumar. 2011) which was published in the Journal of Ethnopharmacology confirmed earlier study results that have attracted supplement companies to this inconspicuous, yet highly ergogenic fungus from the order of the Hypocreales.

The Indian scientists investigated the effect of 200 mg/kg of air-dried cordiceps powder (human equivalent approx. 33mg/kg) to rats for 15 days. The 24 rats were randomized to one out of four groups: control (C), CS supplemented without exercise (CSS), exercise (E, swimming exercise 1h/day without load) and CS supplemented along with exercise (CSS + E) groups. On day 16 all rats were subjected to a exhaustive swimming protocol, in order to differentiate effects of supplementation / training on exercise performance. The results were quite impressive:

Both CS supplementation and supplementation concurrent with exercise improved exercise endurance by 1.79- (P < 0.05) and 2.9-fold (P < 0.01) respectively as compared to placebo rats. CS supplementation concurrent with exercise also increased the swimming endurance by 1.32-fold (P < 0.05) over the exercise group.

What is yet even more interesting, is the data related to the underlying mechanism(s) of these performance improvements:

To study the molecular mechanism of the observed effect, we measured the expression levels of endurance responsive skeletal muscle metabolic regulators AMPK, PGC-1α and PPAR-δ as well as endurance promoting and antioxidant genes like MCT1, MCT4, GLUT4, VEGF, NRF-2, SOD1 and TRX in red gastrocnemius muscle.

Taken together this molecular changes, which took place in trained and untrained animals, are responsible for an upregulation of skeletal muscle metabolism, angiogenesis, better glucose and lactate uptake, as well as adaptations in the anti-oxidant response to exhaustive exercise.

Figure 2: Chemical structure of Cordycepin, the purported
working ingredient in Cordyceps sinensis (Wikipedia)

Combine these results with the recently confirmed (Leu. 2011) stimulatory effect of cordycepin (fig. 2) on Leyding Cells and, via luteinizing hormone, testosterone production and you have a perfect natural ergogenic.

Leptin & AMPK Activation in Muscle - Did Scientists Investigate the Wrong Species?

Actually, this is something I have been reminding people of for years: Human beigns are no mice and although some people may be rats, genetically they are still very different. Usually I put this argument forward if anyone presents me with a study done on rodents that "shows" how bad dietary protein, especially from meat, is for you - thin of it: when was the last time you saw a mouse eating a cow? This time the issue is a little more sophisticated, though...

Australian scientists (Laker. 2010) have recently investigated the effect of leptin on AMP-activated protein kinase (AMPK) in muscle of sheep and (I do not know if to their, but maybe to some of the proclaimed experts surprise) they found that...

[...] leptin infusion reduced (P<0.05) food intake and body weight and it also increased plasma adrenaline concentration at 6 h and 7 days, suggesting increased sympathetic nerve activity. Despite this, and in contrast to rodent studies, central leptin infusion did not increase skeletal muscle AMPKα Thr172phosphorylation or ACCβ Ser221 phosphorylation.

With sheep being genetically closer to human beings than mice, this is an interesting finding and could possible lead into new insights into why leptin, once proclaimed as possible panacea for the obesity epidemic, does work on rodents, but has little positive effect on obese human beings. Hitherto, the most accepted theory is "leptin resistance", which, similar to insulin resistance, is supposed to prevent leptin from doing its magic. This study, however, suggests that there might be genetic issues involved, as well. As always, I will keep you posted...