Supplement Performance - Nitric Oxide Boosters

Cutting-Edge Data from ISSN Conference Proceedings

In humans, multiple cardiovascular regulatory mechanisms have evolved. These mechanisms increase the blood supply to active tissues. Circulatory adjustments are effected by altering the output of the pump (the heart), changing the diameter of the resistance vessels (primarily the arterioles), or altering the amount of blood pooled in capacitance vessels (the veins). The caliber of the arterioles is adjusted in part by autoregulation. However, it’s also increased in active tissues by locally produced vasodilator metabolites. The term vasodilation is generally used to refer to dilation of the resistance vessels.

The endothelium of arterioles contains an enzyme, nitric oxide synthase, which produces nitric oxide (NO) from arginine (amino acid). The NO travels into the smooth muscle cells of the arterioles and activates certain enzymes. This leads to smooth muscle relaxation and thus, vasodilation. Nitroglycerin and other nitro-vasodilators that are of great value in the treatment of angina act in the same manner as NO.

Also, NO plays a prominent role in the production of an erection.¹ NO activates an enzyme called guanylyl cyclase, resulting in increased production of cyclic guanosine monophosphate (cGMP) and cGMP is a potent vasodilator. Injection of inhibitors of NO synthase prevents the erection normally produced by stimulation of the pelvic nerve in experimental animals.¹ Viagra^® inhibits the breakdown of cGMP and has gained worldwide fame for the treatment of impotence.

Recently, nitric oxid boosters (e.g., arginine alpha-ketoglutarate [AKG]) have become popular among serious gym rats. AKG has been purported to increase NO synthesis and thereby enhance blood flow to muscle, in turn leading to greater gains in muscle mass and strength during training.

NO Booster Gets Into the Act

A recent study at the Baylor University (Texas) exercise and sports nutrition lab examined the effects of AAKG supplementation during training on body composition and training adaptations in experienced gym rats.² Thirty-five resistance-trained males were matched according to fat-free mass and randomly assigned to ingest supplements containing either a placebo (fake supplement) or commercial AAKG supplement (MRI´s NO2^®) in a double blind manner. Subjects took four grams of the supplements three times daily (12 grams per day) for eight weeks during standardized training. No significant differences were observed between groups in terms of changes in body mass, fat-free mass, fat mass, or percent body fat. However, changes in bench press one repetition maximum (1-RM) were significantly greater in the AAKG group. According to the authors of this study, results indicate that AAKG supplementation may augment 1-RM strength in response to training, but does not appear to significantly affect body composition.

Another recent study at Baylor´s exercise and sports nutrition lab examined the effects of AAKG supplementation during training on markers of health status.² Again, gym rats took four grams of the supplements three times daily (12 grams per day) for eight weeks during standardized training. Side effects were monitored on a weekly basis. Further, serum and whole blood samples were assayed for a comprehensive panel of clinical health markers. Authors concluded that AAKG supplementation does not appear to adversely affect general markers of health.

The third study at the same lab examined the effects of AAKG supplementation during training on “quality of life” and perceptions about training, health and sexual desire/libido in experienced gym rats.² At zero, four and eight weeks, subjects completed the quality of life questionnaire and a training, health and libido questionnaire. Though non-significant results were reported, a number of interesting trends were observed in response to AAKG supplementation that deserve additional study. As pointed out by the authors, non-significant results could be due to a lack of sample size. The terms “significant” and “non-significant” refer to whether chance may have played a large role in the results of a study. The generally accepted level of significance is P < 0.05, when “P” stands for probability. P is a fraction that expresses the probability that the difference between two means (e.g., placebo group vs. AAKG group) was due to chance variation.

For example, if the P value is 0.10, the probability that the difference was due to chance is 10 percent. When the P value is < 0.05, scientists call the difference “significant” or “statistically significant”, i.e., it’s concluded that the difference is due to the operation of some factor other than chance (e.g., dietary supplementation). It should be noted, however, that statistical significance does not arbitrarily mean physiological significance and the reverse is sometimes true.

Finally, Baylor sports nutritionists examined the effects of ingesting four grams of non-time-released and time-released arginine on blood arginine levels.² Results indicated that non-time-released and time-released arginine supplements have different pharmokinetic patterns that may affect the physiological impact of arginine supplementation.

Bottom Line

AAKG supplementation holds some promise for bodybuilders and other strength-power athletes. AAKG appears to augment 1-RM strength in response to training. Further, AAKG does not appear to adversely affect general markers of health. However, more research is needed before firm conclusions can be drawn.

Protein-Related Bullshit

One of most enduring urban legends in the nutrition world is that high-protein intake destroys your kidneys, liver and bones. Simply stated, that´s a bunch of bullshit! Thus, I recently published a scientific paper entitled “High-protein diets and purported adverse effects: Where is the evidence?” in the