The Alanine-Glucose Cycle: Relevance to the Effects of Exercise on the Brain

The authors of this article [Roe and Mochel, 2006: (http://www.ncbi.nlm.nih.gov/pubmed/16763896)] discussed the fact that skeletal-muscle myocytes normally export some alanine (ALN) and glutamine (GLN) and that the liver may utilize significant amounts of that ALN and GLN. Roe and Mochel (2006) referred to the process as being the "alanine cycle," and the process is also known as the "alanine-glucose cycle." Roe and Mochel (2006) noted that the ALN cycle is a "one-way street" that allows for alanine to be exported from the skeletal muscles and utilized by the liver as a precursor of pyruvate, particularly during strenuous exercise. Exercise is known to increase serum ALN, but that's obviously only one effect that occurs during some types of exercise. Evans et al. (2004) found that the intravenous infusion of L-ALN (that's not the same as beta-alanine, and beta-alanine supplementation can produce symptoms of neuropathy at relatively low dosages, in some cases [Harris et al., 2006: (http://www.ncbi.nlm.nih.gov/pubmed/16554972)]) improved some measures of cognitive functioning in nondiabetic people who were being made artificially hypoglycemic, but it's not clear if the effects were solely due to the entry of ALN into the brain or if the ALN-induced elevations in plasma lactate contributed to the effects [Evans et al., 2004: (http://www.ncbi.nlm.nih.gov/pubmed/15089788)]. Incidentally, oral GLN reliably elevates plasma ALN, and, as a representative article, Déchelotte et al. (1991) found that jejunally-administered GLN elevated plasma ALN in humans [Déchelotte et al., 1991: (http://www.ncbi.nlm.nih.gov/pubmed/1903599)].

That capacity of the skeletal muscles to export GLN and ALN is likely to be relevant to research on the effects of exercise on the brain. These articles don't show the effect as unequivocally as some other articles do [Dalsgaard et al., 2004: (http://jp.physoc.org/content/554/2/571.full)(http://www.ncbi.nlm.nih.gov/pubmed/14608005?dopt=Abstract); Kemppainen et al., 2005: (http://jp.physoc.org/content/568/1/323.full)(http://www.ncbi.nlm.nih.gov/pubmed/16037089?dopt=Abstract)], but the utilization of serum lactate during exercise allows the brain to decrease glucose utilization, and that means that the oxidation of lactate in astrocytes and neurons can exert a "glucose-sparing" effect. It's fairly clear to me that the utilization of lactate becomes more significant during high-intensity exercise than during low-intensity exercise, but the release of lactate from the muscles is also higher. Resistance exercise is likely to ultimately, in the long term, allow the muscles to export substantially more ALN and lactate and GLN than endurance exercise is, and I'm talking about the postexercise period and in the fasted state. Endurance exercise tends to not increase muscle mass (as in the percent lean body mass) very much, and an increase in the efficiency of something like the ALN-glucose cycle requires, in my opinion, some sort of actual increase in muscle tissue. I've discussed some of the details about resistance exercise in past postings.