Choline is an essential nutrient that supports the athletic individual through its role as the precursor of a neurotransmitter, membrane phospholipids, and cellular osmolytes, as well as in methyl-group donation.
These biologic activities are important in muscle performance, recovery from exertion, and in training output.
Choline supports the nervous system that sends signals to exercising muscles. Specifically, choline is a precursor to the neurotransmitter acetylcholine. Choline supports the communication between neurons in the brain and promotes better availability of neurotransmitters for signaling within the brain. Choline also functions as part of phosphatidylcholine, a structural component of the phospholipid membrane of all cells, including glial and neuronal cells. Choline is a precursor to sphingomyelin, which is important to the integrity of neurons and in the metabolism of molecules, including diacylglycerol and ceramide, which function in intracellular signaling.
The level of choline in the brain is directly affected by its levels in plasma, which is supported through dietary intake and supplementation (Wurtman et al, 2009; Babb et al, 2004; Hirsch et al, 1978). Free choline reaches the brain by crossing the blood-brain barrier (Wurtman et al, 2009). Oral intake of choline affects both blood levels of choline and acetylcholine (Hirsch et al, 1978; Cohen and Wurtman, 1975; Cohen and Wurtman, 1976; Zeisel, 1981). In deficiency states, membrane phospholipids and sphingomyelin are broken down so that free choline can support brain functions and provide for its release to the hippocampus (Molinengo et al, 1997). Choline status can also up- or down-regulate the activity of enzymes that synthesize acetylcholine, the neurotransmitter (Cermak et al, 1998). Inadequate choline intake compromises neurotransmission and/or nerve tissue and cellular integrity as the body works to maintain a supply of free choline to the brain.
Maintenance of the nervous system during intense exercise is necessary to drive the continued neural activation of muscles and to delay the onset of "central fatigue", which is associated with periods of sustained muscular usage (Davis, 1996; Meeusen et al, 2006). Decreased choline, and therefore acetylcholine, may be associated with delays in transmission of muscle contraction impulses (Buckman et al, 1999; Zeisel, 1994), enhancing fatigue.
Choline is readily converted by the body to form betaine, an important osmolyte that helps regulate volume changes in cells. Cellular volume changes trigger a series of catabolic and anabolic processes, and need to be regulated (Haussinger, 1996).
Choline is also oxidized in the body to contribute to the cellular "methyl pool". Methyl groups, CH3-, are components that are transferred between biological macromolecules. They are active in numerous metabolic pathways. The methylation of homocysteine converts the cellular metabolite inversely associated with heart health, into an amino acid, methionine. Methionine is involved in muscle building and repair, and is a precursor to other essential metabolic substances, including S-adenosylmethionine. S-adenosylmethionine is involved in the inflammatory response and helps to dispose of cellular homocysteine (James et al, 2002; Detopolou et al, 2008).
Intense and prolonged exercise results in an accumulation of homocysteine in some athletes (Hermann et al, 2003; Joubert and Manore, 2006). Adequate choline supports normal metabolism of homocysteine and regulates its blood levels for optimal health.
Free choline is a precursor to the phospholipid phosphatidylcholine, which is an important component of the structure of very low density lipoproteins (VLDL). The manufacture of VLDL in the liver functions tor package and remove non-polar lipids within the aqueous environment of the blood and moves them away from the liver. VLDLs are the mechanism by which fat is transported to adipose tissue for storage or to the muscles for immediate use (Dumas et al, 2006).
In choline deficiency, there is a decrease in triglyceride export from the liver in VLDLs, resulting in excess fat deposition (steatosis) in that organ (Gruffat et al, 1996). The presence of excess fat in the liver affects its shape, size, and viability (including enzymatic activity) -- leading to liver dysfunction.
Choline deprivation also affects cellular structural integrity and lipid metabolism outside the liver. Cell membranes are catabolized and cellular suicide is activated in muscles without sufficient choline (daCosta et al, 2004). Triglycerides accumulate in choline deficient muscle cells because they are synthesized from the available pool of components (fatty acids, diacylglycerol) scavenged from broken down cell membranes vs. de novo lipogenesis (Michel et al, 2011). Increasing choline directly reverses these effects.
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