I happen to be 30-year-old healthy male who can’t say has trained for a marathon, but if I were then I’d train to build up glycogen in my liver and muscle (1p269). I do this through regular endurance training (1p269) and eating enough carbs to stimulate glycogen synthesis (1p99). Glycogen synthesis happens when plenty of glucose 6-phosphate causes insulin to keep my blood glucose low and the glycogen is stored as a starch for later use (1p99). Liver glycogen, 7 percent of the weight of the liver, helps maintain my blood glucose, and muscle glycogen, 75 percent of total, would be my primary energy source when I start running (1p78). That glycogen is broken down to glucose units by a process of cleaving glycosidic bonds using phosphorolysis called glycogenolysis (1p80). To my body’s inconvenience, however, my glycogen stores are used up after an overnight fast of approximately 12-18 hours (1p256). Glycogenolysis in my muscle and liver will have depleted most if not all my glycogen to give my tissues fuel (1p256)! And I’m a heavy sleeper, so I’d be an early fasting state (1p257).
Glucagon is the hormone that will drive pathways at such a point (1p101). Glucagon kicks in hepatic gluconeogenesis breaking down amino acids from muscle to maintain my plasma glucose (p258), by recycling available lactate provided by red blood cells and muscle, and alanine (turned to pyruvate) from muscle cells, as well as glycerols from lypolysis (1p257;269). If I’m running a morning after a fast, what does my body have to do? My liver may be able to settle with fatty acids from my adipose tissue (although in my case of being too thin, there isn’t too much to go around for beta-oxidation), but my muscles and brain would really want that glucose (1p256;267). Glycolysis would degrade the glucose to pyruvate and, if under aerobic conditions, the pyruvate would be transported to the mitochondria into the TCA cycle; anaerobic conditions owould leave pyruvate converted to lactate (1p82).
Because I’m training as an endurance athlete, I’ d be running short aerobic cycles of 15-minute runs with an exertion below 60 percent VO(2) max and during this time my total fat oxidation would increase attributed to oxidation of muscle triacylglycerols (1p268). Fatty acids would be preferred for any exertion below 50 percent Vo(2) max) (1p269). But with a few, repeated supramaximal sprint bursts and increased exertion to 60-75 percent VO(2) max, then fat can’t be oxidized fast enough and my muscles would have to rely on carbohydrate oxidation (1p268). This is because fatty acids have only two oxygen molecules, not like carbohydrates, which have equal number of oxygen to carbon molecules (1p269). The lack of glycogen can be offset by my body’s acceleration of gluconeogenesis, but without new supply of ingested glucose, then muscle fatigue would set in accompanied by increased lactic acid in the blood due to inadequate oxygen to completely oxidize pyruvate to C02 and H2O (1p269).
To help avoid fatigue, I would be smart to take advantage of eating foods with low-glycemic index carbs before the event as well as an isotonic or hypotonic beverage with a supply of glucose (not slow-absorbing fructose) about 15-20 minutes before training (1p272). After training, I’m free to drink plenty of water and high-glycemic foods to replace glycogen (1p272). A few apples or orange wedges would do the trick (1p272).
Reference List
1. Gropper SS, Smith JL, Groff JL. Advanced Nutrition and Human Metabolism. Belmont, CA: Thomson Wadsworth, 2009.
