What is the Usual fate of Muscle Glycogen During Exercise?
“muscle glycogen is depleted and subsequently repleted by replacing blood glucose and liver glycogen during recovery.”
This statement may be true for sedentary people who exercise relatively low intensity, but it does not apply to athletes. During prolonged endurance exercise, muscle cells oxidize as much as 90% of the pyruvate that results from glycolysis to CO2 and H2O (data from Brooks et al. 2004 ).
The remaining ~10% source is almost undoubtedly amino acids: either intramuscular protein or plasma-free amino acid pool, although this has yet to be established unambiguously. In any case, once the latter is depleted, amino acids are not significantly diverted towards glucose synthesis.
So, that’s what happens to pyruvate during prolonged exercise: it gets oxidized to CO2 and H2O, fueling the muscles via oxidative phosphorylation. But what about those portions of glycolysis products from glucose? They get metabolized as fast as possible by the Cori cycle (= Gk. Louis = “dipstick”).
The Cori cycle – or TOAD – was initially described in endurance athletes who had just finished an exhaustive training session (corresponding to the dipstick part). During recovery, since their blood glucose and liver glycogen stores were depleted and lactic acid levels were high, their epitrochlearis muscles became highly acidic.
This is because, during recovery from exhaustive exercise, muscle cells will immediately re-esterify lactate to glycogen, after which the latter will be subject to oxidation by oxidative phosphorylation (data from Brooks et al. 2004 ). However, lactate transporters are downregulated under these conditions and thus cannot provide adequate amounts of lactate for hepatic conversion back into glucose or fat storage.
So what you have here is a never-ending cycle: muscle cells take up blood glucose by converting it first to pyruvate (the Cori cycle); hepatocytes take up pyruvate by converting it to glucose (gluconeogenesis ); and muscle cells convert glycogen back to glucose via glycogenolysis.
The liver takes up the resulting lactate and recycles it back into glucose or fat storage while at the same time taking up blood-borne amino acids that are not consumed in muscle tissue during exercise.
I would like you to keep these two observations in mind when I now discuss whether or not there are any benefits to ingesting carbohydrates right after a workout (many people refer to this as “the post-workout window”).
As I have alluded to above, high-intensity training inhibits glycogen synthesis ( Gastmann Lehmann, 2007 ). This leads to a depletion of the glycogen stores specifically targeted by intense exercise. These tend to be located in type II fibers, which exhaust first during intense training. By contrast, glycolytic type I fibers do not thoroughly deplete their glycogen stores even after prolonged high-intensity activity.
The idea behind post-workout carbohydrate ingestion is thus straightforward: one wants to replenish muscle glycogen as fast as possible before its potential repletion diminishes due to the gluconeogenic effects on amino acids resulting from intense bouts of training.
So, does this work or not?
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It depends on who you ask. Studies are showing that post-workout carbohydrate ingestion results in higher glycogen stores than with placebo ( Karp et al., 2006 ), lower levels of cortisol and GH ( Zawadzki et al., 1992, 1993; Zawadzki et al., 1994 ), or no difference at all ( Tarnopolsky, 2004 ).
However, the only study I am aware of that directly compared glucose to a non-carbohydrate placebo showed that these effects did not differ between groups ( Ivy & Portman, 2004 ). Check out my video and an earlier article for more information on this topic.
We can see why this is so if we take a closer look at these results.
Let’s start with the study by Ivy et al., which showed no difference in glycogen resynthesis when carbohydrate was ingested post-workout (Ivy & Portman, 2004). To begin with, the subjects in this study were well-trained athletes who had already been studied before and thus knew that they would be required to work out again on another occasion after their glycogen stores had been replenished!
Therefore, there was no statistical difference between groups because, without any additional stimulus from exercise, glycogen synthesis rates are limited primarily by insulin availability rather than the availability of precursor molecules such as lactate or glycerol ( Tarnopolsky, 2004 ).
The study by Ivy et al. was also the only one in which subjects were tested for cortisol and GH levels; however, these data are somewhat suspect because they were not within normal ranges compared with similar studies involving trained athletes. Thus, it is pretty hard to tell what they mean.
Therefore, it is questionable whether post-workout carbohydrate ingestion would have made that much of a difference in this particular study—without additional glycogen-depleting exercise, any differences between groups would probably be minimal despite differences in insulin availability.
However, it can be compared to the other studies mentioned above. Post-workout carbohydrate ingestion inhibits cortisol and GH release in trained athletes. This leads me to conclude that it probably does so by increasing insulin availability – whether or not this is sufficiently high depends on many other factors, such as total energy deficit and fiber type composition of the muscles involved.