Following a glycogen-depleting bout of exercise, trained individuals can resynthesize muscle glycogen more rapidly and to a greater extent than untrained individuals, likely due to a greater GLUT-4 level allowing more glucose transport. The difference in glycogen synthase activity did not appear to be the major factor here. Although the Glycogen synthase I activity was two times higher in the trained subjects immediately after exercise it was not statistically significant. GLUT-4, on the other hand, accounted for 44% of the variance in glycogen accumulation compared to glycogen synthase I accounting for only 27% of the accumulation. During the study it was found that over the elapsed time of 0 to 72 hours after exercise, the rate of glycogen accumulation was correlated with the GLUT-4 concentration in the muscle. It has been found that type I fibers are associated with high GLUT-4 levels and rapid glycogen accumulation and was speculated that fiber types may have affected the results of the study. This reasoning was proven wrong by another study that came to the same conclusion, of higher glycogen rates in trained than untrained rats.

Glucose levels in the blood were lower in the trained individuals because of greater glucose transport into the muscle. There was also less insulin in the blood stream; this is because exercise training helps enhance insulin action after exercise. Then not only are you able to exercise longer without getting sore muscles you are also using less insulin after you finish exercising. So during the first 6 hours after exercise the rate of glucose accumulation was still high.

Many studies have shown that muscle damage can have negative effects on glycogen accumulation, insulin sensitivity, and GLUT-4. Muscle damage did not occur in this study because:

1. Exercise on a cycle ergometer has a low eccentric component
2. The untrained subjects performed a one hour bout of exercise on the cycle ergometer 3 wk before the glycogen depletion bout of exercise, which would have reduced muscle damage during the subsequent depletion ride
3. Although plasma CK values in untrained subjects were higher 48/72 h after exercise compared with pre-exercise values, these 48/72-h values were not significantly higher than in trained subjects, did not correlate with glycogen accumulation at these time points and were not out of the normal range. (Hickner et al.)

There is little muscle damage related to using a cycle, the subjects were exercised before the study began to reduce the amount of damage, and that plasma CK, which is a marker for muscle damage, was not found to be higher in the untrained than the trained and were not related with glycogen accumulation at these specified times.

The glycogen accumulation rates of the trained and untrained subjects between 6 to 48/72 hours were not significantly different. The time between 6-48/72 hours is called the slow phase because most of the glycogen accumulation happens in the first 6 hours. The trained already had higher levels because of the initial accumulation rates in the first 6 hours were greater than the untrained. So there was not a significant difference between the two groups during the slow phase. Glycogen supercompensation, accumulating glycogen over and above the initial levels already in the muscle, could not be determined because tests on the muscles were not performed until after exercise when they could not test for original levels of glycogen, which would have been tested before exercising began.

In the period of 48/72 hours after exercise the mean muscle glycogen concentration in the untrained subjects was 99 mmol/kg, which is in the normal resting range of muscle glycogen (80-100 mmol/kg). But the mean muscle glycogen concentration at 72 hours for the 3 untrained that consumed the diet for 3 days after exercise was 130 mmol/kg, only because the other 3 untrained weren't tested at 72 hours. Overall, the untrained values were always lower than the trained values, which means that the trained always had higher levels of glycogen even at normal resting ranges.

"We conclude that endurance training results in an increased ability to accumulate muscle glycogen after exercise and that this increase is associated with increased GLUT-4 content in trained muscle. This adaptation to training should be beneficial for performance of daily bouts of glycogen-depleting exercise." (Hickner et al.)

Q. Why do we want enhanced insulin action?
A. Enhanced insulin action would increase glucose transport and glycogen synthesis following a glycogen-depleting bout of exercise. As the study showed, the trained individuals were able to replete muscle glycogen stores more rapidly and to a greater extent than were the untrained individuals. As glycogen levels are thought to be an important factor in determining long-term exercise performance, these greater glycogen stores in muscle of the trained individuals would be of advantage during the subsequent exercise bout.

Q. Why do the results have to be statistically different?
A. This is needed to ensure that any differences are real and not due to random chance.