The classical CHO-loading protocol (3
) used by endurance athletes in the 1960s and 1970s has been largely replaced by less demanding modified protocols (24
). Modified protocols include a training taper and may or may not begin with a depletion bout of exercise. Using 13
C MRS to follow the time course of muscle glycogen supercompensation, we demonstrated that moderately trained males achieve greater muscle glycogen concentration and maintain it longer when they follow a modified protocol that begins with a depletion exercise bout. We also found that 20 min of moderate cycle exercise can be performed daily while CHO loading without negatively affecting muscle glycogen supercompensation. Specifically, we found that, when exhaustive cycle exercise was performed and followed by a high-CHO diet (~9 g·kg−1
, ~675–745 g CHO/day), muscle glycogen concentration returned to 103% of baseline within 24 h. Consuming this diet for two more days increased muscle glycogen to 138% of baseline. Muscle glycogen repletion slowed over the next 2 days, peaking at 147% of baseline and persisting until the end of study (day 7
). In contrast, the group that performed only 20 min of cycle exercise (decreasing muscle glycogen to 90% of baseline) and ate the same high-CHO diet showed no change in muscle glycogen at 24 h. Muscle glycogen concentration of the nondepletion group peaked at 72 h (124% of baseline) and was not different from baseline on day 7
. These results agree with earlier findings (2
) that muscle glycogen depletion (i.e., exhaustive exercise) affects the initial rate of muscle glycogen synthesis and the level of repletion (4
Several studies have suggested that when muscle glycogen is severely depleted, glycogen resynthesis is markedly activated (6
). Muscle biopsy studies (6
) have found that when glycogen concentration in the vastus lateralis is decreased to 66–70 mmol/kg wet wt, glycogen synthase activity increases rapidly (6
). More recent studies using MRS reported an increase in the resynthesis rate when muscle glycogen was decreased to 30–40 mmol/l, or 25% of baseline (29
). These findings agree with the rapid glycogen synthesis observed in our depletion group, whose mean postexercise muscle glycogen was 38 ± 6 mmol/l.
Glycogen synthase activity is increased by conversion of its D form to the active I form (8
). Glycogen repletion after exercise is biphasic (21
) and is controlled by the rates of glucose transport and disposal. During the early rapid phase (0–6 h postexercise), glucose transport across the muscle membrane is maximally stimulated and insulin independent (29
). Originally attributed to a “local factor” present in the muscle after exercise (3
), it is now known to result from the translocation of an intracellular pool of the GLUT4 isoform of glucose transporter proteins (9
), possibly secondary to activation of AMP-activated protein kinase (1
). Ren et al. (30
) reported a rapid increase in the number of GLUT4 glucose transport receptors in rats in response to prolonged exercise. Kua et al. (23
) reported that this increase in GLUT4 protein is controlled by both pretranslational and posttranslational mechanisms. This may explain why the depletion group achieved and maintained significantly greater muscle glycogen than the nondepletion group. When provided sufficient glucose, muscle glycogen synthesis continues during the slow phase (6–72 h) so that pre-exercise levels of glycogen can be reached by 24 h. Muscle glycogen can exceed normal levels by 72 h if a high-CHO diet is consumed and exercise is limited. It is well established that, during the slow phase, muscle glycogen can reach 1.5–2.0 times resting levels (16
); however, only a few studies have previously monitored muscle glycogen content longer than 72 h of CHO loading (11
Our second finding has practical applications for competitive endurance athletes who may prefer exercise to rest while CHO loading. Previous research suggests there may be trade-offs associated with continuing training while attempting to achieve and maintain glycogen supercompensation. For example, because the rate of muscle glycogenolysis is most rapid during the early minutes of exercise, even 20 min of moderate-intensity (60–75% O2 peak
) exercise can significantly decrease muscle glycogen by 30–58% (1
). Rapid rates of glycogenolysis also occur with high exercise intensity and high initial muscle glycogen concentrations. In a study comparing two modified CHO-loading protocols (5
), the muscle glycogen of well-trained endurance runners did not differ when they performed 40 min of “easy” daily running instead of resting while CHO loading. Because these researchers did not report the intensity of the exercise or the amount or timing of the postexercise CHO intake, it is difficult to directly compare our findings.
In our study, subjects used only 10–15% of their muscle glycogen during 20 min of daily cycle exercise at 65% O2 peak
. The rate of glycogen resynthesis is maximal during the first 1–2 h postexercise (29
), and maximum resynthesis occurs when 1.5 g glucose/kg body wt is consumed during this period (17
). By consuming a CHO supplement (1.4 g glucose/kg body wt) immediately after exercise, within 24 h our subjects had replaced all of the muscle glycogen used during daily exercise. This demonstrates that an athlete can exercise daily during CHO loading without negatively affecting muscle glycogen supercompensation.
Metabolic and hormonal responses of our subjects were typical for the exercise stress and dietary conditions. The 2-h depletion exercise significantly increased plasma levels of fatty acids and triglycerides consistent with increased lipolysis. Elevated plasma fatty acid levels at 2 h typically occur with endurance exercise combined with glycogen sparing and the absence of lactate accumulation (32
). Plasma lactate levels <2 mM at 2 h indicate that subjects exercising at 65% O2 peak
were below their “lactate threshold.” However, the postsprint plasma lactate concentrations indicate a significant involvement of anaerobic glycolysis. During the first 2 h of cycle exercise, insulin decreased and glucagon increased significantly to maintain glucose availability and was unchanged after the sprints. The hormonal responses of our subjects (e.g., increased plasma epinephrine, norepinephrine, cortisol, and growth hormone) after cycling 2 h at 65% O2 peak
and after the series of intense sprints are consistent with changes typically seen after prolonged exhaustive exercise (32
). There were no significant differences between treatment groups in insulin sensitivity as estimated by homeostasis model assessment-estimated insulin resistance at any point in the study.
CHO-loading studies generally do not measure muscle glycogen in every subject each day, nor do they study the maintenance of supercompensated muscle glycogen. We previously reported that supercompen-sated muscle glycogen can persist for ≥3 days after completion of a classical CHO-loading protocol, if subjects abstain from exercise (11
). The current study is an extension of that work and profiled muscle glycogen during and after subjects completed two modified CHO-loading protocols, which included 20 min of daily cycle exercise.
The potential military application of CHO loading involves possible conditions that would not occur in sports. The most obvious is that missions can be delayed for a variety of reasons and the CHO-loaded personnel may be required to wait several days before deploying. Athletic endurance events, however, are postponed for only minutes, not days. Thus, unlike the sports athlete, military special operations personnel may need to maintain glycogen supercompensation and avoid physical detraining during the period of postponement. The findings of this study may, however, have application to the recreational athlete who could benefit by knowing the time profile of peak muscle glycogen and the effect of daily exercises on super-compensated muscle glycogen.
In conclusion, we have demonstrated that modified CHO-loading protocols that begin with an exhaustive depletion exercise achieve greater muscle glycogen concentrations that will persist longer than nondepletion protocols (e.g., training taper). These findings agree with earlier studies. However, equally important, we demonstrated that 20 min of moderate cycle exercise can be performed daily during all phases of CHO loading. These exercise bouts do not alter the profile muscle glycogen concentrations if a CHO supplement (~1.4 g CHO/kg) is consumed within 30 min after exercise. This suggests that endurance athletes can continue moderate daily exercise while CHO loading and still achieve and maintain muscle glycogen supercompensation.
We thank Carole Franklin, Donna Caseria, and the staff of the Yale/New Haven Hospital General Clinical Research Center for their assistance with this study.