Training with low muscle glycogen enhances fat metabolism in well-trained cyclists

Journal Title (Medline/Pubmed accepted abbreviation):  Med. Sci. Sports Exerc.
Year: 2010
Volume: 42
Number: 11
Page numbers: 2046-2055
doi (if applicable):  10.1249/MSS.0b013e3181dd5070

Summary of Background and Research Design

Background:Muscle glycogen is a primary source of fuel during prolonged exercise. High carbohydrate diets can increase stores of muscle glycogen, increasing the amount of time and/or intensity of an athlete’s workout.
                Exercise induces the transcription and translation of various genes in order for the body to adapt to the training. It is hypothesized that the availability of certain substrates (glycogen and glucose, for example) may influence the regulation of genes involved in exercise-induced adaptation. Therefore, training with low glycogen levels may promote more pronounced transcription of exercise-induced genes and result in more efficient changes in exercise-related physiological parameters.
Yeo et al. (2008) showed that glycogen levels during training decreased practice intensities and did not affect end-study time trial times. They also showed that fat oxidation rates were higher in those training with low glycogen compared to the control group.

Hypothesis/Research Question:The first aim is to confirm recent findings of Yeo et al. The second aim was to rigorously probe the differences in substrate metabolism depending glycogen stores using 13C-labeled palmitate (C16 saturated fatty acid) and deuterated (2H or D) glucose.

Subjects:14 male endurance athletes, age 31 ± 6 y for the high glycogen group and 30 ± 6 y for the low glycogen group

Experimental design:Randomized, independent groups. 

Treatments and protocol: Subjects did not undergo high-intensity interval training for 4 wks before the training protocol. Subjects were pair-matched for VO2max, Wmax, time trial performance, and training history and then randomly assigned to the high- (HIGH) or low-glycogen (LOW) training group. Subjects performed nine aerobic training (AT; 90 min at 70% VO2max) and nine high-intensity interval training sessions (HIT; 8 x 5-min efforts, 1-min recovery) during a 3-wk period. HIGH trained once daily, alternating between AT on day 1 and HIT the following day, whereas LOW trained twice every second day, first performing AT and then, 1 h later, performing HIT.  As such, by performing HIT only 1 hour after completing the AT, the subjects in the LOW group always entered into HIT in a glycogen-depleted state relative to subjects in the HIGH group. Before and after the 3-week training period, the following measures were obtained: resting muscle biopsy (muscle glycogen, and protein contents for GLUT4 glucose transporter, FAT/CD36 (fatty acid translocase), and beta-hydroxyacyl-CoA dehydrogenase ( b -HAD, an enzyme involved in fatty acid oxidation)) , substrate oxidation during steady-state cycling (60 min at 70% VO2max) using labeled glucose and palmitate, plasma glucose and free fatty acids,  and  time trial performance. Subjects were provided with a standard diet consisting of 67.5% carbohydrate (8 g/kg), 13.5% protein, and 19% fat for 24 h before the experimental measures were taken. Subjects were asked to maintain a high carbohydrate diet during the 3-week training session and given instructions on how to do so.

Summary of research findings:
  • Power input during the HIT sessions increased in both groups with time and was higher in the HIGH (mean power output = 323 ± 9 W) versus LOW (mean = 297 ± 8 W, p < 0.05 for time) group. Mean power output in the time trial increased from 271 ± 13 to 298 ± 13 W in HIGH and from 278 ± 11 to 307 ± 10 W in LOW (p < 0.001 for time, no treatment effect).
  • The amount of time required to perform the given specified amount of work in the time trial did not differ significantly: Pre vs. post training times were 62.10 ± 1.49 vs. 56.37 ± 1.17 min in HIGH and 61.90 ± 1.12 vs. 56.12 ± 1.22 min in LOW.
  • There was a significant decrease in the rate of carbohydrate oxidation in LOW and a compensatory increase in fat oxidation, significantly reducing the respiratory exchange ratio (RER). RER was not affected in HIGH. Tracer data showed that plasma glucose and muscle glycogen oxidation dropped after training in LOW.
  • The contribution of substrates to energy expenditure was not altered in HIGH but showed a significant shift away from muscle glycogen in LOW (57 ± 2% before training to 50 ± 2% after training). To compensate, the contribution from muscle-derived triglycerides increased with training in LOW (20 ± 1% to 28 ± 2%, p < 0.05). In agreement with this observation, a 43% increase in the activity of ß-HAD was observed after training with low muscle glycogen.

Interpretation of findings/Key practice applications:

Whole body fat oxidation was increased under a low glycogen training state. An interesting observation is that 3 wks of endurance training under normal glycogen stores did not affect triglyceride utilization but low glycogen training increased the ability of the body to mobilize muscle triglycerides. This shows that different training regimens can be productive in enhancing the body’s adaptation to exercise and, potentially, performance. However, for anaerobic athletes, training at low glycogen levels may be counter-productive since carbohydrate and glycogen oxidation rates correlate highly with performance. At the end of the day, there were no differences in time trial times between LOW and HIGH. Therefore, while the observed changes in fatty acid and carbohydrate oxidation are interesting, it is still premature to recommend this type of approach in training.

Limitations of the research:

It is unclear how the results of this research study might apply to athletes other than cyclists. Further, it is not known to what degree the AT depleted muscle glycogen levels when performed on the same day as HIT in the LOW group.
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