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Updated: Sep 9, 2025

Quantification of Subcellular Glycogen Distribution in Skeletal Muscle Fibers using Transmission Electron Microscopy
Published on: February 7, 2022
Exercise- and diet-induced glycogen depletion impairs performance during one-legged constant-load, high-intensity
Martin Thomassen1, Michael J McKenna2,3,4, Hugo Olmedillas5
1The August Krogh Section for Human Physiology, Department of Nutrition, Exercise and Sports, University of Copenhagen, Copenhagen, Denmark.
Introduction:
The effect of muscle glycogen stores on performance during intense short-duration exercises in humans is unclear. We hypothesized that low initial muscle glycogen levels would impair constant-load intense one-legged knee extensor exercise lasting approximately 5 min and human muscle contractile function, as determined by maximal voluntary contraction (MVC), electrically induced single-twitch maximal force, rate of force development (RFD), and rate of relaxation. Furthermore, alter phosphorylation of the Na+/K+-ATPase (NKA) regulatory proteins AMPK and FXYD1 indicating attenuated NKA activity.
Methods:
With one leg in a glycogen-depleted state and one leg in a glycogen-loaded state, ten healthy young males (age: 25 ± 2 years) performed three intense exercise trials including (i) two-legged cycling for ∼5 min and (ii) 2× one-legged knee extensor exercise to task failure. MVC determination, electrical muscle stimulation, blood sample testing, and vastus lateralis biopsies were performed to assess the muscle composition and function.
Results:
Time to task failure during the one-legged knee-extensor exercise was reduced by approximately 40% (n = 10, P < 0.05) with exercise- and diet-induced glycogen depletion. At rest (n = 10), MVC, twitch force, RFD, and rate of relaxation were unaffected by glycogen content. After exercise to task failure, the single-twitch contractile characteristics were impaired to a greater extent (n = 10, P < 0.05) in the glycogen-loaded leg than in the glycogen-depleted leg, probably induced by longer exercise duration. Concomitantly, MVC (n = 10, except for 15 s: n = 5 and 8) was reduced to similar levels under both conditions. The exercise-induced increase in the nonspecific phosphorylation of FXYD1 (n = 10, P < 0.001), which regulates NKA activity, tended to be greater (n = 10, P = 0.06) in the glycogen-loaded legs, indicating augmented potassium handling.
Conclusion:
Exercise- and diet-induced low muscle glycogen content impairs high-intensity constant-load exercise performance lasting approximately 5 min. This was observed even with concomitantly better single-twitch contractile characteristics and similar reduction in MVC after task failure compared to glycogen-loaded legs. At rest, glycogen levels did not affect MVC and contractile characteristics.
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