Ortenblad, N. (2009). Muscle fatigue in elite cross country skiers: A link between sarcoplasmic reticulum function and glycogen availability? A paper presented at the 14th Annual Congress of the European College of Sport Science, Oslo, Norway, June 24-27.

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The consistent observations that muscle glycogen stores at the beginning of exercise are closely related to endurance capacity and that the point of exhaustion after prolonged exercise coincides with low muscle glycogen levels clearly suggest a role for muscle glycogen in fatigue. However, the link between muscle glycogen and impaired muscle function during fatigue is not well understood and a direct cause-and-effect relationship between muscle glycogen and muscle function remains to be established.

This study presented a system where events in the excitation-contraction coupling are affected by muscle glycogen content and localization. The effect of muscle glycogen content on the sarcoplasmic reticulum function in the arm and leg muscles of elite cross country skiers (N = 10), before, immediately after, and four hours and twenty hours after a fatiguing 15-km race was examined. During the first four hours of recovery the skiers received either water or carbohydrate, and thereafter the same carbohydrate enriched food.

Straight after the race, arm muscle glycogen was reduced to 314% and the sarcoplasmic reticulum Ca2+ release rate had decreased to 852% of initial levels. After a four hour recovery with carbohydrate, the sarcoplasmic reticulum Ca2+ release rate was fully normalized and muscle glycogen had noticeably recovered to 595% of the initial value. When carbohydrate was absent during the first four hours of recovery, the muscle glycogen and the sarcoplasmic reticulum Ca2+ release rate remained low and reduced (292% and 778%, respectively), with both parameters being normalized after the remaining 16 hours of recovery with carbohydrate. Leg-muscle glycogen decreased to a lesser extent (7110% of the initial value) and there were no effects on the sarcoplasmic reticulum Ca2+ release rate. These data demonstrate a strong association between low muscle glycogen levels and muscle excitation-contraction coupling even after long recovery periods where adenine nucleotide levels may be normalized. Additionally, sarcoplasmic reticulum function is estimated in vitro under constant energy levels. Thus, although related to muscle glycogen levels, the impaired sarcoplasmic reticulum function is not due to a diminished energy metabolism at low muscle glycogen levels.

Transmission electron microscopy has revealed that muscle glycogen is located in distinct compartments close to different sites of excitation-contraction coupling. This study showed that 723% of intramuscular glycogen is located in the intermyofibrillar space (between the myofibrils) and 283% in the intramyofibrillar space. In single fibers, the intramyofibrillar glycogen content is positively correlated with fatigue resistance capacity, and intermyofibrillar glycogen is inversely correlated with tetanic half-relaxation time.

Implication. These results demonstrate that two distinct sub-cellular populations of glycogen have different roles in single muscle fiber contractions. This is consistent with the idea that muscle glycogen localization modulates the excitation-contraction coupling, thereby affecting muscle contractility and fatigability.

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