King Grub
2010-12-08, 09:50
Little is known about the precise mechanism that relates skeletal muscle glycogen to muscle fatigue. The aim of the present study was to examine the effect of glycogen on sarcoplasmic reticulum (SR) function in the arm and leg muscles of elite cross-country skiers (n=10, V O2 max 72±2 ml . kg-1 min-1) before, immediately after, and 4h and 22h after a fatiguing 1h ski race. During the first 4hrs recovery, skiers received either water or carbohydrate (CHO) and thereafter all received CHO enriched food. Immediately after the race, arm glycogen was reduced to 31±4% and SR Ca2+ release rate decreased to 85±2% of initial levels. Glycogen noticeably recovered after 4h recovery with CHO (59±5% initial) and the SR Ca2+ release rate returned to pre-exercise levels. However, in the absence of CHO during the first 4h recovery, glycogen and the SR Ca2+ release rate remained unchanged (29±2% and 77±8%, respectively), with both parameters becoming normal after the remaining 18h recovery with CHO. Leg muscle glycogen decreased to a lesser extent (71±10% initial), with no effects on the SR Ca2+ release rate. Interestingly, transmission electron microscopy (TEM) analysis revealed that the specific pool of intramyofibrillar glycogen, representing 10-15% total glycogen, was highly significantly correlated with the SR Ca2+ release rate. These observations strongly indicate that low glycogen and especially intramyofibrillar glycogen, as suggested by TEM, modulate the SR Ca2+ release rate in highly trained subjects. Thus, low glycogen during exercise may contribute to fatigue by causing a decreased SR Ca2+ release rate.
J Physiol. 2010 Dec 6. Role of glycogen availability on SR Ca2+ kinetics in human skeletal muscle.
J Physiol. 2010 Dec 6. Role of glycogen availability on SR Ca2+ kinetics in human skeletal muscle.