TIMOTHY J. FAIRCHILD, ALEX A. ARMSTRONG, ARJUN RAO, HAWK LIU, STEVE LAWRENCE, PAUL A. FOURNIER

There is evidence that active recovery impairs glycogen repletion in skeletal muscles of fasted individuals. Our main goal was to examine the impact of active recovery on the glycogen stores of the different muscle fiber types. Eight endurance-trained individuals cycled for 2.5 min at 130% [OV0312]O(2peak) followed by a 30-s all-out cycling sprint. After exercise, the participants were subjected to either a passive recovery or an active recovery protocol that consisted of pedalling for 45 min at 40% [OV0312]O(2peak). During active recovery, blood lactate and pH returned more rapidly toward preexercise levels than during passive recovery. In contrast, average muscle glycogen content remained at stable levels during active recovery (209 +/- 32 and 202 +/- 30 mmol.kg-1 at 0 and 45 min of recovery, respectively) but increased significantly in response to passive recovery (from 185 +/- 27 to 283 +/- 42 mmol.kg-1). The pattern of change in periodic acid-Schiff staining intensity across muscle fibers suggests that the impact of active recovery on average muscle glycogen content is different from that observed at the levels of the individual muscle fibers, with active recovery having no effect on glycogen resynthesis in Type II muscle fibers but causing glycogen breakdown in Type I muscle fibers. Although active recovery was also associated with higher plasma catecholamines and lower insulin levels, such an unfavorable hormonal environment had no effect on glycogen resynthesis in Type II muscle fibers. Active recovery in comparison to passive recovery does not affect glycogen resynthesis in Type II muscle fibers despite being associated with an unfavorable hormonal environment but results in a marked glycogen mobilization in Type I muscle fibers.