GLYCOGEN DEPLETION ELICITED IN TENUISSIMUS INTRAFUSAL MUSCLE-FIBERS BY STIMULATION OF STATIC GAMMA-AXONS IN THE CAT

The experimental conditions used in this study to elicit glycogen depletion in tenuissimus intrafusal muscle fibers were different from those used by Barker, Emonet-Denand, Harker, Jami and Laporte (1976): the tenuissimus was left in situ; several (4-6) static .gamma.-axons were stimulated together; the blood flow through the muscle was not reduced during the periods of .gamma. stimulation except in 2 experiments; very much longer periods (up to 9 h ) of intermittent stimulation by bursts at 50-500/s were used. Bag1 and bag2 fibers were identified by their different ATPase activities in the B region. In 2 experiments with normal circulation, test responses of several primary endings to short periods of stimulation at 50-100/s were still very strong after stimulation of several static .gamma.-axons for 5 and 9 h, respectively. Glycogen depletion was observed in a large number of chain and bag2 poles but in only 1 of 19 bag1 poles examined. In 2 other experiments with normal circulation, there was a very pronounced reduction of the test responses after stimulation of several static .gamma.-axons for 7 and 9 h, respectively. Nineteen of 24 bag1 poles exhibited zones of depletion. In an experiment in which stimulation was conducted as in Barker et al., i.e, with reduction of muscle blood flow during 1 min periods of stimulation at 50-100/s, the primary endings still gave a strong response after 15 periods of stimulation in contrast with the marked fatigue that was constantly observed in the former study. No depleted intrafusal fibers were found in the spindles of this muscle. In a last experiment, after an initial pattern of stimulation similar to that described above, the new pattern of stimulation, but with periodical reduction of blood flow, was applied, leading to a fatigue of the test responses in 2 h. In the spindles of this muscle 3 of 10 bag1 poles were depleted. The variability of glycogen depletion in bag1 fibers appears to be linked to the degree of spindle fatigue which may develop after static .gamma. stimulation. It seems that in fatigued spindles some factor or factors liberated by the contraction of neighboring fibers may deplete glycogen in bag1 fibers by a non-neural mechanism. When, in spite of a prolonged stimulation of static .gamma.-axons, no fatigue of the test responses develops, zones of depletion in bag1 fibers, possibly of neural origin, are very rare although a large proportion of bag2 and chain fibers are depleted.