Glycogen depletion elicited in tenuissimus intrafusal muscle fibres by stimulation of static gamma‐axons in the cat.

In this study the experimental conditions used to elicit glycogen depletion in tenuissimus intrafusal muscle fibres were different from those used by Barker, Emonet-Dénand, Harker, Jami 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 two experiments; very much longer periods (up to 9 h) of intermittent stimulation by bursts at 50-500/s were used. Bag1 and bag2 fibres were identified by their different ATPase activities in the B region. In two 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 one of nineteen bag1 poles examined. In two 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. Out of twenty-four bag1 poles examined, nineteen exhibited zones of depletion. In an experiment in which stimulation was conducted as in Barker et al. (1976), 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 fifteen periods of stimulation in contrast with the marked 'fatigue' that was constantly observed in the former study. No depleted intrafusal fibres 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 three out of ten bag1 poles were depleted. The variability of glycogen depletion in bag1 fibres 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 neighbouring fibres may deplete glycogen in bag1 fibres 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 fibres--possibly of neural origin--are very rare, although a large proportion of bag2 and chain fibres are depleted.