THE RECOVERY PROCESS AFTER FATIGUE OF MAMMALIAN SKELETAL MUSCLE IN THE NORMAL AND IN THE DIABETIC ANIMAL
Authors: Milroy T. H. 
Published: December 2014

In the most extreme case of fatigue produced by stimulation for one hour (Table III.) the characteristic changes were—the entrance of water, the loss of some phosphate, the depletion of the glycogen store, the low lactacidogen (B—A) value, and, for stimulated muscle, the low lactic acid percentage. On testing this muscle under fluoride there was almost complete loss in the power of esterification. Next in order of severity is the example given in Table IV. Here there was again the increase in water, the depletion of glycogen, and a great diminution in the power of esterification under fluoride, but neither the hexose phosphate nor the lactic acid showed the low values of the first example. Following this in severity comes the stimulated muscle of Table I., then that of Table VI., and last of Table II. The less fatigued, or the more excitable the muscle, the less was the loss in glycogen, the higher the lactic acid value, the better the esterification under fluoride, and the smaller the increase in the water content. The recovery process was of the same type in all the experiments. It was quite evident even in the most exhausted muscle of the normal animal, and it was characterised by a reversal of the fatigue changes, the loss of the excess water, good storage of glycogen, increase in the hexose phosphate, decrease in lactic acid and a very great improvement in esterification under fluoride (Table III.). This recovery process began very quickly in the normal animal, so that within eight minutes after a stimulation which had almost exhausted the glycogen store, there was a good deposition of this polysaccharide in the muscle. At the same time the water and the lactic acid showed the usual decrease, but esterification under fluoride still remained very poor (Table IV.). Perhaps the most striking recovery changes were to be seen after a less prolonged period of stimulation, twenty minutes. In an experiment of this kind, after a period of twenty minutes' rest, all the characteristic signs of improvement were present (Table VI.), namely, decrease in the water and the lactic acid, along with great improvement in esterification under fluoride and an increase in the glycogen value.

The example given in Table V. showed that the last process to recover completely was the esterification under fluoride. The excess water and lactic acid in this case had been removed, the glycogen and hexose phosphate had returned to the normal level, while esterification both of the pre‐existing and of the added phosphate had lagged slightly behind the normal.

In the depancreatised animal the disturbances in glycolysis depend upon the extent to which the glycogen store in the muscles has been encroached upon, that is to say, upon the severity of the diabetic condition. In the example given in Table VII., the glycogen store, even before stimulation, was probably low. Certainly after twenty minutes' stimulation the muscles only contained an extremely small quantity of the polysaccharide, and, as a result, the esterification and the lactic acid production were much below the values for the normal animal after the same stimulation period (Table VI.). The most marked departure from the normal is, however, seen in the subsequent resting period. After a twenty‐minute “recovery” period the muscle showed practically no improvement as regards glycogen storage, and only an insignificant increase in esterification under fluoride. Apart from the usual loss of water and fall in lactic acid there were no other evident signs of true recovery. Another type of diabetic animal is dealt with in Table VIII. Here the muscle before stimulation had quite a good store of glycogen, although the liver was exhausted and the hyperglycwmia at a high level. The water content of the muscle was lower than normal. For muscle with such a good glycogen store, and the lactacidogen also at a high level, esterification under fluoride was not nearly so good as in the unstimulated muscles of the normal animal. In the recovery period after stimulation the contrast between the diabetic and the normal animal becomes more evident. As the muscle was not examined immediately after stimulation, one cannot tell how far the muscle glycogen had fallen, but even if the thirty‐five‐minute stimulation had led almost to complete exhaustion, the storage of 2.4 mg. glycogen per gramme muscle within a resting period of half an hour would have been below the normal. Esterification under fluoride, both in the case of the pre‐existing and of the added phosphate, was also below the value met with in normal recovering muscle. That the muscles of this diabetic animal could, however, esterify without fluoride is evident from the lactacidogen values (B—A), and therefore it is probable that the accumulation of the ester is in part due to the processes following esterification being interfered with. The unstimulated muscles of this animal behaved somewhat like those of a slightly fatigued normal animal, while those of the preceding depancreatised case, even when allowed to rest after a short period of stimulation, showed practically none of the improvement which always occurs under normal conditions.

I am very much indebted to Dr
Myra K. Beattie and Miss
Florence Beattie for assistance in carrying out analyses.