Serious contaminant in "ultra pure" grades of sucrose.

might account for the apparent absence of stretch reflexes at expected latencies in human subjects reported by several investigators (10). The pause between a monosynaptic response to stretch and a later increase in electromyographic activity may be due to a preponderance of inhibition from Golgi organs, as has been suggested for the respiratory system (11). Preliminary results with standing human subjects have shown a definite inhibitory period in the electromyogram recorded from ankle extensors when these muscles are stretched by rotating a platform (12). In conclusion, we demonstrate that autogenetic reflexes can compensate for variations in muscular stiffness revealed when responses to large stretches and releases are compared. Our data also show that the stiffness in response to large stretches can be greatly increased by autogenetic reflexes. The former observation supports the hypothesis that these reflexes compensate for variations in the mechanical properties of a muscle, whereas the latter supports the hypothesis that they compensate for variations in load. Our data do not allow us to distinguish which function is more important. The evidence reviewed in the preceding paragraph favors a higher gain of force feedback in normal animals. If this is true, compensation for variations in muscle properties would be greater, whereas compensation for variations in load would be less. T. RICHARD NICHOLS JAMES C. HouK* Department of Physiology, Harvard Medical School, Boston, Massachusetts 02115