  The involuntary force fluctuations associated with physiological (as distinct
from pathological) tremor are an unavoidable component of human motor control.
While the origins of the physiological tremor are known to depend on muscle
afferentation, it is possible that the mechanical properties of muscle-tendon
systems also affect its generation, amplification and maintenance. In this
paper, we investigated the dependence of physiological tremor during tonic,
isometric plantarflextion torque at 30% of maximum at three ankle angles. The
amplitude of physiological tremor increased as calf muscles shortened in
contrast to the stretch reflex whose amplitude decreases as muscle shortens. We
used a closed-loop simulation model of afferented muscle to explore the
mechanisms responsible for this behavior. We demonstrate that changing muscle
lengths does not suffice to explain our experimental findings. Rather, the
model consistently required the modulation of gamme-static fusimotor drive to
produce increases in physiological tremor with muscle shortening--while
successfully replicating the concomitant reduction in stretch reflex amplitude.
This need to control gamma-static fusimotor drive explicitly as a function of
muscle length has important implication. First, it permits the amplitudes of
physiological tremor and stretch reflex to be decoupled. Second, it postulates
neuromechanical interaction that require length-dependent gamma drive
modulation to be independent from alpha drive to the parent muscle. Lastly, it
suggests that physiological tremor can be used as a simple, non-invasive
measure of the afferent mechanisms underlying healthy motor function, and their
disruption in neurological conditions.
