A theory is presented to explain how accurate, single-joint movements are controlled. The theory applies to movements across different distances, with different inertial loads, toward targets of different widths over a wide range of experimentally manipulated velocities. The theory is based on three propositions. (1) Movements are planned according to “strategies” of which there are at least two: a speed-insensitive (SI) and a speed-sensitive (SS) one. (2) These strategies can be equated with sets of rules for performing diverse movement tasks. The choice between SI and SS depends on whether movement speed and/or movement time (and hence appropriate muscle forces) must be constrained to meet task requirements. (3) The electromyogram can be interpreted as a low-pass filtered version of the controlling signal to the motoneuron pools. This controlling signal can be modelled as a rectangular excitation pulse in which modulation occurs in either pulse amplitude or pulse width. Movements to different distances and with loads are controlled by the SI strategy, which modulates pulse width. Movements in which speed must be explicitly regulated are controlled by the SS strategy, which modulates pulse amplitude. The distinction between the two movement strategies reconciles many apparent conflicts in the motor control literature.

1. Normal human subjects made discrete elbow flexions and extensions in the horizontal plane from a stationary initial position to visually defined targets at different distances with a constant inertial load or made flexions to a visually defined target with different inertial loads. We measured joint angle, acceleration, and electromyograms (EMGs) from two agonist and two antagonist muscles. 2. Subjects were instructed to move their limbs accurately but quickly to the targets. Movements of greater distances or lesser loads were performed at higher velocities. 3. Peak inertial torque, acceleration and velocity, movement time, and integrated, rectified EMG were all highly correlated with the task variables, distance and inertial load. We show that peak inertial torque can be used as a linking variable that is almost sufficient to explain all correlations between the tasks, the EMG, and movement kinematics. 4. The rate at which subjects initially developed torque to accelerate their movements was invariant over changes in the value of either task variable. The rising phase of the agonist EMG was also independent of the distance or load moved. 5. Two components were distinguished in the antagonist EMG. The first had a relatively constant latency and amplitude. It terminated on the onset of the second and larger component at a latency that was delayed as both distance and load increased. 6. The integrated, rectified antagonist EMG was proportional to inertial load and peak decelerating torque for changes in inertial load. When target distance varied, proportionality between peak decelerating torque and antagonist EMG could be found if correction was made for the effects of muscle length on the torque-EMG relationship. 7. We propose organizing principles for the control of single-joint human movements in which tasks are performed by one of two strategies. These are called speed-insensitive and speed-sensitive strategies. 8. A model is described in which movements made under a speed-insensitive strategy are executed by controlling the duration and the relative timing of amplitude invariant patterns of activation to the spinal motoneuron pools.

1. Normal human subjects made discrete flexions of the elbow over a fixed distance in the horizontal plane from a stationary initial position to a visually defined target. We measured joint angle, acceleration, and electromyograms (EMGs) from two agonist and two antagonist muscles. 2. Changes in movement speed were elicited either by explicit instruction to the subject or by adjusting the target width. Instructions always required accurately stopping in the target zone. 3. Peak inertial torques and accelerations, movement times, and integrated EMGs were all highly correlated with speed. We show that inertial torque can be used as a linking variable that is almost sufficient to explain all correlations between the task, the EMG, and movement kinematics. 4. When subjects perform tasks that require control of movement speed, they adjust the rate at which torque is developed by the muscles. This rate is modulated by the way in which the muscles are activated. The rate at which joint torque develops is correlated with the rate at which the agonist EMG rises as well as with integrated EMG. 5. The antagonist EMG shows two components. The latency of the first is 30-50 ms and independent of movement dynamics. The latency of the second component is proportional to movement time. The rate of rise and area of both components scale with torque. 6. We propose organizing principles for the control of single-joint movements in which tasks are performed by one of two strategies. These are called speed-insensitive and speed-sensitive strategies. 7. A model is proposed in which movements made under a speed-sensitive strategy are executed by controlling the intensity of an excitation pulse delivered to the motoneuron pool. The effect is to regulate the rate at which joint torque, and consequently acceleration, increases. 8. Movements of variable distance, speed, accuracy, and load are shown to be controlled by one of two consistent sets of rules for muscle activation. These rules apply to the control of both the agonist and antagonist muscles. Rules of activation lead to distinguishable patterns of EMG and torque development. All observable changes in movement kinematics are explained as deterministic consequences of these effects.

1. Sudden dorsiflexions and plantarflexions of the foot were imposed on normal human subjects under various states of voluntary activity. 2. Under conditions of constant muscle contraction, the myotatic reflex in soleus and lateral gastrocnemius muscles is linearly and highly correlated with the rate of muscle stretch. The slope of this curve characterizes part of the reflex arc "gain." 3. The gain is linearly proportional to the level of tonic voluntary activation. 4. The gain is reduced by tonic contraction of antagonists. 5. The above statements can be summarized by the following equation (formula: see text), where d theta/dt is the rate of joint rotation. Ts and Tat are measures of voluntary contraction (tension) of all the extensor and flexor muscles acting at the ankle. The term S represents the level of preexisting spinal excitability that can be altered by prior instruction to the subject. 6. A phasic voluntary contraction of the soleus muscle, which leads to muscle shortening, will alter the reflex gain. The gain initially increases with increasing rates of shortening, but at higher rates the gain is reduced. This is in contradiction to the observation for tonic activation as stated above and may be due to an inability of the coactivated fusimotor system to produce sufficiently rapid cocontraction of the spindle fibers. 7. During lengthening of a muscle caused by voluntary contraction of its antagonists, the myotatic reflex gain is reduced. 8. The above facts are interpreted to imply that a functional role for the myotatic reflex in the leg extensors is limited to conditions of postural maintenance or slow, precise movement. During rapid movement, the myotatic reflex is ineffective and load-compensating reactions are mediated by longer latency loops. 9. The duration of the myotatic reflex EMG is from 10 to 40 ms, too brief to be a simple response to a velocity-sensing receptor organ. Either the response is in large measure due to the initial burst of spindle activity that occurs at the start of a ramp stretch, or motoneuron pool dynamics act as a high-pass filter on afferent inputs. 10. In the anterior tibial muscle, the relationships between stretch velocity and reflex amplitude and tonic voluntary contraction and reflex gain are qualitatively similar to those found in the ankle extensors.

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