Tip a virtual platform under a real 3D ankle. Discover why one muscle gets more drive while its partner gets less, follow the spinal circuit, and change one connection to see the difference.
Enable JavaScript to change the conditions and run the interactive experiment.
Your nervous system coordinates muscles. In one stretch-response pathway, it increases drive to a stretched muscle and reduces drive to its opposing partner. That reduction is called inhibition. Try removing the connection and compare both outputs.
Keep the same stretch. Remove only the inhibitory connection. Which output changes in our completed model?
The direct branch still adds the same calf drive. Removing the selected inhibitory branch leaves the opposing output at its background value. That is a circuit comparison, not a pain or balance prediction.
A muscle spindle is a sensory structure inside a muscle. When the calf muscle–tendon arrangement is lengthened by the platform, spindle input can change. Our enlarged spindle is a locator illustration. Its brightness represents a selected teaching stage, not measured nerve firing.
Soleus, at the back of the lower leg, contributes to pointing the toes downward: plantarflexion. Tibialis anterior, in front, contributes to lifting them: dorsiflexion. These are opposing actions at the ankle. Many other muscles, body loads and control pathways also contribute during real movement.
It is a way to trace an input through a nervous-system pathway to an output. The selected stretch example begins with sensory input, includes spinal connections and ends with motor output. The phrase does not mean that every reflex has one identical circuit or that the brain is always absent.
A sensory branch excites the motor pool of the stretched muscle. Another branch excites an inhibitory interneuron. That neuron reduces drive in the opposing motor pool. The inhibition is a connection within the nervous system; it is not a special inhibitory motor nerve switching off the muscle itself.
The direct spinal branch shown here need not wait for a conscious decision. But the brain can influence spinal circuits, and some fast feedback responses include cortical processing. Automatic does not mean the nervous system above the spinal cord is uninvolved.
Skin-evoked withdrawal starts with a different input and recruits other pathways. Human experiments show that stimulation at different sole locations can produce different muscle-response patterns. A stretch pathway is useful to understand, but it is not a complete diagram of every protective movement.
Sensory fibers enter through dorsal, or posterior, roots. The sensory cell body is in a dorsal-root ganglion outside the cord; it is not an extra compulsory relay between two neurons. Motor axons leave through ventral, or anterior, roots. Our detached diagram has dorsal at the top and ventral at the bottom. It does not align spinal segments with vertebral levels.
The selected direct Ia afferent-to-motor-neuron branch has one central synapse. The reciprocal branch includes an inhibitory interneuron, giving two central synapses. Both include additional events elsewhere, including the neuromuscular junction. Neither count is a complete description of every stretch-related response.
Let u be authored stretch input from 0 to 1, b background drive, and g be 1 with the inhibitory connection or 0 with it removed. At the completed teaching stage: calf drive = clamp(b + 0.5u); opposing drive = clamp(b − 0.3gu). Clamp keeps outputs in [0,1]. The gains 0.5 and 0.3 are chosen for a readable comparison. They are not fitted nerve, EMG, force or movement measurements. During playback we reveal the result in stages, on an illustrative clock.
Crone and colleagues studied reciprocal ankle pathways in 60 humans in 1987 using conditioned H reflexes. Assuming symmetric central connections, they inferred about 1 ms of additional central delay relative to monosynaptic Ia excitation. That comparison does not measure the whole time from an everyday stimulus to movement, and it says nothing about when someone becomes aware of pain.
Pruszynski and colleagues combined human and rhesus-monkey experiments in 2011 to investigate rapid multijoint feedback and motor-cortex contributions. This evidence expands the simple spinal picture. It does not make our ankle illustration a model of every arm response or assign one delay to all people.
Suzuki and colleagues compared crossed cutaneous effects on a soleus H reflex in humans. They found facilitation while standing at selected conditioning-to-test intervals, but suppression during early stance in walking. The measured endpoint was electrically probed reflex excitability, not whole-leg force. Gervasio and colleagues separately studied crossed responses during walking and distinguished measured data from modeled afferent activity.
Nociception concerns neural processing of potentially tissue-damaging input. Pain is a personal sensory and emotional experience. Experimental reflex measures and reported pain can dissociate. This lesson neither assigns a pain score nor tests a learner’s neurological function.
Body motion changes sensory input. Spinal pathways, brain pathways and muscle mechanics together contribute to responses. The ankle reveals a coordination principle, while actual balance needs much more than two output bars.
A robot controller can compare a desired condition with sensor input and adjust its outputs. This is a useful engineering analogy for feedback. A two-motor program is not a biological reflex circuit, and muscles have their own changing mechanical properties.
An electrical muscle recording, a joint movement and a person’s report answer different questions. Research and clinical tests need controlled procedures and interpretation; watching or moving this model is not such a test.
Draw two boxes: “toes down” and “toes up.” Put or draw two counters in each. Counters represent model drive. They do not measure muscle force.
Draw a “stretch input” card. Connect it directly to the toes-down box. Draw a second route through a card labeled “inhibitory relay,” ending at the toes-up box.
Our rules are: the direct route adds one counter; the inhibitory route removes one. Before moving anything, predict both final counts and explain the reason.
Activate the input card. Add one counter to toes down and remove one from toes up. You now have three and one. Compare both with the starting counts.
Reset to two counters in each box. Cover the inhibitory route and repeat the same input. Toes down reaches three again; toes up stays at two. Which connection explains the difference?
Explain excitation and inhibition to a partner. The counters show the signs of a small circuit. They cannot predict real movement, response time, strength or pain. Those require different evidence.
Can reducing one output change the result without changing the other?
This is a paper model, not a body test. An adult can prepare large squares, or simply draw and cross out counters. No tapping tendons, painful contact, electrical stimulation or sudden loads. No movement is required.
Ventral motor root Motor axons leave through ventral roots. Dorsal roots carry sensory input; the central canal is not the outgoing muscle-signal route. See FIPAT in the source record.
Reduces drive in the opposing motor pool The sensory branch excites this interneuron, whose output inhibits the target motor pool. The skeletal motor output itself remains excitatory at muscle. Day et al. supports the reciprocal-pathway distinction.
The model has more opposing drive Only the first claim is calculated here. The platform sets foot pose; no whole-body balance or pain is predicted.
The input and recruited circuit change A muscle spindle supplies the main example. Skin input recruits other pathways and location-dependent patterns, as examined by Andersen et al.
No; some fast feedback includes cortical processing A direct spinal branch need not wait for a decision. Other fast feedback pathways can include cortex, as tested by Pruszynski et al.
No; task and pathway matter Suzuki et al. found different crossed effects on a tested H reflex during standing and early stance in walking. That is a context comparison, not a universal rule for leg force.
No; those are different intervals Crone et al. compared selected central pathway delays under an assumption. Sensory travel, motor travel and movement are not all included in that extra central interval.
No Pain is personal. Reflex measures and reported pain can dissociate; the IASP definition and Edwards et al. support keeping those measures distinct.
Crone et al. studied 60 humans using conditioned soleus and tibialis-anterior H reflexes. The extra central delay was inferred under a symmetry assumption; our drive gains are not taken from their data.
Crone et al. · Journal of Physiology, 1987Original human forearm conditioning experiments; corroborating pathway evidence, not ankle-specific simulation constants.
Day et al. · Journal of Physiology, 1984Original recordings from human muscle spindle afferents during vibration, length and movement conditions. The lesson does not reproduce their firing rates.
Burke et al. · human spindle recordings, 1976Original human foot-sole electrical-stimulation study. Not every withdrawal response is one universal activation pattern.
Andersen et al. · human leg withdrawal, 1999Primary human and rhesus-monkey experiments on multijoint feedback control. Distinguish these experimental tasks from the modeled ankle.
Pruszynski et al. · Nature, 2011Human conditioned soleus H-reflex measurements. The 100–130 ms intervals are between conditioning and test stimuli, not natural movement onset delays.
Suzuki et al. · Experimental Brain Research, 2014Gervasio et al. 2017, PLOS ONE 12(1):e0168557. Complete Figure 3 documents the setup and is reused under CC BY 4.0. This paper is separate from Suzuki’s standing/walking comparison.
Gervasio et al. · PLOS ONE, 2017Sherrington’s own 1932 Nobel lecture. Historical animal experiments are not direct human measurements or the origin of our authored numerical gains.
Sherrington · original Nobel lecture, 1932FIPAT Terminologia Neuroanatomica. Terminology guides the detached functional diagram; it does not validate authored geometry.
FIPAT · Terminologia NeuroanatomicaBodyParts3D, © The Database Center for Life Science licensed under CC Attribution 4.0 International. Current owner license updated February 2025; source selections and changes are recorded in the manifest.
DBCLS · BodyParts3D license and attributionIASP’s definition distinguishes personal pain experience from nociception. No pain prediction or self-test is offered.
IASP · revised definition of painEdwards et al. original human study of task-related arousal, reflex threshold and pain ratings. The lesson uses the distinction, not a personal calibration.
Edwards et al. · Journal of Psychophysiology, 2006Independent subject review is pending.
Read the sources and model assumptions
Interactive explorationSlide a texture beneath a finger. See the contact change, compare a moving touch with a steady one, and zoom from skin to a real sensing protein. Discover how touch differs from pain.
Interactive explorationNudge a membrane, discover when a spike appears, test its recovery, and cross a chemical synapse. Then inspect a real potassium-channel structure.
Move a load closer to an elbow on a transparent teaching arm. See the force change, then explore how muscles can work without visible movement.