A hypothesis is forwarded regarding the role of secondary spindle afferents and the FRA (flexor reflex afferents) in motor control. The hypothesis is based on evidence (cf. Lundberg et al. 1987a, b) summarized in 9 introductory paragraphs. Group II excitation. It is postulated that subsets of excitatory group II interneurones (transmitting disynaptic group II excitation to motoneurones) may be used by the brain to mediate motor commands. It is assumed that the brain selects subsets of interneurones with convergence of secondary afferents from muscles whose activity is required for the movement. During movements depending on coactivation of static gamma-motoneurones impulses in secondary afferents may servo-control transmission to alpha-motoneurones at an interneuronal level. The large group II unitary EPSPs in interneurones are taken to indicate that, given an adequate interneuronal excitability, impulses in single secondary afferents may fire the interneurone and produce EPSPs in motoneurones; interneuronal transmission would then be equivalent to that in a monosynaptic pathway but with impulses from different muscles combining into one line. It is postulated that impulses in the FRA are evoked by the active movements and that the role of the multisensory convergence from the FRA onto the group II interneurones is to provide the high background excitability which allows the secondary spindle afferents to operate as outlined above. The working hypothesis is put forward that a movement governed by the excitatory group II interneurones is initiated by descending activation of these interneurones, but is maintained in a later phase by the combined effect of FRA activity evoked by the movement and by spindle secondaries activated by descending activation of static gamma-motoneurones. As in the original "follow up length servo" hypothesis (Rossi 1927; Merton 1953), we assume that a movement at least in a certain phase can be governed from the brain solely or mainly via static gamma-motoneurones. However, our hypothesis implies that the excitatory group II reflex connexions have a strength which does not allow transmission to motoneurones at rest and that the increase in the gain of transmission during an active movement is supplied by the movement itself. Group II inhibition. It is suggested that the inhibitory reflex pathways like the excitatory ones have subsets of interneurones with limited group II convergence. When higher centres utilize a subset of excitatory group II interneurones to evoke a given movement, there may mobilize inhibitory subsets to inhibit muscles not required in the movement.(ABSTRACT TRUNCATED AT 400 WORDS)