Human motor fatigability as evoked by repetitive movements results from a gradual breakdown of surround inhibition.
Motor fatigability emerges when demanding tasks are executed over an extended period of time. Here, we used repetitive low-force movements that cause a gradual reduction in movement speed (or 'motor slowing') to study the central component of fatigability in healthy adults. We show that motor slowing is associated with a gradual increase of net excitability in the motor network and, specifically, in primary motor cortex (M1), which results from overall disinhibition. Importantly, we link performance decrements to a breakdown of surround inhibition in M1, which is associated with high coactivation of antagonistic muscle groups. This is consistent with the model that a loss of inhibitory control might broaden the tuning of population vectors such that movement patterns become more variable, ill-timed and effortful. We propose that the release of inhibition in M1 is an important mechanism underpinning motor fatigability and, potentially, also pathological fatigue as frequently observed in patients with brain disorders.
['Bächinger|Marc|M|0000-0002-3726-542X', 'Lehner|Rea|R|0000-0002-6497-2875', 'Thomas|Felix|F|', 'Hanimann|Samira|S|', 'Balsters|Joshua|J|0000-0001-9856-6990', 'Wenderoth|Nicole|N|0000-0002-3246-9386']
D000328:Adult D004569:Electroencephalography D005221:Fatigue D005260:Female D006225:Hand D064368:Healthy Volunteers D006801:Humans D008279:Magnetic Resonance Imaging D008297:Male D008959:Models, Neurological D009044:Motor Cortex D009068:Movement D055815:Young Adult
human repetitive movements motor slowing fatigue electrophysiology functional magnetic resonance imaging neuroscience transcranial magnetic stimulation