Department of Health Sciences and Technology, Neural Control of Movement Lab, Zurich, Switzerland; Neuroscience Center Zurich (ZNZ), University of Zurich, Federal Institute of Technology Zurich, University and Balgrist Hospital Zurich, Zurich, Switzerland
Department of Health Sciences and Technology, Neural Control of Movement Lab, Zurich, Switzerland; Neuroscience Center Zurich (ZNZ), University of Zurich, Federal Institute of Technology Zurich, University and Balgrist Hospital Zurich, Zurich, Switzerland
Felix Thomas
Department of Health Sciences and Technology, Neural Control of Movement Lab, Zurich, Switzerland; Neuroscience Center Zurich (ZNZ), University of Zurich, Federal Institute of Technology Zurich, University and Balgrist Hospital Zurich, Zurich, Switzerland
Samira Hanimann
Department of Health Sciences and Technology, Neural Control of Movement Lab, Zurich, Switzerland
Department of Health Sciences and Technology, Neural Control of Movement Lab, Zurich, Switzerland; Department of Psychology, Royal Holloway University of London, Egham, United Kingdom
Department of Health Sciences and Technology, Neural Control of Movement Lab, Zurich, Switzerland; Neuroscience Center Zurich (ZNZ), University of Zurich, Federal Institute of Technology Zurich, University and Balgrist Hospital Zurich, Zurich, Switzerland
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.
