Muscle fatigue is an exercise-induced reduction in maximal voluntary muscle force. It may arise not only because of peripheral changes at the level of the muscle, but also because the central nervous system fails to drive the motoneurons adequately. Evidence for “central” fatigue and the neural mechanisms underlying it are reviewed, together with its terminology and the methods used to reveal it. Much data suggest that voluntary activation of human motoneurons and muscle fibers is suboptimal and thus maximal voluntary force is commonly less than true maximal force. Hence, maximal voluntary strength can often be below true maximal muscle force. The technique of twitch interpolation has helped to reveal the changes in drive to motoneurons during fatigue. Voluntary activation usually diminishes during maximal voluntary isometric tasks, that is central fatigue develops, and motor unit firing rates decline. Transcranial magnetic stimulation over the motor cortex during fatiguing exercise has revealed focal cha...

Spinal and Supraspinal Factors in Human Muscle Fatigue

https://www.cs.cmu.edu/~hgeyer/Teaching/R16-899B/Papers/Winter95Gait&Posture.pdf

Human balance and posture control during standing and walking

Exercise: a behavioral intervention to enhance brain health and plasticity

Skeletal muscles adapt to changes in their workload by regulating fibre size by unknown mechanisms. The roles of two signalling pathways implicated in muscle hypertrophy on the basis of findings in vitro, Akt/mTOR (mammalian target of rapamycin) and calcineurin/NFAT (nuclear factor of activated T cells), were investigated in several models of skeletal muscle hypertrophy and atrophy in vivo. The Akt/mTOR pathway was upregulated during hypertrophy and downregulated during muscle atrophy. Furthermore, rapamycin, a selective blocker of mTOR, blocked hypertrophy in all models tested, without causing atrophy in control muscles. In contrast, the calcineurin pathway was not activated during hypertrophy in vivo, and inhibitors of calcineurin, cyclosporin A and FK506 did not blunt hypertrophy. Finally, genetic activation of the Akt/mTOR pathway was sufficient to cause hypertrophy and prevent atrophy in vivo, whereas genetic blockade of this pathway blocked hypertrophy in vivo. We conclude that the activation of the Akt/mTOR pathway and its downstream targets, p70S6K and PHAS-1/4E-BP1, is requisitely involved in regulating skeletal muscle fibre size, and that activation of the Akt/mTOR pathway can oppose muscle atrophy induced by disuse.

Akt/mTOR pathway is a crucial regulator of skeletal muscle hypertrophy and can prevent muscle atrophy in vivo.

Neuronal plasticity is a central theme of modern neurobiology, from cellular and molecular mechanisms of synapse formation in Drosophila to behavioural recovery from strokes in elderly humans. Although the methods used to measure plastic responses differ, the stimuli required to elicit plasticity are thought to be activity-dependent. In this article, we focus on the neuronal changes that occur in response to complex stimulation by an enriched environment. We emphasize the behavioural and neurobiological consequences of specific elements of enrichment, especially exercise and learning.

Neural consequences of environmental enrichment.

Co-contractions in antagonistic hindlimb muscles during simulated step cycle rates

The contribution of individual muscles to the ankle moment produced in the cat hindlimb

Changes in myonuclear number in rat plantaris fibers following ten weeks of functional overload.: 792

A number of neurorehabilitative strategies have demonstrated efficacy in enhancing the recovery of sensorimotor function after a spinal cord injury (SCI). Combinations of task-specific motor training, epidural electrical stimulation of the spinal cord, and pharmacological interventions such as the administration of serotonergic agonists have resulted in remarkable improvements of locomotor and/or postural functions in rats with a complete SCI. Similar results are emerging in human patients with severe spinal cord damage. Synergistic amelioration of the loss of sensorimotor function through combinatorial approaches, i.e., the use of two or more interventions simultaneously, indicates that individual interventions can have both specific and complementary influences. For example, electrical stimulation applied at distinct rostrocaudal locations or agonists to specific receptor subtypes administered systemically tune unique aspects of locomotor movements. When administered simultaneously, the effects of these interventions can combine synergistically and result in significantly greater improvements in locomotor performance than either intervention alone. In addition, the use of robotic assistance during motor training, in particular in an “assist-as-needed” mode that allows a normal amount of variability in performing the task as opposed to a repetitive rigid training mode, can strongly enhance the effect of locomotor rehabilitation. We suggest that all of these interventions are enabling factors. They enable spinal neural circuitries to interpret task-specific sensory input and use this information in a feedforward manner to produce appropriate motor responses. Continued advancement in the development and refinement of such neurorehabilitative interventions will ensure progress towards improving the quality of life of individuals with a SCI or other severe sensorimotor dysfunctions.

Roland R. Roy

Papers

Co-contractions in antagonistic hindlimb muscles during simulated step cycle rates

The contribution of individual muscles to the ankle moment produced in the cat hindlimb

Changes in myonuclear number in rat plantaris fibers following ten weeks of functional overload.: 792

Multisystem Neurorehabilitation in Rodents with Spinal Cord Injury

An analysis of the spatial distribution of muscle fibers within the territory of a motor unit