Spinal and supraspinal control of motor function during maximal eccentric muscle contraction: Effects of resistance training

Abstract

HighlightsNeuromuscular activity is suppressed during maximal eccentric muscle contraction in untrained subjects, evidenced by decreased electromyography signal amplitude, attenuated evoked H-reflex responses, increased autogenic motor neuron inhibition, and decreased excitability in descending corticospinal motor pathways.Heavy-load resistance training yields marked gains in eccentric muscle strength owing to increased excitability of spinal motor neurons, decreased presynaptic or postsynaptic inhibition of spinal motor neurons, and likely also involving elevated descending motor drive from supraspinal centers.Increased eccentric muscle strength induced by heavy-load resistance training provides an important basis for enhanced neuromuscular performance in athletes, as well as nonathletes, including older adults and clinical patients.

Influence of fascicle strain and corticospinal excitability during eccentric contractions on force loss

“…This decrease in MEP/M, together with the reduction in other neural parameters (e.g. EMG activity, voluntary activation) during maximal voluntary eccentric contractions compared with other contraction types is well established in untrained subjects and underlines the specific neural control involved during eccentric contractions (for recent reviews, see Aagaard, ; Duchateau & Enoka, ). Hence, the MEP/M ecc/iso ratio was calculated to evaluate the ability of an individual to activate VL through the corticospinal pathway; the lower the MEP/M ecc/iso , the greater the corticospinal inhibitions during eccentric contractions.…”

“…They concluded that mechanical sensory feedback would play only a minor role in modulating neural pathways during eccentric contractions, but the specific neural strategy observed during active muscle lengthening would instead lie on central controls. As previously discussed (Aagaard, ; Duchateau & Enoka, ), it is possible that spinal processes other than disynaptic inhibitory postsynaptic potentials from Ib afferents and monosynaptic excitatory postsynaptic potentials from Ia afferents were responsible for the corticospinal inhibitions (e.g. recurrent inhibition).…”

“…Conversely, individuals with a reduced corticospinal excitability of VL at long muscle lengths during eccentric contractions were resilient to muscle damage. A decrement in MEP/M might arise from a decrease in the responsiveness of cortical neurons to motor cortex stimulation and/or changes in peripheral afferent inputs to α‐motoneurons (Aagaard, ; Duclay et al., ; Gruber et al., ). It is possible that this relationship was not associated with any physiological causes of muscle damage, but it might be that these results suggest that corticospinal excitability measured at long muscle lengths during the first eccentric contraction was related, in part, to the extent of subsequent muscle damage.…”

“…Given that the present study found no correlation ( r 2 = 0.02) between the duration of CSP at 100 deg, which represents intracortical inhibitory processes (Duchateau & Enoka, ), and the reduction in MVC torque at 24 h postexercise, it might be suggested that the present relationship found between corticospinal excitability and muscle damage arose from spinal rather than supraspinal processes. As discussed in recent reviews (Aagaard, ; Duchateau & Enoka, ), several neural mechanisms might be involved in reducing neuromuscular activity during maximal voluntary eccentric contractions and participating in protection from muscle damage. Briefly, presynaptic inhibition of Ia terminals (Duclay et al., ) and recurrent inhibition mediated by Renshaw cells (Barrué‐Belou, Marque, & Duclay, ; Duchateau & Enoka, ; Duclay et al., ) are the best candidates that seem to play a significant role in adjusting motoneuronal activity at the spinal level during maximal voluntary eccentric contractions.…”

Autogenic recurrent Renshaw inhibition is elevated in human spinal motor neurones during maximal eccentric muscle contraction in vivo

“…As stated by Barrué‐Belou et al cortical and spinal neural mechanisms involved in the modulation of the neural drive during eccentric contraction have previously been investigated by comparing the effect of muscle contraction type (i) on the motor evoked potential elicited by transcranial magnetic stimulation (TMS), (ii) on the cervicomedullary motor evoked potential (CMEP) and (iii) on the Hoffmann reflex (H‐reflex, V‐wave) obtained by electrical stimulation of the peripheral motor nerve (for recent reviews, see Duchateau and Enoka, and Aagaard). Specifically, when assessing spinal mechanisms responsible for the inability to fully active motor neurones during maximal eccentric muscle actions, reduced evoked H‐reflex responses consistently have been observed for lengthening compared to isometric or shortening contractions performed at both maximal and submaximal effort, indicating suppressed motor neurone excitability and/or an elevated levels of presynaptic or postsynaptic inhibition.…”