Facilitation–inhibition control of motor neuronal persistent inward currents in young and older adults

A well-coordinated facilitation–inhibition control of motor neuronal persistent inward currents (PICs) via diffuse neuromodulation and local inhibition is essential to ensure motor units discharge at required times and frequencies. Present best estimates indicate that PICs are reduced in older adults; however, it is not yet known whether PIC facilitation–inhibition control is also altered with ageing. We investigated the responses of PICs to (i) a remote handgrip contraction, which is believed to diffusely increase serotonergic input onto motor neurones, and (ii) tendon vibration of the antagonist muscle, which elicits reciprocal inhibition, in young and older adults. High-density surface electromyograms were collected from soleus and tibialis anterior of 18 young and 26 older adults during triangular-shaped plantar and dorsiflexion contractions to 20 % (handgrip experiments) and 30 % (vibration experiments) of maximum torque (rise-decline rate of 2 % / s). A paired-motor-unit analysis was used to calculate ∆F, which is assumed to be proportional to PIC strength. ΔF increased in both soleus (0.55 peaks per second (pps), 16.0 %) and tibialis anterior (0.42 pps, 11.4 %) after the handgrip contraction independent of age. Although antagonist tendon vibration reduced ΔF in soleus (0.28 pps, 12.6 %) independent of age, less reduction was observed in older (0.42 pps, 10.7 %) than young adults (0.72 pps, 17.8 %) in tibialis anterior. Our data indicate a preserved ability of older adults to amplify PICs following a remote handgrip contraction, during which increased serotonergic input onto the motor neurones is expected, in both lower leg muscles. However, PIC deactivation in response to reciprocal inhibition was impaired with ageing in tibialis anterior despite being preserved in soleus. (Figure presented.). Key points: Motor neuronal persistent inward currents (PICs) are facilitated via diffuse neuromodulation and deactivated by local inhibition to ensure motor units discharge at required times and frequencies, allowing normal motor behaviour. PIC amplitudes appear to be reduced with ageing; however, it is not known whether PIC facilitation–inhibition control is also altered. Remote handgrip contraction, which should diffusely increase serotonergic input onto motor neurones, facilitated PICs similarly in both soleus and tibialis anterior of young and older adults. Antagonist tendon vibration, which induces reciprocal inhibition, reduced PICs in soleus in both young and older adults but had less effect in tibialis anterior in older adults. Data from lower-threshold motor units during low-force contractions suggest that PIC facilitation is preserved with ageing in soleus and tibialis anterior. However, the effect of reciprocal inhibition on the contribution of PICs to motor neurone discharge seems reduced in tibialis anterior but preserved in soleus

Ageing reduces persistent inward current contribution to motor neurone firing: Potential mechanisms and the role of exercise

Nervous system deterioration is a primary driver of age-related motor impairment. The motor neurones, which act as the interface between the central nervous system and the muscles, play a crucial role in amplifying excitatory synaptic input to produce the desired motor neuronal firing output. For this, they utilise their ability to generate persistent (long-lasting) depolarising currents that increase cell excitability, and both amplify and prolong the output activity of motor neurones for a given synaptic input. Modulation of these persistent inward currents (PICs) contributes to the motor neurones’ capacities to attain the required firing frequencies and rapidly modulate them to competently complete most tasks. Thus, PICs are crucial for adequate movement generation. Impairments in intrinsic motor neurone properties can impact motor unit firing capacity, with convincing evidence indicating that the PIC contribution to motor neurone firing is reduced in older adults. Indeed, this could be an important mechanism underpinning the age-related reductions in strength and physical function. Furthermore, resistance training has emerged as a promising intervention to counteract age-associated PIC impairments, with changes in PICs being correlated with improvements in muscular strength and physical function after training. In this review, we present the current knowledge of the PIC magnitude decline during ageing and discuss whether reduced serotonergic and noradrenergic input onto the motor neurones, voltage-gated calcium channel dysfunction or inhibitory input impairments are candidates that: (i) explain age-related reductions in the PIC contribution to motor neurone firing and (ii) underpin the enhanced PIC contribution to motor neurone firing following resistance training in older adults. (Figure presented.)

Neuromuscular factors contributing to reductions in muscle force after repeated, high-intensity muscular efforts

Multiple neuromuscular processes contribute to the loss of force production following repeated, high-intensity muscular efforts; however, the relative contribution of each process is unclear. In Experiment 1, 16 resistance trained men performed six sets of unilateral isometric plantar flexor contractions of the right leg (3 s contraction/2 s rest; 85% maximal voluntary contraction torque; 90-s inter-set rest) until failure with and without caffeine ingestion (3 mg kg-1) on two separate days. Corticospinal excitability and cortical silent period (cSP) were assessed before and immediately, 10 and 20 min after the exercise. In Experiment 2, electrically evoked tetanic force and persistent inward current (PIC)-mediated facilitation of the motor neuron pool (estimated using neuromuscular electrical stimulation with tendon vibration) were assessed before and after the same exercise intervention in 17 resistance trained men. Results showed decreases in peak plantar flexion torque (Experiment 1: -12.2%, Experiment 2: -16.9%), electrically evoked torque (20 Hz -15.3%, 80 Hz -15.3%, variable-frequency train -17.9%), and cSP (-3.8%; i.e., reduced inhibition) post-exercise which did not recover by 20 min. Electromyographic activity (EMG; -6%), corticospinal excitability (-9%), and PIC facilitation (-24.8%) were also reduced post-exercise but recovered by 10 min. Caffeine ingestion increased torque and EMG but did not notably affect corticospinal excitability, PIC amplification, or electrically evoked torque. The data indicate that a decrease in muscle function largely underpins the loss of force after repeated, high-intensity muscular efforts, but that the loss is exacerbated immediately after the exercise by simultaneous decreases in corticospinal excitability and PIC amplitudes at the motor neurons

Rate of torque development and striatal shape in individuals with prodromal Huntington\u27s disease

The aim of the present study was to quantify explosive joint torque or the ability to develop joint torque rapidly, typically measured as the rate of torque development, in individuals with prodromal Huntington’s disease and healthy controls and its associations with measures of disease burden and striatal pathology. Twenty prodromal Huntington’s disease and 19 healthy control individuals volunteered for this study. Plantar flexor isometric rate of torque development values were evaluated using isokinetic dynamometry. Pathological changes in striatal shape were evaluated using magnetic resonance imaging. Disease burden was evaluated using the disease burden score and cytosine-adenine-guanine age product score. No statistical differences in the rate of torque development were observed between individuals with prodromal Huntington’s disease and healthy controls. However, significant associations were observed between the rate of torque development values and measures of disease burden (r = −0.42 to −0.69) and striatal pathology (r = 0.71–0.60) in individuals with prodromal Huntington’s disease. We found significant associations between lower rate of torque development values and greater striatal shape deflation and disease burden and striatal pathology in individuals with prodromal Huntington’s disease. While no significant differences in the rate of torque development were found between prodromal Huntington’s disease and healthy controls, the noted associations suggest that differences may emerge as the disease advances, which should be investigated longitudinally in future studies

Static Stretching Reduces Motoneuron Excitability:The Potential Role of Neuromodulation

Prolonged static muscle stretching transiently reduces maximal muscle force, and this force loss has a strong neural component. In this review, we discuss the evidence suggesting that stretching reduces the motoneuron's ability to amplify excitatory drive. We propose a hypothetical model in which stretching causes physiological relaxation, reducing the brainstem-derived neuromodulatory drive necessary to maximize motoneuron discharge rates.</p

Interpreting Signal Amplitudes in Surface Electromyography Studies in Sport and Rehabilitation Sciences

Surface electromyography (sEMG) is a popular research tool in sport and rehabilitation sciences. Common study designs include the comparison of sEMG amplitudes collected from different muscles as participants perform various exercises and techniques under different loads. Based on such comparisons, researchers attempt to draw conclusions concerning the neuro- and electrophysiological underpinning of force production and hypothesize about possible longitudinal adaptations, such as strength and hypertrophy. However, such conclusions are frequently unsubstantiated and unwarranted. Hence, the goal of this review is to discuss what can and cannot be inferred from comparative research designs as it pertains to both the acute and longitudinal outcomes. General methodological recommendations are made, gaps in the literature are identified, and lines for future research to help improve the applicability of sEMG are suggested

Neurophysiological mechanisms underpinning stretch-induced force loss

It is well known that prolonged passive muscle stretch reduces maximal muscle force production. There is a growing body of evidence suggesting that adaptations occurring within the nervous system play a major role in this stretch-induced force reduction. This article reviews the existing literature, and some new evidence, regarding acute neurophysiological changes in response to passive muscle stretching. We discuss the possible contribution of supra-spinal and spinal structures to the force reduction after passive muscle stretch. In summary, based on the recent evidence reviewed we propose a new hypothesis that a disfacilitation occurring at the motoneuronal level after passive muscle stretch is a major factor affecting the neural efferent drive to the muscle and, subsequently, its ability to produce maximal force

Effects of three neuromuscular electrical stimulation methods on muscle force production and neuromuscular fatigue

This study compared the acute responses of three neuromuscular electrical stimulation (NMES) methods on muscle torque-time integral (TTI) and neuromuscular fatigue. Narrow-pulse (0.2 ms; NP), wide-pulse (1 ms; WP), and tendon vibration superimposed onto wide-pulse (WP + VIB)-NMES conditions were applied to sixteen healthy individuals (n = 16) in three separate sessions in a randomized order. Stimulation intensity was set to elicit 20% of maximal voluntary contraction (MVC); the stimulus pattern comprised four sets of 20 repetitions (5 s On and 5 s Off) with a one-minute inter-set interval. TTI was measured for each NMES condition and MVC, voluntary activation (VA), peak twitch torque (Peaktwitch), and peak soleus (EMGSOL), medial (EMGMG), and lateral gastrocnemius (EMGLG) electromyography were measured before and immediately after each NMES condition. TTI was higher during WP + VIB (19.63 ± 6.34 MVC.s, mean difference = 3.66, p twitch forces decreased (p ≤ 0.001) immediately after all conditions. No changes were observed for VA (p = 0.365). EMGSOL amplitude reduced (p = 0.040) only after NP, yet EMGLG and EMGMG amplitudes decreased immediately after all conditions (p = 0.003 and p = 0.013, respectively). WP + VIB produced a higher TTI than WP and NP-NMES, with similar amounts of neuromuscular fatigue across protocols. All NMES protocols induced similar amounts of peripheral fatigue and reduced EMG amplitudes.</p

The back squat and the power clean: Elicitation of different degrees of potentiation

Purpose: To compare the acute effects of back squats and power cleans on sprint performance. Methods: Thirteen elite junior rugby league players performed 20-m linear sprints before and 7 min after 2 different conditioning activities or 1 control condition. The conditioning activities included 1 set of 3 back squats or power cleans at 90% 1-repetition maximum. A 2 × 2 repeated-measures ANOVA was used to compare preconditioning and postconditioning changes in sprint performance. Results: Both the back-squat and power-clean conditioning activities demonstrated a potentiation effect as indicated by improved sprint time (back squat: P =.001, ES = -0.66; power cleans: P =.001, ES = -0.92), velocity (back squat: P =.001, ES = 0.63; power cleans: P =.001, ES = 0.84), and average acceleration over 20 m (back squat: P =.001, ES = 0.70; power cleans: P =.001, ES = 1.00). No potentiation effect was observed after the control condition. Overall, the power clean induced a greater improvement in sprint time (P =.042, ES = 0.83), velocity (P =.047, ES = 1.17), and average acceleration (P =.05, ES = 0.87) than the back squat. Conclusions: Back-squat and power-clean conditioning activities both induced improvements in sprint performance when included as part of a potentiation protocol. However, the magnitude of improvement was greater after the power cleans. From a practical perspective, strength and conditioning coaches should consider using power cleans rather than back squats to maximize the performance effects of potentiation complexes targeting the development of sprint performance