A matter of nerves

Regrowing new body parts requires neural input to restore appropriately sized limbs in salamanders.

Behaviour of Motor Units during Submaximal Isometric Contractions in Chronically Strength-Trained individuals

Neural and morphological adaptations combine to underpin the enhanced muscle strength following prolonged exposure to strength training, although their relative importance remains unclear. We investigated the contribution of motor unit (MU) behaviour and muscle size to submaximal force production in chronically strength-trained athletes (ST) vs. untrained controls (UT). Sixteen ST (age, 22.9±3.5 yr; training experience, 5.9±3.5 yr) and fourteen UT (age, 20.4±2.3 yr) performed maximal voluntary isometric force (MViF) and ramp contractions (at 15, 35, 50, 70%MViF) with elbow flexors, whilst high-density surface EMG (HDsEMG) was recorded from the biceps brachii (BB). Recruitment thresholds (RT) and discharge rates (DR) of MUs identified from the submaximal contractions were assessed. The neural drive-to-muscle gain was estimated from the relation between changes in force (ΔFORCE, i.e. muscle output) relative to changes in MU DR (ΔDR, i.e. neural input). BB maximum anatomical cross-sectional area (ACSAMAX) was also assessed by MRI. MViF (+64.8% vs. UT, P<0.001) and BB ACSAMAX (+71.9%, P<0.001) were higher in ST. Absolute MU RT was higher in ST (+62.6%, P<0.001), but occurred at similar normalized forces. MU DR did not differ between groups at the same normalized forces. The absolute slope of the ΔFORCE-ΔDR relationship was higher in ST (+66.9%, P=0.002), whereas it did not differ for normalized values. We observed similar MU behaviour between ST athletes and UT controls. The greater absolute force-generating capacity of ST for the same neural input, demonstrates that morphological, rather than neural, factors are the predominant mechanism for their enhanced force generation during submaximal efforts.

Costs of position, velocity, and force requirements in optimal control induce triphasic muscle activation during reaching movement

The nervous system activates a pair of agonist and antagonist muscles to determine the muscle activation pattern for a desired movement. Although there is a problem with redundancy, it is solved immediately, and movements are generated with characteristic muscle activation patterns in which antagonistic muscle pairs show alternate bursts with a triphasic shape. To investigate the requirements for deriving this pattern, this study simulated arm movement numerically by adopting a musculoskeletal arm model and an optimal control. The simulation reproduced the triphasic electromyogram (EMG) pattern observed in a reaching movement using a cost function that considered three terms: end-point position, velocity, and force required; the function minimised neural input. The first, second, and third bursts of muscle activity were generated by the cost terms of position, velocity, and force, respectively. Thus, we concluded that the costs of position, velocity, and force requirements in optimal control can induce triphasic EMG patterns. Therefore, we suggest that the nervous system may control the body by using an optimal control mechanism that adopts the costs of position, velocity, and force required; these costs serve to initiate, decelerate, and stabilise movement, respectively.

Entorhinal cortical Island cells regulate temporal association learning with long trace period

Temporal association learning (TAL) allows for the linkage of distinct, nonsynchronous events across a period of time. This function is driven by neural interactions in the entorhinal cortical–hippocampal network, especially the neural input from the pyramidal cells in layer III of medial entorhinal cortex (MECIII) to hippocampal CA1 is crucial for TAL. Successful TAL depends on the strength of event stimuli and the duration of the temporal gap between events. Whereas it has been demonstrated that the neural input from pyramidal cells in layer II of MEC, referred to as Island cells, to inhibitory neurons in dorsal hippocampal CA1 controls TAL when the strength of event stimuli is weak, it remains unknown whether Island cells regulate TAL with long trace periods as well. To understand the role of Island cells in regulating the duration of the learnable trace period in TAL, we used Pavlovian trace fear conditioning (TFC) with a 60-sec long trace period (long trace fear conditioning [L-TFC]) coupled with optogenetic and chemogenetic neural activity manipulations as well as cell type-specific neural ablation. We found that ablation of Island cells in MECII partially increases L-TFC performance. Chemogenetic manipulation of Island cells causes differential effectiveness in Island cell activity and leads to a circuit imbalance that disrupts L-TFC. However, optogenetic terminal inhibition of Island cell input to dorsal hippocampal CA1 during the temporal association period allows for long trace intervals to be learned in TFC. These results demonstrate that Island cells have a critical role in regulating the duration of time bridgeable between associated events in TAL.

JNK activation in TA and EDL muscle is load-dependent in rats receiving identical excitation patterns

As the excitation–contraction coupling is inseparable during voluntary exercise, the relative contribution of the mechanical and neural input on hypertrophy-related molecular signalling is still poorly understood. Herein, we use a rat in-vivo strength exercise model with an electrically-induced standardized excitation pattern, previously shown to induce a load-dependent increase in myonuclear number and hypertrophy, to study acute effects of load on molecular signalling. We assessed protein abundance and specific phosphorylation of the four protein kinases FAK, mTOR, p70S6K and JNK after 2, 10 and 28 min of a low- or high-load contraction, in order to assess the effects of load, exercise duration and muscle-type on their response to exercise. Specific phosphorylation of mTOR, p70S6K and JNK was increased after 28 min of exercise under the low- and high-load protocol. Elevated phosphorylation of mTOR and JNK was detectable already after 2 and 10 min of exercise, respectively, but greatest after 28 min of exercise, and JNK phosphorylation was highly load-dependent. The abundance of all four kinases was higher in TA compared to EDL muscle, p70S6K abundance was increased after exercise in a load-independent manner, and FAK and JNK abundance was reduced after 28 min of exercise in both the exercised and control muscles. In conclusion, the current study shows that JNK activation after a single resistance exercise is load-specific, resembling the previously reported degree of myonuclear accrual and muscle hypertrophy with repetition of the exercise stimulus.

Loss of direct adrenergic innervation after peripheral nerve injury causes lymph node expansion through IFN-γ

Peripheral nerve injury can cause debilitating disease and immune cell–mediated destruction of the affected nerve. While the focus has been on the nerve-regenerative response, the effect of loss of innervation on lymph node function is unclear. Here, we show that the popliteal lymph node (popLN) receives direct neural input from the sciatic nerve and that sciatic denervation causes lymph node expansion. Loss of sympathetic, adrenergic tone induces the expression of IFN-γ in LN CD8 T cells, which is responsible for LN expansion. Surgery-induced IFN-γ expression and expansion can be rescued by β2 adrenergic receptor agonists but not sensory nerve agonists. These data demonstrate the mechanisms governing the pro-inflammatory effect of loss of direct adrenergic input on lymph node function.

The costs of positon, velocity and force requirements in optimal control induce triphasic muscle activation during reaching movement

The nervous system activates a pair of agonist and antagonist muscles to determine the muscle activation pattern for a desired movement. Although there is a problem with redundancy, it is solved immediately, and movements are generated with characteristic muscle activation patterns in which antagonistic muscle pairs show alternate bursts with a triphasic shape. To investigate the requirements for deriving this pattern, this study simulated arm movement numerically by adopting a musculoskeletal arm model and an optimal control based on the minimization of neural input. The simulation reproduced the triphasic electromyogram (EMG) pattern observed in a reaching movement using a cost function that considered three terms: end-point position, velocity, and force required. The first, second and third bursts of muscle activity were generated by the cost terms of position, velocity and force, respectively. Thus we concluded that the costs of position, velocity and force requirements in optimal control can induce triphasic EMG patterns. Therefore we suggest that the nervous system may control the body by using an optimal control mechanism that adopts the costs of position, velocity and force required, which serve to initiate, decelerate and stabilize movement, respectively.

A unified model of the task-evoked pupil response

The pupil dilates and re-constricts following task events. It is popular to model this task-evoked pupil response as a linear transformation of event-locked impulses, the amplitudes of which are used as estimates of arousal. We show that this model is incorrect, and we propose an alternative model based on the physiological finding that a common neural input drives saccades and pupil size. The estimates of arousal from our model agreed with key predictions: arousal scaled with task difficulty and behavioral performance but was invariant to trial duration. Moreover, the model offers a unified explanation for a wide range of phenomena: entrainment of pupil size and saccade occurrence to task timing, modulation of pupil response amplitude and noise with task difficulty, reaction-time dependent modulation of pupil response timing and amplitude, a constrictory pupil response time-locked to saccades, and task-dependent distortion of this saccade-locked pupil response.

Training-Induced Acute Neuromuscular Responses to Military Specific Test during a Six-Month Military Operation

Limited data are available regarding strength and endurance training adaptations to occupational physical performance during deployment. This study assessed acute training-induced changes in neuromuscular (electromyography; EMG) and metabolic (blood lactate, BLa) responses during a high-intensity military simulation test (MST), performed in the beginning (PRE) and at the end (POST) of a six-month crisis-management operation. MST time shortened (145 ± 21 vs. 129 ± 16 s, −10 ± 7%, p < 0.001) during the operation. Normalized muscle activity increased from PRE to POST in the hamstring muscles by 87 ± 146% (116 ± 52 vs. 195 ± 139%EMGMVC, p < 0.001) and in the quadriceps by 54 ± 81% (26 ± 8 vs. 40 ± 20%EMGMVC, p < 0.001). In addition, higher acute BLa values were measured after MST during POST. Changes in BLa and EMG suggested an increased neural input and metabolic rate during POST MST, likely leading to faster performance times at the end of the operation. High EMG values throughout the different phases of MST suggested that despite the anaerobic nature of the test, the soldiers were able to maintain their voluntary muscle activation level until the end of the test. This indicates only limited neural fatigue during the two-minute high-intensity military specific performance. While learning effect may explain some part of the improvement in the MST performance times, combined strength and endurance training three times per week may improve neuromuscular performance in occupationally relevant tasks.