Training History-Dependent Functional Role of EMG Model-Predicted Antagonist Moments in Knee Extensor Moment Generation in Healthy Young Adults

Resistance training (RT) improves the skeletal muscle’s ability to generate maximal voluntary force and is accompanied by changes in the activation of the antagonist muscle which is not targeted primarily by RT. However, the nature and role of neural adaptation to RT in the antagonist muscle is paradoxical and not well understood. We compared moments, agonist muscle activation, antagonist activation, agonist-antagonist coactivation, and electromyographic (EMG) model-predicted moments generated by antagonist hamstring muscle coactivation during isokinetic knee extension in leg strength-trained (n = 10) and untrained (n = 11) healthy, younger adults. Trained vs. untrained adults were up to 58% stronger. During knee extension, hamstring activation was 1.6-fold greater in trained vs. untrained adults (p = 0.022). This hamstring activation produced 2.6-fold greater model-predicted antagonist moments during knee extension in the trained (42.7 ± 19.55 Nm) vs. untrained group (16.4 ± 12.18 Nm; p = 0.004), which counteracted (reduced) quadriceps knee extensor moments ~43 Nm (0.54 Nm·kg−1) and by ~16 Nm (0.25 Nm·kg−1) in trained vs. untrained. Antagonist hamstring coactivation correlated with decreases and increases, respectively, in quadriceps moments in trained and untrained. The EMG model-predicted antagonist moments revealed training history-dependent functional roles in knee extensor moment generation.

Antagonist surface electromyogram decomposition and the case of the missing motor units

Reece & Herda (2021) reported that an antagonist muscle exhibited an organized motor unit (MU) recruitment scheme during isometric elbow flexion contractions. This control scheme, however, differed from the typical MU control scheme in that MU firing rates did not change between force levels (40% and 70% MVC) in the triceps brachii when it acted as an antagonist to isometric elbow flexion. Here we suggest technological considerations with evidence that may have affected these findings. Additionally, we highlight how this paper offers a promising starting point from which further insight into antagonist MU behaviour can be gathered non-invasively, and suggest future research directions to improve our understanding of MU activity of antagonist muscles in the upper limb.

Abnormal center of mass feedback responses during balance: A potential biomarker of falls in Parkinson’s disease

Although Parkinson disease (PD) causes profound balance impairments, we know very little about how PD impacts the sensorimotor networks we rely on for automatically maintaining balance control. In young healthy people and animals, muscles are activated in a precise temporal and spatial organization when the center of body mass (CoM) is unexpectedly moved that is largely automatic and determined by feedback of CoM motion. Here, we show that PD alters the sensitivity of the sensorimotor feedback transformation. Importantly, sensorimotor feedback transformations for balance in PD remain temporally precise, but become spatially diffuse by recruiting additional muscle activity in antagonist muscles during balance responses. The abnormal antagonist muscle activity remains precisely time-locked to sensorimotor feedback signals encoding undesirable motion of the body in space. Further, among people with PD, the sensitivity of abnormal antagonist muscle activity to CoM motion varies directly with the number of recent falls. Our work shows that in people with PD, sensorimotor feedback transformations for balance are intact but disinhibited in antagonist muscles, likely contributing to balance deficits and falls.

Antagonist Muscle Co-Activation during Kettlebell Single Arm Swing Exercise

The purpose of this study was to determine the muscle activation and co-activation of selected muscles during the kettlebell single arm swing exercise. To the best of our knowledge, this is the first study investigating the muscle co-activation of a kettlebell single arm swing exercise. Nine volunteers participated in the present study (age: 22.6 ± 3.8 years; body mass: 80.4 ± 9.2 kg; height: 175.6 ± 7.5 cm). The electrical muscle activity of eight right agonist/antagonist muscles (AD/PD, ESL/RA, ESI/EO, and GM/RF) were recorded using a surface EMG system (Myon m320RX; Myon, Switzerland) and processed using the integrated EMG to calculate a co-activation index (CoI) for the ascending and descending phases. A significant effect of the ascending and descending phases on the muscles’ CoI was observed. Post hoc analyses showed that the co-activation was significantly higher in the descending phase compared to that in the ascending phase of AD/PD CoI (34.25 ± 18.03% and 24.75 ± 13.03%, p < 0.001), ESL/RA CoI (34.97 ± 17.86% and 24.19 ± 10.32%, p < 0.001), ESI/EO CoI (41.14 ± 10.72% and 30.87 ± 11.26%, p < 0.001), and GM/RF CoI (27.49 ± 12.97% and 34.98 ± 14.97%, p < 0.001). In conclusion, the co-activation of the shoulder muscles varies within the kettlebell single arm swing. The highest level of co-activation was observed in the descending phase of AD/PD and GM/RF CoI, and the lowest level of co-activation was observed during the descending phase, ESL/RA and ESI/EO CoI. In addition, the highest level of co-activation was observed in the ascending phase of ESL/RA and ESI/EO CoI, and the lowest level of co-activation was observed during the ascending phase, AD/PD and GM/RF CoI. The co-activation index could be a useful method for the interpretation of the shoulder and core muscles’ co-activity during a kettlebell single arm swing.

An examination of a potential organized motor unit firing rate and recruitment scheme of an antagonist muscle during isometric contractions

The primary purpose of the present study is to determine if an organized control scheme exists for the antagonist muscle during steady isometric torque. A secondary focus is to better understand how firing rates of the antagonist muscle changes from a moderate- to higher-contraction intensity. Fourteen subjects performed two submaximal isometric trapezoid muscle actions of the forearm flexors that included a linearly increasing, steady force at both 40% and 70% maximum voluntary contraction, and linearly decreasing segments. Surface electromyographic signals of the biceps and triceps brachii were collected and decomposed into constituent motor unit action potential trains. Motor unit firing rate vs. recruitment threshold, motor unit action potential amplitude vs. recruitment threshold, and motor unit firing rate vs. action potential amplitude relationships of the biceps brachii (agonist) and triceps brachii (antagonist) muscles were analyzed. Moderate- to-strong relationships (|r| ³ 0.69) were present for the agonist and antagonist muscles for each relationship with no differences between muscles (p = 0.716, 0.428, 0.182). The y-intercepts of the motor unit firing rate vs. recruitment threshold relationship of the antagonist did not increase from 40% to 70% maximal voluntary contractions (p = 0.96), unlike for the agonist (p = 0.009). The antagonist muscle exhibits a similar motor unit control scheme to the agonist. Unlike the agonist, however, the firing rates of the antagonist did not increase with increasing intensity. Future research should investigate how antagonist firing rates adapt to resistance training and changes in antagonist firing rates in the absence of peripheral feedback.

No effect of passive stretching on neuromuscular function and maximum force-generating capacity in the antagonist muscle

Purpose The present study investigated whether or not passive stretching increases the force-generating capacity of the antagonist muscle, and the possible neuromuscular mechanisms behind. Methods To this purpose, the neuromuscular function accompanying the force-generating capacity was assessed in 26 healthy male volunteers after passive stretching and in a control session. Before and after passive intermittent static stretching of the plantar flexors consisting of five sets × 45 s + 15 s-rest, maximum voluntary isometric contraction (MVC) and surface electromyographic root mean square (sEMG RMS) were measured in the tibialis anterior (the antagonist muscle). Additionally, evoked V wave, H-reflex, and M wave were elicited by nerve stimulation at rest and during MVC. Ankle range of motion (ROM) and plantar flexors MVC and EMG RMS were measured to check for the effectiveness of the stretching manoeuvre. Results No change in MVC [p = 0.670; effect size (ES) − 0.03] and sEMG RMS/M wave during MVC (p = 0.231; ES − 0.09) was observed in the antagonist muscle after passive stretching. Similarly, no change in V wave (p = 0.531; ES 0.16), H-reflex at rest and during MVC (p = 0.656 and 0.597; ES 0.11 and 0.23, respectively) and M wave at rest and during MVC (p = 0.355 and 0.554; ES 0.04 and 0.01, respectively) was observed. An increase in ankle ROM (p < 0.001; ES 0.55) and a decrease in plantar flexors MVC (p < 0.001; ES − 1.05) and EMG RMS (p < 0.05; ES − 1.72 to − 0.13 in all muscles) indicated the effectiveness of stretching protocol. Conclusion No change in the force-generating capacity and neuromuscular function of the antagonist muscle after passive stretching was observed.

Corticomuscular Coherence and Motor Control Adaptations after Isometric Maximal Strength Training

Strength training (ST) induces corticomuscular adaptations leading to enhanced strength. ST alters the agonist and antagonist muscle activations, which changes the motor control, i.e., force production stability and accuracy. This study evaluated the alteration of corticomuscular communication and motor control through the quantification of corticomuscular coherence (CMC) and absolute (AE) and variable error (VE) of the force production throughout a 3 week Maximal Strength Training (MST) intervention specifically designed to strengthen ankle plantarflexion (PF). Evaluation sessions with electroencephalography, electromyography, and torque recordings were conducted pre-training, 1 week after the training initiation, then post-training. Training effect was evaluated over the maximal voluntary isometric contractions (MVIC), the submaximal torque production, AE and VE, muscle activation, and CMC changes during submaximal contractions at 20% of the initial and daily MVIC. MVIC increased significantly throughout the training completion. For submaximal contractions, agonist muscle activation decreased over time only for the initial torque level while antagonist muscle activation, AE, and VE decreased over time for each torque level. CMC remained unaltered by the MST. Our results revealed that neurophysiological adaptations are noticeable as soon as 1 week post-training. However, CMC remained unaltered by MST, suggesting that central motor adaptations may take longer to be translated into CMC alteration.

Effect of Prophylactic Knee Bracing on Anterior Cruciate Ligament Agonist and Antagonist Muscle Forces During Perturbed Walking

Background: Anterior cruciate ligament (ACL) injuries most commonly occur after a perturbation. Prophylactic knee braces (PKBs) are off-the-shelf braces designed to prevent and reduce the severity of knee injuries during sports, yet their effectiveness has been debated. Purpose: To identify differences in ACL agonist and antagonist muscle forces, during braced and unbraced conditions, while walking with the application of unexpected perturbations. Study Design: Controlled laboratory study. Methods: A total of 20 recreational athletes were perturbed during walking at a speed of 1.1 m/s, and motion analysis data were used to create patient-specific musculoskeletal models. Static optimization was performed to calculate the lower-limb muscle forces. Statistical parametric mapping was used to compare muscle forces between the braced and unbraced conditions during the stance phase of the perturbed cycle. Results: The brace reduced muscle forces in the quadriceps (QUADS), gastrocnemius (GAS), and soleus (SOL) but not in the hamstrings. The peak QUADS muscle force was significantly lower with the brace versus without at 49% to 60% of the stance phase (28.9 ± 12.98 vs 14.8 ± 5.06 N/kg, respectively; P < .001) and again at 99% of the stance phase (1.7 ± 0.4 vs 3.6 ± 0.13 N/kg, respectively; P = .049). The SOL muscle force peak was significantly lower with the brace versus without at 25% of the stance phase (1.9 ± 1.7 vs 4.6 ± 3.4 N/kg, respectively; P = .031) and at 39% of the stance phase (1.9 ± 1.4 vs 5.3 ± 5.6 N/kg, respectively; P = .007). In the GAS, there were no significant differences between conditions throughout the whole stance phase except between 97% and 100%, where the braced condition portrayed a smaller peak force (0.23 ± 0.13 vs 1.4 ± 1.1 N/kg for unbraced condition; P = .024). Conclusion: These findings suggested that PKBs that restrict knee hyperextension and knee valgus/varus motion can alter neuromuscular patterns, which result in a reduction of QUADS force. Clinical Relevance: Understanding the way PKBs alter muscle function and knee mechanics can provide invaluable information that will help in making decisions about their use. Further studies should investigate different types of braces and perturbations to evaluate the effectiveness of PKBs.

How Well Do Commonly Used Co-contraction Indices Approximate Lower Limb Joint Stiffness Trends During Gait for Individuals Post-stroke?

Muscle co-contraction generates joint stiffness to improve stability and accuracy during limb movement but at the expense of higher energetic cost. However, quantification of joint stiffness is difficult using either experimental or computational means. In contrast, quantification of muscle co-contraction using an EMG-based Co-Contraction Index (CCI) is easier and may offer an alternative for estimating joint stiffness. This study investigated the feasibility of using two common CCIs to approximate lower limb joint stiffness trends during gait. Calibrated EMG-driven lower extremity musculoskeletal models constructed for two individuals post-stroke were used to generate the quantities required for CCI calculations and model-based estimation of joint stiffness. CCIs were calculated for various combinations of antagonist muscle pairs based on two common CCI formulations: Rudolph et al. (2000) (CCI1) and Falconer and Winter (1985) (CCI2). CCI1 measures antagonist muscle activation relative to not only total activation of agonist plus antagonist muscles but also agonist muscle activation, while CCI2 measures antagonist muscle activation relative to only total muscle activation. We computed the correlation between these two CCIs and model-based estimates of sagittal plane joint stiffness for the hip, knee, and ankle of both legs. Although we observed moderate to strong correlations between some CCI formulations and corresponding joint stiffness, these associations were highly dependent on the methodological choices made for CCI computation. Specifically, we found that: (1) CCI1 was generally more correlated with joint stiffness than was CCI2, (2) CCI calculation using EMG signals with calibrated electromechanical delay generally yielded the best correlations with joint stiffness, and (3) choice of antagonist muscle pairs significantly influenced CCI correlation with joint stiffness. By providing guidance on how methodological choices influence CCI correlation with joint stiffness trends, this study may facilitate a simpler alternate approach for studying joint stiffness during human movement.