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 change 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 versus recruitment threshold, motor unit action potential amplitude versus recruitment threshold, and motor unit firing rate versus action potential amplitude relationships of the biceps brachii (agonist) and triceps brachii (antagonist) muscles were analyzed. Moderate- to-strong relationships (|r| ≥ 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 versus 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.NEW & NOTEWORTHY This is the first study to explore a potential motor unit control scheme and quantify changes in firing rates with increasing intensity of an antagonist muscle during isometric contractions. We demonstrate that the antagonist muscle possesses an organized motor unit firing rate and recruitment scheme similar to the agonist muscle during isometric forearm flexion, but unlike the agonist muscle, there was no significant increase in firing rates from a moderate- to higher-intensity isometric contraction.

An examination of motor unit firing rates during steady torque of maximal efforts with either an explosive or slower rate of torque development.

NEW FINDINGS: What is the central question of this study? The aim was to explore agonist and antagonist motor unit firing rates during maximal efforts performed with either an explosive or a slower rate of torque development. What is the main finding and its importance? The antagonist muscle presented a motor unit firing rate relationship similar to the agonist muscle. Additionally, the motor units of both muscles exhibited higher firing rates during explosive maximal contractions than during maximal contractions performed at a slower rate of torque development. These results could prove useful to future research analysing the effects of age, disease, resistance training and/or fatigue-related alterations to motor unit firing rates. ABSTRACT: The primary purpose of the present study was to examine motor unit (MU) firing rates in agonist and antagonist muscles during periods of steady, maximal efforts using explosive and slower rates of torque development. A secondary purpose was to analyse the MU firing rate versus action potential amplitude relationships of the agonist and antagonist muscles during maximal efforts. Thirteen subjects (mean ± SD; age, 21.2 ± 3.6 years; mass 81.1 ± 21.3 kg; and stature, 177.1±9.9 cm) performed two maximal isometric trapezoid muscle actions of the elbow flexors that included either an explosive or a slower, linearly increasing rate (ramp) of torque development. Surface EMG signals of the biceps brachii (BB) and triceps brachii (TB) muscles were collected and decomposed into their constituent MU action potential trains. The MU firing rate versus action potential amplitude relationships of the BB (agonist) and TB (antagonist) muscles were analysed. Moderate to strong relationships (|r| ≥ 0.65) were present for the explosive and ramp contractions in the agonist and antagonist muscles. Firing rates of smaller and larger MUs were higher during the explosive [mean ± SD; agonist = 18.1 ± 6.9 pulses per second (pps), antagonist = 22.0±3.9 pps] than the ramp (agonist = 14.0 ± 5.1 pps, antagonist = 18.3 ± 4.4 pps) contractions for the agonist (P = 0.013) and antagonist muscles (P = 0.007). The antagonist muscle exhibits a similar MU firing rate versus action potential amplitude relationship to the agonist muscle at maximal efforts. Future research should investigate the effects of short-term resistance training on antagonist firing rates and the involvement of peripheral feedback on firing rates during maximal efforts performed at various rates of torque development.

Effects of low-load resistance training with blood flow restriction on muscle fiber myofibrillar and extracellular area.

Blood flow restriction applied during low-load resistance training (LL-BFR) induces a similar increase in the cross-sectional area of muscle fibers (fCSA) compared to traditional high-load resistance training (HL-RT). However, it is unclear whether LL-BFR leads to differential changes in myofibrillar spacing in muscle fibers and/or extracellular area compared to HL-RT. Therefore, this study aimed to investigate whether the hypertrophy of type I and II fibers induced by LL-BFR or HL-RT is accompanied by differential changes in myofibrillar and non-myofibrillar areas. In addition, we examined if extracellular spacing was differentially affected between these two training protocols. Twenty recreationally active participants were assigned to LL-BFR or HL-RT groups and underwent a 6-week training program. Muscle biopsies were taken before and after the training period. The fCSA of type I and II fibers, the area occupied by myofibrillar and non-myofibrillar components, and extracellular spacing were analyzed using immunohistochemistry techniques. Despite the significant increase in type II and mean (type I + II) fCSA (p < 0.05), there were no significant changes in the proportionality of the myofibrillar and non-myofibrillar areas [∼86% and ∼14%, respectively (p > 0.05)], indicating that initial adaptations to LL-BFR are primarily characterized by conventional hypertrophy rather than disproportionate non-myofibrillar expansion. Additionally, extracellular spacing was not significantly altered between protocols. In summary, our study reveals that LL-BFR, like HL-RT, induces skeletal muscle hypertrophy with proportional changes in the areas occupied by myofibrillar, non-myofibrillar, and extracellular components.

Myofiber hypertrophy adaptations following 6 weeks of low-load resistance training with blood flow restriction in untrained males and females.

The effects of low-load resistance training with blood flow restriction (BFR) on hypertrophy of type I/II myofibers remains unclear, especially in females. The purpose of the present study is to examine changes in type I/II myofiber cross-sectional area (fCSA) and muscle CSA (mCSA) of the vastus lateralis (VL) from before (Pre) to after (Post) 6 wk of high-load resistance training (HL; n = 15, 8 females) and low-load resistance training with BFR (n = 16, 8 females). Mixed-effects models were used to analyze fCSA with group (HL, BFR), sex (M, F), fiber type (I, II), and time (Pre, Post) included as factors. mCSA increased from pre- to posttraining (P < 0.001, d = 0.91) and was greater in males compared with females (P < 0.001, d = 2.26). Type II fCSA increased pre- to post-HL (P < 0.05, d = 0.46) and was greater in males compared with females (P < 0.05, d = 0.78). There were no significant increases in fCSA pre- to post-BFR for either fiber type or sex. Cohen's d, however, revealed moderate effect sizes in type I and II fCSA for males (d = 0.59 and 0.67), although this did not hold true for females (d = 0.29 and 0.34). Conversely, the increase in type II fCSA was greater for females than for males after HL. In conclusion, low-load resistance training with BFR may not promote myofiber hypertrophy to the level of HL resistance training, and similar responses were generally observed for males and females. In contrast, comparable effect sizes for mCSA and 1-repetition maximum (1RM) between groups suggest that BFR could play a role in a resistance training program.NEW & NOTEWORTHY This is the first study, to our knowledge, to examine myofiber hypertrophy from low-load resistance training with blood flow restriction (BFR) in females. Although this type of training did not result in myofiber hypertrophy, there were comparable increases in muscle cross-sectional area compared with high-load resistance training. These findings possibly highlight that males and females respond in a similar manner to high-load resistance training and low-load resistance training with BFR.