Changes in muscle fiber conduction velocity, mean power frequency, and mean EMG voltage during prolonged submaximal contractions

Average muscle fiber conduction velocity, mean power frequency, and mean EMG voltage have been measured in human vastus lateralis during prolonged isometric knee extensions at 10, 20, 30, and 40% of the maximum knee extension force. During contractions at 10 and 20% of maximum force, conduction velocity and mean power frequency rose as the contraction progressed, whereas the conduction velocity and mean power frequency fell at 30 and 40% of the maximum force. The mean EMG voltage rose during the contractions, with steeper increases for higher forces. It is argued that two principal factors influence the EMG during prolonged submaximal contractions: firstly, the fatigue of current active motor units, and, secondly, recruitment of fresh motor units. These factors act in opposition to muscle fiber conduction velocity. Recruitment gives an increase in average conduction velocity, whereas fatigue provokes a slowing in conduction velocity.     

Muscle fiber conduction velocity and mean power spectrum frequency in neuromuscular disorders and in fatigue.

This study investigated the relation of muscle fiber conduction velocity (MFCV) to difference power spectrum mean frequency (MF), their fatigue trends, and differences between their values and their fatigue trends in various neuromuscular disorders. Electromyographic interference pattern was recorded inside the biceps in continuous isometric maximal voluntary contractions. Each subject was encouraged to pull for as long as possible. Fatigue was calculated as percent of time to complete inability to sustain contraction. The MFCV was computed by cross-correlation. The MF was computed by differencing, windowing, FFT, squaring of coefficient, and repeat averaging. There were 33 healthy, 86 polyneuropathic, 28 myasthenic, 13 myotonic, and 32 myopathic patients. Both MFCV and MF changed significantly with fatigue--the MFCV linearly, while the MF in a markedly nonlinear fashion. Both were found to be insensitive to the end stages of muscle fatigue--the MFCV did not change its slope toward complete fatigue, and the MF did not change at all beyond the 40% fatigue point. A statistically sound fatigue regression equation was derived for each, and a nonlinear equation was found to best describe their relationship. Neither MFCV nor its fatigue changes were found to be significantly different across the neuromuscular disorders. The MF, however, was found to be significantly different in some neuromuscular disorders in both its average values and fatigue trends. This study showed, in contrast to the literature, a nonlinear relationship between MFCV and MF. It also shows that neither the MFCV nor the MF had reasonable diagnostic power on its own; however, the MF was very promising to serve as an adjunct to other variables.     

Response to high-intensity eccentric muscle contractions in persons with myopathic disease

Although the response to intense eccentric muscle contractions is well described in normal subjects, concern exists about possible untoward effects in persons with myopathic diseases. We investigated 14 subjects with slowly progressive muscular dystrophies including myotonic muscular dystrophy (n = 9), facioscapulohumeral dystrophy (n = 2), limb-girdle syndrome (n = 2), and Becker muscular dystrophy (n = 1). Control subjects consisted of 18 able-bodied persons. Subjects performed two sets of eight maximal-effort eccentric repetitions of the elbow flexors, with measurement of maximal concentric strength, serum creatine kinase, resting and flexed arm angle, arm circumference, and soreness at days 0, 3, and 7. Although the myopathic group had less initial strength, both groups demonstrated a similar response to the protocol over 7 days. Both groups had a significant rise in serum creatine kinase, which was still elevated at 7 days (P < 0.05). The control group demonstrated a slightly greater injury response in terms of soreness, resting and flexed arm angles, and arm swelling. Both groups of subjects appeared to respond similarly to an acute bout of eccentric contractions. However, the potential long-term effects of this type of exercise in persons with myopathic diseases remains unknown.     

Impact of initial muscle length on force deficit following lengthening contractions in mammalian skeletal muscle

The purpose of this study was to determine whether initial muscle length influenced the extent of isometric force deficit following 20 in vitro lengthening contractions of the soleus muscle from Fischer 344 rats. Force deficit was evaluated following one of five protocols: (1) lengthening contractions from optimal muscle length (Lo) to 120% Lo; (2) lengthening contractions from 80% Lo to Lo; (3) lengthening contractions from Lo to 120% Lo but with a stimulation frequency that elicited the same force as protocol 2; (4) 20 isometric contractions at Lo; (5) 20 stretches +/- 20% Lo in inactive muscle. Following lengthening contractions, extent of force deficit significantly differed between protocols 1, 2, and 3 (P < 0.05). Maximal isometric force (Po) was decreased by approximately 32%, approximately 8%, and approximately 15% in protocols 1, 2, and 3, respectively. In contrast, neither isometric contractions nor passive stretching (protocols 4 and 5) resulted in any reduction in Po. Irrespective of muscle length, the extent of force deficit was highly correlated (R = -0.774, P < 0.001) with peak force during active lengthening. Thus, the magnitude of isometric force deficit following lengthening contractions is influenced by both initial muscle length and peak force development. These findings have important practical implications for both exercise conditioning and rehabilitation, which are discussed.     

Quadriceps low‐frequency fatigue and muscle pain are contraction‐type‐dependent

Eccentric contractions are thought to induce greater low‐frequency fatigue (LFF) and delayed‐onset muscle soreness (DOMS) than concentric contractions. In this study we induced a similar amount of eccentric quadriceps muscle fatigue during either a concentric or eccentric fatigue task to compare LFF and DOMS. Subjects (n = 22) performed concentric or eccentric fatigue tasks using 75% of the pre‐fatigue maximal voluntary contraction (MVC) torque, and both tasks ended when the MVC eccentric torque decreased by 25% pre‐fatigue. When subjects reached the failure criterion during the eccentric and concentric tasks, the concentric MVC was 78 ± 9.8% and 64 ± 8.4% of initial, respectively. LFF was greater after the concentric than the eccentric protocols (22 ± 12.4% and 15 ± 7.6% increase, respectively; P < 0.01). DOMS was over 100% greater for the eccentric protocol. These results indicate that DOMS is not dependent on the events that contribute to LFF. Muscle Nerve, 2010     

Correlation between muscle metabolism and changes in M-wave and surface electromyogram: Dynamic constant load leg exercise in untrained subjects

In untrained subjects exercising on a cycle at constant work loads presented at a sub- or suprathreshold level, reduced M wave amplitude with lengthening of duration was measured in vastus lateralis muscle during and after suprathreshold exercise. M wave changes were correlated with increased blood lactate concentration. At the two work load levels, the increase in root mean square of EMG was rapidly closely adjusted to that of oxygen consumption, confirming the reality of adaptative reflex mechanisms in leg muscles during cycling. © 1997 John Wiley & Sons, Inc. Muscle Nerve 20:1197–1199, 1997     

Recovery of strength is dependent on mTORC1 signaling after eccentric muscle injury

Introduction: Eccentric contractions may cause immediate and long‐term reductions in muscle strength that can be recovered through increased protein synthesis rates. The purpose of this study was to determine whether the mechanistic target‐of‐rapamycin complex 1 (mTORC1), a vital controller of protein synthesis rates, is required for return of muscle strength after injury. Methods: Isometric muscle strength was assessed before, immediately after, and then 3, 7, and 14 days after a single bout of 150 eccentric contractions in mice that received daily injections of saline or rapamycin. Results: The bout of eccentric contractions increased the phosphorylation of mTORC1 (1.8‐fold) and p70s6k1 (13.8‐fold), mTORC1's downstream effector, 3 days post‐injury. Rapamycin blocked mTORC1 and p70s6k1 phosphorylation and attenuated recovery of muscle strength (～20%) at 7 and 14 days. Conclusion: mTORC1 signaling is instrumental in the return of muscle strength after a single bout of eccentric contractions in mice. Muscle Nerve 54 : 914–924, 2016     

Ultrastructural changes after concentric and eccentric contractions of human muscle

Four normal subjects performed a 20 min step test using a step of the same relative height. During the test the quadriceps muscle of one leg contracted concentrically throughout by stepping up, while the contralateral muscle contracted eccentrically by controlling the step down. Thus both muscles performed the same amount of work. Three subjects had bilateral needle biopsies just prior to exercise. All four had bilateral biopsies immediately after exercise, and 24-48 hours later when the muscles which had contracted eccentrically were painful. The samples were examined by light and electron microscopy. No abnormalities were seen in pre-exercise samples nor after exercise in muscles which had contracted concentrically. The muscles which had contracted eccentrically showed some damage immediately after exercise. In the samples taken 24-48 hours after exercise the damage was more marked and involved a greater percentage of fibres. In view of the known differences between these types of contractions it is suggested that the initial damage is mechanically induced. The exacerbation of damage with time could be due to mechanical or chemical factors.     

Electrodiagnosis and muscle biopsy in asymptomatic hyperckemia

Purpose/aim of the study: An increased serum level of creatine kinase (CK) in asymptomatic individuals is a diagnostic challenge, as it may be associated with either physiological conditions, such as exercise or even signal an ominous neuromuscular disease at a presymptomatic stage. The electromyogram (EMG) and the muscle biopsy play a key role in the evaluation of asymptomatic hyperckemia. The objective of this study was to investigate asymptomatic individuals with increased CK levels. Materials and methods: We comparatively studied EMG, quantitative EMG and muscle biopsy in asymptomatic clinically normal individuals with repeatedly increased CK levels. Results: Conventional EMG was abnormal in 76% of patients, while quantitative EMG showed abnormal results in 88.9%. Muscle biopsy was diagnostic in 28%, one patient had neurogenic findings, 40% showed non-specific changes and 28% had normal results. Conclusions: EMG and especially quantitative EMG are highly sensitive in detecting subclinical neuromuscular diseases, whereas muscle biopsy may better contribute in the final diagnosis. No strong correlations were found between histological abnormalities and electrophysiological data, but further research is needed.     

Bradykinesia,muscle weakness and reduced muscle power in Parkinson's disease

Muscle power (force × velocity) could clarify the relationship between weakness and bradykinesia in Parkinson's disease (PD). The aims of this study were to determine if patients with PD were weaker and/or less powerful in their leg extensor muscles than a neurologically normal control group and to determine the relative contributions of force and movement velocity/bradykinesia to muscle power in PD. Forty patients with PD and 40 controls were assessed. Strength in Newtons (N) was measured as the heaviest load the participant could lift. Power in Watts (W) was measured by having the participant perform lifts as fast as possible. The PD group were 172 N weaker (95% CI 28–315) and 124 W less powerful at peak power (95% CI 32–216) than controls. However, velocity at maximal power was only reduced compared with controls when lifting light to medium loads. When lifting heavy loads bradykinesia was no longer apparent in the PD group. These results suggest that reduced muscle power in PD at lighter loads arises from weakness and bradykinesia combined, but at heavier loads arises only from weakness. The absence of bradykinesia in the PD group when lifting heavy loads warrants further investigation. © 2009 Movement Disorder Society     

Excitation frequency and muscle fatigue: electrical responses during human voluntary and stimulated contractions.

Changes in the electrical activity of the human adductor pollicis muscle during fatiguing maximal voluntary contractions (MVCs) were compared to those resulting from equal periods of maximal ulnar nerve stimulation at different frequencies. In each case the force and smoothed, rectified EMG (SRE) were monitored continuously, and the area of the evoked surface action potential (SAP) was measured at intervals. During high-frequency stimulation (50 and 80 Hz), both the SRE and SAP area increased in the first 10 to 20 s, thereafter declining to very low values. With low-frequency stimulation (20 Hz), both increased gradually throughout the contraction. The increases in SAP area were related to a slowing of conduction velocity. In all experiments in which the frequency of stimulation was constant, changes in the SRE and SAP area mirrored one another. In sustained MVCs, the rate of force loss was less than during high-frequency stimulation. SAPs evoked by periodic single maximal shocks to the nerve increased initially in area but then remained relatively constant. The SRE no longer paralleled the SAP; it generally increased initially, but then declined roughly in proportion to the force. When the nerve was maximally stimulated at a progressively reduced frequency (80 to 20 Hz), force loss and SAP area were similar to those recorded during an MVC. The SRE was also similar in form. It is concluded that (a) during continuous high-frequency stimulation, much of the fatigue is due to failure of electrical propagation, probably largely at the muscle fiber membrane; and (b) in voluntary contractions where no similar failure was observed, muscle fatigue is minimized by a progressive reduction in motor unit activation.     

Peak power of muscles injured by lengthening contractions

Excessive or extreme lengthening contractions have a well-characterized depressive effect on skeletal muscle isometric force. In addition to producing force, active muscles must often shorten in order to meet the power requirements of locomotion and other physical activities. However, the impact of lengthening contractions on muscle power is poorly understood. We evaluated the effect of 20 isometric contractions or 20 lengthening contractions (20% strain at 1.5 fiber lengths/s) on the force-velocity-power relationships of mouse soleus muscles in vitro at 35 degrees C. Pre- and posttreatment data were obtained as the muscles shortened through their optimal length (Lo). The isometric treatment did not alter Lo, the curvature of the force-velocity relationship (a/Po), or soleus maximal shortening velocity (Vmax), whereas peak force (Po) displayed a slow, time-dependent decline of 10% across the experiments. Following the lengthening treatment, Lo increased by 6%, a/Po increased by 22%, and Vmax and Po fell by 24% and 26%, respectively. Under optimal conditions for producing power, muscles damaged by lengthening contractions attained 22% less force and shortened 20% more slowly than before damage. Consequently, soleus peak power fell 37% after lengthening, a 2.5-fold greater decline than noted for the isometric treatment. Under the conditions studied here, the excessive power loss following lengthening contractions was due to force and velocity deficits of approximately equal relative magnitude. Because power represents the ability of the muscle to perform work, reductions in both force and shortening velocity should be considered when evaluating and treating lengthening-induced skeletal muscle injuries.     

Effect of caffeine ingestion on torque and muscle activity during resistance exercise in men

Introduction: We examined the effect of caffeine ingestion on muscle torque production and muscle activity at different contraction speeds in trained men. Methods: 10 men (mean age ± SD = 22 ± 1.1 years) volunteered to participate. A double‐blind, randomized cross‐over design was used. Sixty minutes postingestion of caffeine (6 mg kg^?1) or placebo, participants completed 6 repetitions of isokientic knee extension at 3 angular velocities (30°s^?1, 150°s^?1, 300°s^?1) from which peak torque was determined. Electromyographic activity of the vastus medialis was also collected. Results: Repeated measures analysis of variance indicated that muscle torque production was significantly higher (P = 0.02) with caffeine compared with placebo. A significant (P = 0.02) substance by velocity interaction for muscle activity indicated significantly higher vastus medialis muscle activity in the presence of caffeine versus placebo, and this difference was amplified as angular velocity increased. Conclusions: Acute caffeine ingestion improves muscle performance and increases muscle activity during short‐duration maximal dynamic contractions. Muscle Nerve 50: 523–527, 2014     

Surface electromyogram potentials of motor units; Relationship between potential size and unit location in a large human skeletal muscle

The muscle fibers of a motor unit are spread over only part of the total transverse cross section of a skeletal muscle. As a consequence, both the geometric and electrical centers of different units are distributed throughout the cross section. It follows that the estimate of a unit's size, if based on its surface potential measured by an electrode placed on the skin above the muscle, will depend on a number of variables; most specifically, the properties of the volume conductor and the “unit center-to-electrode” distance. An experimental approach to the problem of “depth normalization” of unit potentials is described. The approach is based on the use of a multielectrode and approximate geometric reconstruction of the unit's intramuscular course. The experimental findings are generalized to cross sections of various geometry. The approach is applied to an evaluation of both the size distribution and the size-threshold relationship of the human tibialis anterior muscle.     

Lengthening our perspective: Morphological,cellular, and molecular responses to eccentric exercise

The response of skeletal muscle to unaccustomed eccentric exercise has been studied widely, yet it is incompletely understood. This review is intended to provide an up‐to‐date overview of our understanding of how skeletal muscle responds to eccentric actions, with particular emphasis on the underlying molecular and cellular mechanisms of damage and recovery. This review begins by addressing the question of whether eccentric actions result in physical damage to muscle fibers and/or connective tissue. We next review the symptomatic manifestations of eccentric exercise (i.e., indirect damage markers, such as delayed onset muscle soreness), with emphasis on their relatively poorly understood molecular underpinnings. We then highlight factors that potentially modify the muscle damage response following eccentric exercise. Finally, we explore the utility of using eccentric training to improve muscle function in populations of healthy and aging individuals, as well as those living with neuromuscular disorders. Muscle Nerve 49 : 155–170, 2014     

Inflammation-induced leukocyte accumulation in injured skeletal muscle: role of mast cells

Inflammation consequent to muscle damage is characterized by an accumulation of leukocytes. Our aim in this study was to determine whether mast cells can modulate inflammation-induced leukocyte trafficking. One approach consisted of giving rats a mast cell-degranulating agent, CMP 48/80, prior to a protocol of lengthening contractions inducing inflammation without neutrophil accumulation; in parallel, other rats were given the mast cell-stabilizing agent, cromolyn, prior to injecting muscle with bupivacaine, which induces neutrophil accumulation. Damage was evaluated through measurement of contractile force and inflammation using histochemical and immunohistochemical methods. Stimulation with CMP 48/80 increased the proportion of degranulated mast cells significantly and neutrophil accumulation occurred with lengthening contractions. With bupivacaine, accumulation of neutrophils decreased by 70% when degranulation was inhibited. These results indicate that mast cells are important in the process governing leukocyte trafficking in skeletal muscle trauma and that targeting their inhibition could be an attractive alternative for control of inflammation.     

Mechanomyographic and electromyographic responses to eccentric muscle contractions

Little is known regarding the modulation of torque during eccentric muscle actions. Mechanomyographic (MMG) and electromyographic (EMG) signals have been used to examine motor control strategies. The purpose of this study was to examine the MMG and EMG amplitude and frequency in relation to torque during eccentric muscle contractions. Eight women performed eccentric leg extension muscle contractions at 10-100% of peak torque (PT). A piezoelectric crystal contact sensor and bipolar surface electrodes were placed on the vastus medialis to detect the MMG and EMG signals. Polynomial regression analyses indicated that EMG amplitude (r(2)=0.994) and MMG wavelet center frequency (CF) (r(2)=0.846) increased linearly to 100% eccentric PT, whereas there were no significant relationships for EMG wavelet CF or MMG amplitude and eccentric torque. These results suggested that eccentric torque is primarily modulated through changes in motor unit firing rate.     

The effects of strength,aerobic, and concurrent exercise on skeletal muscle damage in rats

Introduction: In this study we examined oxidative stress and skeletal muscle damage resulting from acute strength, aerobic, or concurrent exercise in rats. Methods: The animals were divided into control (C), strength (SE), aerobic (AE), and combined (CE) exercise groups. They were euthanized at 3 different time‐points (6, 24, and 48 h) after acute exercise. Results: SE exercise rats had increased dichlorofluorescein oxidation at 6 h post‐exercise and decreased superoxide dismutase activity at all time‐points. Glutathione peroxidase activity and sulfhydryl levels were increased in the AE group at 48 h post‐exercise. Serum lactate dehydrogenase activity was increased in the SE and CE groups at 24 h and in the AE group at 48 h. Echo intensity was elevated at 24 h for all groups. Conclusions: Forty‐eight hours was sufficient for complete recovery from oxidative stress and muscle damage in the SE and CE groups, but not in the AE group. Muscle Nerve 50 : 79–86, 2014