Repeated sprint training in hypoxia induces specific skeletal muscle adaptations through S100A protein signaling.

Athletes increasingly engage in repeated sprint training consisting in repeated short all-out efforts interspersed by short recoveries. When performed in hypoxia (RSH), it may lead to greater training effects than in normoxia (RSN); however, the underlying molecular mechanisms remain unclear. This study aimed at elucidating the effects of RSH on skeletal muscle metabolic adaptations as compared to RSN. Sixteen healthy young men performed nine repeated sprint training sessions in either normoxia (FIO2 = 0.209, RSN, n = 7) or normobaric hypoxia (FIO2 = 0.136, RSH, n = 9). Before and after the training period, exercise performance was assessed by using repeated sprint ability (RSA) and Wingate tests. Vastus lateralis muscle biopsies were performed to investigate muscle metabolic adaptations using proteomics combined with western blot analysis. Similar improvements were observed in RSA and Wingate tests in both RSN and RSH groups. At the muscle level, RSN and RSH reduced oxidative phosphorylation protein content but triggered an increase in mitochondrial biogenesis proteins. Proteomics showed an increase in several S100A family proteins in the RSH group, among which S100A13 most strongly. We confirmed a significant increase in S100A13 protein by western blot in RSH, which was associated with increased Akt phosphorylation and its downstream targets regulating protein synthesis. Altogether our data indicate that RSH may activate an S100A/Akt pathway to trigger specific adaptations as compared to RSN.

Motoneuron persistent inward current contribution to increased torque responses to wide-pulse high-frequency neuromuscular electrical stimulation.

PURPOSE: To assess the effect of a remote handgrip contraction during wide-pulse high-frequency (WPHF) neuromuscular electrical stimulation (NMES) on the magnitude of extra torque, progressive increase in torque during stimulation, and estimates of the persistent inward current (PIC) contribution to motoneuron firing in the plantar flexors. METHODS: Ten participants performed triangular shaped contractions to 20% of maximal plantar flexion torque before and after WPHF NMES with and without a handgrip contraction, and control conditions. Extra torque, the relative difference between the initial and final torque during stimulation, and sustained electromyographic (EMG) activity were assessed. High-density EMG was recorded during triangular shaped contractions to calculate ∆F, an estimate of PIC contribution to motoneuron firing, and its variation before vs after the intervention referred to as ∆F change score. RESULTS: While extra torque was not significantly increased with remote contraction (WPHF + remote) vs WPHF (+ 37 ± 63%, p = 0.112), sustained EMG activity was higher in this condition than WPHF (+ 3.9 ± 4.3% MVC EMG, p = 0.017). Moreover, ∆F was greater (+ 0.35 ± 0.30 Hz) with WPHF + remote than control (+ 0.03 ± 0.1 Hz, p = 0.028). A positive correlation was found between ∆F change score and extra torque in the WPHF + remote (r = 0.862, p = 0.006). DISCUSSION: The findings suggest that the addition of remote muscle contraction to WPHF NMES enhances the central contribution to torque production, which may be related to an increased PIC contribution to motoneuron firing. Gaining a better understanding of these mechanisms should enable NMES intervention optimization in clinical and rehabilitation settings, improving neuromuscular function in clinical populations.

M-wave changes caused by brief voluntary and stimulated isometric contractions.

INTRODUCTION: Under isometric conditions, the increase in muscle force is accompanied by a reduction in the fibers' length. The effects of muscle shortening on the compound muscle action potential (M wave) have so far been investigated only by computer simulation. This study was undertaken to assess experimentally the M-wave changes caused by brief voluntary and stimulated isometric contractions. METHODS: Two different methods of inducing muscle shortening under isometric condition were adopted: (1) applying a brief (1 s) tetanic contraction and (2) performing brief voluntary contractions of different intensities. In both methods, supramaximal stimulation was applied to the brachial plexus and femoral nerves to evoke M waves. In the first method, electrical stimulation (20 Hz) was delivered with the muscle at rest, whereas in the second, stimulation was applied while participants performed 5-s stepwise isometric contractions at 10, 20, 30, 40, 50, 60, 70, and 100% MVC. The amplitude and duration of the first and second M-wave phases were computed. RESULTS: The main findings were: (1) on application of tetanic stimulation, the amplitude of the M-wave first phase decreased (~ 10%, P < 0.05), that of the second phase increased (~ 50%, P < 0.05), and the M-wave duration decreased (~ 20%, P < 0.05) across the first five M waves of the tetanic train and then plateaued for the subsequent responses; (2) when superimposing a single electrical stimulus on muscle contractions of increasing forces, the amplitude of the M-wave first phase decreased (~ 20%, P < 0.05), that of the second phase increased (~ 30%, P < 0.05), and M-wave duration decreased (~ 30%, P < 0.05) as force was raised from 0 to 60-70% MVC force. CONCLUSIONS: The present results will help to identify the adjustments in the M-wave profile caused by muscle shortening and also contribute to differentiate these adjustments from those caused by muscle fatigue and/or changes in Na+-K+ pump activity.

Muscle fibre conduction velocity varies in opposite directions after short- vs. long-duration muscle contractions.

INTRODUCTION: The effects of muscle contractions on muscle fibre conduction velocity have normally been investigated for contractions of a given duration and intensity, with most studies being focused on the decline on conduction velocity during/after prolonged contractions. Herein, we perform a systematic analysis of the changes in conduction velocity after voluntary contractions of different durations and intensities. METHODS: Conduction velocity was estimated in the vastus lateralis before and after knee extensor isometric maximal voluntary contractions (MVCs) of 1, 3, 6, 10, 30 and 60 s, and after brief (3 s) contractions at 10, 30, 50, 70, and 90% of MVC force. Measurements were made during the 10-min period following each contraction. RESULTS: (1) Conduction velocity was increased immediately after (1 s) the MVCs of brief (≤ 10 s) duration (12 ± 2%, P < 0.05), and then returned rapidly (within 15 s) to control levels; (2) the extent of the increase in conduction velocity was similar after the 3-s, 6-s, and 10-s MVCs (P > 0.05); (3) the magnitude of the increase in conduction velocity after a brief contraction augmented with the intensity of the contraction (increases of 4.6, 7.7, 11.4, 14.8, and 15.2% for contractions at 10, 30, 50, 70, and 90% of MVC force, respectively); (4) conduction velocity was not decreased immediately after the 30-s MVC (P > 0.05); and (5) conduction velocity did not reach its minimum 1 s after the long (≥ 30 s) MVCs. CONCLUSIONS: Brief (≤ 10 s) muscle contractions induce a short-term increase in conduction velocity, lasting 15 s, while long (≥ 30 s) contractions produce a long-term decrease in conduction velocity, lasting more than 2 min.

The Muscle-Brain Axis and Neurodegenerative Diseases: The Key Role of Mitochondria in Exercise-Induced Neuroprotection.

Regular exercise is associated with pronounced health benefits. The molecular processes involved in physiological adaptations to exercise are best understood in skeletal muscle. Enhanced mitochondrial functions in muscle are central to exercise-induced adaptations. However, regular exercise also benefits the brain and is a major protective factor against neurodegenerative diseases, such as the most common age-related form of dementia, Alzheimer's disease, or the most common neurodegenerative motor disorder, Parkinson's disease. While there is evidence that exercise induces signalling from skeletal muscle to the brain, the mechanistic understanding of the crosstalk along the muscle-brain axis is incompletely understood. Mitochondria in both organs, however, seem to be central players. Here, we provide an overview on the central role of mitochondria in exercise-induced communication routes from muscle to the brain. These routes include circulating factors, such as myokines, the release of which often depends on mitochondria, and possibly direct mitochondrial transfer. On this basis, we examine the reported effects of different modes of exercise on mitochondrial features and highlight their expected benefits with regard to neurodegeneration prevention or mitigation. In addition, knowledge gaps in our current understanding related to the muscle-brain axis in neurodegenerative diseases are outlined.

Dynamic MR imaging of the skeletal muscle in young and senior volunteers during synchronized minimal neuromuscular electrical stimulation.

OBJECTIVE: Neuromuscular electrical stimulation (NMES)-induced isometric contraction is feasible during MRI and can be combined with acquisition of volumetric dynamic MR data, in a synchronous and controlled way. Since NMES is a potent resource for rehabilitation, MRI synchronized with NMES presents a valuable validation tool. Our aim was to show how minimal NMES-induced muscle contraction characterization, as evaluated through phase-contrast MRI, differs between senior and young volunteers. MATERIALS AND METHODS: Simultaneous NMES of the quadriceps muscle and phase-contrast imaging were applied at 3 T to 11 senior (75 ± 3 years) and 12 young volunteers (29 ± 7 years). A current sufficient to induce muscle twitch without knee extension was applied to both groups. RESULTS: Strain vectors were extracted from the velocity fields and strain datasets were compared with non-parametric tests and descriptive statistics. Strain values were noticeably different between both groups at both current intensities and significant differences were observed for similar current level. DISCUSSION: In conclusion, NMES-synchronized MRI could be successfully applied in senior volunteers with strain results clearly different from the younger volunteers. Also, differences within the senior group were detected both in the magnitude of strain and in the position of maximum strain pixels.

Toxic doses of caffeine are needed to increase skeletal muscle contractility.

Discrepant results have been reported regarding an intramuscular mechanism underlying the ergogenic effect of caffeine on neuromuscular function in humans. Here, we reevaluated the effect of caffeine on muscular force production in humans and combined this with measurements of the caffeine dose-response relationship on force and cytosolic free [Ca2+] ([Ca2+]i) in isolated mouse muscle fibers. Twenty-one healthy and physically active men (29 ± 9 yr, 178 ± 6 cm, 73 ± 10 kg, mean ± SD) took part in the present study. Nine participants were involved in two experimental sessions during which supramaximal single and paired electrical stimulations (at 10 and 100 Hz) were applied to the femoral nerve to record evoked forces. Evoked forces were recorded before and 1 h after ingestion of 1) 6 mg caffeine/kg body mass or 2) placebo. Caffeine plasma concentration was measured in 12 participants. In addition, submaximal tetanic force and [Ca2+]i were measured in single mouse flexor digitorum brevis (FDB) muscle fibers exposed to 100 nM up to 5 mM caffeine. Six milligrams of caffeine per kilogram body mass (plasma concentration ~40 µM) did not increase electrically evoked forces in humans. In superfused FDB single fibers, millimolar caffeine concentrations (i.e., 15- to 35-fold above usual concentrations observed in humans) were required to increase tetanic force and [Ca2+]i. Our results suggest that toxic doses of caffeine are required to increase muscle contractility, questioning the purported intramuscular ergogenic effect of caffeine in humans.

Sarcolemmal membrane excitability during repeated intermittent maximal voluntary contractions.

NEW FINDINGS: What is the central question of this study? Is impaired membrane excitability reflected by an increase or by a decrease in M-wave amplitude? What is the main finding and its importance? The magnitude of the M-wave first and second phases changed in completely different ways during intermittent maximal voluntary contractions, leading to the counterintuitive conclusion that it is an increase (and not a decrease) of the M-wave first phase that reflects impaired membrane excitability. ABSTRACT: The study was undertaken to investigate separately the changes in the first and second phases of the muscle compound action potential (M-wave) during 4 min of intermittent maximal voluntary contractions (MVCs) of the quadriceps. M-waves were evoked by supramaximal single electrical stimulation to the femoral nerve delivered in the resting periods between 48 successive MVCs of 3 s. The amplitude, duration and area of the M-wave first and second phases were measured separately, together with muscle conduction velocity and MVC force. During the intermittent MVCs, the amplitude of the M-wave first phase increased uninterruptedly for the first 3 min (12-16%, P < 0.05) and stabilized thereafter, whereas the second phase initially increased for 55-75 s (11-22%, P < 0.05), but decreased subsequently. The enlargement of the first phase occurred in parallel with an increase in its duration, and concomitantly with a decline in conduction velocity (maximal cross-correlations, 0.89-0.97; time lag, 0 s). Also, a significant temporal association was found between the amplitude of the first phase and MVC force (time lag, 0 s; maximal cross-correlations, 0.85-0.97). Conversely, there was no temporal association between the second phase amplitude and conduction velocity or MVC force (time lag, 73-117 s; maximal cross-correlations, 0.65-0.77). It is concluded that the enlargement of the M-wave first phase is the electrical manifestation of impaired muscle membrane excitability. The results highlight the importance of independently analysing the first and second phases, as only the first phase can be used reliably to detect changes in membrane excitability, while the second might be affected by muscle architecture.

Neuromuscular evaluation of arm-cycling repeated sprints under hypoxia and/or blood flow restriction.

PURPOSE: This study aimed to determine the effects of hypoxia and/or blood flow restriction (BFR) on an arm-cycling repeated sprint ability test (aRSA) and its impact on elbow flexor neuromuscular function. METHODS: Fourteen volunteers performed an aRSA (10 s sprint/20 s recovery) to exhaustion in four randomized conditions: normoxia (NOR), normoxia plus BFR (NBFR), hypoxia (FiO2 = 0.13, HYP) and hypoxia plus BFR (HBFR). Maximal voluntary contraction (MVC), resting twitch force (Db10), and electromyographic responses from the elbow flexors [biceps brachii (BB)] to electrical and transcranial magnetic stimulation were obtained to assess neuromuscular function. Main effects of hypoxia, BFR, and interaction were analyzed on delta values from pre- to post-exercise. RESULTS: BFR and hypoxia decreased the number of sprints during aRSA with no significant cumulative effect (NOR 16 ± 8; NBFR 12 ± 4; HYP 10 ± 3 and HBFR 8 ± 3; P < 0.01). MVC decrease from pre- to post-exercise was comparable whatever the condition. M-wave amplitude (- 9.4 ± 1.9% vs. + 0.8 ± 2.0%, P < 0.01) and Db10 force (- 41.8 ± 4.7% vs. - 27.9 ± 4.5%, P < 0.01) were more altered after aRSA with BFR compared to without BFR. The exercise-induced increase in corticospinal excitability was significantly lower in hypoxic vs. normoxic conditions (e.g., BB motor evoked potential at 75% of MVC: - 2.4 ± 4.2% vs. + 16.0 ± 5.9%, respectively, P = 0.03). CONCLUSION: BFR and hypoxia led to comparable aRSA performance impairments but with distinct fatigue etiology. BFR impaired the muscle excitation-contraction coupling whereas hypoxia predominantly affected corticospinal excitability indicating incapacity of the corticospinal pathway to adapt to fatigue as in normoxia.

Neuromuscular adaptations to wide-pulse high-frequency neuromuscular electrical stimulation training.

PURPOSE: No studies have evaluated the potential benefits of wide-pulse high-frequency (WPHF) neuromuscular electrical stimulation (NMES) despite it being an interesting alternative to conventional NMES. Hence, this study evaluated neuromuscular adaptations induced by 3 weeks of WPHF NMES. METHODS: Ten young healthy individuals (training group) completed nine sessions of WPHF NMES training spread over 3 weeks, whereas seven individuals (control group) only performed the first and last sessions. Plantar flexor neuromuscular function (maximal voluntary contraction (MVC) force, voluntary activation level, H reflex, V wave, contractile properties) was evaluated before the first and last training sessions. Each training session consisted of ten 20-s WPHF NMES contractions (pulse duration: 1 ms, stimulation frequency: 100 Hz) interspaced by 40 s of recovery and delivered at an intensity set to initially evoke ~ 5% of MVC force. The averaged mean evoked forces produced during the ten WPHF NMES-evoked contractions of a given session as well as the sum of the ten contractions force time integral (total FTI) were computed. RESULTS: Total FTI (+ 118 ± 98%) and averaged mean evoked forces (+ 96 ± 91%) increased following the 3-week intervention (p < 0.05); no changes were observed in the control group. The intervention did not induce any change (p > 0.05) in parameters used to characterize plantar flexor neuromuscular function. CONCLUSION: Three weeks of WPHF NMES increased electrically evoked forces but induced no other changes in plantar flexor neuromuscular properties. Before introducing WPHF NMES clinically, optimal training program characteristics (such as frequency, duration and intensity) remain to be identified.

Three weeks of sprint interval training improved high-intensity cycling performance and limited ryanodine receptor modifications in recreationally active human subjects.

PURPOSE: Mechanisms underlying the efficacy of sprint interval training (SIT) remain to be understood. We previously reported that an acute bout of SIT disrupts the integrity of the sarcoplasmic reticulum (SR) Ca2+ release channel, the ryanodine receptor 1 (RyR1), in recreationally active human subjects. We here hypothesize that in addition to improving the exercise performance of recreationally active humans, a period of repeated SIT sessions would make the RyR1 protein less vulnerable and accelerate recovery of contractile function after a SIT session. METHODS: Eight recreationally active males participated in a 3-week SIT program consisting of nine sessions of four-six 30-s all-out cycling bouts with 4 min of rest between bouts. RESULTS: Total work performed during a SIT session and maximal power (Wmax) reached during an incremental cycling test were both increased by ~ 7.5% at the end of the training period (P < 0.05). Western blots performed on vastus lateralis muscle biopsies taken before, 1 h, 24 h and 72 h after SIT sessions in the untrained and trained state showed some protection against SIT-induced reduction of full-length RyR1 protein expression in the trained state. SIT-induced knee extensor force deficits were similar in the untrained and trained states, with a major reduction in voluntary and electrically evoked forces immediately and 1 h after SIT (P < 0.05), and recovery after 24 h. CONCLUSIONS: Three weeks of SIT improves exercise performance and provides some protection against RyR1 modification, whereas it does not accelerate recovery of contractile function.

Test-retest reliability of wide-pulse high-frequency neuromuscular electrical stimulation evoked force.

INTRODUCTION: We compare forces evoked by wide-pulse high-frequency (WPHF) neuromuscular electrical stimulation (NMES) delivered to a nerve trunk versus muscle belly and assess their test-retest intraindividual and interindividual reliability. METHODS: Forces evoked during 2 sessions with WPHF NMES delivered over the tibial nerve trunk and 2 sessions over the triceps surae muscle belly were compared. Ten individuals participated in 4 sessions involving ten 20-s WPHF NMES contractions interspaced by 40-s recovery. Mean evoked force and force time integral of each contraction were quantified. RESULTS: For both nerve trunk and muscle belly stimulation, intraindividual test-retest reliability was good (intraclass correlation coefficient > 0.9), and interindividual variability was large (coefficient of variation between 140% and 180%). Nerve trunk and muscle belly stimulation resulted in similar evoked forces. DISCUSSION: WPHF NMES locations might be chosen by individual preference because intraindividual reliability was relatively good for both locations. Muscle Nerve 57: E70-E77, 2018.

Clinical Use of Neuromuscular Electrical Stimulation for Neuromuscular Rehabilitation: What Are We Overlooking?

The clinical success of neuromuscular electrical stimulation (NMES) for neuromuscular rehabilitation is greatly compromised by the poor consideration of different physiological and methodological issues that are not always obvious to the clinicians. Therefore, the aim of this narrative review is to reexamine some of these fundamental aspects of NMES using a tripartite model perspective. First, we contend that NMES does not actually bypass the central nervous system but results in a multitude of neurally mediated responses that contribute substantially to force generation and may engender neural adaptations. Second, we argue that too much emphasis is generally placed on externally controllable stimulation parameters while the major determinant of NMES effectiveness is the intrinsically determined muscle tension generated by the current (ie, evoked force). Third, we believe that a more systematic approach to NMES therapy is required in the clinic and this implies a better identification of the patient-specific impairment and of the potential "responders" to NMES therapy. On the basis of these considerations, we suggest that the crucial steps to ensure the clinical effectiveness of NMES treatment should consist of (1) identifying the neuromuscular impairment with clinical assessment and (2) implementing algorithm-based NMES therapy while (3) properly dosing the treatment with tension-controlled NMES and eventually amplifying its neural effects.

Determinants, analysis and interpretation of the muscle compound action potential (M wave) in humans: implications for the study of muscle fatigue.

The compound muscle action potential (M wave) has been commonly used to assess the peripheral properties of the neuromuscular system. More specifically, changes in the M-wave features are used to examine alterations in neuromuscular propagation that can occur during fatiguing contractions. The utility of the M wave is based on the assumption that impaired neuromuscular propagation results in a decrease in M-wave size. However, there remains controversy on whether the size of the M wave is increased or decreased during and/or after high-intensity exercise. The controversy partly arises from the fact that previous authors have considered the M wave as a whole, i.e., without analyzing separately its first and second phases. However, in a series of studies we have demonstrated that the first and second phases of the M wave behave in a different manner during and after fatiguing contractions. The present review is aimed at five main objectives: (1) to describe the mechanistic factors that determine the M-wave shape; (2) to analyze the various factors influencing M-wave properties; (3) to emphasize the need to analyze separately the first and second M-wave phases to adequately identify and interpret changes in muscle fiber membrane properties; (4) to advance the hypothesis that it is an increase (and not a decrease) of the M-wave first phase which reflects impaired sarcolemmal membrane excitability; and (5) to revisit the involvement of impaired sarcolemmal membrane excitability in the reduction of the force generating capacity.

Short vs. long pulses for testing knee extensor neuromuscular properties: does it matter?

PURPOSE: The present study aimed at comparing knee extensor neuromuscular properties determined with transcutaneous electrical stimulation using two pulse durations before and after a standardized fatigue protocol. METHODS: In the first sub-study, 19 healthy participants (ten women and nine men; 28 ± 5 years) took part to two separate testing sessions involving the characterization of voluntary activation (twitch interpolation technique), muscle contractility (evoked forces by single and paired stimuli), and neuromuscular propagation (M-wave amplitude from vastus lateralis and vastus medialis muscles) obtained at supramaximal intensity with a pulse duration of either 0.2 or 1 ms. The procedures were identical in the second sub-study (N = 11), except that neuromuscular properties were also evaluated after a standardized fatiguing exercise. Electrical stimulation was delivered through large surface electrodes positioned over the quadriceps muscle and a visual analog scale was used to evaluate the discomfort to paired stimuli evoked at rest. RESULTS: There was no difference between pulse durations in the estimates of voluntary activation, neuromuscular propagation, and muscle contractility both in the non-fatigued and fatigued states. The discomfort associated with supramaximal paired electrical stimuli was also comparable between the two pulse durations. CONCLUSIONS: It appears that 0.2- and 1-ms-long pulses provide a comparable evaluation of knee extensor neuromuscular properties.

Ryanodine receptor fragmentation and sarcoplasmic reticulum Ca2+ leak after one session of high-intensity interval exercise.

High-intensity interval training (HIIT) is a time-efficient way of improving physical performance in healthy subjects and in patients with common chronic diseases, but less so in elite endurance athletes. The mechanisms underlying the effectiveness of HIIT are uncertain. Here, recreationally active human subjects performed highly demanding HIIT consisting of 30-s bouts of all-out cycling with 4-min rest in between bouts (≤3 min total exercise time). Skeletal muscle biopsies taken 24 h after the HIIT exercise showed an extensive fragmentation of the sarcoplasmic reticulum (SR) Ca(2+) release channel, the ryanodine receptor type 1 (RyR1). The HIIT exercise also caused a prolonged force depression and triggered major changes in the expression of genes related to endurance exercise. Subsequent experiments on elite endurance athletes performing the same HIIT exercise showed no RyR1 fragmentation or prolonged changes in the expression of endurance-related genes. Finally, mechanistic experiments performed on isolated mouse muscles exposed to HIIT-mimicking stimulation showed reactive oxygen/nitrogen species (ROS)-dependent RyR1 fragmentation, calpain activation, increased SR Ca(2+) leak at rest, and depressed force production due to impaired SR Ca(2+) release upon stimulation. In conclusion, HIIT exercise induces a ROS-dependent RyR1 fragmentation in muscles of recreationally active subjects, and the resulting changes in muscle fiber Ca(2+)-handling trigger muscular adaptations. However, the same HIIT exercise does not cause RyR1 fragmentation in muscles of elite endurance athletes, which may explain why HIIT is less effective in this group.

New insights into the potentiation of the first and second phases of the M-wave after voluntary contractions in the quadriceps muscle.

INTRODUCTION: We investigated the mechanisms underlying the potentiation of the first and second phases of the compound action potential (M-wave) after conditioning contractions. METHODS: M-waves were evoked in the knee extensors before and after isometric maximal voluntary contractions (MVCs) of 1 s, 3 s, 6 s, 10 s, 30 s, and 60 s. The amplitude, duration, and area of the M-wave first and second phases were measured during the 10-min period after each contraction. RESULTS: The magnitude of the M-wave first phase was enlarged only after MVCs of 30 s and 60 s, whereas the second phase increased after all MVCs, regardless of their duration. The enlargement of the first phase remained for longer than 2 min, whereas the potentiation of the second phase lasted only 20 s. CONCLUSIONS: Potentiation of the first phase is the result of fatigue-induced membrane changes, whereas enlargement of the second phase is probably related to shortening of muscle fascicles. Muscle Nerve 55: 35-45, 2017.

Different recoveries of the first and second phases of the M-wave after intermittent maximal voluntary contractions.

PURPOSE: We investigated the recovery of muscle electrical properties after intermittent intense exercise by examining separately the first and second phases of the muscle compound action potential (M-wave). METHODS: M-waves and mechanical twitches were obtained using femoral nerve stimulation throughout the 30-min recovery period following 48 successive intermittent 3-s MVCs. The amplitude, duration, and area of the M-wave first and second phases, and the peak twitch force were measured from the knee extensors. RESULTS: The amplitudes of both the first and second M-wave phases were increased immediately after exercise (P < 0.05), but, whereas the first phase remained enlarged for 5 min after exercise, the increase of the second phase only lasted for 10 s. After 30 min of recovery, the amplitude, area, and duration of both the first and second phases were decreased compared to control values (10-20%, P < 0.05). A significant temporal association was found between the changes in the amplitude and duration of the M-wave first phase (maximal cross correlations, 0.9-0.93; time lag, 0 s). A significant, negative temporal relation was found between the amplitude of the M-wave first phase and the peak twitch force during recovery (P < 0.05). CONCLUSIONS: The prolonged enlargement of the M-wave first phase during recovery seems primarily related to fatigue-induced changes in membrane properties, whereas the extremely short recovery of the second phase might be related to changes in muscle architectural features. It is concluded that muscle excitability is impaired even after intermittent fatiguing contractions which allow partial clearance of extracellular K+.

Effects of glenoid inclination and acromion index on humeral head translation and glenoid articular cartilage strain.

BACKGROUND: Previous clinical studies have reported associations between glenoid inclination (GI), the acromion index (AI), and the critical shoulder angle (CSA) on the one hand and the occurrence of glenohumeral osteoarthritis and supraspinatus tendon tears on the other hand. The objective of this work was to analyze the correlations and relative importance of these different anatomic parameters. METHODS: Using a musculoskeletal shoulder model developed from magnetic resonance imaging scans of 1 healthy volunteer, we varied independently GI from 0° to 15° and AI from 0.5 to 0.8. The corresponding CSA varied from 20.9° to 44.1°. We then evaluated humeral head translation and critical strain volume in the glenoid articular cartilage at 60° of abduction in the scapular plane. These values were correlated with GI, AI, and CSA. RESULTS: Humeral head translation was positively correlated with GI (R = 0.828, P < .0001), AI (R = 0.539, P < .0001), and CSA (R = 0.964, P < .0001). Glenoid articular cartilage strain was also positively correlated with GI (R = 0.489, P = .0004) but negatively with AI (R = -0.860, P < .0001) and CSA (R = -0.285, P < .0473). CONCLUSIONS: The biomechanical shoulder model is consistent with clinical observations. The prediction strength of CSA is confirmed for humeral head translation and thus presumably for rotator cuff tendon tears, whereas the AI seems more appropriate to evaluate the risk of glenohumeral osteoarthritis caused by excessive articular cartilage strain. As a next step, we should corroborate these theoretical findings with clinical data.

Differences in the recruitment curves obtained with monopolar and bipolar electrode configurations in the quadriceps femoris.

INTRODUCTION: We sought to verify whether the stimulation intensity at which M-wave amplitude reaches a plateau actually corresponds to full motor unit activation in monopolar and bipolar configurations. METHODS: M-waves and twitches were evoked using femoral nerve stimulation of gradually increasing intensity in 21 subjects. Recruitment curves corresponding to the amplitude of the first phase (AmpliFIRST ) and peak-to-peak amplitude (AmpliPP ) of the M-wave were obtained in the vastus lateralis, vastus medialis, and rectus femoris in monopolar and bipolar configurations. RESULTS: In all muscles, bipolar M-waves and twitches reached plateau at a significantly lower stimulus intensity compared with monopolar M-waves (P < 0.05). The different behavior of monopolar and bipolar M-waves with stimulus intensity was found for both AmpliFIRST and AmpliPP . CONCLUSIONS: In a bipolar configuration, the stimulus intensity at which M-waves plateau should be increased by at least 10%-20% to achieve complete motor unit recruitment. Muscle Nerve 54: 118-131, 2016.