Central Activation Failure Research Articles

The effect of obesity on central activation failure during ankle fatigue: a pilot investigation

ABSTRACT Background: In a forward-directed oscillation, individuals who are obese may be at higher risk of falls due to weaker ankle dorsiflexor muscles as the prime controllers of the balance recovery. Muscle recovery may be negatively affected by fatigue at either the central (activation) and/or peripheral (contraction) levels. Additional body weight support, as required with obesity, may increase lower extremity muscle fatigue development. Purpose: The objective of this pilot study was to quantify the relationship between body mass index (BMI) and fatigue symptoms quantified as endurance time, torque loss, and central activation failure for the tibialis anterior. Methods: Twenty-two young males (mean BMI = 27.0 kg/m2; range: 20.5–36.7 kg/m2) completed maximum voluntary isometric contractions (MVICs) of the ankle dorsiflexors before (pre-MVIC) and after (post-MVIC) a sustained isometric fatiguing task at 60% of their strength. Electrical stimulation was superimposed during each MVIC to identify central activation failure. Results: Pre-fatigue central activation was equivalent across participants. However, BMI and pre-MVIC explained 59% of the variation in central activation failure after the fatiguing task as well as 29% of the variation in endurance time. In fact, a significant effect of obesity on central activation failure was observed with fatigue. Finally, 43% of the torque loss following fatigue variation was explained only with pre-MVIC. Conclusions: The findings of this pilot investigation indicate that endurance and central activation after fatigue may be impaired with increased BMI. This finding may aid in the evaluation of falls mechanisms and the development of falls prevention strategies.

Reliability of the Superimposed-Burst Technique in Patients With Patellofemoral Pain: A Technical Report

The superimposed-burst (SIB) technique is commonly used to quantify central activation failure after knee-joint injury, but its reliability has not been established in pathologic cohorts. To assess within-session and between-sessions reliability of the SIB technique in patients with patellofemoral pain. Descriptive laboratory study. University laboratory. A total of 10 patients with self-reported patellofemoral pain (1 man, 9 women; age = 24.1 ± 3.8 years, height = 167.8 ± 15.2 cm, mass = 71.6 ± 17.5 kg) and 10 healthy control participants (3 men, 7 women; age = 27.4 ± 5.0 years, height = 173.5 ± 9.9 cm, mass = 78.2 ± 16.5 kg) volunteered. Participants were assessed at 6 intervals spanning 21 days. Intraclass correlation coefficients (ICCs [3,3]) were used to assess reliability. Quadriceps central activation ratio, knee-extension maximal voluntary isometric contraction force, and SIB force. The quadriceps central activation ratio was highly reliable within session (ICC [3,3] = 0.97) and between sessions through day 21 (ICC [3,3] = 0.90-0.95). Acceptable reliability of knee extension (ICC [3,3] = 0.75-0.91) and SIB force (ICC [3,3] = 0.77-0.89) was observed through day 21. The SIB technique was reliable for clinical research up to 21 days in patients with patellofemoral pain.

Direct and indirect measurement of neuromuscular fatigue in Canadian football players.

This study assessed the effects of a fatiguing game simulation (G-Sim) on the balance of collegiate Canadian football players. The purpose of the study was to evaluate postural control as a potential tool for monitoring neuromuscular fatigue (NMF) in collision-based team sports. Fifteen male Canadian football players were recruited (mean±SD: age 21.8±1.6 years, weight 97.6±14.7 kg). Indirect NMF measures (postural sway and countermovement jump (CMJ)) were performed 24 h before (TBase), immediately before (TPre) and after (TPost), and 24 h (T24) and 48 h after (T48) a Canadian football G-Sim. Peak isometric knee extensor torque of a maximal voluntary contraction (MVC) and electrically evoked tetani at 20 Hz (P20) and 80 Hz (P80) were also recorded as direct NMF measures at TBase, TPre, TPost, and T48. At TPost, we observed significant declines in MVC, P20, and the MVC/P80 ratio (-15.3%, -15.7%, and -12.1%, respectively; n=12) along with reductions in CMJ takeoff velocity and peak power (-6.9% and -6.5%, respectively; n=12) and larger area of the center of pressure trajectory (95.2%; n=10) during a 60-s postural sway task. All variables were no longer different than baseline by T48. Acute neuromuscular impairment in this cohort is likely attributable to alterations in excitation-contraction coupling due to structural damage and central activation failure. Congruency between the direct and indirect measures of NMF suggests monitoring postural sway has the potential to identify both neuromuscular and somatosensory alterations induced by acute game-induced fatigue in collision-based team sports players.

Post-stroke fatigue: a deficit in corticomotor excitability?

The pathophysiology of post-stroke fatigue is poorly understood although it is thought to be a consequence of central nervous system pathophysiology. In this study we investigate the relationship between corticomotor excitability and self-reported non-exercise related fatigue in chronic stroke population. Seventy first-time non-depressed stroke survivors (60.36 ± 12.4 years, 20 females, 56.81 ± 63 months post-stroke) with minimal motor and cognitive impairment were included in the cross-sectional observational study. Fatigue was measured using two validated questionnaires: Fatigue Severity Scale 7 and Neurological Fatigue Index - Stroke. Perception of effort was measured using a 0-10 numerical rating scale in an isometric biceps hold-task and was used as a secondary measure of fatigue. Neurophysiological measures of corticomotor excitability were performed using transcranial magnetic stimulation. Corticospinal excitability was quantified using resting and active motor thresholds and stimulus-response curves of the first dorsal interosseous muscle. Intracortical M1 excitability was measured using paired pulse paradigms: short and long interval intracortical inhibition in the same hand muscle as above. Excitability of cortical and subcortical inputs that drive M1 output was measured in the biceps muscle using a modified twitch interpolation technique to provide an index of central activation failure. Stepwise regression was performed to determine the explanatory variables that significantly accounted for variance in the fatigue and perception scores. Resting motor threshold (R = 0.384; 95% confidence interval = 0.071; P = 0.036) accounted for 14.7% (R(2)) of the variation in Fatigue Severity Scale 7. Central activation failure (R = 0.416; 95% confidence interval = -1.618; P = 0.003) accounted for 17.3% (R(2)) of the variation in perceived effort score. Thus chronic stroke survivors with high fatigue exhibit high motor thresholds and those who perceive high effort have low excitability of inputs that drive motor cortex output. We suggest that low excitability of both corticospinal output and its facilitatory synaptic inputs from cortical and sub-cortical sites contribute to high levels of fatigue after stroke.

The Role of Central and Peripheral Muscle Fatigue in Postcancer Fatigue: A Randomized Controlled Trial

ContextPostcancer fatigue is a frequently occurring problem, impairing quality of life. Little is known about (neuro)physiological factors determining postcancer fatigue. It may be hypothesized that postcancer fatigue is characterized by low peripheral muscle fatigue and high central muscle fatigue. ObjectivesThe aims of this study were to examine whether central and peripheral muscle fatigue differ between fatigued and non-fatigued cancer survivors and to examine the effect of cognitive behavioral therapy (CBT) on peripheral and central muscle fatigue of fatigued cancer survivors in a randomized controlled trial. MethodsSixteen fatigued patients in the intervention group (CBT) and eight fatigued patients in the waiting list group were successfully assessed at baseline and six months later. Baseline measurements of 20 fatigued patients were compared with 20 non-fatigued patients. A twitch interpolation technique and surface electromyography were applied, respectively, during sustained contraction of the biceps brachii muscle. ResultsMuscle fiber conduction velocity (MFCV) and central activation failure (CAF) were not significantly different between fatigued and non-fatigued patients. Change scores of MFCV and CAF were not significantly different between patients in the CBT and waiting list groups. Patients in the CBT group reported a significantly larger decrease in fatigue scores than patients in the waiting list group. ConclusionPostcancer fatigue is neither characterized by abnormally high central muscle fatigue nor by low peripheral muscle fatigue. These findings suggest a difference in the underlying physiological mechanism of postcancer fatigue vs. other fatigue syndromes.

Stimulated Contractions Delay and Prolong Central Fatigue Compared With Voluntary Contractions in Men

Voluntary and stimulated contractions are commonly used in sports training and rehabilitation, and it is well known that both these kinds of contractions generate central fatigue. However, to date, there is a lack of research on the comparison of the mechanisms by which these 2 exercises induce central disturbances. Central fatigue can be characterized by central activation failure during maximal voluntary contraction (MVC). Superimposition of an electrical stimulation onto MVC has been used to detect central activation failure. Completeness of activation has been quantified by the central activation ratio (CAR) = MVC/(MVC + stimulated force). The aim was not only to evaluate the CAR immediately after fatiguing voluntary (VOL) and stimulated (STIM) contractions but also to compare recovery duration over different time periods (prefatigue: PRE condition; immediate postfatigue: POST condition; after a 5-minute recovery: POST 5 condition; after a 30-minute recovery: POST 30 condition) (n = 18). Results showed that in the POST condition, the CAR is more affected for the VOL contractions than for the STIM contractions (p < 0.001). The CAR was affected for the STIM contractions only in the POST 5 condition (p < 0.05). In the POST 30 condition, the CAR was incomplete for the STIM contractions, whereas it was complete for the VOL contractions (p < 0.01). In conclusion, the VOL contractions alter the CAR more than the STIM contractions immediately after their completion. However, the effects of the STIM contractions on the CAR are delayed and prolonged.

Passive-heat stress does not induce muscle fatigue, central activation failure or changes in intracortical properties of wrist flexors

This study evaluated the effect of passive-heat stress on the neuromuscular properties of the wrist flexor muscles, which are commonly used in manual labour hand tasks. A combination of techniques were utilised, involving nerve stimulation and paired-pulse transcranial magnetic stimulation to assess changes in muscle strength, contractile properties, fatigue-resistance and central activation as well as indices of intracortical excitability in 10healthy humans who were exposed to a passive heat stress protocol as well as a normothermia control protocol. Passive-heat stress increased core body temperature ∼1°C (37.2 ± 0.4 to 38.2 ± 0.4°C ; p < 0.01), mean skin temperature (34.5 ± 0.7°C to 37.3 ± 1.1°C; p < 0.01), and heart rate (79.5 ± 20.0 to 110.0 ± 23.0 beats/min; p = 0.04). No effect was observed on muscle strength, contractile properties, muscle fatigability, central activation orindices of intracortical excitability (p > 0.05). These data indicate that allowing internal temperatures of workers to increase ≤1.0°C does not affect neuromuscular properties of the wrist flexors. Statement of Relevance: Exercise-heat stress has been shown to reduce human performance and exacerbate muscle fatigue. However, lessis known about passive-heat stress, especially during milder heat stress encountered in many occupational settings. Accordingly, the effect of occupationally relevant passive-heat stress on the neuromuscular properties of thewristflexors was examined.

Commentaries on Viewpoint: Can muscle size fully account for strength differences between children and adults?

# {#article-title-2} to the editor: As comprehensively explained in their Viewpoint article ([1][1]), the answer to the question posed in the title has received conflicting answers. Since the contractile machinery in children is the same as that in adults, there is no reason to believe that

Lack of quadriceps dysfunction in women with early knee osteoarthritis

Quadriceps dysfunction, specifically weakness and central activation failure (CAF), has been implicated in the development and progression of knee osteoarthritis (OA), though few data are available to confirm its presence in early OA. The purpose of this study was to determine the presence and magnitude of quadriceps dysfunction in those with and without early knee OA. Thirty-five female volunteers were classified into two groups, OA (n=22) and control (n=13), based on the presence [Kellgren-Lawrence (K-L) grade 2] or absence (K-L grade 0-1) of mild OA, respectively. Isometric quadriceps strength and central activation ratio (CAR) were assessed and compared between groups utilizing a one-way ANOVA. Frequency statistics and Fisher's exact test were used to compare the percentage of women with and without CAF between groups. Quadriceps strength (control: 1.47+/-0.62 Nm/kg; OA: 1.30+/-0.62 Nm/kg; p=0.45) was not significantly different for women with and without mild OA. Further, the CAR (control: 0.91+/-0.07; OA: 0.87+/-0.12; p=0.19) did not differ between groups; however, women in both groups presented with CAF (control: 54%; OA: 73%; p=0.29). Our results suggest that the women with mild osteoarthritis do not present with quadriceps dysfunction.

Evidence Of Central And Peripheral Fatigue After A Functional Fatigue Protocol

Muscle fatigue often occurs during athletic participation, and may lead to injury. The mechanisms that produce muscular fatigue during intermittent, multi-directional exercise (e.g., soccer or basketball) remain unknown. We propose that central activation failure (CAF) will account for a major portion of the decrease in muscle force production that occurs during a functional fatigue protocol (FFP) designed to simulate high-level activities. PURPOSE: To determine the extent of central and peripheral fatigue during a FFP in unimpaired individuals. METHODS: Fourteen (7 M, 7 F) recreationally-active participants volunteered for this study (age: 21±2years, height: 175±9cm, mass: 68±8kg). The FFP consisted of a maximum-effort timed 90m agility course and 5 standing broad jumps for maximum distance. The FFP was repeated (with a 5-sec rest between each repetition) until the time to complete the agility course exceeded 150% of the initial repetition. Voluntary (MVC) and electrically-elicited (EEC) peak isometric quadriceps torque, and maximum vertical jump height (VJ), were measured pre- and post-FFP. Central fatigue was assessed by using the twitch superimposition technique to measure CAF in the quadriceps. A 130V, 10 pulse train of electrical impulses (lasting 100ms) were delivered via two electrodes placed over the quadriceps during a 3s MVC. Peak torque was calculated 100ms prior to, and immediately after the initiation of the electrical pulses. CAF was calculated as the change in peak torque (EEC-MVC) divided by the EEC torque. Peripheral fatigue was assessed by examining the change in EEC torque. Paired t-tests and bivariate correlations were performed to analyze the results between conditions. RESULTS: CAF increased post-fatigue (pre:3.5±2.8%; post:10.2±6.2%, p = 0.004). Both MVC (166.4±40.1Nm to 139.1±42.3Nm, p = 0.010) and EEC (172.7±41.8Nm to 153.7±40.7Nm, p = 0.018) decreased post-fatigue. The change in CAF was highly correlated to the loss of MVC torque (r = 0.797), explaining 59.4% of the variance (p = 0.002). VJ also decreased post-fatigue (48.5±8.3cm to 45.4±11.8cm, p = 0.034). CONCLUSION: This FFP produces significant levels of central and peripheral fatigue and decreases isometric quadriceps force and VJ height. The loss of voluntary muscle force is significantly related to the change in CAF.

Alteration of neuromuscular function in squash

The alteration in neuromuscular function of knee extensor muscles was characterised after a squash match in 10 trained players. Maximal voluntary contraction (MVC) and surface EMG activity of vastus lateralis (VL) and vastus medialis (VM) muscles were measured before and immediately after a 1-h squash match. M-wave and twitch contractile properties were analysed following single stimuli. MVC declined (280.5 ± 46.8 vs. 233.6 ± 35.4 N m, −16%; P < 0.001) after the exercise and this was accompanied by an impairment of central activation, as attested by decline in voluntary activation (76.7 ± 10.4 vs. 71.3 ± 9.6%, −7%; P < 0.05) and raw EMG activity of the two vastii (−17%; P < 0.05), whereas RMS/M decrease was lesser (VL: −5%; NS and VM: −12%; P = 0.10). In the fatigued state, no significant changes in M-wave amplitude (VL: −9%; VM: −5%) or duration were observed. Following exercise, the single twitch was characterised by lower peak torque (−20%; P < 0.001) as well as shorter half-relaxation time (−13%; P < 0.001) and reduced maximal rate of twitch tension development (−23%; P < 0.001) and relaxation (−17%; P < 0.05). A 1-h squash match play caused peripheral fatigue by impairing excitation–contraction coupling, whereas sarcolemmal excitability seems well preserved. Our results also emphasise the role of central activation failure as a possible mechanism contributing to the torque loss observed in knee extensors. Physical conditioners should consider these effects when defining their training programs for squash players.

Different types of fatigue in patients with facioscapulohumeral dystrophy, myotonic dystrophy and HMSN-I. Experienced fatigue and physiological fatigue

Although fatigue is a common symptom in neuromuscular disorders, little is known about different types of fatigue. Sixty-five FSHD, 79 adult-onset MD and 73 HMSN type I patients were studied. Experienced fatigue was assessed with the CIS-fatigue subscale. Physiological fatigue was measured during a 2-min sustained maximal voluntary contraction of the biceps brachii muscle using the twitch interpolation technique to assess central activation failure (CAF) and peripheral fatigue. Experienced fatigue, CAF and peripheral fatigue appeared to be predominantly separate types of fatigue.

Contrasting Influences of Age and Sex on Muscle Fatigue

Greater resistance to muscle fatigue has been observed in women versus men and in older versus young individuals. As suggested mechanisms for these differences include task intensity and duty cycle, the purpose of this study was to evaluate fatigue in healthy young and older men and women during maximum-effort isometric contractions with a 70% duty cycle (7 s of contraction, 3 s of rest). We hypothesized that no differences in fatigue would be observed across age or sex, in contrast to studies incorporating lower duty cycles. The protocol was carried out on ankle dorsiflexors of older (73 +/- 1 yr) and younger (25 +/- 1 yr) men and women. Volitional and stimulated force, compound muscle action potential, and muscle contractile responses were collected before, during, and immediately after the fatigue protocol. These measurements allowed for assessment of fatigue as well as central and peripheral activation. At baseline, older subjects had longer force half-relaxation times and less twitch potentiation than younger subjects, consistent with a slower muscle phenotype. During contractions, younger subjects fatigued more than older subjects did, with no differences between men and women. Central activation decreased similarly in all groups with fatigue. There were no fatigue-related differences in peripheral excitation or contractile properties attributable to age or sex. These data indicate that age-related differences in fatigue are observed even during intermittent MVC with a high duty cycle, and that these differences are independent of central and peripheral activation. Further, it seems that sex-based differences in both fatigue and central activation failure were abolished with this duty cycle. Overall, these results suggest that age- and sex-based differences in fatigue arise from distinct mechanisms.

Motor performance during and following acute alcohol intoxication in healthy non-alcoholic subjects

Chronic alcohol abuse has adverse effects on skeletal muscle, and reduced muscle strength is frequently seen in chronic alcoholics. In this study the acute effects of moderate alcohol intoxication on motor performance was evaluated in 19 non-alcoholic healthy subjects (10 women, 9 men). A randomised double-blinded placebo controlled design was applied to subjects receiving alcohol in juice and pure juice at two separate test periods. Isokinetic and isometric muscle strength and endurance were determined before, during, 24 and 48 h after the ingestion of alcohol in juice and juice (placebo). To detect a reduced activation of the central motor pathways superimposed external electrical stimulations during voluntary contractions were applied. Creatine kinase (CK) was measured to detect any alcohol-induced changes in sarcolemmal integrity. No change was seen in isokinetic as well as in isometric muscle performance during or following the alcohol intoxication as compared to the non-alcoholic condition. Also, no central activation failure was observed. No significant difference in CK increment was observed comparing the alcoholic- and non-alcoholic condition. In conclusion, a single episode of moderate alcohol intoxication (1,4 g/l) does not impair motor performance, and no accelerated exercise-induced muscle damage is seen.

Neuromuscular fatigue during a prolonged intermittent exercise: Application to tennis

The time course of alteration in neuromuscular function of the knee extensor muscles was characterized during a prolonged intermittent exercise. Maximal voluntary contraction (MVC) and surface EMG activity of both vastii were measured during brief interruptions before ( T 0), during (30, 60, 90, 120, 150 and 180 min: T 30, T 60, T 90, T 120, T 150, T 180) and 30 min after ( T +30) a 3 h tennis match in 12 trained players. M-wave and twitch contractile properties were analyzed following single stimuli. Short tetani at 20 Hz and 80 Hz were also applied to six subjects at T 0 and T 180. Significant reductions in MVC ( P < 0.05; −9%) and electromyographic activity normalized to the M wave for both vastii ( P < 0.01) occurred with fatigue at T 180. No significant changes in M-wave duration and amplitude nor in twitch contractile properties were observed. The ratio between the torques evoked by 20 Hz and 80 Hz stimulation declined significantly ( P < 0.001; −12%) after exercise. Central activation failure and alterations in excitation–contraction coupling are probable mechanisms contributing to the moderate impairment of the neuromuscular function during prolonged tennis playing.

Changes In Motoneuron Pool Excitability During Prolonged Tennis Playing

Previous studies dedicated to prolonged continuous exercise have shown that central activation failure occurred with fatigue. However, it is still unknown whether decreased voluntary activation is associated with modulations at both spinal and/or supraspinal levels, particularly during long duration (> 2 h) intermittent activities. PURPOSE: To examine the time course of alteration in neural process (spinal loop properties) during prolonged tennis playing by using combined measurements of soleus (SOL)-evoked H-reflex and V-wave responses. METHODS: A series of neuromuscular tests were performed during brief interruptions (< 10 min) every 30 min during a 3 h tennis match in 12 well-trained players. To examine potential impairment in central drive, changes in SOL EMG activity divided by the M-wave amplitude (RMS/M) as well as muscle activation (VA) were quantified during maximal voluntary contraction (MVC) of plantar flexors. SOL maximal H-reflex and M-wave potentials were evoked at rest (i.e. Hmax and Mmax, respectively). During MVC, a supramaximal stimulus was used to record the SOL superimposed maximal M-wave (Msup) and V-wave (V). Peripheral fatigue was assessed by examining the characteristics of the M-wave and the twitch contractile properties. RESULTS: MVC torque declined significantly (P < 0.001) by ∼15% after 90 min of exercise. Decrease in torque was accompanied by a progressive reduction in VA and RMS/M that reached significance (P < 0.001) at the end of the exercise (−10 and −22%, respectively). The change in MVC was correlated with the modification of VA (r = 0.77; P < 0.05). Similarly, Hmax/Mmax (P < 0.001) and V/Msup (P < 0.05) ratios were altered with fatigue. Significant reductions (P < 0.01) in M-wave and peak twitch amplitudes occurred throughout the exercise. CONCLUSIONS: It can be concluded that central activation failure and alterations of neuromuscular propagation and excitation-contraction coupling are key mechanisms contributing to the impairment of the neuromuscular function during prolonged tennis playing. These novel findings indicate that the decrease in torque induced by this type of long duration intermittent activity is specifically modulated by neural mechanisms at the spinal level. This emphasizes the role of presynaptic inhibition via group III and IV muscle afferents.

Time Course of Central Fatigue Transfer ability

Fatigue is defined as any contraction-induced reduction in the ability to generate maximal muscle force or power output. Central and peripheral components contribute to the development of muscle fatigue. The possibility of central fatigue transferability from the fatigued to the unfatigued knee extensors has been established previously in our laboratory; however the time course of this event was not evident. PURPOSE: Establish the time course of central fatigue transferability and assess the contribution of spinal excitability to central activation failure. METHODS: Twelve untrained male volunteers participated in the experiment. Central fatigue was induced with a series of sub maximal, intermittent isometric voluntary contractions (30% MVC, 0.6 duty cycle) of the knee extensors of one limb. The superimposed twitch technique was used to measure changes in voluntary activation. Alterations in force-generating capacity were monitored with brief MVC performed periodically on both limbs before, during, and after the fatiguing protocol. Surface electromyography (EMG and M wave) from vastus lateralis (VL) as well as twitch contractile properties from the knee extensors were obtained throughout the fatigue protocol from both limbs. The fatigue-related changes in spinal excitability were assessed by measuring the duration of the mixed nerve silent period (SP). Two-way repeated measures ANOVA were used to analyze the pooled data. RESULTS: The average length of the fatigue protocol was 58.2±15.5 min. Central and peripheral components contributed to the 40% (p<0.01) reduction in MVC in the fatigued limb. Central fatigue was partially transferred to the unfatigued side. This was represented by 10% (p<0.03) decline in MVC together with 4.5% (p<0.01) reduction in voluntary activation. The transferability of central fatigue occurred within the first 15 min of the fatigue protocol. The SP duration was not altered in either limb throughout the experiment. CONCLUSION: The time course of central fatigue transferability was during the first 15 min of the fatigue protocol. Since spinal excitability remained unchanged, it leads us to conclude that some supraspinal mechanism(s) were responsible for the transfer of central fatigue.

Contribution of central and peripheral factors to residual fatigue in Guillain–Barré syndrome

Many patients with Guillain-Barré syndrome (GBS) suffer from severe residual fatigue that has an uncertain basis. We determined the relative contribution of peripheral and central factors during a 2-min fatiguing sustained maximal voluntary contraction (MVC) in 10 neurologically well-recovered GBS patients and 12 age- and sex-matched healthy controls. Physiological fatigue was defined as the decline of voluntary force during an MVC of the biceps brachii. Relative amounts of peripheral fatigue and central activation failure were determined combining voluntary force and force responses to electrical stimulation. Surface electromyography was used to determine muscle-fiber conduction velocity. During the first minute of sustained MVC, peripheral fatigue developed more slowly in patients than in controls. Central fatigue only occurred in patients. The muscle-fiber conduction velocity was higher in patients. The initial MVC, decrease of MVC, initial force response, and initial central activation failure did not significantly differ between the groups. Although peripheral mechanisms cannot be excluded in the pathogenesis of residual fatigue after GBS, these results suggest that central changes are involved. This study thus provides further insight into the factors contributing to residual fatigue in GBS patients.

Experienced and physiological fatigue in neuromuscular disorders

ObjectiveFatigue has been described as a typical symptom of neurological diseases. It might be caused both by changes at the peripheral and at the central level. This study measured the level of experienced fatigue and physiological correlates of fatigue in three genetically defined neuromuscular disorders. MethodsSixty-five facioscapulohumeral dystrophy (FSHD), 79 classical myotonic dystrophy (DM), 73 hereditary motor and sensory neuropathy type I (HMSN) patients and 24 age-matched healthy controls made a 2-min sustained maximal voluntary contraction of the biceps brachii muscle. Experienced fatigue at the current moment was assessed with the abbreviated fatigue questionnaire just before the physiological measurement. Peripheral fatigue was quantified by comparing the amplitudes of an initial and a final stimulated force response during rest. Muscle fibre conduction velocity was determined from a 5-channel surface EMG recording in order to show peripheral changes during the contraction. Central aspects of fatigue were measured using superimposed electrical endplate stimulation. ResultsPatients showed an increased level of experienced fatigue. Total physiological and peripheral fatigue were smaller in patients compared to controls, and central fatigue was normal. The most interesting result of this study was the presence of a large central activation failure (CAF) in all groups of neuromuscular patients; they showed CAF values of 36–41% already directly at the start of sustained contraction, whereas the control group showed only 12%. CAF slightly correlated with the level of experienced fatigue just before the test. ConclusionsThe cause of the large CAF in patients is unclear. Reduced concentration, motivation or effort can lead to lower central activation. In neuromuscular patients especially fear of physical activity or fear to damage the muscle or nerve tissue may contribute. Besides, also physiological feedback mechanisms or changes at the motocortical level may be a cause of reduced central activation. SignificanceFor the clinician it is important to know that experienced fatigue is part of the clinical spectrum of neuromuscular patients. Besides, the weakness in these patients is aggravated by reduced central activation. Potentially, both problems could be subject of an intervention.

Neuromuscular Activation in Conventional Therapeutic Exercises and Heavy Resistance Exercises: Implications for Rehabilitation

Central activation failure and muscular atrophy are common after knee joint injury. Thus, exercises that aim to stimulate muscular hypertrophy and increase neural drive to the muscle fibers should be used during rehabilitation. This study examined the level of knee joint neuromuscular activation during 4 conventional therapeutic exercises (quadriceps femoris muscle setting, manual lateralization of the patella, rhythmic stabilization, and the pelvic bridging exercise) and 4 heavy resistance exercises (free-weight squat with a barbell, horizontal seated leg press, isolated knee extension with a cam mechanism, and isolated hamstring muscle curl) in young, untrained men who were healthy. Thirteen male subjects (mean age=25.3 years, SD=3.0) with no previous history of knee injury participated in the study. Neuromuscular activation during the exercises was defined as the root-mean-square (RMS) electromyographic (EMG) signal normalized to the peak RMS EMG signal of a maximal isometric muscle contraction. Low levels of neuromuscular activation were found during all conventional exercises (<35%). A limitation may be that only a few of many different conventional exercises were investigated. The highest level of neuromuscular activation (67%-79%) was observed during the open kinetic chain resistance exercises (isolated knee extension and hamstring muscle curl). None of the conventional exercises or heavy resistance exercises were found to preferentially activate the vastus medialis muscle over the vastus lateralis muscle. The results indicate that heavy resistance exercises should be included in rehabilitation programs to induce sufficient levels of neuromuscular activation to stimulate muscle growth and strength.