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PubMed2004

An EMG fractal indicator having different sensitivities to changes in force and muscle fatigue during voluntary static muscle contractions.

During a sustained contraction, electromyographic signals (EMGs) undergo a spectral compression. This fatigue behaviour induces a shift of the mean and the median frequencies to lower frequencies. On the other hand, several studies conclude that the mean/median frequency can increase, decrease or remain constant with an increasing force level. Such inconsistency is embarrassing since the fatigue state may be influenced by the force level. In this paper, we propose a frequency indicator which is sensitive to the force level independently of the fatigue state evaluated at 70% of the maximal voluntary contraction. Ten healthy volunteers participated in the study and both surface EMGs (from the short head of the biceps brachii) and force signals were measured. This study compared force and fatigue effects on the EMGs during short (3-s) isometric contractions at different strength intensities and during a sustained isometric contraction until exhaustion. The EMGs partly show 1/falpha spectral behaviours since their power spectral densities may experimentally fit with two linear segments in a log-log representation. The measured "right" slope produces variations of force as 20 times the variations of fatigue. 1/falpha Behaviour may be related to stochastic fractals. This fractal indicator is a new frequency indicator that is thus complementary to other known classical frequency indicators when studying force during unknown fatigue states.

Adult↗

PubMed1993

Muscle fatigue: clinical implications for fatigue assessment and neuromuscular electrical stimulation.

Muscle fatigue can be defined as a decrease in the force-generating ability of a muscle that resulted from recent activity. Recent studies of muscle fatigue are reviewed that are relevant to two areas of interest to physical therapists: clinical assessment of muscle fatigue and neuromuscular electrical stimulation. Volitional and electrical tests have been used to quantify muscle fatigue. Several variations on each type of test are discussed, as are the possible sites in which fatigue might occur. The rate of fatigue during the therapeutic application of electrical stimulation of skeletal muscle is much greater than that seen during volitional contractions. Factors contributing to this phenomenon are examined. The unique requirements affecting how stimulus variables can be manipulated to minimize muscle fatigue in three specific therapeutic uses of neuromuscular electrical stimulation are addressed.

Electric Stimulation↗

PubMed2006

Intensity-dependent effect of body tilt angle on calf muscle fatigue in humans.

Body tilt angle affects the fatigue of human calf muscle at a high contractile force (i.e. 70 %MVC); but the range of forces across which this effect occurs is not known and we sought to determine this in the present study. Fourteen men performed intermittent calf muscle contractions at either 30, 40, 50 and 60 %MVC (Group 1 n = 7) or at 80 and 90 %MVC (Group 2 n = 7). Two tests were performed at each intensity in the supine (tilt angle = 0 degrees) and inclined head-up position (tilt angle = 67 degrees). MVC was measured prior to and during each calf exercise test, and the linear rate of decline in MVC during each test was used to estimate muscle fatigue. MVC prior to each test was unaffected by body tilt angle in Groups 1 and 2. In Group 1 muscle fatigue was significantly lower in the inclined than supine position at 50 %MVC (0.10 +/- 0.05 vs. 0.19 +/- 0.10 N s(-1)) and 60 %MVC (0.22 +/- 0.20 vs. 0.36 +/- 0.33 N s(-1)); but there was no significant difference in fatigue at 30 %MVC (0.07 +/- 0.06 vs. 0.07 +/- 0.07 N s(-1)) and 40 %MVC (0.12 +/- 0.07 vs. 0.18 +/- 0.08 N s(-1)). In Group 2, muscle fatigue was significantly lower in the inclined compared with the supine position at 80 %MVC (0.90 +/- 0.50 vs. 1.49 +/- 0.87 N s(-1)) and 90 %MVC (1.19 +/- 0.47 vs. 1.79 +/- 0.78 N s(-1)). These data demonstrate that the postural effect on calf muscle fatigue during intermittent contractions is manifest at moderate to very high forces, but that it does not occur at low forces.

Adult↗

PubMed2001

Is there a relationship between muscle fatigue resistance and cardiovascular responses to isometric exercise in mild chronic heart failure?

BACKGROUND: Exercise intolerance in chronic heart failure (CHF) may be due to altered fatigue resistance and muscle afferent input to the cardiovascular system from dysfunctional skeletal muscle. AIM: To determine whether calf muscle fatigue resistance was associated with the magnitude of a muscle afferent driven cardiovascular response to isometric exercise. METHODS AND RESULTS: Cardiovascular responses were recorded in eight stable CHF patients (ejection fraction 20-40%) and nine healthy, age-matched controls during voluntary and electrically evoked isometric plantar flexion and post-exercise circulatory occlusion. The force developed by the plantar flexors during a 2-min submaximal electrically evoked fatigue test was measured. There was no relationship between ischaemic muscle fatigue and cardiovascular changes during and after voluntary contraction in either group nor evoked contraction in the CHF group. In the control group, the change in diastolic blood pressure (DBP) at the end of evoked contraction was related to the severity of fatigue at 90 s and 120 s (FI=0.01DeltaDBP+0.3, r=0.81, P<0.05 and FI=0.02DeltaDBP+0.8, r=0.84, P<0.01, respectively). CONCLUSION: Muscle fatigue resistance did not relate to the magnitude of the cardiovascular stress generated by isometric exercise of the same muscle in these patients.

Blood Pressure↗

PubMed2000

Excitatory lung reflex may promote inspiratory muscle fatigue in the rabbit.

BACKGROUND: Inspiratory muscle fatigue is common in severe pulmonary diseases and develops when the inspiratory effort quotient, which is the mean inspiratory pressure over maximal inspiratory pressure (PI/PIMAX), exceeds a critical value. If PIMAX is unchanged, increased PI will promote muscle fatigue. PI can be expressed as (k x VT/Cdyn) x (TI/TTOT), where k is a constant, VT is tidal volume, Cdyn is dynamic lung compliance, and TI/TTOT is inspiratory duty cycle, which is inspiratory time over the period of a respiratory cycle. The excitatory lung reflex (ELR), which can be evoked by inflammatory mediators (e.g., H2O2) or hypertonic saline to cause a vagally mediated neural hyperpnea and tachypnea, may be one of the mechanisms to promote inspiratory muscle fatigue. METHODS: To investigate whether the ELR can promote inspiratory muscle fatigue I conducted experiments in anesthetized and open-chest rabbits whose lungs were made motionless. The duty cycle, amplitude of the phrenic neurogram (which is closely correlated with VT), and burst rate were examined after initiation of the ELR by injection of hypertonic saline (8.1%, 0.1 mL) into the lung parenchyma. RESULTS: The duty cycle, amplitude, and burst rate of the phrenic activity increased by 36 +/- 7, 15 +/- 3, and 40 +/- 8% (n = 9; P < 0.01), respectively. The responses were abolished by bilateral vagotomy. CONCLUSIONS: Because Cdyn and PIMAX did not change, the ELR increased the duty cycle, phrenic amplitude, and burst rate, therefore activation of this reflex may promote inspiratory muscle fatigue and may precipitate ventilatory failure.

Animals↗

PubMed2003

Habitual level of physical activity and muscle fatigue of the elbow flexor muscles in older men.

Reduced muscle performance, related to the loss of muscle mass and strength, is a common and natural part of ageing. Nevertheless, it is generally believed that regular participation in activities of moderate intensity may slow down these age-related changes. This study investigated the relationship between the habitual level of physical activity (PA), assessed by the modified Baecke Questionnaire, and the mechanical and fatigue characteristics of the right elbow flexor muscles, m. biceps brachii and m. brachioradialis, in men over the age of 55 years. Muscle fatigue was quantified both by measuring the maximal voluntary contraction (MVC) torque before and after a sustained isometric contraction at 25% MVC until exhaustion, and also by the temporal changes observed in the surface electromyographic (EMG) signal recorded during the fatigue task. Results showed a decreased MVC torque at the end of the fatiguing contraction. After 20 min of recovery, the MVC force was still significantly lower than the pre-fatigue value, except for the most active subjects. Typical myoelectrical indications of fatigue were also observed: a shift in the frequency spectrum of the signal towards lower frequencies accompanied by an increase in the EMG amplitude. We concluded from this study that the level of PA was related to the absolute isometric MVC values and the measurement of neuromuscular efficiency after 20 min of recovery, but did not influence the indications of muscle fatigue during an isometric fatigue task.

Aged↗

PubMed2000

Nonlinear time-course of lumbar muscle fatigue using recurrence quantifications.

Isometric skeletal muscle fatigue is usually assumed to be a linear process based upon the monotonic decrease in spectral frequency of the EMG. Since spectral analysis by fast Fourier transform (FFT) constitutes a linear transformation of the data, the present study was designed to reevaluate the time-course of muscle fatigue with a nonlinear tool, recurrence quantification analysis (RQA). Surface EMG recordings were obtained from the multifidus muscle of 17 human subjects during isometric posture-holding of the upper torso. The process of muscle fatigue was found to be linear for 59% of the subjects by FFT criteria, but nonlinear for 76% by RQA criteria. As a demonstrative control, both slow and fast transients occurring within a nonlinear mathematical process could be accurately depicted by RQA, but not by FFT. It is concluded that assessment of EMG patterns by nonlinear techniques can give insight into the time-course of fatiguing muscles attributed to the summation of several nonlinear and competing processes.

Adult↗

PubMed2003

Evaluation of shoulder proprioception following muscle fatigue.

OBJECTIVE: To investigate the effect of shoulder muscle fatigue on glenohumeral proprioception. DESIGN: A repeated proprioception test was performed. BACKGROUND: The role of conditioning and fatigue in sport injuries remains controversial. It has been hypothesized that proprioceptive information plays an important role in joint stabilization and that muscle fatigue may alter proprioceptive ability. However, the effect of shoulder muscle fatigue on glenohumeral proprioception is still controversial. METHODS: Eleven normal subjects (mean age 27.3 years) participated in this study. Proprioception tests (on the dominant shoulder) were performed in which proprioception of the active reproduced and passive reproduced shoulder position was measured using an isokinetic dynamometer and a proprioception testing apparatus, respectively. The speed of active repositioning was at 2 deg/s and passive repositioning was at 0.5 deg/s. The mean value of maximum voluntary contraction and the number of repetitions for muscle fatigue were recorded. Post-fatigue proprioception test was started within 3 min after muscle fatigue. RESULTS: There was no significant difference of shoulder proprioception between pre- and post-fatigue determinations of passive repositioning in shoulder internal rotation, passive repositioning in external rotation and active repositioning in internal rotation. There was a significant difference between pre- and post-fatigue determination of active repositioning in external shoulder rotation (mean degrees: 2.57 (SD 1.02) vs. 4.96 (SD 1.73), P<0.05). CONCLUSION: Shoulder proprioception in active repositioning in external rotation was major affected by muscle mechanoreceptors in the presence of muscle fatigue. RELEVANCE: This study revealed that the shoulder proprioception after muscle fatigue in active repositioning in shoulder external rotation was affected more sensitively by the muscle mechanoreceptors than the joint mechanoreceptors. Increasing resistance of muscle fatigue would increase the shoulder proprioceptive ability.

Adaptation, Psychological↗

PubMed2001

Pulmonary function subsequent to expiratory muscle fatigue in healthy humans.

One of the mechanisms proposed to explain the decrement in pulmonary function often seen after exercise is fatigue of the expiratory muscles. To test the hypothesis that expiratory muscle fatigue alters lung function, several indices of pulmonary function were measured before and after expiratory muscle fatigue was induced by expiratory loaded breathing. Eight subjects completed a fatigue trial (EF) in which expiratory threshold loaded breathing was performed at an initial resistance equal to 80 % of their maximal expiratory pressure (MEP), at a respiratory rate of 13 bpm, and a duty cycle (T(I)/T(Tot)) of 0.33. MEP was taken at predefined intervals throughout the loaded breathing protocol, and loaded breathing was discontinued when MEP was less than 80 % of each subject's pre EF trial MEP (T(Lim)). FVC, FEV(1.0), FEF(25 %), FEF(25-75 %), and maximal inspiratory and expiratory pressures (MIP and MEP) were taken prior to, immediately after, and at 5, 10, and 15 min post fatigue. On a separate day a control trial (CON) was performed that was identical to each subjects EF trial with the exception that no expiratory load was utilized. At T(Lim) MEP was significantly reduced (p < 0.001) by 23.5 % from the pre-expiratory loaded breathing value (183.1 +/- 39.56 to 140.13 +/- 30.45 mmHg), whereas it remained unchanged during the CON trial (191.06 +/- 44.18 to 188.06 +/- 43.50 mmHg). FVC measured prior to and immediately after T(Lim) remained unchanged following both the EF (5349.45 +/- 1130.8 to 5387.43 +/- 1139.92 mL) and CON trials (5287.75 +/- 1220.29 and 5352.78 +/- 1191.30 mL). These results suggest that any expiratory muscle fatigue developed during exercise by itself does not result in altered pulmonary function. However, any interactions between expiratory muscle fatigue and other consequences of exercise that may alter lung function cannot be ruled out.

Adult↗

PubMed2002

Respiratory muscle fatigue.

The contribution of respiratory muscle fatigue to the development of ventilatory failure has been the subject of considerable interest and has stimulated much research. Experimental studies in dogs have shown respiratory muscle fatigue to be a cause of ventilatory failure in both cardiogenic and septic shock models. In clinical conditions resulting in acute or chronic hypercapnia, respiratory muscle fatigue is believed to occur; however, the specific role of fatigue has been difficult to prove.

Animals↗

PubMed1991

The roles of ion fluxes in skeletal muscle fatigue.

Intense muscle contractions result in large changes in the intracellular concentrations of electrolytes. The purpose of this study was to examine the contributions of changes in intracellular strong ions to calculated changes in steady-state membrane potential (Em) and muscle intracellular H+ concentration ([H+]i). A physicochemical model is used to examine the origin of the changes in [H+]i during intense muscle contraction. The study used the isolated perfused rat hindlimb intermittently stimulated to contract at high intensity for 5 min. This resulted in significant K+ depletion of both slow (soleus) and fast (white gastrocnemius, WG) muscle fibers and a release of K+ and lactate (Lac-) into venous perfusate. The major contributor to a 12- to 14-mV depolarization of Em in soleus and WG was the decrease in intracellular K+ concentration ([K+]i). The major independent contributors to [H+]i are changes in the concentrations of strong and weak ions and in CO2. Significant decreases in the strong ion difference [( SID]i) in both soleus and WG contributed substantially to the increase in [H+]i during stimulation. In WG the model showed that the decrease in [SID]i accounted for 35% of the increase in [H+]i (133-312 nequiv/L; pHi = 6.88-6.51) at the end of stimulation. Of the main contributors to decreased [SID]i, increased [Lac-]i and decreased [K+]i contributed 40 and 60%, respectively, to increased [H+]i, whereas a decrease in [PCr2-]i contributed to reduced [H+]i. It is concluded that decreased muscle [K+]i during intense contractions is the single most important contributor to reduced Em and increased [H+]i. Depletion of PCr2- simultaneous to the changes in [Lac-]i and [K+]i prevents larger increases in [H+]i and helps maintain the intracellular acid-base state.

Animals↗

PubMed2003

Diaphragm pacing during prolonged mechanical ventilation of the lungs could prevent from respiratory muscle fatigue.

UNLABELLED: Respiratory muscle fatigue after prolonged mechanical ventilation of the lungs is a common occurrence. This is probably due to disuse atrophy. The standard technique used to overcome this problem is to gradually wean the patient from the respirator over the course of several days or weeks. HYPOTHESIS: based on experience with the rehabilitation of skeletal muscles during long-term immobilisation of the extremities following trauma or surgery and on experience with diaphragm pacing in quadriplegics, intermittent electrical or magenetic stimulation of the diaphragm while the lungs are still being mechanically ventilated may be beneficial. The result of such stimulation would be to preserve the dysfunctioning diaphragm from atrophy. CONSEQUENCES: dependence on the respirator, length of intubation time, risk of complications and length of stay in the ICU would be considerably reduced.

Diaphragm↗

PubMed1991

Respiratory muscle fatigue limiting physical exercise?

Inspiratory muscle fatigue has been documented during loaded breathing or acute respiratory failure, but its role in exercise limitation is still undetermined. Electromyographic (EMG) signs of diaphragmatic fatigue develop in normal subjects hyperventilating above 70% of maximal voluntary ventilation (MVV), a ventilatory level commonly attained at peak exercise. EMG signs of diaphragmatic fatigue also occur during high power cycling exercise in normal subjects and chronic obstructive pulmonary disease (COPD) patients. However, a loss of respiratory muscle strength has rarely been documented following strenuous physical exercise with techniques independent of the subjects' collaboration. Prior inspiratory muscle fatigue decreases exercise tolerance in normal subjects but its effect is largely unknown in COPD patients. Respiratory muscle rest by negative pressure ventilation was reported to improve exercise tolerance in COPD, but this beneficial effect was not confirmed by controlled studies. The effect of inspiratory muscle training on exercise tolerance is still undefined by existing data, in part because of differences in methods and selection criteria between studies. Although respiratory muscle fatigue may occur during exercise, it is not clearly established whether interventions directed at respiratory muscles may improve exercise tolerance in COPD.

Electromyography↗

PubMed1987

Ineffective breathing pattern related to respiratory muscle fatigue.

In brief, preliminary research suggests that respiratory muscle fatigue contributes to the clinical manifestations of CAL and is associated with changes in breathing patterns. The specific mechanisms for changes in breathing patterns have not been clearly elucidated. Moreover, the mechanisms of respiratory muscle fatigue remain unclear, and clinical methods for diagnosing respiratory muscle fatigue are inconclusive. Until we improve our understanding of respiratory muscle fatigue, interventions are mostly directed toward preventing respiratory muscle fatigue by improving respiratory muscle function. One way to achieve this goal is by inspiratory muscle training. However, further research is needed to elucidate the physiologic mechanisms, clinical implications, and therapeutic interventions for respiratory muscle fatigue so that we can improve the associated ineffective breathing patterns.

Breathing Exercises↗

PubMed1996

Gum chewing and jaw muscle fatigue and pains.

To study possible associations between gum chewing and fatigue and pains in the jaw muscles, eight healthy adults performed prolonged idling, prolonged unilateral chewing of gum, and brief vigorous clenching of the teeth (MVC). Through surface electromyography (EMG), the authors monitored the cumulative (microV.s) as well as the average rates (microV.s-1) of contractile activities in the right and left masseter muscles. During 10 min of idling there was an absence of muscle fatigue and muscle pains when the EMG rates of the right and left masseter muscles were 2% and 3%, respectively, of those required to elicit isometric muscle pains through MVC. During 10 min of right-sided gum chewing at a rate of 1.2 Hz, the majority of subjects (75%) experienced weak jaw muscle fatigue-not jaw muscle pains-when the EMG rates of the right and left masseter muscles were 38% and 19%, respectively, of those required to elicit isometric pains through MVC. In comparison with 10 min of idling, the weak muscle fatigue of 10 min of unilateral gum chewing appeared when the total contractile activities of the right and left masseter muscles were increased by 1664% and 519%, respectively. It seemed as if prolonged unilateral gum chewing and previous pain-releasing MVC caused some sensitization of muscle nociceptors which, in turn, aggravated subsequent isometric jaw muscle pains elicited through MVC. Even though the right masseter muscle was the most frequent site of clinical fatigue and pains, the authors found no evidence supporting the theoretical foundation of the myofascial pain/dysfunction syndrome.

Adult↗

PubMed2007

Muscle fatigue changes cutaneous suppression of propriospinal drive to human upper limb muscles.

Some voluntary drive reaches human upper limb muscles via cervical propriospinal premotoneurones. Stimulation of the superficial radial nerve can inhibit these premotoneurones selectively and the resultant suppression of voluntary drive to motoneurones changes on-going electromyographic (EMG) activity. We investigated whether muscle fatigue changes this cutaneous-induced suppression of propriospinal drive to motoneurones of upper limb muscles. EMG was recorded from the extensors and flexors of the wrist and elbow. In the first study (n = 10 subjects), single stimuli (2 x perception threshold; 2PT) to the superficial radial nerve were delivered during contraction of the wrist extensors, before and after sustained fatiguing contractions of wrist extensors. In the second study (n = 10), similar stimuli were applied during elbow extension, before and during fatigue of elbow extensors. In the final study (n = 10), trains of three stimuli (2PT) were delivered during contractions of wrist extensors, before and while they were fatigued. With fatigue of either the wrist or elbow extensors, EMG suppression to single cutaneous stimuli increased significantly (by approximately 75%) for the fatigued muscle (P < 0.05). Conversely, in the other muscles, which were coactivated but not principally involved in the task, inhibition decreased or facilitation increased. Trains of stimuli produced greater suppression of on-going wrist extensor EMG than single stimuli and this difference persisted with fatigue. A control study of the H reflex in extensor carpi radialis showed that the mechanism responsible for the altered EMG suppression in fatigue was not at a motoneurone level. The findings suggest that the proportion of descending drive mediated via the disynaptic propriospinal pathway or the excitability of inhibitory interneurones projecting to propriospinal neurones increases substantially to fatigued muscles, but decreases to other active muscles. This pattern of changes may maintain coordination during multimuscle movements when one group of muscles is fatigued.

Adult↗

PubMed2003

Inhibition of muscle spindle afferent activity during masseter muscle fatigue in the rat.

The influence of muscle fatigue on the jaw-closing muscle spindle activity has been investigated by analyzing: (1) the field potentials evoked in the trigeminal motor nucleus (Vmot) by trigeminal mesencephalic nucleus (Vmes) stimulation, (2) the orthodromic and antidromic responses evoked in the Vmes by stimulation of the peripheral and central axons of the muscle proprioceptive afferents, and (3) the extracellular unitary discharge of masseter muscle spindles recorded in the Vmes. The masseter muscle was fatigued by prolonged tetanic masseter nerve electrical stimulation. Pre- and postsynaptic components of the potentials evoked in the Vmot showed a significant reduction in amplitude following muscle fatigue. Orthodromic and antidromic potentials recorded in the Vmes also showed a similar amplitude decrease. Furthermore, muscle fatigue caused a decrease of the discharge frequency of masseter muscle spindle afferents in most of the examined units. The inhibition of the potential amplitude and discharge frequency was strictly correlated with the extent of muscle fatigue and was mediated by the group III and IV afferent muscle fibers activated by fatigue. In fact, the inhibitory effect was abolished by capsaicin injection in the masseter muscle that provokes selective degeneration of small afferent muscle fibers containing neurokinins. We concluded that fatigue signals originating from the muscle and traveling through capsaicin-sensitive fibers are able to diminish the proprioceptive input by a central presynaptic influence. In the second part of the study, we examined the central projection of the masseter small afferents sensitive to capsaicin at the electron-microscopic level. Fiber degeneration was induced by injecting capsaicin into the masseter muscle. Degenerating terminals were found on the soma and stem process in Vmes and on the dendritic tree of neurons in Vmot. This suggests that small muscle afferents may influence the muscle spindle activity through direct synapses on somata in Vmes and on dendrites of neurons in Vmot.

Action Potentials↗

PubMed1993

Mechanisms of muscle fatigue.

The concept of muscle fatigue as a factor limiting muscle performance has evolved into one in which fatigue is avoided in order to protect the muscle from injury induced by over stimulation. No one mechanism accounts for all the changes in muscle performance occurring during fatigue. Research on pathophysiological factors limiting force production or shortening capacity during the fatigue process has widened to detailed electrophysiologic, metabolic and molecular aspects. All are extensively reviewed in the present paper. The known mechanisms are likely to be interdependent, synergistic, and integrated. A careful interpretation of individual research is implied, particularly when data from experimental animal models are translated to human beings.

Action Potentials↗