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At least 19 recordsLinked to original sources
PubMed2006

The effects of lumbar massage on muscle fatigue, muscle oxygenation, low back discomfort, and driver performance during prolonged driving.

An increasing dependence of society on automobiles for both work and leisure and the corresponding increase in time spent seated in the car has been correlated with a greater risk of low back pain and absence from work (Porter and Gyi 2002). This study examined the effects of three types of lumbar massage units on seating comfort, muscle fatigue, muscle oxygenation, muscle blood flow and driving performance during a 1 h simulated driving task. Electromyographic (EMG) signals were recorded from the right and left thoracic and lumbar erector spinae musculature. Average EMG (AEMG), mean power frequency (MPF), gaps and amplitude probability distribution function (APDF) parameters were analysed from the three massage seats and compared to a control seat. Near infrared spectroscopy (NIRS) and skin temperature from the right thoracic and lumbar erector spinae were used as an indication of muscle oxygenation and blood flow throughout the driving task. Ratings of perceived discomfort were used to assess driver discomfort, and driving performance was assessed by calculating mean lap times for the duration of each driving trial. The results showed statistically significant increases in skin temperature compared with the control seat after 60 min of driving. The NIRS results reflected these trends although the results were not statistically significant. AEMG and MPF measures showed no significant differences between the seats. MPF measures were found to increase over time, effects attributed to increases in muscle temperature. Gaps and APDF analyses revealed greater rest times and lower activation levels, respectively, with the control seat, which could result in increased loading of passive structures. This study demonstrated the beneficial effects of lumbar massage systems in increasing muscle blood flow and oxygenation. Although EMG parameters were not significantly different, the trends support the significant blood flow results. Future research should include longer driving times and adjustments in EMG measures to account for the effects of increasing muscle temperature on AEMG and MPF measures.

Adult↗
PubMed1995

Variable-frequency stimulation patterns for the optimization of force during muscle fatigue. Muscle wisdom and the catch-like property.

Muscle wisdom is the process whereby the activation rates of motor units are modulated by the central nervous system to optimize the force during sustained voluntary contractions. During maximal voluntary contractions the activation rates decline as the muscle fatigues. No similar decline has been observed during submaximal contractions. Subsequent chapters explore the potential mechanisms for muscle wisdom. In this chapter, a historical background on the development of ideas on muscle wisdom is first presented. Next, artificial wisdom, the procedure used to optimize force during an electrically imposed tetanus by progressively reducing the stimulation frequency as the muscle fatigues, is discussed. Finally, recent studies are described in which fatigue was delayed and reduced by the use of variable-frequency stimulus trains that elicit the catch-like property of muscle.

Evoked Potentials↗
PubMed2000

Muscle fatigue and muscle injury.

The purpose of this review is to acquaint the reader with the neurobiology of muscle fatigue. Muscle fatigue is a complex, multifactorial process. The authors have covered the chain of events bringing about skeletal muscle contraction and the manner in which fatigue may affect each step. Advances in technology continue to increase understanding of central fatigue. Many excellent studies of peripheral fatigue have been designed to delineate the mechanisms that influence the excitation-contraction coupling, energy supply, and force generation processes. Although much of this work has considered mechanisms in isolation, different mechanisms may be responsible under different conditions. Fatigue is a common complaint among patients with a variety of neuromuscular and metabolic diseases. Armed with an enhanced knowledge of the mechanisms of muscle fatigue, one can more fully recognize the signs and symptoms of metabolic disorders and neuromuscular diseases and use diagnostic testing. The clinician should anticipate the role of muscle fatigue in injury and focus on injury prevention strategies, especially during the restorative phase of rehabilitation. As a clinician-scientist concerned with optimizing patients' and athletes' performance, one must design ways to identify, measure, and treat muscle fatigue. Beyond illustrating what is currently known about muscle fatigue, the authors hope this review inspires the reader to solve problems of great clinical importance to patients and athletes alike.

Animals↗
PubMed2001

Challenging the role of pH in skeletal muscle fatigue.

Muscle fatigue is frequently defined as a temporary loss in force- or torque-generating ability because of recent, repetitive muscle contraction (1). The development of this temporary loss of force is a complex process and results from the failure of a number of processes, including motor unit recruitment and firing rate, chemical transmission across the neuromuscular junction, propagation of the action potential along the muscle membrane and T tubules, Ca2+ release from the sarcoplasmic reticulum (SR), Ca2+ binding to troponin C, and cross-bridge cycling (for detailed reviews, see Bigland-Ritchie and Woods(1), McLester(2), and Favero(3)). Muscle fatigue may limit the time a person can stand, the distance a person can ambulate, or the number of stairs a person can ascend or descend. In practical terms, however, we cannot know what actually leads to a decline in function for a given patient. For a phenomenon that may have profound clinical implications, muscle fatigue often receives inadequate attention in physiology textbooks, many of which contain a page or less of information on the entire topic (4-8). In addition, many textbooks report that muscle fatigue is mainly the result of a decrease in pH within the muscle cell due to a rise in hydrogen ion concentration ([H+]) resulting from anaerobic metabolism and the accumulation of lactic acid (6-8). Recent literature, however, contradicts this assertion (9-10). The purpose of this update, therefore, is to provide a brief review of the role of pH in the development of muscle fatigue.

Animals↗
PubMed2006

The effect of random modulation of functional electrical stimulation parameters on muscle fatigue.

Muscle contractions induced by functional electrical stimulation (FES) tend to result in rapid muscle fatigue, which greatly limits activities such as FES-assisted standing and walking. It was hypothesized that muscle fatigue caused by FES could be reduced by randomly modulating parameters of the electrical stimulus. Seven paraplegic subjects participated in this study. While subjects were seated, FES was applied to quadriceps and tibialis anterior muscles bilaterally using surface electrodes. The isometric force was measured, and the time for the force to drop by 3 dB (fatigue time) and the normalized force-time integral (FTI) were determined. Four different modes of FES were applied in random order: constant stimulation, randomized frequency (mean 40 Hz), randomized current amplitude, and randomized pulsewidth (mean 250 micros). In randomized trials, stimulation parameters were stochastically modulated every 100 ms in a range of +/-15% using a uniform probability distribution. There was no significant difference between the fatigue time measurements for the four modes of stimulation. There was also no significant difference in the FTI measurements. Therefore, our particular method of stochastic modulation of the stimulation parameters, which involved moderate (15%) variations updated every 100 ms and centered around 40 Hz, appeared to have no effect on muscle fatigue. There was a strong correlation between maximum force measurements and stimulation order, which was not apparent in the fatigue time or FTI measurements. It was concluded that a 10-min rest period between stimulation trials was insufficient to allow full recovery of muscle strength.

Action Potentials↗
PubMed2005

Reductions in interhemispheric motor cortex functional connectivity after muscle fatigue.

Muscle fatigue has been known to differentially affect the activation level of the primary motor cortices (MIs) of the brain's two hemispheres. Whether this fatigue-related decoupling influence on the motor cortical signals extends beyond the motor action to the after-fatigue-task resting state is unknown. This question can be addressed by analyzing functional connectivity (FC) of low-frequency oscillations of resting-state functional MRI (fMRI) signals of the MIs. Low-frequency oscillations (<0.08 Hz) have been detected in many fMRI studies and appear to be synchronized between functionally related areas. These patterns of FC have been shown to differ between normal and various pathological states. The purpose of this study was to examine muscle fatigue-induced resting-state interhemispheric motor cortex FC changes in healthy subjects. We hypothesized that muscle fatigue would create a temporary "disrupted state" in the brain, and would decrease resting state interhemispheric motor cortical FC. Ten healthy subjects performed repetitive unilateral handgrip contractions that induced significant muscle fatigue, with resting state fMRI data collected before and after the task. After excluding two subjects due to gross head motion, interhemispheric motor cortex FC was assessed by cross-correlating the MI fMRI signal time courses. We found that the number of significant interhemispheric correlations in the MI fMRI signals decreased significantly after the performance of the fatigue task. These results suggest that resting state interhemispheric motor cortex FC may be used as an index of recovery from fatigue.

Adult↗
PubMed1992

Neurobiology of muscle fatigue.

Muscle fatigue encompasses a class of acute effects that impair motor performance. The mechanisms that can produce fatigue involve all elements of the motor system, from a failure of the formulation of the descending drive provided by suprasegmental centers to a reduction in the activity of the contractile proteins. We propose four themes that provide a basis for the systematic evaluation of the neural and neuromuscular fatigue mechanisms: 1) task dependency to identify the conditions that activate the various mechanisms; 2) force-fatigability relationship to explore the interaction between the mechanisms that results in a hyperbolic relationship between force and endurance time; 3) muscle wisdom to examine the association among a concurrent decline in force, relaxation rate, and motor neuron discharge that results in an optimization of force; and 4) sense of effort to determine the role of effort in the impairment of performance. On the basis of this perspective with an emphasis on neural mechanisms, we suggest a number of experiments to advance our understanding of the neurobiology of muscle fatigue.

Animals↗
PubMed2003

Wavelet analysis of surface electromyography to determine muscle fatigue.

Muscle fatigue is often a result of unhealthy work practice. It has been known for some time that there is a significant change in the spectrum of the electromyography (EMG) of the muscle when it is fatigued. Due to the very complex nature of this signal however, it has been difficult to use this information to reliably automate the process of fatigue onset determination. If such a process implementation were feasible, it could be used as an indicator to reduce the chances of work-place injury. This research report on the effectiveness of the wavelet transform applied to the EMG signal as a means of identifying muscle fatigue. We report that with the appropriate choice of wavelet functions and scaling factors, it is possible to achieve reliable discrimination of the fatigue phenomenon, appropriate to an automated fatigue identification system.

Algorithms↗
PubMed2001

Spinal and supraspinal factors in human muscle fatigue.

Muscle fatigue is an exercise-induced reduction in maximal voluntary muscle force. It may arise not only because of peripheral changes at the level of the muscle, but also because the central nervous system fails to drive the motoneurons adequately. Evidence for "central" fatigue and the neural mechanisms underlying it are reviewed, together with its terminology and the methods used to reveal it. Much data suggest that voluntary activation of human motoneurons and muscle fibers is suboptimal and thus maximal voluntary force is commonly less than true maximal force. Hence, maximal voluntary strength can often be below true maximal muscle force. The technique of twitch interpolation has helped to reveal the changes in drive to motoneurons during fatigue. Voluntary activation usually diminishes during maximal voluntary isometric tasks, that is central fatigue develops, and motor unit firing rates decline. Transcranial magnetic stimulation over the motor cortex during fatiguing exercise has revealed focal changes in cortical excitability and inhibitability based on electromyographic (EMG) recordings, and a decline in supraspinal "drive" based on force recordings. Some of the changes in motor cortical behavior can be dissociated from the development of this "supraspinal" fatigue. Central changes also occur at a spinal level due to the altered input from muscle spindle, tendon organ, and group III and IV muscle afferents innervating the fatiguing muscle. Some intrinsic adaptive properties of the motoneurons help to minimize fatigue. A number of other central changes occur during fatigue and affect, for example, proprioception, tremor, and postural control. Human muscle fatigue does not simply reside in the muscle.

Animals↗
PubMed1995

Muscle fatigue and muscle length interaction: effect on the EMG frequency components.

Muscle fatigue can be identified by a decrease in the frequency components of the EMG signal, typically represented by a fall in the center frequency (fc). In addition, changes in muscle length have been demonstrated to independently alter the EMG fc. What remains unknown is the interaction between muscle fatigue and muscle length changes on the EMG fc. To address this question, a human biceps model of muscle fatigue, consisting of repetitive non-isometric contractions until task failure was studied. EMG signals from the biceps brachii were acquired via surface electrodes, and muscle length was determined by recording elbow angle. Five subjects developed biceps fatigue by repeating contractions of 50% maximal force until task failure. Fatigue produced a decrease in EMG fc at all muscle lengths. For the first three quarters of fatigue development there was a similar degree of reduction in EMG fc at all muscle lengths. But as task failure approached, there was a greater reduction in EMG fc at the shortest muscle length relative to the longest muscle length (41% reduction from baseline versus 30% reduction from baseline, respectively). The effect of muscle length independent of fatigue was such that a 20% increase in length would result in approximately an 18% fall in EMG fc. In conclusion, during fatigue development muscle length significantly influences the EMG fc, and it may be an important factor to consider when utilizing the EMG fc to detect muscle fatigue.

Adult↗
PubMed1995

The role of intracellular acidosis in muscle fatigue.

Muscle fatigue is often accompanied by an intracellular acidosis of variable size. The variability reflects the involvement of different metabolic pathways, the presence or absence of blood flow and the effectiveness of pH-regulating pathways. Intracellular acidosis affects many aspects of muscle cell function; for instance it reduces maximal Ca(2+)-activated force and Ca2+ sensitivity, slows the maximal shortening velocity and prolongs relaxation. However, acidosis is not the only metabolic change in fatigue which causes each of the above, and there are important aspects of muscle fatigue (e.g., the failure of Ca2+ release) which do not appear to be caused by acidosis.

Acidosis↗
PubMed2001

Effects of agonist and antagonist muscle fatigue on muscle coactivation around the knee in pubertal boys.

In many activities the knee joint flexes and extends actively with the involvement of both knee extensor and flexor muscle groups. Consequently the examination of the muscle activity during reciprocal movements may provide useful information on the function of these two muscle groups during fatigued conditions. Therefore, the purpose of this study was to examine the activity of antagonist muscles during a reciprocal isokinetic fatigue test of the knee extensors and flexors. Fifteen healthy pubertal males (age 13.8+/-0.8 years) performed 22 maximal isokinetic concentric efforts of the knee extensors at 60 degrees s(-1). The EMG activity of vastus medialis (VM), vastus lateralis (VL) and biceps femoris (BF) was recorded using surface electrodes. The motion ranged from 100 to 0 degrees of knee flexion. The average moment and average EMG (AEMG) at 10-30 degrees, 31-50 degrees, 51-70 degrees and 71-90 degrees angular position intervals were calculated for each repetition. Twenty efforts were further analyzed. Two-way repeated measures analysis of variance (ANOVA) tests indicated a significant decline of moment during the test (p<0.025). The VM and VL AEMG at longer muscle lengths increased significantly as the test progressed whereas the AEMG at short muscle lengths (10-30 degrees ) did not significantly change. The agonist AEMG of BF during the first repetition demonstrated a significant increase after the ninth repetition (p<0.025). The antagonist AEMG of all muscles did not change significantly during the test. These results indicate that there is consistent antagonist activity during both extension and flexion phases of an isokinetic reciprocal fatigue test. It can be concluded that during an isokinetic reciprocal fatigue test, both knee extensors and flexors are fatigued. However, this condition does not have a significant effect on the EMG patterns of these muscles when acting as antagonists during the test.

Adolescent↗
PubMed1995

The importance of ATPase microenvironment in muscle fatigue: a hypothesis.

A broadly held opinion is that fatigue is not due to an insufficient supply of ATP to the energy consuming mechanisms because tissue [ATP] always remains at least one order of magnitude higher than Km for ATP of any ATPase. In general these findings also suggest that ATP consumption is well balanced with ATP regeneration even in the fatigued muscles. This balance is achieved by down-regulation of ATP consumption. Potentially this down-regulation could be accomplished by any product of the ATPase reaction and the role of Pi and H+ accumulation in this regulation has been discussed in the literature. The purpose of this paper is to describe known compartmentalization of ATP regeneration systems in muscle cell, their importance in the regulation of [adenine nucleotide] in the vicinity of ATPases and how such local ATP regeneration maybe important in the etiology of muscle fatigue. Available experimental evidence suggests that the binding of creatine kinase and glycolytic enzymes in the vicinity of sites where ATP is hydrolyzed and functional coupling between these ATP regenerating mechanisms and ATPase can generate ATPase microenvironments that have an important role in the regulation of ATPase function. Main function of this ATP regeneration is to keep the local ADP/ATP ratios favorable for ATPase function, which seems to be especially important when ATPase turnover is high. Unfortunately, the maximum rate of local ATP regeneration relative to that of ATP hydrolysis in vivo is not known, mainly because in vitro determinations underestimate this value due to a decrease in the fractional of loosely abound enzyme to the preparation during isolation procedure.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenine Nucleotides↗
PubMed2006

Assessment of muscle fatigue using sonomyography: muscle thickness change detected from ultrasound images.

Muscle fatigue is an exercise-induced reduction in maximal voluntary muscle force. As the surface electromyography (SEMG) can be used to estimate the features of neuromuscular activations associated with muscle contractions, it has been widely employed as an objective tool to evaluate muscle fatigue. On the other hand, ultrasound imaging can inherently provide the morphological information of individual muscle, thus the architectural changes of muscles during fatigue can be obtained. In this study, we demonstrated the feasibility of using the dimensional change of muscles detected by ultrasound images, named as sonomyography (SMG), to characterize the behavior of muscles when they were in fatigue. The SEMG signals of the muscles were also recorded simultaneously and used for comparison. The right biceps brachii muscles of 8 normal young male adult subjects were tested for 30s under 80% of the maximal voluntary isometric contraction. The muscle fatigue was indicated by the change of the root-mean-square (RMS) and median frequency (MDF) of the SEMG signals. The results showed that the SEMG RMS had a linear increase with time with a rate of 2.9+/-1.9%/s (mean+/-S.D.), while the MDF decreased linearly with a rate of -0.60+/-0.26Hz/s. The muscle thickness, detected from the ultrasound images, continuously increased during the muscle fatigue but with a nonlinear increase with time, which was rapid during the initial 8.1+/-2.1s with a mean deformation rate of 0.30+/-0.19%/s and then became slower with a rate of 0.067+/-0.024%/s up to 20s after the contraction. The muscle deformation at 20s was 3.5+/-1.6%. The results demonstrated that the architectural change of muscles detected using SMG could potentially provide complementary information for SEMG for the muscle fatigue assessment.

Adult↗
PubMed1992

Effect of inspiratory muscle fatigue on inspiratory muscle relaxation rates in healthy subjects.

Simple methods to diagnose inspiratory muscle fatigue in the clinical setting would be of considerable benefit. Inspiratory muscle relaxation rates are known to slow following induction of fatigue. Inspiratory muscle relaxation rates have been measured following a short sharp inspiratory effort against an occluded airway (sniffmouth) or through the unoccluded nostrils (sniffnostrils). Relaxation rates in the absence of fatigue are faster when sniffs are performed through the unoccluded nostrils. While both methods have been shown to be capable of detecting inspiratory muscle fatigue, there may be quantitative or qualitative differences between the two techniques in their ability to detect fatigue similar to the differences observed in the fresh state. Accordingly, we measured relaxation rates with the two sniff techniques in five healthy naive male subjects before and after induction of fatigue. Inspiratory muscle fatigue was induced by threshold loading at 80 percent of Pesmax until the subjects were unable to generate the target pressure. For those trials in which sniffnostrils were performed, the maximum relaxation rate from the esophageal pressure curve (MRRes) was significantly decreased following induction of fatigue in nine of ten trials, while the exponential time constant (taues) was significantly increased in all ten trials. In contrast, for those trials in which sniffmouth were performed, the MRRes was significantly decreased following induction of fatigue in only six of ten trials. Similarly, taues was significantly increased following induction of fatigue in only six of ten trials. In addition, the magnitude of change in the MRR or tau following induction of fatigue was quantitatively greater with sniffnostrils compared with sniffmouth. Similar findings were obtained when relaxation rates were measured from the diaphragmatic pressure tracing. In conclusion, changes in relaxation rate following induction of fatigue were quantitatively greater and more consistently observed when sniffs were performed through the unoccluded nostrils rather than against an occluded airway.

Adult↗
PubMed1996

Fusimotor system in muscle fatigue.

Evidence is reviewed that a reflex increase in fusimotor activity develops during fatiguing muscle contraction in decerebrate and/or spinal cats. This phenomenon is apparently due to an increased inflow from small-diameter afferents that is elicited by metabolic products liberated and/or accumulated in the muscle tissue. It occurs in fusimotor neurones to the contracting muscle as well as in those to its close synergists, inactive remote muscle groups, and in a smaller number of those to antagonist muscles. It is finely modulated by afferent inflow of other origin and results in changes of muscle spindle outflow and responsiveness. According to the magnitude and time course of the responses, the fusimotor-spindle system might contribute to: (1) optimization of skeletomotor activity directed to the contracting muscle so as to relieve the fatigue-induced changes in its contractile properties; (2) spreading of activity to initially inactive muscle groups when the agonist gets fatigued; (3) providing more information to skeletomotor neurones and higher motor centres both during and after the fatiguing contraction until the muscle recovers. However, it remains to be assessed whether such a reflex increase plays a role in muscle fatigue in intact animals and/or humans.

Animals↗
PubMed2006

The frequency of alternate muscle activity is associated with the attenuation in muscle fatigue.

Alternate muscle activity between synergist muscles has been demonstrated during low-level sustained contractions [< or =5% of maximal voluntary contraction (MVC) force]. To determine the functional significance of the alternate muscle activity, the association between the frequency of alternate muscle activity during a low-level sustained knee extension and the reduction in knee extension MVC force was studied. Forty-one healthy subjects performed a sustained knee extension at 2.5% MVC force for 1 h. Before and after the sustained knee extension, MVC force was measured. The surface electromyogram was recorded from the rectus femoris (RF), vastus lateralis (VL), and vastus medialis (VM) muscles. The frequency of alternate muscle activity for RF-VL, RF-VM, and VL-VM pairs was determined during the sustained contraction. The frequency of alternate muscle activity ranged from 4 to 11 times/h for RF-VL (7.0 +/- 2.0 times/h) and RF-VM (7.0 +/- 1.9 times/h) pairs, but it was only 0 to 2 times/h for the VL-VM pair (0.5 +/- 0.7 times/h). MVC force after the sustained contraction decreased by 14% (P < 0.01) from 573.6 +/- 145.2 N to 483.3 +/- 130.5 N. The amount of reduction in MVC force was negatively correlated with the frequency of alternate muscle activity for the RF-VL and RF-VM pairs (P < 0.001 and r = 0.65 for both) but not for the VL-VM pair. The results demonstrate that subjects with more frequent alternate muscle activity experience less muscle fatigue. We conclude that the alternate muscle activity between synergist muscles attenuates muscle fatigue.

Adaptation, Physiological↗