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Respiratory muscle fatigue after marathon running.

Respiratory muscle fatigue has been demonstrated in the laboratory as well as in pathological states, but whether it occurs in healthy individuals under physiological conditions is unknown. To determine whether fatigue of the respiratory muscles may develop with endurance exercise, we measured spirometry and respiratory muscle strength and endurance in four runners before and after completion of a marathon race (42.2 km). Strength was assessed by measuring maximal inspiratory (PImax) and expiratory (PEmax) pressures and transdiaphragmatic pressure during inspiratory capacity (PdiIC); endurance was determined by measuring maximal voluntary ventilation (MVV). After marathon running (mean time, 3 h 24 min) there was no change in forced vital capacity, inspiratory capacity, or flow rates from prerace values. Decreases were observed between pre- and postrace PImax (165.8 +/- 11.0 vs. 138.5 +/- 7.6 cmH2O; P less than 0.01) PEmax (240.0 +/- 20.4 vs. 173.0 +/- 22.6 cmH2O; P less than 0.05), PdiIC (78.8 +/- 11.6 vs. 63.3 +/- 7.0 cmH2O; P less than 0.10), and MVV (178 +/- 24.2 vs. 161.2 +/- 23.2 l/min; P less than 0.005). The decrements in respiratory muscle strength and endurance suggest the development of respiratory muscle fatigue after marathon running.

Adult↗

Role of phosphate and calcium stores in muscle fatigue.

Intensive activity of muscles causes a decline in performance, known as fatigue, that is thought to be caused by the effects of metabolic changes on either the contractile machinery or the activation processes. The concentration of inorganic phosphate (P(i)) in the myoplasm ([P(i)](myo)) increases substantially during fatigue and affects both the myofibrillar proteins and the activation processes. It is known that a failure of sarcoplasmic reticulum (SR) Ca(2+) release contributes to fatigue and in this review we consider how raised [P(i)](myo) contributes to this process. Initial evidence came from the observation that increasing [P(i)](myo) causes reduced SR Ca(2+) release in both skinned and intact fibres. In fatigued muscles the store of releasable Ca(2+) in the SR declines mirroring the decline in SR Ca(2+) release. In muscle fibres with inoperative creatine kinase the rise of [P(i)](myo) is absent during fatigue and the failure of SR Ca(2+) release is delayed. These results can all be explained if inorganic phosphate can move from the myoplasm into the SR during fatigue and cause precipitation of CaP(i) within the SR. The relevance of this mechanism in different types of fatigue in humans is considered.

Animals↗

Subjective and objective evaluation of shoulder muscle fatigue.

In order to relate EMG signs of localized muscle fatigue to subjectively perceived muscle fatigue, a study was undertaken on 20 healthy volunteers exposing their right trapezius muscle by raising the arm to 90 degrees of abduction. Every person performed two contractions: 0 kg hand load during 5 min and 2 kg hand load during 2.5 min. Surface EMG was recorded and analysed with respect to RMS amplitude and mean power frequency (MPF). Subjective muscle fatigue was estimated with a psychophysical rating scale (Borg's CR-10 Scale). At high load level we found a significant correlation between MPF and the CR-scores (r = -0.46), but at low load level there was no correlation. At high load level there was a linear decrease of MPF with increasing load dose, but at low load level the MPF did not change, despite significant subjective fatigue. There was a linear rise of the CR-score with increasing load dose, more pronounced at high load level. It was concluded, that at low load levels common in working life, MPF and subjective scores seem to provide different fatigue information. Moreover, the MPF did not seem to work as a valid estimator of muscle fatigue at this low load level. Caution is recommended if it is to be used in static low-load situations.

Adult↗

Comparison of quantitative analysis and fractal analysis of center of pressure based on muscle fatigue.

To examine the influence of muscle fatigue on center of pressure displacement during quiet standing using quantitative and fractal analyses, 12 healthy young men and women did the exercise stress test on the triceps surae muscle until fatigued. Subjects were measured for body stability for 60 sec. before and after the exercise. Quantitative analysis showed that center-of-pressure parameters for distance, velocity, amplitude distribution, and mean vector length of sway in the anterior/posterior direction changed significantly after muscle fatigue but not on the periodic parameters. This result suggested that quantitative analysis may identify the effects of muscle fatigue on the parameters that show displacement in the anterior/posterior direction of center of pressure. Fractal analysis indicated the value of critical point coordinates increased after muscle fatigue. This analysis can clarify the fundamental postural control strategy and time-series characteristics of postural sway which cannot be identified by spectral analysis.

Adult↗

Adaptation of the precentral cortical command to elbow muscle fatigue.

The control exerted by individual motor cortical cells on their fatigued target muscles was assessed by analyzing the discharge patterns and electromyographic (EMG) postspike effects of cortical cells in monkeys making repeated forceful, but submaximal, isometric flexions of the elbow to produce fatigue. Two monkeys were trained to perform self-paced isometric contractions (for longer than 2 s) at forces greater than 35% maximal contraction, with three sets of 20 consecutive contractions; the first and last sets were at the same force level. Pairs of EMG electrodes were implanted in the biceps brachii, brachioradialis, and triceps brachii. The cortical cell discharges were modulated with the active and passive movements of the elbow and produced consistent EMG postspike effects during isometric contraction. Muscle fatigue was assessed as a statistically significant (P < 0.05) drop in the mean power frequency of the EMG power spectrum in one or both flexors in the last set of contractions. Clear signs of muscular fatigue occurred in 20 different experimental sessions. Before fatigue, cortical cells were classified as phasic-tonic (18), phasi-cramp (three), or tonic (five). Twenty cells briskly fired to passive elbow extension, and 9 also responded to passive flexion. Only 6 cells showed a decreased discharge to passive extension. A 22-30% increase in the contraction force produced a higher discharge frequency in 13 cells, and a lower frequency in 5 cells. All cells exerted EMG postspike effects in their target muscles: 20 cells facilitated the flexors, and some of these also inhibited (3 cells) or cofacilitated (5 cells) the extensor; the other 6 cells had mixed effects: 5 of them inhibited at least one flexor, and 1 cell only facilitated the extensor. Most cells (24/26) still produced EMG postspike effects in their target muscles during fatigue, and the number of facilitated muscles increased: 21 cells facilitated the flexors, and 12 of them cofacilitated the extensor. Only 3 cells still inhibited the flexors and were tonic cells. The cortical cell firing frequency increased during fatigue in 13 cells and decreased in 8 cells. Increases involved 10 cells excited by passive elbow extension. Fourteen cells showed parallel changes in firing frequency with fatigue and force, and 9 of these cells facilitated both extensors and flexors in fatigue. Increases were found in 8 cells, decreases in 5 cells and no change in 1 cell. As muscle afferents provide substantial information to cortical cells, which in turn establish functional linkages with their target muscles before and during fatigue, the changes in cell firing frequencies during fatigue demonstrate the active participation of the motor cortex in the control of compensation for the peripheral adjustments concomitant with muscle fatigue.

Adaptation, Physiological↗

An electromyographic index for localized muscle fatigue.

A new method for objective quantification of localized muscle fatigue is described. The method is based on power spectrum analysis of myoelectric signals obtained from the fatigued muscle. It permits real-time investigations and yields statistically based criteria for the occurrence of fatigue. The findings are interpreted in terms of muscle action potential conduction velocity changes and rate of the fatigue development.

Action Potentials↗

Calcium exchange hypothesis of skeletal muscle fatigue: a brief review.

Skeletal muscle fatigue is often associated with diminished athletic performance and work productivity as well as increased susceptibility to injury. The exact cause of muscle fatigue probably involves a number of factors which influence force production in a manner dependent on muscle fiber type and activation pattern. However, a growing body of evidence implicates alterations in intracellular Ca2+ exchange as a major role in the fatigue process. These changes are thought to occur secondary to reductions in the rates of Ca2+ uptake and release by the sarcoplasmic reticulum (SR). This hypothesis is based on the finding that peak myoplasmic Ca2+ concentration ([Ca2+]i) is reduced as force declines during fatigue. In addition, direct measurements of Ca2+ uptake and release show that fatiguing activity causes intrinsic alterations in the functional properties of the SR. We also propose that fatigue-induced alterations in Ca2+ exchange may be beneficial, reducing the rate of energy utilization by the muscle fiber and preventing irreversible damage to the cell.

Adenosine Diphosphate↗

[Muscle fatigue. Metabolic changes in muscle mass].

Strenuous physical activity results in depressed muscle function characterised by diminished force production, reduced speed and slowed relaxation. Studies of isolated muscle fibres have shown reduced force to be due to a combination of impaired cross-bridge function, reduced Ca(2+)-sensitivity and decreased Ca(2+)-release. The first two changes are caused by an accumulation of inorganic phosphate and a lowering of pH as a result of increased energy metabolism; the cause of the reduced Ca(2+)-release is unclear. Reduced speed is due to lowered pH and possibly to an increase in ADP (adenosine diphosphate). Slowed relaxation appears to be due to metabolically induced changes both in Ca(2+)-reuptake and cross-bridge function.

Calcium↗

The influence of muscle length on muscle fibre conduction velocity and development of muscle fatigue.

The influence of muscle (vastus lateralis) length on the muscle fibre conduction velocity (MFCV) and on muscle fatigue was studied in 8 healthy volunteers. In experiment 1, the electromyographic (EMG) responses were evoked by electrical stimulation of the motor point and recorded by a surface electrode array aligned along the muscle fibre direction. The MFCV (determined by cross-correlation) was measured at knee flexions of 5 degrees (full extension), 45 degrees, 90 degrees and 120 degrees with 3 different extension torques. The MFCV declined with increasing muscle length and increased with increasing background torque at knee flexions from 5 degrees to 90 degrees. From 90 degrees to 120 degrees knee flexion of MFCV tended to increase. In experiment 2, the EMG activity at a static fatiguing contraction (80% MVC) was measured at 45 degrees and 90 degrees knee flexion. The EMG was measured until the subject gave up contracting the muscle (endurance). The largest increase in the RMS amplitude and the fastest decreases in the mean power frequency (MPF) and MFCV were found at 90 degrees flexion. The MVC at 45 degrees knee flexion was 35% lower than at 90 degrees and the time until endurance was approximately twice as long for the 45 degrees contraction. The results indicate that muscle length is an important parameter for the propagation velocity of action potentials and for the development of static muscle fatigue.

Action Potentials↗

The effects of muscle fatigue on neuromuscular function and anterior tibial translation in healthy knees.

We investigated the effect of quadriceps and hamstring muscle fatigue on anterior tibial translation and muscle reaction time in 10 healthy subjects. The six men and four women had an average age of 21.3 years and had no known pathologic knee conditions. Each patient underwent a knee examination, arthrometer measurements of tibial translation, subjective functional assessment, and an anterior tibial translation stress test before and after quadriceps and hamstring muscle-fatiguing exercise. The recruitment order of the lower extremity muscles in response to anterior tibial translation did not change with muscle fatigue. However, the results showed an average increase of 32.5% in anterior tibial translation (range, 11.4% to 85.2%) after fatigue. Muscle responses in the gastrocnemius, hamstring, and quadriceps originating at the spinal cord and cortical level showed significant slowing and, in some cases, an absence of activity after the quadriceps and hamstring muscles were fatigued. The increases in displacement after fatigue strongly correlated (0.62 to 0.96) with a delay in cortical-level activity (intermediate and voluntary). Muscle fatigue, which appears to affect the dynamic stability of the knee, alters the neuromuscular response to anterior tibial translation. Therefore, fatigue may play an important role in the pathomechanics of knee injuries in physically demanding sports.

Adult↗

Failure of neuromuscular transmission and contractility during muscle fatigue.

In previous studies of muscle fatigue, tension was monitored from whole muscle, while action potentials were recorded from a few muscle fibers. To compare more accurately changes in these responses, an in vitro fluid electrode technique was employed to record the action potential of whole muscle simultaneously with tension during fatigue induced by nerve stimulation in the rat extensor digitorum longus (EDL), soleus, and diaphragm muscles. In each muscle, tension declined from the start of stimulation, while action potential amplitude initially increased slightly and then declined most rapidly in EDL, more slowly in diaphragm, and most slowly in soleus. Direct stimulation of the fatigued muscle produced the greatest increase in tension in EDL, next in diaphragm, and least in soleus. These results indicate that while failure of excitation-contraction coupling or of the contractile mechanism is the initial cause of fatigue in all the muscles studied, and remains the predominant cause throughout in the soleus muscle, failure of neuromuscular transmission plays an important role in fatigue after the first 15 seconds in EDL, and to a lesser extent, after the first 90 seconds in diaphragm.

Action Potentials↗

Evaluation of skeletal muscle fatigue in patients with heart failure.

Exertional fatigue is a major limiting symptom in patients with heart failure. Nevertheless, the mechanism responsible for this fatigue remains unclear. Reduced skeletal muscle blood flow, altered muscle oxidative enzymes, decreased muscle mass and altered muscle contractility have all been implicated but the precise contribution of these factors remains to be determined. Clinically, the severity of muscle fatigue is usually determined from the patient history. This approach is unreliable since symptoms reported during normal daily activities correlate poorly with objective measures of exercise performance. The degree of perceived fatigue noted during formal exercise testing also correlates poorly with objective measures of muscle behavior, such as blood lactate levels. Cardiopulmonary exercise testing can be used to identify the onset of lactate release, or the anaerobic threshold, and therefore provides more objective information about muscle behavior. However, an increase in blood lactate does not necessarily indicate muscle fatigue. Surface recordings of muscle electromyograms during exercise permits detection of increasing EMG signal, an indicator of fatigue. This technique is potentially valuable but is technically challenging. Finally, muscle fatigue can be assessed by monitoring developed tension during repetitive contractions of the quadriceps muscle. This index of muscle fatigability correlates relatively closely with maximal exercise performance and provides the best index of fatigue currently available. However, further studies are needed to document the clinical utility of this methodology.

Cardiac Output, Low↗

Climatic stress in the workplace: its effect on thermoregulatory responses and muscle fatigue in female workers.

The present study was designed to determine the differences in thermoregulatory responses and the levels of muscle fatigue in the seated worker, performing a task involving a light metabolic load (typing), versus the standing worker, undertaking a task of a heavier metabolic load (lifting), in different climatic conditions (neutral and hot, humid). The results showed that environmental heat significantly influenced the cardiovascular and thermoregulatory systems in workers performing both light and heavy work tasks. In addition, environmental heat was shown to influence the magnitude of the frequency shift during the fatiguing muscle contraction in the typists rather than the lifters. These results suggest that: (1) performance of even sedentary workers performing a light manual task may be deleteriously affected by environmental heat; and (2) environmental heat may be of secondary importance to the nature of the task investigated on the level of muscle fatigue.

Journal Article↗

The reliability of monopolar and bipolar fine-wire electromyographic measurement of muscle fatigue.

Bipolar intramuscular wire electrodes and spectral analysis of the electromyographic signal have been used to measure fatigue in muscles that cannot be studied with surface electrodes. Intramuscular electrodes can detect a greater range of frequencies from muscle, obtain a less distorted signal, and are therefore felt to be more sensitive to detecting fatigue. To determine the reliability and sensitivity of electrode placement (with a fixed distance) for assessing muscle fatigue, we placed three intramuscular electrodes in and two surface electrodes on the biceps brachii of 30 healthy male subjects. With these electrodes, we devised eight configurations that were analyzed separately for reliability. Subjects performed four, 30-s isometric fatiguing contractions divided between two testing sessions. Mean and median frequency of the power density spectrum were plotted against time. Linear regression was performed to obtain slopes, which were used as indicators of fatigue. The bipolar surface electrode configuration displayed mean and median frequency intrasession and mean frequency intersession reliability for slope. All four bipolar fine-wire configurations had mean and median frequency intrasession reliability (P < or 0.05). Only three of the four bipolar fine-wire configurations approached mean frequency intersession reliability, and none fo the four displayed median frequency intersession reliability. the configuration with distal bipolar intramuscular electrodes placed 1 cm apart was the most reliable intramuscular technique. The bipolar fine-wire configuration studied showed a trend toward better reliability than monopolar fine-wire configurations. No intramuscular technique, however, was reliable enough for clinical use in the study of fatigue.

Adolescent↗

Correlation between electromyographic spectral changes and subjective assessment of lumbar muscle fatigue in subjects without pain from the lower back.

OBJECTIVE: The purpose of this study was to correlate objective measurements of muscle fatigue in the lower back to the subject's own assessment of fatigue. DESIGN: Muscle fatigue in the lower back was assessed in healthy subjects using electromyography (EMG), endurance time and the Borg scale. BACKGROUND: Muscle fatigue, measured with EMG and endurance time, in the lower back, is significant for patients with pain in the lower back. METHODS: Fifty healthy subjects participated. EMG was detected from the lumbar extensor muscles during a modified Sørensen's test, an isometric contraction for the back extensors until exhaustion. During the test, subjects rated their subjective fatigue on a Borg CR-10 scale. RESULTS: Borg scale ratings correlated with endurance time (0.68) and EMG median- and mean power frequency slopes (0.41-0.50). At a Borg rating of 3, median- and mean power frequency and endurance time were reduced by 30%. At a Borg rating of 5, median- and mean power frequency and endurance time were reduced by 50%. At a Borg rating of 7, median- and mean power frequency and endurance time were reduced by 60-70%. CONCLUSIONS: Significant correlation between the Borg scale, EMG and endurance time suggests a close relationship between subjective and objective assessment of muscle fatigue.

Adult↗

Expiratory muscle fatigue in normal subjects.

We examined expiratory muscle fatigue during expiratory resistive loading in 11 normal subjects. Subjects breathed against expiratory resistances at their own breathing frequency and tidal volume until exhaustion or for 60 min. Respiratory muscle strength was assessed from both the maximum static expiratory and inspiratory mouth pressures (PEmax and PImax). At the lowest resistance, PEmax and PImax measured after completion of the expiratory loaded breathing were not different from control values. With higher resistance, both PEmax and PImax were decreased (P less than 0.05), and the decrease lasted for greater than or equal to 60 min. The electromyogram high-to-low frequency power ratio for the rectus abdominis muscle decreased progressively during loading (P less than 0.01), but the integrated EMG activity did not change during recovery. Transdiaphragmatic pressure during loading was increased 3.6-fold compared with control (P less than 0.05). These findings suggest that expiratory resistive loaded breathing induces muscle fatigue in both expiratory and inspiratory muscles. Fatigue of the expiratory muscles can be attributed directly to the high work load and that of the inspiratory muscles may be related to increased work due to shortened inspiratory time.

Adult↗

Modeling of muscle fatigue using Hill's model.

A new model incorporating muscle fatigue has been developed to predict the effect of muscle fatigue on the force-time relationship of skeletal muscle by using the PAK-program. Differential equations in the incremental form have been implemented into Hill's muscle model. In order to describe the effect of muscle fatigue and recovery on skeletal muscle behaviors, a set of equations in terms of three phenomenological parameters which are a fatigue curve under sustained maximal activation, a recovery curve and an endurance function were developed. With reference to existing models and experimental results, the input parameters for fatigue curve under sustained maximal activation and endurance function were determined. The model has been investigated under an isometric condition. The effects of different shapes of the recovery curves have also been considered in this model. Validation of the model has been performed by comparing the predicted results with the experimental data from an existing literature.

Action Potentials↗

Respiratory muscle fatigue: a cause of respiratory failure?

1. The question whether respiratory muscle fatigue ever causes respiratory failure is over 40 years old, but we still have no definitive answer to this question. Skeletal muscle fatigue occurs when the rate of energy consumption of the muscle is greater than the energy supplied, so that energy stores are utilized and eventually become depleted. 2. Five factors which are important in the development of muscle fatigue (a, the tension developed by the muscle; b, the maximum tension the muscle can develop; c, the energy stored within the muscle; d, the energy supplied to the muscle; e, the efficiency of the muscle). These can be affected in many diseases, so disposing to fatigue, thus respiratory muscle fatigue is likely to be a common occurrence. 3. Respiratory muscle fatigue can in principle easily be diagnosed at the bedside by application of a simple electromyographic technique used to detect fatigue in other skeletal muscles.

Electromyography↗