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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

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

The consequences of diaphragmatic muscle fatigue in the newborn infant.

We have previously demonstrated that diaphragmatic muscle fatigue can be diagnosed in infants from spectral frequency analysis of the surface diaphragmatic electromyogram. This requires a digital computer, but the analysis takes several days. Spectral frequency changes, however, can be accurately reflected by band pass filtering and expressing the ratio of high-frequency power to low-frequency power. A fall in this ratio of greater than 20% indicates muscle fatigue. Using a simple analog device to obtain this ratio permits the results to be immediately available; we have used this method to study weaning from mechanical ventilators in ten infants. With a successful weaning step there is no significant change in the ratio, whereas an unsuccessful weaning step invariably leads to a decrease in the ratio of greater than 20%, which precedes CO2 retention and clinical deterioration. These data indicate that diaphragmatic muscle fatigue plays an important role in the infant's response to lung disease. Monitoring of the high/low frequency ratio may be helpful in weaning infants from assisted ventilation.

Computers, Analog

Muscle fatigue and its relation to lactate accumulation and LDH activity in man.

The lactate concentration in different muscle fibre types was determined in biopsy specimens from human vastus lateralis muscle after 30 and 60 s of maximal dynamic leg exercise. In addition, muscle fibre type distribution, total lactate dehydrogenase (LDH) activity, and isozymes of LDH were determined. In accordance with previous studies (Thorstensson and Karlsson 1976, Nilsson et al. 1977) it was found that an increasing proportion of slow twitch (ST) fibres corresponded to better sustained muscle force. Lactate was found preferentially in fast twitch (FT) fibres after 30 s, but after 60 s this difference was abolished. Differences between the two main muscle fibre types in muscle lactate, total LDH activity, and M-LDH activity were correlated to muscle fatigue. It was concluded that lactate or associated pH changes primarily in FT fibres could be one factor responsible for the impaired muscle function.

Adult

Composition of vacuoles and sarcoplasmic reticulum in fatigued muscle: electron probe analysis.

Electron probe analysis, cryo-ultramicrotomy, and freeze-substitution were used to determine the nature of vacuolation and the subcellular composition in fatigued frog skeletal muscle fibers. The vacuoles caused by fatigue were part of the T-tubule system and contained high concentrations of NaCl. The calcium concentration in the terminal cisternae was higher than previously measured normal resting values. Mitochondrial calcium content was relatively low (mean +/- SEM, 2 +/- 2 mmol/kg dry weight). Fiber NaCl was increased. It is concluded that fatigue is not due to the depletion of calcium stores from the terminal cisternae or to uncoupling of mitochondria due to calcium loading but may be caused by multiple mechanisms including failure of the T-tubule action potential.

Animals

Muscle fatigue.

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Animals

[Interaction of catecholamines and corticosteroids during the process of muscle fatigue].

After prolonged (8 hrs) swimming, the level of corticosteroids was reduced and the contents of aldosterone and DOC in the blood was increased in the rats. At incubation of these rats' adrenals in the L-thyrosine substratum the synthesis of adrenaline was reduced. Addition of hydrocortisone, prednisolone and corticosterone into the medium as well as in vivo administration of these increased the adrenaline synthesis in swimming rats and did not alter it in intact rats. Neither in vitro addition of aldosterone nor in vivo administration of ACTH activated the process. The activating effect of glucocorticoids was absent at incubation of the adrenals with L-DOPA and L-noradrenaline. Synthesis of cathecholamines in the heart of swimming rats in the presence of L-thyrosine and L-DOPA as precnrsors was suppressed; neither was it restored by administration of corticosteroids both in vitro and in vivo. This suggests that one of the reasons for suppression of the catecholamine synthesis in adrenals at obvious physical fatigue is the decrease of the glucocorticoid activity.

Adrenal Cortex Hormones

Fatigue of inspiratory muscles and their synergic behavior.

The time (tlim) required to produce inspiratory muscle fatigue was measured in five normal subjects breathing at functional residual capacity (FRC) against a variety of high inspiratory resistive loads. In every breathing test the subjects generated with each inspiration a mouth pressure (Pm) that was a predetermined fraction of maximum Pm (Pmmax). They continued breathing until they were unable to generate this Pm. The Pm/Pmmax that could be generated indefinitely (Pmcrit) was around 60%. The inspiratory power output at that level of breathing was 6.6 kg.m/min (Wcrit). In three of those subjects the same experiment was conducted at an end-expiratory volume of FRC + one-half inspiratory capacity (1/2IC). The higher lung volume was actively maintained by the subjects watching end-expiratory transpulmonary pressure on an oscilloscope. For any fraction of the maximum mouth pressure at FRC + 1/2IC (Pm'max), tlim was shorter than FRC. Pmcrit decreased to 30% Pm'max and Wcrit to 2.6 kg.m/min. Monitoring the abdominal pressure revealed that the contribution of the diaphragm and intercostal accessory muscles alternated in time, possibly postponing the onset of fatigue.

Diaphragm

Some subjective-experiential parameters in experimental tooth clenching in man.

Experimental tooth clenching was performed by fourteen human subjects in order to determine the onset of the subjective sensations of jaw muscle fatigue and jaw muscle pains, the ability to endure jaw muscle pains, and other discomforts. During production of maximal voluntary isometric tension by the elevator jaw muscles the fatigue threshold (x = 31 s), the pain threshold (x = 55 s), and the pain tolerance (x = 118 s) of tooth clenching did not vary significantly intraindividually, whereas this was so interindividually. There might have existed psychological relationships between the three parameters, but they might also have been influenced by the same physiological cause. The weak to intense discomforts were localized to the face, and primarily to the jaw muscles, and after determination of the pain tolerance they disappeared in about 90 s.

Adult