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Query: UMLS:C0015672 (
fatigue
)
51,768
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
H+ accumulation at the sarcolemma is believed to play a key role in determining the electrophysiological correlates of
fatigue
. This paper describes an in vitro method to externally manipulate muscle pH while measuring the resultant effect on surface-detected median frequency (MDF) and conduction velocity (CV) parameters. Hamster muscle diaphragm strips (n = 8) were isolated with the phrenic nerve intact and placed in an oxygenated Krebs bath (26 degrees C). The muscle was clamped to a noncompliant load cell to measure isometric contractile tension. Tetanic contraction was developed via 40-Hz supermaximal stimulation of the phrenic nerve. Differential signals were recorded from three electromyogram (EMG) detection surfaces for computation of CV (via the phase shift in the EMG signals) and MDF. Repeated trials were conducted at bath pHs of 7.4, 7.0, and 6.6. Bath pH was altered by aerating predetermined concentrations of O2 and
CO2
into the bath. Decreases in bath pH resulted in decreases in both initial MDF and initial CV. The differences in initial MDF and initial CV were significant (P less than 0.001) for each of the bath pH conditions. In general, the change in bath pH resulted in an equal percent change in initial MDF and initial CV. This suggests that the change in bath pH caused a decrease in CV without significantly altering the fundamental shape of the M wave. In contrast, the EMG was altered differently during stimulated contractions. During stimulation, the rate of decay of CV was 65% of the rate of decay of MDF.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:pH-induced effects on median frequency and conduction velocity of the myoelectric signal. 176 86
1. Single muscle fibres were dissected from the toe muscles of Xenopus laevis and microinjected with Fura-2 to measure myoplasmic calcium concentration ([Ca2+]i). Injected fibres were illuminated at 340 and 380 nm and the ratio of the resulting fluorescence at 505 nm (the Fura-2 ratio) was taken as a measure of [Ca2+]i. Fibres were fatigued at 21 degrees C by repeated tetani until developed tension had fallen to 50% of control. 2. Tetanic tension declined monotonically during fatiguing stimulation, whereas the tetanic Fura-2 ratio first increased and then declined. At the 10th tetanus, tension was 87% of control whereas the Fura-2 ratio was 106% of control. At the end of fatiguing stimulation, where tension was around 50% of control, the tetanic Fura-2 ratio was reduced to 71%. The rate of decline of both tension and the Fura-2 ratio after a tetanus slowed during
fatigue
. During recovery, the tension and the tetanic Fura-2 ratio recovered in parallel. 3. The resting Fura-2 ratio increased throughout
fatigue
reaching 237% of control when tension had declined to 50%. There was a rapid phase of recovery, complete within 1 min, by which time the resting Fura-2 ratio was 198% of control. Subsequent recovery was slower and took 20-30 min to reach a stable level which was 121% of control. 4. The resting Fura-2 ratio towards the end of fatiguing stimulation was greater than the tetanic Fura-2 ratio in the early part of recovery although there was no detectable increase of resting tension during fatiguing stimulation. This observation suggests that the Ca2+ sensitivity of the contractile proteins was reduced at the end of fatiguing stimulation. 5. Plots of the tetanic tension against tetanic Fura-2 ratios throughout fatiguing stimulation and recovery also suggested that Ca2+ sensitivity was reduced during fatiguing stimulation when compared to recovery. 6. The increases in resting [Ca2+]i caused by raised [K+]o (from 2.5 to 10 mM) and/or by application of 15%
CO2
were much less than those produced by fatiguing stimulation. Much of the elevated [Ca2+]i in
fatigue
could be reversed by application of dantrolene (25 microM). 7. The results suggest that both reduced tetanic [Ca2+]i and reduced Ca2+ sensitivity contribute to the decline of tension during
fatigue
.(ABSTRACT TRUNCATED AT 400 WORDS)
...
PMID:Changes in tetanic and resting [Ca2+]i during fatigue and recovery of single muscle fibres from Xenopus laevis. 184 42
1. Single, intact muscle fibres from the flexor brevis foot muscle of the mouse have been fatigued at 25 degrees C by 350 ms, 70 Hz stimulation trains, initially delivered every 3.8 s and then at stepwise decreasing intervals until tension was down to about 30% of the original (Po). Rested fibres generated a specific force of 372 +/- 8.4 kPa (mean +/- S.E.M., n = 25). 2. Endurance, defined as time to attain 0.5 Po, varied from 2.5 to 24 min, with the majority of fibres falling in the range 4-8 min, corresponding to 70-160 tetani. In all fibres where it was followed, tension recovery after cessation of stimulation was 90% or better. 3. Tetanic force declined in a characteristic way during fatiguing stimulation: initially tension fell to about 0.85 Po during eight to fourteen tetani (phase 1), then followed a long period of nearly steady tension generation (phase 2) and finally there was a rapid force decline (phase 3). 4. Caffeine (15 or 25 mM) caused a slight potentiation of tetanic force in the rested state (4.7 +/- 0.9%, n = 21) and slowed relaxation. No change in resting tension was seen with caffeine at concentrations up to 25 mM. 5. Caffeine (15-25 mM) caused a rapid and dramatic increase in tetanic force when applied to severely fatigued fibres: force output rose from 29.8 +/- 1.5 to 82.5 +/- 1.2% (n = 13) of Po. During phase 2 force potentiation with caffeine was much smaller. 6. A 10 s pause resulted in a large, transient force increase when imposed during phase 3 but had little effect on force production during phase 2. 7. Intracellular acidosis, induced by superfusion with Tyrode solution gassed with 30%
CO2
instead of the normal 5% (extracellular pH 6.5 vs. 7.3), resulted in a fall in tetanic tension to about 0.85 Po (n = 7). This depression could to some extent be counteracted by 15 mM-caffeine, which brought tension back to about 0.90 Po. 8. It is concluded that there are at least two mechanisms for force decline during fatiguing stimulation: one which manifests itself early and is likely to be related to cross-bridge function and another representing deficient Ca2+ handling which becomes prominent at a later stage. For severe
fatigue
(0.3 Po) the latter mechanism is dominant.
...
PMID:Force decline due to fatigue and intracellular acidification in isolated fibres from mouse skeletal muscle. 190 15
1. In the preceding paper we analysed the force decline in
fatigue
of isolated mouse muscle fibres. Using the same preparation and stimulation scheme we have now examined another aspect of muscle
fatigue
, namely slowing of relaxation. 2. Relaxation at the end of a tetanic contraction can usually be divided into two phases, an initial nearly linear force decline, followed by an exponential phase. We have analysed the initial phase in terms of decline rate and duration. In rested fibres the decline rate after a 350 ms tetanus was not affected by a 30% reduction of tetanic tension (obtained by decreasing the stimulation frequency). 3. Relaxation became gradually slower during fatiguing stimulation with a maximum reduction at the time when tetanic tension was reduced to about 75% of the original (end of phase 2, see preceding paper). At this time the decline rate of the linear phase had fallen to 55.2 +/- 2.9% (mean +/- S.E.M., n = 25) and its duration had increased to 151.3 +/- 14.2% of the control (unfatigued 350 ms, 70 Hz tetanus). 4. Short rest periods (duration = 10s), given at various times during fatiguing stimulation, resulted in a clear, but partial, normalization of the relaxation parameters; at the time of maximum slowing the mean decline rate increased from 50.3 to 58.7% and the duration decreased from 167.9 to 144.0% of the control (n = 14). 5. The influence of intracellular acidosis on relaxation was studied by exposing rested fibres to 30%
CO2
instead of the normal 5%. This resulted in a decline rate of 43.0 +/- 2.6% and a duration of 221.1 +/- 13.1% of the control (n = 7). 6. In amphibian muscle relaxation is known to become gradually slower during a single, prolonged tetanus. The existence of such an effect also in the present preparation was studied by giving 'interrupted' tetani with a total duration of about 2 s. In rested fibres the mean rate of relaxation was found to fall from 140.9 to 71.8% (n = 11) of the control (end of 350 ms stimulation) with a time constant of about 0.5 s. Thus, a marked slowing during a long tetanus occurs also in mammalian muscle. 7. A distinct slowing of relaxation during prolonged tetani was observed also in the fatigued and in the acidified state. Under these two conditions the mean rate of relaxation fell from 87.0 to 34.0% (n = 3) and from 74.0 to 23.0% (n = 5) of the control, respectively, with time constants similar to that in the rested state.(ABSTRACT TRUNCATED AT 400 WORDS)
...
PMID:Slowing of relaxation during fatigue in single mouse muscle fibres. 190 16
A prospective evaluation of the prevalence of
CO2
retention and its relationship to lung mechanics and inspiratory muscle strength was carried out in 311 clinically stable patients with chronic obstructive pulmonary disease (COPD). Of these patients 32.8% had hypercapnia (PaCO2 greater than or equal to 43 mm Hg). PaCO2 was directly related to lung resistance (RL; r = 0.53) and inversely related to FEV1 (r = 0.53) and to an expression of the dead space/tidal volume ratio (1 - VD/VT) (r = 0.48). RL was found to be a major determinant of the mean intrathoracic pressure swing developed during inspiration (PI) at rest (r = 0.85). Maximal inspiratory pressure (PImax) was found to improve the predictive value for PaCO2 of several mechanical loads, with RL/PImax the best predictor (r = 0.57). The prevalence of hypercapnia increased from virtually 0 to 100% with increases in the RL/PImax value and was higher in the obese subjects at intermediate RL/PImax values, probably because of the burden placed on the respiratory muscles by chest wall mass loading. Our results show that chronic alveolar hypoventilation is likely to develop in COPD patients who have a combination of high inspiratory loads and inspiratory muscle weakness. hypercapnia may be one strategy available to avoid overloading of the inspiratory muscles leading to
fatigue
and possible irreversible failure.
...
PMID:Inspiratory muscle dysfunction and chronic hypercapnia in chronic obstructive pulmonary disease. 202 40
Hypoxic, hypercapnic acidosis (HHA) decreases tension and enhances
fatigue
in hamster diaphragm in vitro. We hypothesized that theophylline would decrease the harmful effect of HHA. Hamster diaphragm strips were studied in Krebs solution aerated with 21% O2 and 12%
CO2
. The force-frequency responses and the tension and relaxation of brief, submaximal contractions were studied. Mild
fatigue
was produced by a series of 45 submaximal contractions, after which recovery of force was followed for 15 min. Theophylline (0.55 mM) was added at the time of exposure to HHA (early theophylline) in half the strips and at the end of the
fatigue
run (late theophylline) in the others. In contrast to our hypothesis, early theophylline had a limited effect on force production in unfatigued HHA diaphragm strips and resulted in lower force production in the recovery period. Late theophylline improved force in the recovery period for low-frequency contractions. Thus the effect of theophylline in the setting of HHA depended on the time it was added and was beneficial only if added after the muscle stopped contracting.
...
PMID:The effect of theophylline on hypoxic, hypercapnic hamster diaphragm muscle in vitro. 202 50
The pattern of oxygen (O2) consumption (VO2), carbon dioxide (
CO2
) production (VCO2), ventilatory and metabolic responses during and in recovery from supine bicycle exercise was examined in 18 patients with recent myocardial infarction. An increase in VO2 with increasing work load was accomplished by proportional increases in both cardiac output and the arteriovenous O2 difference. During recovery, however, the arteriovenous O2 difference rapidly decreased below levels at rest, whereas VO2 and cardiac output remained elevated, indicating that VO2 during recovery further depended on relatively high cardiac output. The ratio of VCO2 to VO2 further increased after exercise, suggesting that such cardiac output contributed to the remaining high
CO2
flow to the lung and therefore enhanced ventilation. Increased arterial catecholamines during exercise remained elevated for the first 5 minutes of recovery. Arterial lactate during this period continued to increase and resulted in profound metabolic acidosis, causing alveolar hyperventilation after exercise. These results suggest that during recovery from exercise, cardiopulmonary responses remain enhanced because of continuing high cardiac output, resulting in subsequent high
CO2
flow to the lung and metabolic acidosis, and that this may be associated with profound
fatigue
or dyspnea after exercise.
...
PMID:Oxygen utilization, carbon dioxide elimination and ventilation during recovery from supine bicycle exercise 6 to 8 weeks after acute myocardial infarction. 203 36
The force-velocity relation of frog sartorius muscle was observed during slow stretch and during shortening in solutions with and without
CO2
at extracellular pH (pHo) 6.9 and pHo 7.5 (5 degrees C). Less force was produced with
CO2
than without
CO2
during stretch, during shortening, and under isometric conditions. Compared with pHo 7.5, the effects were greater at pHo 6.9, where the concentration of
CO2
, a permeant acid, was greater and would cause a greater acidification of intracellular pH (pHi). The reduction of force caused by
CO2
was smaller during stretch than during shortening or isometric contraction. This result indicates that the crossbridge states specific to stretch retain their ability to produce force better under acidic conditions than those characteristic of shortening and isometric conditions. This difference between stretch and shortening suggests that there may be compensating changes in the pattern of motor unit activity during
fatigue
in vivo.
...
PMID:Force during stretch and shortening of frog sartorius muscle: effects of intracellular acidification due to increased carbon dioxide. 211 94
In ten lightly anaesthetized dogs breathing spontaneously, we studied diaphragmatic force generation (Pdi 10, 30, 100 Hz and single twitch) and ventilatory control (P 0, 1, Vt/Ti and respiratory frequency). We found
CO2
retention proportional to hypothermia (Fig. 3). The TP was not changed while VMxA and VMxD decreased (Table 1). High frequency
fatigue
and low frequency potentiation were found (Fig. 1, 2). These changes do not explain
CO2
retention which correlated with fall in central drive (P 0, 1, Vt/Ti, Fig. 3, 4) and respiratory timing (respiratory frequency, Fig. 4).
...
PMID:[Diaphragmatic strength and ventilatory control in experimental hypothermia]. 213 Feb 40
Continuous monitoring of important respiratory indices has the potential for predicting catastrophes and for providing an opportunity for the timely institution of lifesaving measures. Pulmonary gas exchange can be assessed by indices derived from arterial blood gas measurements, but these are limited by their invasive and intermittent nature. Intra-arterial electrodes that provide a continuous recording of blood gases are under development and appear very promising. Specially designed pulmonary artery catheters permit continuous recording of mixed venous O2 saturation, whereas continuous, non-invasive recordings of arterial oxygenation can be obtained with pulse oximetry and transcutaneous electrodes. A satisfactory method of monitoring
CO2
tension does not exist. Measurements of respiratory drive can be obtained at the bedside, but their clinical usefulness remains unknown. Assessment of respiratory muscle strength is helpful in determining the need for mechanical ventilation, but a practical method of diagnosing respiratory muscle
fatigue
remains elusive. Recordings of the airway pressure waveform, calculation of thoracic compliance, and detailed examination of the pattern of breathing are helpful in assessing pulmonary mechanics. Although respiratory monitoring provides much useful information, it does not substitute for careful bedside examination.
...
PMID:Respiratory monitoring during mechanical ventilation. 219 1
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