Low-frequency Fatigue Research Articles

Is post-tetanic potentiation, low frequency fatigue (LFF) and pre-contractile depression (PCD) coexistent in intermittent isometric exercises of maximal intensity?

The aim of our experiment was to test the hypothesis that the performance of maximal isometric exercise every 20 s would reduce the intermediate frequency force, i.e. the force that appears while stimulating the muscle at 15 and 20 Hz, and would produce less decrease the force at 10 and 50 Hz, while Pt would increase. Such changes in stimulated force should demonstrate the coexistence of potentiation, low frequency fatigue (LFF) and 'post-contractile depression' (PCD). The quadriceps muscle of 14 healthy men (aged 19-37 years) was studied. The results have shown, that during isometric exercise of maximal intensity there was significant (P < 0.05) decrease in P15 and P20, increase in Pt, however, MVC and P10 and P50 was unchanged (P > 0.05). LFF manifested itself most significantly which is evident from decrease in P20/P50. During recovery after work there was significant increase in LFF and decrease in P50 which is indicative of the manifestation of PCD. Besides, there was significant (P < 0.05) decrease immediately after exercise in RTP20 and RTP50, while no changes in T50 and RT. There were no significant changes (P > 0.05) however, either in RTP20 and RTP50 or in T50 and RT 20 min after exercise if compared to the initial and immediately post-exercise values.

Electrical stimulation of human tibialis anterior: (A) contractile properties are stable over a range of submaximal voltages; (B) high- and low-frequency fatigue are inducible and reliably assessable at submaximal voltages.

To investigate the validity and reliability of submaximal voltage stimulation for assessing the 'fresh' contractile properties of human tibialis anterior muscle (TA) and the efficacy of such stimulation in inducing and assessing high- and low-frequency fatigue. (A) Contractile properties of fresh TA were assessed in six normal volunteers using multifrequency stimulation trains (comprising 2 seconds at each of 10, 20 and 50 Hz, arranged contiguously) over a range of submaximal voltages. (B) On three separate occasions, fatigue was induced in the TA of 10 normal volunteers by means of a 3-minute unbroken sequence of the described multifrequency stimulation trains, delivered at a 'standardized' submaximal voltage. This fatiguing protocol was preceded by discrete multifrequency stimulation trains, at the same standardized voltage, but followed by discrete multifrequency trains delivered over a range of submaximal voltages (which included the standardized voltage). In experiment A the 10:50 Hz and 20:50 Hz force ratios were analysed for between-voltages variability using coefficients of variation (CVs), and for trends using Friedman tests and post-hoc Wilcoxon tests. In experiment B low-frequency fatigue was detected using 10:50 Hz and 20:50 Hz force ratios derived from the discrete multifrequency trains. High-frequency fatigue was calculated from the decline in high-frequency force which occurred during the fatiguing protocol itself. Each parameter was assessed for between-days repeatability using CVs. In experiment A the 'fresh' 10:50 Hz force ratio was clearly unreliable at voltages which generated <10% of maximal voluntary contractile force (MVC) (CV< or =29.7%), but was reasonably reliable at voltages which generated 20-30% of MVC (CV < or = 11.5%; p = 0.847). The 'fresh' 20:50 Hz force ratio was,in contrast, extremely reliable throughout the tested voltage range (CV< or =5.8%; p = 0.636) in fresh muscle. In experiment B paired t-tests indicated that the fatiguing protocol induced significant high-frequency fatigue (p <0.0037) and low-frequency fatigue (p <0.0008 for 'fresh' versus 'fatigued' 10:50 Hz force ratio; p <0.0001 for 'fresh' versus 'fatigued' 20:50 Hz force ratio). In muscle thus fatigued, the 20:50 Hz force ratio was extremely reliable in the 20-33% of MVC range (CV < or =7.3%; p = 0.847). Between-days repeatability was poor for the 10:50 Hz force ratio in both fresh and fatigued muscle (CV < or =23.8 and 44.4% respectively), but was highly acceptable for both voluntary and stimulated fatigue indices and for the 20:50 Hz force ratio, the latter in both fresh and fatigued muscle. These results confirm the validity and reliability of submaximal voltages in assessing contractile properties (including low-frequency fatiguability) and inducing fatigue of human TA.

The influence of loading frequency on the high-temperature fatigue behavior of a Nicalon-fabric-reinforced polymer-derived ceramic-matrix composite

Fiber-reinforced ceramic-matrix composites are under development for high-temperature structural applications. These applications involve fatigue loading under a wide range of frequencies. To date, high-temperature fatigue experiments have typically been performed at loading frequencies of 10 Hz or lower. At higher frequencies, a strong effect of loading frequency on fatigue life has been demonstrated for certain CMC`s tested at room temperature. The fatigue life of CMC`s with weak fiber-matrix interfaces typically decreases as the loading frequency increases. This decrease is attributed to frictional heating and frequency dependent interface and fiber damage. More recently, it has been shown that the room temperature fatigue life of a Nicalon-fabric-reinforced composite with a strong interface (SYLRAMIC{trademark}) appears to be independent of loading frequency. The high-temperature low-frequency fatigue behavior of the SYLRAMIC composite has also been investigated. For a fatigue peak stress {sigma}{sub peak} above a proportional limit stress of 70 MPa, the number of cycles to failure N{sub f} decreased with an increase in {sigma}{sub peak}. The material endured more than 10{sup 6} cycles for {sigma}{sub peak} below 70 MPa. In this paper, the influence of loading frequency on the high-temperature fatigue behavior of the SYLRAMIC composite is reported. It will be shown that themore » fatigue limit is unaffected by the loading frequency, that the number of fatigue cycles to failure N{sub f} increases with an increase in frequency, and that the time to failure t{sub f} decreases with an increase in frequency.« less

High frequency diaphragmatic fatigue detected with paired stimuli in humans.

The purpose of this study was to determine whether high frequency fatigue was present in the diaphragm after intense whole body endurance exercise. We used bilateral phrenic nerve stimulation (BPNS) before and during recovery from whole body exercise to detect fatigue in the diaphragm. To detect high frequency fatigue we used paired stimuli at 10, 20, 50, 70, and 100 Hz frequency and determined the transdiaphragmatic pressure (Pdi) response to the second stimulation (T2). The subjects (N = 10) exercised at 93.3 +/- 2.3% of their VO2max for 9.9 +/- 0.5 min. The Pdi response to "twitch" and 10 Hz "tetanic" stimulation was decreased immediately after exercise versus pre-exercise values (-23.4 +/- 3.3%). The T2 amplitude was substantially reduced at all frequencies immediately after exercise (-28.0%), but by 30 min into recovery the T2 amplitude at 70 and 100 Hz was not different from pre-exercise values. In contrast, at 10 and 20 Hz the T2 response was still significantly reduced. We interpret these data to mean that high frequency fatigue as well as low frequency fatigue were present in the diaphragm after intense whole body endurance exercise.

Mechanisms underlying the slow recovery of force after fatigue: importance of intracellular calcium.

Recovery of force production after an intense bout of activity may sometimes take several days, especially at low activation frequencies ('low frequency fatigue'). This slow recovery can also be observed in isolated muscle and single muscle fibres. The origin of the force deficit is failure of excitation-contraction coupling at the level of the triads. The most likely cause of the failure is an elevated intracellular Ca2+ level, but the site of action of Ca2+ is unclear. Available evidence does not support the involvement of Ca2+-activated proteases. Ca2+-induced damage to mitochondria or swelling of t-tubules do not seem to be causative factors. Other mechanisms are discussed, including possible detrimental effects of Ca2+-activated lipases, calmodulin, and reactive oxygen species.

Muscle fatigue and induction of stress protein genes: a dual function of reactive oxygen species?

Definitive characterization of the mechanisms of skeletal muscle fatigue is still an area of active investigation. One emerging theory concerns a role for the reactive oxygen species (ROS) produced primarily as a consequence of elevated rates of mitochondrial respiration. It has been theorized that the long-lasting effects of low-frequency fatigue (LFF) can be attributed to disruption of some stage of the excitation contraction coupling (ECC) process. Recent evidence suggests that ROS likely denature one or more proteins directly associated with the sarcoplasmic reticulum (SR) Ca2+ release mechanism. Given the potential of ROS to damage intracellular proteins during subsequent bouts of muscle contractions, the capacity of preexisting antioxidant pathways may be complemented by the synthesis of inducible heat-stress proteins (HSPs). HSPs collectively function to maintain cellular protein conformation during stressful proteotoxic insults. The goal of this article is to illustrate how recent findings suggest a dual role of ROS generated during muscle contractions.

The effects of fatigue on the torque-frequency curve of the human paralysed soleus muscle

An advanced understanding of the torque-generating properties of the chronically paralysed soleus muscle may be instrumental in developing improved methods to activate human paralysed muscle. We established the shape of the torque-frequency curve before and after fatigue of the human paralysed soleus muscle. After fatigue, the normalized torque-frequency curve was shifted to the right, suggesting a higher frequency was required to generate the same relative torque. Low frequency fatigue (LFF) consisting of reduced torques at low frequencies and normal torques at higher frequencies was demonstrated. Conversely, the acutely paralysed soleus muscle was found to be fatigue-resistant and showed no shift in the torque-frequency curve. The muscle activation history (potentiation), LFF, and changing contractile speeds may affect the torque-frequency curve after fatigue. These factors may also play an important role in the development of optimal methods to activate paralysed muscle to attenuate fatigue.

Fatigue-induced changes in group IV muscle afferent activity: differences between high- and low-frequency electrically induced fatigues

Recordings of group IV afferent activity of tibialis anterior muscle were performed in paralysed rabbits during runs of electrically induced fatigue produced by direct muscle stimulation at a high (100 Hz, high-frequency fatigue HFF) or a low rate (10 Hz, low-frequency fatigue LFF). In addition to analysis of afferent nerve action potentials, muscle force and compound muscle action potentials (M waves) elicited by direct muscle stimulation with single shocks were recorded. Changes in M wave configuration were used as an index of the altered propagation of membrane potentials and the associated efflux of potassium from muscle fibers. The data show that increased group IV afferent activity occurred during LFF as well as HFF trials and developed parallel with force failure. Enhanced afferent activity was significantly higher during LFF (maximal Δf impulses=249±35%) than HFF (147±45%). No correlation was obtained between the responses of group IV afferents to LFF or to pressure exerted on tibialis anterior muscle. On the other hand, decreased M wave amplitude was minimal with LFF while it was pronounced with HFF. Close correlations were found between fatigue-induced activation of group IV afferents and decreases in force or M wave amplitude, but their strength was significantly higher with LFF compared to HFF. Thus, electrically induced fatigue activates group IV muscle afferents with a prominent effect of low-frequency stimulation. The mechanism of muscle afferent stimulation does not seem to be due to the sole increase in extracellular potassium concentration, but also by the efflux of muscle metabolites, present during fatiguing contractions at low rate of stimulation.

Role of intracellular calcium and metabolites in low-frequency fatigue of mouse skeletal muscle.

We have examined the extent to which prolonged reductions in low-frequency force (i.e., low-frequency fatigue) result from increases in intracellular free Ca2+ concentration ([Ca2+]i) and alterations in muscle metabolites. Force and [Ca2+]i were measured in mammalian single muscle fibers in response to short, intermediate, and long series of tetani that elevated the [Ca2+]i-time integral to 5, 17, and 29 microM x s, respectively. Only the intermediate and long series resulted in prolonged (>60 x min) reductions in Ca2+ release and low-frequency fatigue. When fibers recovered from the long series of tetani without glucose, Ca2+ release was reduced to a greater extent and force was reduced at high and low frequencies. These findings indicate that the decrease in sarcoplasmic reticulum Ca2+ release associated with fatigue has at least two components: 1) a metabolic component, which, in the presence of glucose, recovers within 1 h, and 2) a component dependent on the elevation of the [Ca2+]i-time integral, which recovers more slowly. It is this Ca2+-dependent component that is primarily responsible for low-frequency fatigue.

Diaphragm performance during maximal voluntary ventilation in chronic obstructive pulmonary disease.

In normal subjects 2 min of maximal voluntary hyperventilation results in failure of tension generation and low-frequency fatigue of the diaphragm. Patients with severe chronic obstructive pulmonary disease (COPD) do not develop diaphragm fatigue during exhaustive treadmill exercise despite excessive inspiratory muscle loading and we hypothesized that they might be relatively resistant to the development of diaphragm fatigue during maximal ventilation. In six patients with severe COPD (mean FEV1 0.671) we therefore loaded the diaphragm using 2 min of maximal isocapnic ventilation (MIV). Initial mean ventilation was 28.6 L/min and diaphragm pressure-time product (PTPdi) 602 cm H2O x s/min; these values were sustained throughout MIV without significant decline. Mean twitch transdiaphragmatic pressure (Tw Pdi) was 19.7 cm H2O 25 min after a control run and 20.5 cm H2O at the same time after MIV [corrected]. Compared with normal subjects previously studied in our laboratory (Hamnegard, C.-H., et al. Eur. Respir. J. 1996;9:241-247) the reduction in PTPdi was disproportionately greater than the reduction in Tw Pdi. We conclude that, unlike normal subjects, 2 min of MIV causes neither failure of diaphragm performance nor low-frequency diaphragm fatigue in patients with severe COPD. It is likely that the diaphragm makes a relatively limited contribution to the generation of maximal levels of ventilation in severe COPD.

Phosphorylation of myosin and twitch potentiation in fatigued skeletal muscle

Phosphorylation of myosin regulatory light chain (R-LC) increases the sensitivity of skinned skeletal muscle fibers to low Ca2+ activation. The purpose of this study was to determine whether phosphorylation of R-LC-mediated increases in Ca2+ sensitivity provides a molecular basis for potentiated twitch forces observed during fatigue of intact mammalian skeletal muscle. Tetanic stimulation for 120 s reduced peak tetanic force (Po) of mouse extensor digitorum longus (EDL) muscle by 74 +/- 2%. Despite high frequency fatigue (HFF), Pt was potentiated by 18 +/- 3% when R-LC phosphorylation (in moles phosphate per mole R-LC) was increased from 0.11 +/- 0.05 (rest) to 0.52 +/- 0.04 by 15 s of stimulation. Thereafter Pt declined below resting values despite high levels for R-LC phosphorylation (0.80 +/- 0.04 after 120 s of stimulation). In separate experiments, 10 min of stimulation, which reduced Po and Pt by 80 +/- 2 and 67 +/- 3%, respectively, was used to induce low frequency fatigue (LFF) in mouse EDL muscle. During LFF, long-lasting reductions in Pt were evident despite near-normal levels for Po (79 +/- 2 and 98 +/- 2% of controls, respectively). Application of conditioning stimuli (CS) increased R-LC phosphate content of fatigued muscles from 0.15 +/- 0.03 (rest) to 0.56 +/- 0.03 (stimulated) and potentiated Pt by 26 +/- 2% compared with LFF. Twitch potentiation during LFF was transient, lasting only as long as R-LC was phosphorylated above resting values for fatigued muscles. Overall, our data showing potentiated twitch forces concomitant with elevations in R-LC phosphate content during either HFF or LFF of mouse EDL muscle suggest that this molecular event counters reduced twitch forces during these forms of fatigue. Our results may be explained by R-LC phosphorylation induced increases in Ca2+ sensitivity for twitch force production in fatigued muscle.

EXERCISE-INDUCED HIGH FREQUENCY DIAPHRAGM FATIGUE 528

The purpose of this study was to determine if high frequency diaphragmatic fatigue was present after intense whole body endurance exercise. We have adapted the paired stimuli technique (Yan et al., Eur. Respir J. 6: 211-218, 1993), to determine changes in the transdiaphragmatic pressure (Pdi) response to low and high frequency supramaximal bilateral phrenic nerve stimulation(BPNS) before and after intense whole body endurance exercise. Subjects (N=6) exercised for 10.6 ±0.5 min until volitional fatigue at 93.3±2.3% of VO2max. BPNS Pdi was measured at FRC using single twitch, tetanic 10 Hz (4 stimuli in 400 ms) and paired stimuli at 10, 20, 50, 70 and 100 Hz frequencies before exercise, immediately after exercise, 30 min and 60 min post-exercise. The paired stimuli data were analyzed by subtracting the ensemble averaged Pdi twitch response from each of the paired supramaximal stimulation. The residual Pdi was the response to the second high frequency stimulus (T2). Low frequency fatigue was shown by the mean percent decrease in the supramaximal BPNS Pdi (twitch and tetanic 10 Hz) which was-20.4 ±5.1%, immediately after exercise. It did not recover until > 60 min post exercise. The paired stimuli Pdi (at 50, 70, 100 Hz) were decreased from pre-exercise control by an average of 24.2 ±2.1% immediately following exercise. Four of six subjects T2 amplitude recovered to pre-exercise levels by 30 min post-exercise. These data suggest that the diaphragm experienced high frequency fatigue following intense whole body endurance exercise. Intense whole body endurance exercise not only caused peripheral fatigue in the diaphragm but also may cause nerve transmission disruptions at the muscle membrane.

The role of elevations in intracellular [Ca2+] in the development of low frequency fatigue in mouse single muscle fibres.

1. Intracellular free calcium concentration ([Ca2+]i) and force were measured in isolated single skeletal muscle fibres from mice. The aim was to determine the extent to which elevations in [Ca2+]i during various stimulation protocols affected subsequent muscle performance. 2. A protocol of repeated tetanic stimulation which elevated [Ca2+]i and caused a large decline in force (fatigue) had a [Ca2+]-time integral of 36.4 +/- 8.1 microM s. A protocol of repeated tetani at a lower duty cycle (stimulation) caused only a small decline in force (9-16%) but elevated the [Ca2+]-time integral to 16.7 +/- 2.8 and 24.9 +/- 1.6 microM s in the absence and presence of 10 mM caffeine, respectively. Caffeine alone raised the [Ca2+]-time integral to 20.3 +/- 3.4 microM s. 3. Following the fatigue protocol there was a proportionately greater loss of force at low stimulation frequencies (30 and 50 Hz) compared with high frequencies (100 Hz) which persisted for up to an hour. This pattern of force loss could be attributed to a uniform reduction in [Ca2+]i at all frequencies. Similar effects were observed after elevating [Ca2+]i with the caffeine + stimulation protocol but were not observed after stimulation or caffeine alone. The higher [Ca2+]-time integrals during the fatigue and caffeine + stimulation protocols suggest that some threshold for [Ca2+]i must be reached before these effects are observed. 4. The reductions in low frequency force induced by the fatigue and caffeine + stimulation protocols were not due to decreased Ca2+ sensitivity or to decreases in maximum force-generating capacity of the contractile proteins and therefore are due to a failure of Ca2+ release. 5. The Ca(2+)-activated neutral protease (calpain) inhibitor calpeptin was not effective in preventing the effects of caffeine + stimulation indicating that the reduction in Ca2+ release was not due to calpain-mediated hydrolysis of the Ca2+ release channel. 6. Our findings indicate that low frequency fatigue results from increases in [Ca2+]i during fatigue and that these elevations in [Ca2+]i activate some process which leads to failure of excitation-contraction (E-C) coupling and Ca2+ release.

High-and low-frequency fatigue revisited.

Changes in excitation-contraction coupling have long been recognized as possible causes of the failure in function which occurs in fatigued muscle. High-frequency fatigue is characterized by an excessive loss of force at high frequencies of stimulation and rapid recovery when the frequency is reduced. Frequencies in excess of 50 Hz are rarely seen with voluntary activation of human muscle, and for this reason there has been some doubt as to whether high-frequency fatigue is a significant feature of normal activity. Recent experiments have shown that with 30 Hz stimulation there is a more rapid loss of force if the muscle is held isometric in a shortened position and the fatigue is rapidly reversed if the muscle is re-extended, even under ischaemic conditions. These findings are consistent with the accumulation of K+ in the t-tubules and interfibre spaces of the muscle. Low-frequency fatigue is characterized by a relative loss of force at low frequencies of stimulation and a slow recovery over the course of hours or even days. There is evidence from intracellular measurements that low-frequency fatigue is due to a reduction in Ca2+ release. However, there is a possibility that in the fatiguing exercise, the end sarcomeras of the fibre overextend and damage those in the middle section of the fibre. In this situation the active sarcomas would be working at a shorter length than predicted from the overall fibre length and the force-frequency curve will be shifted to the right. Measurements of the length-tension relationship of muscles damaged by stretching are consistent with this happening.

Slow recovery of force in single skeletal muscle fibres

After a bout of intense exercise, especially in untrained persons recovery of muscle force is often slow. Force depression is much more marked at low frequencies of stimulation than at high frequencies ("low-frequency fatigue') and recovery can take more than 1 day. Delayed force recovery is also seen in single muscle fibres from frog and mouse after fatigue induced by repeated, brief contractions. Evidence from our own and other laboratories indicates that the impairment is unlikely to result from metabolic changes and points to a defect in excitation-contraction coupling. We demonstrate that the likely site of failure is in the coupling between t-tubule depolarization and release of Ca2+ from the SR. The causative agent appears to be a localized increase in cytoplasmic Ca2+ which initiates some disruptive process, which can, however, be fully reversed, albeit slowly. Our experimental evidence does not support the involvement of Ca(2+)-activated proteases. Attempts to clarify the possible role of Ca(2+)-activated lipases (phospholipase A2) and Ca2+/calmodulin have been hampered by side-effects of available inhibitors. Efforts to clarify how Ca2+ exerts its effects are continuing.

Botulinum-induced muscle paralysis alters metabolic gene expression and fatigue recovery.

We evaluated the physiological, histochemical, and biochemical consequences of inhibiting contractile activity in rat skeletal muscles with botulinum toxin A (BTX). Contractile activity was entirely eliminated 12-18 h after a single, focal, intramuscular injection of BTX into the rat tibialis anterior muscle (TA). Neuromuscular transmission remained completely inhibited for 10-12 days, then slowly recovered. BTX-treated muscles exhibited a lower resistance to both high- and low-frequency fatigue at 7 and 14 days after injection, but contractile force recovered more rapidly in treated TA after fatigue. Treated TA showed a twofold increase in the activity of the triglyceride hydrolase enzyme lipoprotein lipase (LPL) and a comparable increase in the relative abundance of LPL steady-state mRNA. In contrast, there was a 28% reduction in protein levels of the muscle isozyme of glycogen phosphorylase (MGP) and a 70% decrease in relative MGP transcript levels. Similar changes in relative transcript levels of LPL and MGP were observed in the predominantly fast-twitch extensor digitorum longus after BTX injection, but relative LPL and MGP mRNA levels were not altered in predominantly slow-twitch soleus. Histochemical evidence indicated that fast-twitch glycolytic fibers had increased lipid content. These biochemical alterations were reversed 120 days after BTX treatment despite persistent atrophy.

Effect of varying inspired oxygen concentration on diaphragm glutathione metabolism during loaded breathing.

Recent studies have suggested that loaded breathing elicits alterations in diaphragmatic glutathione levels that may be mediated by free radicals and may also be linked to the development of diaphragm fatigue. While free-radical generation in a number of pathophysiologic conditions is known to be a function of ambient oxygen concentrations, the effect of varying inspired oxygen concentration on the diaphragmatic response to loaded breathing (i.e., on diaphragm fatigue and glutathione levels) has not been studied. In this study, we compared the effect of loaded breathing, continued until respiratory arrest in decerebrate rats breathing room air (RA), with the effect of the same load on animals breathing 100% oxygen (O2). After arrest, the animals' diaphragms were excised, force generation was assessed in vitro, and diaphragmatic levels of reduced glutathione (GSH) and oxidized glutathione (GSSG) were determined. Similar measurements were made on unloaded control animals. We found both similarities and differences in the response to loading in O2- and RA-breathing animals. O2-breathing loaded animals had a greater load endurance, lower blood pressure at the end of loading, higher carbon dioxide levels, and greater high-frequency fatigue at the conclusion of loaded trials than did RA-breathing animals. The degree of low-frequency fatigue was similar, however, in the O2- and RA-breathing loaded groups (i.e, twitch force averaged 7.9 +/- 0.6, 8.4 +/- 0.5, 3.8 +/- 0.9, and 4.5 +/- 0.8 N/cm2, respectively, in the RA/unloaded, O2/unloaded, RA/loaded, and O2/loaded groups, p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Exhaustive treadmill exercise does not reduce twitch transdiaphragmatic pressure in patients with COPD.

Reduced diaphragm contractility has been described in normal subjects after whole body endurance exercise, and it indicates low frequency fatigue (LFF); it is unknown whether LFF is of clinical importance. We therefore studied the effect of treadmill exercise to exhaustion on diaphragm contractility in six patients with severe chronic obstructive pulmonary disease (COPD) (mean FEV1, 0.71, 27% predicted). The subjects first performed a short (control), treadmill walk and then, after resting, a second walk to a state of severe dyspnea. Cervical magnetic stimulation of the phrenic nerve roots was performed at the start of the study and 20 and 30 min after each walk. The twitch transdiaphragmatic pressure (Tw Pdi) was reproducible (mean coefficient of variation, 5.3%; range, 2 to 12.5%). Mean Twi Pdis were 18.4 cm H2O at baseline and 19.6 cm H2O and 19.2 cm H2O 20 and 30 min after the control walk. At the same times after the exhaustive walk, mean Tw Pdis were 19.6 and 20.4 cm H20. Tw Pdi was not reduced by exhaustive treadmill walking (p > 0.9), and a power calculation showed that the study had a 95% chance of detecting a 10% fall at the 5% significance level. We conclude that Tw Pdi is not reduced when patients with severe COPD walk to a state of extreme breathlessness and that therefore low frequency fatigue of the diaphragm does not occur.

Submaximal-exercise-induced impairment of human muscle to develop and maintain force at low frequencies of electrical stimulation

The aim of this study was to test the hypothesis that low intensity exercise-induced low frequency fatigue is caused by failure of excitation-contraction coupling. Changes in knee extension torque at 5, 10, 15, 20 and 50 Hz electrical stimulation of quadriceps muscle in ten healthy, young, male subjects were recorded during 20-min voluntary exercise followed by 60-min recovery. In seven of the ten subjects, changes in torque during 3 min of 10-Hz stimulation were recorded 2 min and 20 min after 20 min voluntary exercise. Exercise was performed at 30% of maximal voluntary contraction with a contraction plus relaxation period of 6 plus 4 s. Torque at 5, 10, 15, 20 and 50-Hz stimulation at the end of exercise was reduced to mean 91.0 (SEM 5.4)%, 68.7 (SEM 5.4)%, 67.2 (SEM 3.9)%, 66.5 (SEM 4.5)% and 74.7 (SEM 4.3)% of control values, respectively. During the first 30 s of the 3 min 10-Hz stimulation, torque was reduced in exercised muscle and increased in nonfatigued muscle. The reduction in torque was more marked 20 min after exercise than after 2 min. In conclusion, the pattern of depression and recovery of muscle force observed was in agreement with the hypothesis that the main cause of low intensity exercise-induced low frequency fatigue is an impairment of excitation-contraction coupling.

Influence of prestraining on high temperature, low frequency fatigue crack growth in superalloys: Zheng, D., Rosenberger, A. and Ghonem, H. Mater. Sci. Eng. A (15 Mar. 1993) A161 (1), 13–21

Influence of prestraining on high temperature, low frequency fatigue crack growth in superalloys: Zheng, D., Rosenberger, A. and Ghonem, H. Mater. Sci. Eng. A (15 Mar. 1993) A161 (1), 13–21