scholarly journals Recovery of central and peripheral neuromuscular fatigue after exercise

2017 ◽  
Vol 122 (5) ◽  
pp. 1068-1076 ◽  
Author(s):  
T. J. Carroll ◽  
J. L. Taylor ◽  
S. C. Gandevia
Keyword(s):  
Muscle Function ◽  
Time Course ◽  
Central Fatigue ◽  
Exercise Bout ◽  
Complete Recovery ◽  
Peripheral Fatigue ◽  
Partial Recovery ◽  
Long Duration ◽  
Intracellular Ca ◽  
Generating Capacity

Sustained physical exercise leads to a reduced capacity to produce voluntary force that typically outlasts the exercise bout. This “fatigue” can be due both to impaired muscle function, termed “peripheral fatigue,” and a reduction in the capacity of the central nervous system to activate muscles, termed “central fatigue.” In this review we consider the factors that determine the recovery of voluntary force generating capacity after various types of exercise. After brief, high-intensity exercise there is typically a rapid restitution of force that is due to recovery of central fatigue (typically within 2 min) and aspects of peripheral fatigue associated with excitation-contraction coupling and reperfusion of muscles (typically within 3–5 min). Complete recovery of muscle function may be incomplete for some hours, however, due to prolonged impairment in intracellular Ca2+ release or sensitivity. After low-intensity exercise of long duration, voluntary force typically shows rapid, partial, recovery within the first few minutes, due largely to recovery of the central, neural component. However, the ability to voluntarily activate muscles may not recover completely within 30 min after exercise. Recovery of peripheral fatigue contributes comparatively little to the fast initial force restitution and is typically incomplete for at least 20–30 min. Work remains to identify what factors underlie the prolonged central fatigue that usually accompanies long-duration single joint and locomotor exercise and to document how the time course of neuromuscular recovery is affected by exercise intensity and duration in locomotor exercise. Such information could be useful to enhance rehabilitation and sports performance.

Interactions between intracellular calcium and phosphate in intact mouse muscle during fatigue

2011 ◽  
Vol 111 (2) ◽  
pp. 358-366 ◽  
Author(s):  
D. G. Allen ◽  
E. Clugston ◽  
Y. Petersen ◽  
I. V. Röder ◽  
B. Chapman ◽  
...  
Keyword(s):  
Tibialis Anterior Muscle ◽  
Complete Recovery ◽  
Force Transducer ◽  
Partial Recovery ◽  
Initial Value ◽  
Intact Mouse ◽  
Mouse Muscle ◽  
Intracellular Ca ◽  
Intracellular Phosphate ◽  
Distal Tendon

Fatigue was studied in intact tibialis anterior muscle of anesthetized mice. The distal tendon was detached and connected to a force transducer while blood flow continued normally. The muscle was stimulated with electrodes applied directly to the muscle surface and fatigued by repeated (1 per 4 s), brief (0.4 s), maximal (100-Hz stimulation frequency) tetani. Force declined monotonically to 49 ± 5% of the initial value with a half time of 36 ± 5 s and recovered to 86 ± 4% after 4 min. Intracellular phosphate concentration ([Pi]) was measured by 31P-NMR on perchloric acid extracts of muscles. [Pi] increased during fatigue from 7.6 ± 1.7 to 16.0 ± 1.6 mmol/kg muscle wet wt and returned to control during recovery. Intracellular Ca2+ was measured with cameleons whose plasmids had been transfected in the muscle 2 wk before the experiment. Yellow cameleon 2 was used to measure myoplasmic Ca2+, and D1ER was used to measure sarcoplasmic reticulum (SR) Ca2+. The myoplasmic Ca2+ during tetani declined steadily during the period of fatigue and showed complete recovery over 4 min. The SR Ca2+ also declined monotonically during fatigue and showed a partial recovery with rest. These results show that the initial phase of force decline is accompanied by a rise in [Pi] and a reduction in the tetanic myoplasmic Ca2+. We suggest that both changes contribute to the fatigue. A likely cause of the decline in tetanic myoplasmic Ca2+ is precipitation of CaPi in the SR.

Temporal relationships of ventilatory failure, pump failure, and diaphragm fatigue

1996 ◽  
Vol 81 (1) ◽  
pp. 238-245 ◽  
Author(s):  
C. S. Sassoon ◽  
S. E. Gruer ◽  
G. C. Sieck
Keyword(s):  
Time Course ◽  
Central Fatigue ◽  
Blood Gases ◽  
Respiratory Arrest ◽  
Peripheral Fatigue ◽  
Respiratory Drive ◽  
Pump Failure ◽  
Arterial Blood ◽  
Ventilatory Failure ◽  
Resistive Loads

The time course of ventilatory failure, pump failure, and diaphragm peripheral fatigue was determined during the application of external inspiratory resistive loads (IRL) in anesthetized rabbits. Pump failure is defined as the inability of the diaphragm to sustain the expected force under IRL. To assess contractile fatigue, transdiaphragmatic pressures (Pdi) generated by bilateral phrenic nerve stimulation at 75 Hz (Pdi-75) and 20 Hz (Pdi-20) were measured. The amplitude of evoked diaphragm electromyographic (EMG) signals was measured to assess neurotransmission failure. The rate of rise of spontaneous diaphragm EMG was used as an index of respiratory drive. Ventilation was evaluated together with arterial blood gases. During IRL the rate of rise of spontaneous diaphragm EMG increased, and there was a progressive hypercapnic acidosis and hypoxemia, indicating ventilatory failure. In contrast, Pdi-75 and Pdi-20 were stable until the time of respiratory arrest (apnea), when they decreased by 34 and 45%, respectively. The amplitude of evoked diaphragm EMG signals remained unchanged throughout the IRL and decreased only slightly at the time of apnea. We conclude that IRL induces progressive ventilatory failure long before any contractile fatigue of the diaphragm or pump failure occurs. This suggests that ventilatory failure is due to central fatigue, whereas pump failure (apnea) is attributable to multiple factors.

scholarly journals Convective oxygen transport and fatigue

2008 ◽  
Vol 104 (3) ◽  
pp. 861-870 ◽  
Author(s):  
Markus Amann ◽  
Jose A. L. Calbet
Keyword(s):  
Central Fatigue ◽  
Peripheral Fatigue ◽  
Healthy Human ◽  
Reduction In Force ◽  
Fatigue Development ◽  
Inhibitory Feedback ◽  
Generating Capacity ◽  
Exercise Fatigue ◽  
Acute And Chronic Exposure ◽  
Rate Of Accumulation

During exercise, fatigue is defined as a reversible reduction in force- or power-generating capacity and can be elicited by “central” and/or “peripheral” mechanisms. During skeletal muscle contractions, both aspects of fatigue may develop independent of alterations in convective O2delivery; however, reductions in O2supply exacerbate and increases attenuate the rate of accumulation. In this regard, peripheral fatigue development is mediated via the O2-dependent rate of accumulation of metabolic by-products (e.g., inorganic phosphate) and their interference with excitation-contraction coupling within the myocyte. In contrast, the development of O2-dependent central fatigue is elicited 1) by interference with the development of central command and/or 2) via inhibitory feedback on central motor drive secondary to the peripheral effects of low convective O2transport. Changes in convective O2delivery in the healthy human can result from modifications in arterial O2content, blood flow, or a combination of both, and they can be induced via heavy exercise even at sea level; these changes are exacerbated during acute and chronic exposure to altitude. This review focuses on the effects of changes in convective O2delivery on the development of central and peripheral fatigue.

Electrically-induced quadriceps fatigue in the contralateral leg impairs ipsilateral knee extensors performance

2021 ◽  
Author(s):  
Fabio Giuseppe Laginestra ◽  
Markus Amann ◽  
Emine Kirmizi ◽  
Gaia Giuriato ◽  
Chiara Barbi ◽  
...  
Keyword(s):  
Muscle Activation ◽  
Central Fatigue ◽  
Endurance Performance ◽  
Voluntary Exercise ◽  
Peripheral Fatigue ◽  
Knee Extensors ◽  
Motor Drive ◽  
Time To Exhaustion ◽  
Crossover Effect ◽  
The Impact

Muscle fatigue induced by voluntary exercise, which requires central motor drive, causes central fatigue that impairs endurance performance of a different, non-fatigued muscle. This study investigated the impact of quadriceps fatigue induced by electrically-induced (no central motor drive) contractions on single-leg knee-extension (KE) performance of the subsequently exercising ipsilateral quadriceps. On two separate occasions, eight males completed constant-load (85% of maximal power-output) KE exercise to exhaustion. In a counterbalanced manner, subjects performed the KE exercise with no pre-existing quadriceps fatigue in the contralateral leg on one day (No-PreF), while on the other day, the same KE exercise was repeated following electrically-induced quadriceps fatigue in the contralateral leg (PreF). Quadriceps fatigue was assessed by evaluating pre- to post-exercise changes in potentiated twitch force (ΔQtw,pot; peripheral-fatigue), and voluntary muscle activation (ΔVA; central-fatigue). As reflected by the 57±11% reduction in electrically-evoked pulse force, the electrically-induced fatigue protocol caused significant knee-extensors fatigue. KE endurance time to exhaustion was shorter during PreF compared to No-PreF (4.6±1.2 vs 7.7±2.4 min; p<0.01). While ΔQtw,pot was significantly larger in No-PreF compared to PreF (-60% vs -52%, p<0.05), ΔVA was greater in PreF (-14% vs -10%, p<0.05). Taken together, electrically-induced quadriceps fatigue in the contralateral leg limits KE endurance performance and the development of peripheral fatigue in the ipsilateral leg. These findings support the hypothesis that the crossover-effect of central fatigue is mainly mediated by group III/IV muscle afferent feedback and suggest that impairments associated with central motor drive may only play a minor role in this phenomenon.

Acute effects of repetitive depolarization on sodium current in chick myocytes

1991 ◽  
Vol 260 (6) ◽  
pp. H1810-H1818
Author(s):  
M. R. Gold ◽  
G. R. Strichartz
Keyword(s):  
Time Course ◽  
Sodium Current ◽  
Complete Recovery ◽  
Acute Effects ◽  
Na Current ◽  
Patch Clamp Technique ◽  
Membrane Hyperpolarization ◽  
Atrial Cells ◽  
Whole Cell Patch Clamp ◽  
Recovery From Inactivation

Acute effects of repetitive depolarization on the inward Na+ current (INa) of cultured embryonic chick atrial cells were studied using the whole cell patch-clamp technique. Stimulation rates of 1 Hz or greater produced a progressive decrement of peak INa. With depolarizations to 0 mV of 150-ms duration, applied at 2 Hz from a holding potential of -100 mV, the steady-state decrement was approximately 20%. The magnitude of this effect increased with stimulation frequency and with test potential depolarization and decreased with membrane hyperpolarization. Analysis of INa kinetics revealed that reactivation was sufficiently slow to preclude complete recovery from inactivation with interpulse intervals less than 1,000 ms. Moreover, reactivation accelerated markedly with membrane hyperpolarization, in parallel with the response to repetitive stimulation. The multiexponential time course of recovery of peak INa from repetitive depolarization was similar to that observed after single stimuli; however, there was a shift toward a greater proportion of current recovering with the slower of two time constants. It is concluded that incomplete recovery from inactivation is responsible for the decrement in INa observed with short interpulse intervals.

scholarly journals Factors affecting the appearance of the hump charge movement component in frog cut twitch fibers.

1991 ◽  
Vol 98 (2) ◽  
pp. 315-347 ◽  
Author(s):  
C S Hui
Keyword(s):  
Time Course ◽  
Extreme Case ◽  
Complete Recovery ◽  
Creatine Phosphate ◽  
Boltzmann Distribution ◽  
Distribution Functions ◽  
Charge Movement ◽  
Factors Affecting ◽  
Gap Technique ◽  
Voltage Dependent

Charge movement was measured in frog cut twitch fibers with the double Vaseline gap technique. Five manipulations listed below were applied to investigate their effects on the hump component (I gamma) in the ON segments of TEST minus CONTROL current traces. When external Cl-1 was replaced by MeSO3- to eliminate Cl current, I gamma peaked earlier due to a few millivolts shift of the voltage dependence of I gamma kinetics in the negative direction. The Q-V plots in the TEA.Cl and TEA.MeSO3 solutions were well fitted by a sum of two Boltzmann distribution functions. The more steeply voltage-dependent component (Q gamma) had a V approximately 6 mV more negative in the TEA.MeSO3 solution than in the TEA.Cl solution. These voltage shifts were partially reversible. When creatine phosphate in the end pool solution was removed, the I gamma hump disappeared slowly over the course of 20-30 min, partly due to a suppression of Q gamma. The hump reappeared when creatine phosphate was restored. When 0.2-1.0 mM Cd2+ was added to the center pool solution to block inward Ca current, the I gamma hump became less prominent due to a prolongation in the time course of I gamma but not to a suppression of Q gamma. When the holding potential was changed from -90 to -120 mV, the amplitude of I beta was increased, thereby obscuring the I gamma hump. Finally, when a cut fiber was stimulated repetitively, I gamma lost its hump appearance because its time course was prolonged. In an extreme case, a 5-min resting interval was insufficient for a complete recovery of the waveform. In general, a stimulation rate of once per minute had a negligible effect on the shape of I gamma. Of the five manipulations, MeSO3- has the least perturbation on the appearance of I gamma and is potentially a better substitute for Cl- than SO2-(4) in eliminating Cl current if the appearance of the I gamma hump is to be preserved.

Impact of ejection on magnitude and time course of ventricular pressure-generating capacity

1993 ◽  
Vol 265 (3) ◽  
pp. H899-H909 ◽  
Author(s):  
D. Burkhoff ◽  
P. P. De Tombe ◽  
W. C. Hunter
Keyword(s):  
Time Course ◽  
Cardiac Cycle ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Time Varying ◽  
Generating Capacity ◽  
Ejection Phase ◽  
Time Point ◽  
Ventricular Dynamics

This study focuses on elucidating how ventricular afterloading conditions affect the time course of change of left ventricular pressure (LVP) throughout the cardiac cycle, with particular emphasis on revealing specific limitations in the time-varying elastance model of ventricular dynamics. Studies were performed in eight isolated canine hearts ejecting into a simulated windkessel afterload. LVP waves measured (LVPm) during ejection were compared with those predicted (LVPpred) according to the elastance theory. LVPm exceeded LVPpred from a time point shortly after the onset of ejection to the end of the beat. The instantaneous difference between LVPm and LVPpred increased steadily as ejection proceeded and reached between 45 and 65 mmHg near end ejection. This was in large part due to an average 35-ms prolongation of the time to end systole (tes) in ejecting compared with isovolumic beats. The time constant of relaxation was decreased on ejecting beats so that, despite the marked prolongation of tes, the overall duration of ejecting contractions was not greater than that of isovolumic beats. The results demonstrate a marked ejection-mediated enhancement and prolongation of ventricular pressure-generating capacity during the ejection phase of the cardiac cycle with concomitant acceleration of relaxation. None of these factors are accounted for by the time-varying elastance theory.

Effect of Phasic Activation on Endplate Potential in Rat Diaphragm

1999 ◽  
Vol 82 (6) ◽  
pp. 3030-3040 ◽  
Author(s):  
Michelle Moyer ◽  
Erik van Lunteren
Keyword(s):  
Time Course ◽  
Complete Recovery ◽  
Stimulation Frequency ◽  
Drop Out ◽  
Rat Diaphragm ◽  
Continuous Stimulation ◽  
Intermittent Stimulation ◽  
Rate Of Decline ◽  
Phasic Activation

Neuromuscular junction endplate potentials (EPPs) decrease quickly and to a large extent during continuous stimulation. The present study examined the hypothesis that EPP rundown recovers rapidly, thereby substantially preserving neurotransmission during intermittent compared with continuous stimulation. Studies were performed in vitro on rat diaphragm, using μ-conotoxin to allow recording of normal-sized EPPs from intact fibers. During continuous 5- to 100-Hz stimulation, EPP amplitude declined with a biphasic time course. The initial fast rate of decline was modulated substantially by stimulation frequency, whereas the subsequent slow rate of decline was relatively frequency independent. During intermittent 5- to 100-Hz stimulation (duty cycle 0.33), EPP amplitude declined rapidly during each train, but recovered substantially by the onset of the following train. The intra-train declines were substantially greater than the inter-train declines in EPP amplitude. Intra-train reductions in EPP amplitude were stimulation frequency dependent, based on both the total decline and rate constant of EPP decline. In contrast, the degree of recovery from train to train was independent of stimulation frequency, indicating low frequency dependence of inter-train rundown. The substantial recovery of EPP amplitude in between trains resulted in greater cumulative EPP size during intermittent compared with continuous stimulation. During continuous stimulation, EPP drop-out was only seen during 100-Hz stimulation; this was completed mitigated during intermittent stimulation. Miniature EPP size was unaffected by either continuous or intermittent stimulation. The pattern of rapid intra-train rundown and slow inter-train rundown of EPP size during intermittent stimulation is therefore due to rapid changes in the magnitude of neurotransmitter release rather than to axonal block or postsynaptic receptor desensitization. These findings indicate considerable rundown of EPP amplitudes within a stimulus train, with near complete recovery by the onset of the next train. This substantially attenuates the decrement in EPP amplitude during intermittent compared with continuous stimulation, thereby preserving the integrity of neurotransmission during phasic activation.

Fatigue of intermittent submaximal voluntary contractions: central and peripheral factors

1986 ◽  
Vol 61 (2) ◽  
pp. 421-429 ◽  
Author(s):  
B. Bigland-Ritchie ◽  
F. Furbush ◽  
J. J. Woods
Keyword(s):  
No Reduction ◽  
Rest Period ◽  
Central Fatigue ◽  
Voluntary Contraction ◽  
Adductor Pollicis ◽  
M Wave ◽  
Generating Capacity ◽  
Target Force ◽  
Voluntary Contractions ◽  
Muscle Contractile

Central and peripheral factors were studied in fatigue of submaximal intermittent isometric contractions of the human quadriceps and soleus muscles. Subjects made repeated 6 s, 50% maximal voluntary contractions (MVC) followed by 4 s rest until the limit of endurance (Tlim). Periodically, a fatigue test was performed. This included a brief MVC, either a single shock or 8 pulses at 50 Hz during a rest period and a shock superimposed on a target force voluntary contraction. At Tlim, the MVC force had declined by 50%, usually in parallel with the force from stimulation at 50 Hz. The twitches superimposed on the target forces declined more rapidly, disappearing entirely at Tlim. In similar experiments on adductor pollicis, no reduction of the evoked M wave was seen. The results suggest that, during fatigue of quadriceps and adductor pollicis induced by this protocol, no central fatigue was apparent, but some was seen in soleus. Thus the reduced force-generating capacity could result mainly or entirely from failure of the muscle contractile apparatus.

scholarly journals Measurement of the dynamics of stimulation and inhibition of steroidogenesis in isolated rat adrenal cells by using column perfusion

1974 ◽  
Vol 142 (2) ◽  
pp. 287-294 ◽  
Author(s):  
P. J. Lowry ◽  
Colin McMartin
Keyword(s):  
Cyclic Amp ◽  
Time Course ◽  
Acth Stimulation ◽  
Duration Of Action ◽  
Adrenal Cells ◽  
Small Column ◽  
Long Duration ◽  
Full Effect ◽  
Rapid Fall

Isolated adrenal cells were perfused in a small column by using Bio-Gel polyacrylamide beads as an inert supporting matrix, and the time-course of the response to various stimuli was observed by measuring fluorogenic 11-hydroxycorticosteroids in the effluent. A small but significant response was observed 1 min after stimulation with physiological concentrations of ACTH (adrenocorticotrophin), but the response did not start to build up rapidly for 3–4min and eventually reached a plateau after 9–10min. A similar pattern of events was observed for the decay of the steroid output on removal of ACTH. ACTH analogues, including one with a long duration of action in vivo, were found to produce responses with similar kinetics. However, cyclic AMP caused a more rapid increase in steroidogenesis and its effects were more short-lived after withdrawal. If, as present evidence suggests, cyclic AMP is produced rapidly after ACTH stimulation the delayed build-up of the steroidogenic response to ACTH would indicate that cyclic AMP may not be the intracellular mediator. When inhibitors were applied during ACTH stimulation, aminoglutethimide, which blocks mitochondrial conversion of cholesterol into pregnenolone (3β-hydroxypregn-5-en-20-one), caused a rapid fall in steroid output (1 min), whereas cycloheximide took longer to achieve its full effect. Nevertheless, the response had fallen by 50% in 2 min, indicating a much shorter half-life than that previously reported for the labile protein implicated in steroidogenesis. In addition the rapid response to cyclic AMP makes it unlikely that steroid production is induced as a result of initiation of protein synthesis. This suggests that the labile protein plays an obligatory but permissive role in the development of the response. Column perfusion has proved to be a simple technique which can readily yield accurate data on responses of cells to stimulants and inhibitors.

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