Changes in muscle afferents, motoneurons and motor drive during muscle fatigue

2000 ◽  
Vol 83 (2-3) ◽  
pp. 106-115 ◽  
Author(s):  
Janet L. Taylor ◽  
Jane E. Butler ◽  
S. C. Gandevia
Keyword(s):  
Muscle Fatigue ◽  
Muscle Afferents ◽  
Motor Drive

scholarly journals Opioid-mediated muscle afferents inhibit central motor drive and limit peripheral muscle fatigue development in humans

2009 ◽  
Vol 587 (1) ◽  
pp. 271-283 ◽  
Author(s):  
Markus Amann ◽  
Lester T. Proctor ◽  
Joshua J. Sebranek ◽  
David F. Pegelow ◽  
Jerome A. Dempsey
Keyword(s):  
Muscle Fatigue ◽  
Muscle Afferents ◽  
Motor Drive ◽  
Peripheral Muscle ◽  
Fatigue Development

The pathophysiology of McArdle's disease: clues to regulation in exercise and fatigue

1986 ◽  
Vol 61 (2) ◽  
pp. 391-401 ◽  
Author(s):  
S. F. Lewis ◽  
R. G. Haller
Keyword(s):  
Skeletal Muscle ◽  
Muscle Fatigue ◽  
Muscle Afferents ◽  
Common Denominator ◽  
Circulatory Response ◽  
Mcardle's Disease ◽  
O2 Transport ◽  
Mcardle’S Disease ◽  
Muscle Phosphorylase ◽  
Response To Exercise

Muscle phosphorylase deficiency (McArdle's disease) has conventionally been considered a disorder of glycogenolysis, and the associated impairment in oxidative metabolism has been largely overlooked. Muscle glycogen normally is the primary oxidative fuel at exercise work loads requiring more than 75–80% of maximal O2 uptake (VO2max). Evidence is presented to support the hypothesis that a limited flux through the Embden-Myerhof pathway in McArdle's disease reduces the capacity to generate NADH required to support a normal VO2max. The extent of the oxidative defect is substrate dependent; i.e., it can be partially corrected by increasing the availability of alternative oxidative substrates (e.g., glucose, free fatty acids) to working muscle. Experiments employing modification of substrate availability closely link the hyperkinetic circulatory response to exercise (i.e., an abnormally large increase in O2 transport to skeletal muscle) and the premature muscle fatigue and cramping of McArdle patients with their oxidative impairment and suggest that a metabolic common denominator in these abnormal responses may be a pronounced decline in the muscle phosphorylation potential ([ATP]/[ADP][Pi]). The hyperkinetic circulation likely is mediated by the local effects on metabolically sensitive skeletal muscle afferents and vascular smooth muscle of K+, Pi, or adenosine or a combination of these substances released excessively from working skeletal muscle. The premature muscle fatigue and cramping of McArdle patients does not appear to be due to depletion of ATP but is associated with an increased accumulation of Pi and probably ADP in skeletal muscle. Accumulations of Pi and ADP are known to inhibit the myofibrillar, Ca2+, and Na+-K+-ATPase reactions.

Effects of muscle fatigue on mechanically sensitive afferents of slow conduction velocity in the cat triceps surae

1991 ◽  
Vol 65 (2) ◽  
pp. 360-370 ◽  
Author(s):  
L. Hayward ◽  
U. Wesselmann ◽  
W. Z. Rymer
Keyword(s):  
Muscle Contraction ◽  
Muscle Fatigue ◽  
Surface Pressure ◽  
Muscular Contraction ◽  
Muscle Afferents ◽  
Triceps Surae ◽  
Spontaneous Discharge ◽  
Primary Role ◽  
Mechanical Stimuli ◽  
Group Iii

1. Group III and IV muscle afferents have been shown to be sensitive to both mechanical stimuli and metabolic and thermal changes in muscle. To establish the potential role of slowly conducting muscle afferents in regulating motor output during fatigue, we recorded from mechanically sensitive group III and nonspindle group II afferents originating in the triceps surae in barbiturate-anesthetized cats. We evaluated the response of these afferents to tetanic muscle contraction, stretch, and surface pressure, before, during, and after fatigue. 2. Our results show that muscle fatigue both increases spontaneous discharge in these mechanically sensitive afferents and sensitizes their response to muscle stretch, surface pressure, and, in a few instances, muscle contraction. These fatigue-induced changes typically occurred after 5-10 min of submaximal fatiguing stimulation. 3. During recovery from muscle fatigue, several contraction-sensitive free nerve endings, which had become sensitized to contractions during fatigue, remained sensitized after 20-30 min of rest. 4. The results of this study provide support for the hypothesis that fatigue-induced excitation of slowly conducting afferents is significant in mediating fatigue-induced inhibition of motoneuron output. However, our finding that the discharge of many slowly conducting mechanoreceptor afferents declines during the initial phase of fatigue argues against a primary role for these afferents in mediating the initial decline in motoneuron rate that is so prominent in fatiguing maximum voluntary muscular contraction.

ASICs are required for immediate exercise-induced muscle pain and are downregulated in sensory neurons by exercise training

2020 ◽  
Vol 129 (1) ◽  
pp. 17-26
Author(s):  
Tahsin Khataei ◽  
Anne Marie S. Harding ◽  
Mahyar Janahmadi ◽  
Maram El-Geneidy ◽  
Hamid Agha-Alinejad ◽  
...  
Keyword(s):  
Ion Channels ◽  
Exercise Training ◽  
Muscle Fatigue ◽  
Sensory Neurons ◽  
Negative Feedback ◽  
Exercise Performance ◽  
Muscle Pain ◽  
Muscle Afferents ◽  
Acid Sensing Ion Channels ◽  
Exercise Induced

Exercise performance can be limited by the sensations of muscle fatigue and pain transmitted by muscle afferents. It has been proposed that exercise training abrogates these negative feedback signals. We found that acid-sensing ion channels (ASICs) are required for immediate exercise-induced muscle pain (IEIP). Moreover, exercise training prevented IEIP and was correlated with downregulation of ASICs in sensory neurons.

Respiratory load compensation. III. Role of spinal cord afferents

1993 ◽  
Vol 75 (2) ◽  
pp. 682-687 ◽  
Author(s):  
D. T. Frazier ◽  
F. Xu ◽  
L. Y. Lee ◽  
R. F. Taylor
Keyword(s):  
Spinal Cord ◽  
Muscle Afferents ◽  
Motor Drive ◽  
Dorsal Spinal Cord ◽  
Load Compensation ◽  
Dorsal Rhizotomy ◽  
Before And After ◽  
Bilateral Vagotomy ◽  
Adult Cats

In a previous study, we reported that inspiratory tracheal occlusion (TO) significantly inhibited the motor drive to the diaphragm in a decerebellated bilaterally vagotomized preparation (J. Appl. Physiol. 75:675–681, 1993). The hypothesis to be tested in the present study was that respiratory muscle afferents activated by inspiratory TO provided the inputs responsible for the observed inhibition. Adult cats were anesthetized, tracheotomized, and instrumented with diaphragm electromyographic (EMGdi) recording electrodes. The cerebellum, vagi, and dorsal spinal cord (C2-T2) were surgically exposed. Inspiratory TO was applied before and after cold blockade of the dorsal cord (C6) or dorsal root (C3–6) transection in the intact and decerebellated vagotomized cat. Respiratory timing (inspiratory and expiratory duration) was determined from the EMGdi record, and the peak integrated EMGdi (integral of EMGdi) response was used as an index of respiratory motor drive. Our results showed that 1) cold blockade at the dorsal C6 level in an intact preparation significantly increased the peak of the integral of EMGdi response to TO and was reversible upon rewarming; 2) as previously reported, decerebellation coupled with bilateral vagotomy significantly decreased the peak integral of EMGdi response to TO with no effect on timing; 3) cold blockade (-1 degree C) of the dorsal cord at C6 significantly attenuated this inhibition, and subsequent dorsal rhizotomy at C3–6 completely abolished this inhibition; and 4) decerebellation, cold blockade of the dorsal cord (C6), and dorsal rhizotomy (C3–6) did not significantly affect baseline values in bilaterally vagotomized cats.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals The physiological basis of neuromuscular fatigue during high intensity exercise

2017 ◽  
Vol 3 (2) ◽  
pp. 1-3
Author(s):  
Faryal Zahir ◽  
Radha Budhwar ◽  
Gabrielle Gonsalves ◽  
Lily Green ◽  
Aliza Barua
Keyword(s):  
Muscle Fatigue ◽  
Motor Unit ◽  
High Intensity ◽  
Muscle Fibers ◽  
Central Fatigue ◽  
Muscle Afferents ◽  
Neuromuscular Fatigue ◽  
High Intensity Exercise ◽  
Peripheral Fatigue ◽  
Group Iii

Introduction Neuromuscular fatigue refers to a reduction in maximal force generation capacity, and is categorized as central and peripheral. Central fatigue is defined as a reduction in the ability of the central nervous system to voluntarily activate muscles, and peripheral fatigue indicates a decrease in the contractile strength of muscle fibers. During high intensity exercise, motor neurons are involved in the recruitment of type IIB muscle fibers as they are fast-twitch, high glycolytic, and have low aerobic capacity. Furthermore, group III and IV muscle afferents detect the physiological circumstances in the body and convey signals to the brain that influence the onset of central and peripheral fatigue. Methods A PRISMA flow diagram was created to record relevant studies found from scholarly databases. Inclusion criteria required studies from 2005 to 2017, and subject grouping headings required key terms indicating that the presence of central and peripheral fatigue was analyzed on healthy adult subjects performing exercise. To ensure that high quality studies were analyzed, each article was independently rated using the National Institute of Health Quality Assessment Tool criteria. Discussion During low intensity exercise, asynchronous motor unit recruitment is involved in delaying the onset of muscle fatigue. However, this is not apparent in high intensity exercises, as maximal motor unit firing is required in order to sustain a maximal level of force output. Persistent firing of action potentials to maintain muscle contraction results in acetylcholine depletion at the motor end plate, initiating the process of central fatigue. Furthermore, due to prolonged metabolite accumulation in skeletal muscle fibers, group III and IV afferents convey signals to the motor cortex and cause a reduction in the action potential conduction velocities along the contracting muscle. This leads to the onset of peripheral fatigue. As high intensity exercise proceeds, electromyogram (EMG) measurements display this as an increase in amplitude to reflect heightened motor unit recruitment and a compressed power density spectrum alongside a decreased centre frequency. This is determined by the innervated muscle fiber’s conduction velocity and subsequent variations in the action potential waveform shape. Conclusion A record of current studies systematically display the overview of muscle fatigue and its underlying mechanisms during exercise. However, further research is yet to be conducted for a more comprehensive understanding regarding the onset and recovery of neuromuscular fatigue in varied population demographics and physiological circumstances. Likewise, the distinctive roles of group III and IV muscle afferents in supraspinal stimulation require further investigation in order to gain a holistic understanding of their involvement in central fatigue and resistance training. Additional research in this subject matter is currently being explored through technology involving imaging studies, as they have potential to elucidate motor cortex activity alongside other regions of the brain and portray neuromuscular muscle fatigue eminently.

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