The role of capsaicin‐sensitive muscle afferents in fatigue‐induced modulation of the monosynaptic reflex in the rat

Pettorossi, Vito Enrico; Torre, G. Della; Bortolami, R.; Brunetti, O

doi:10.1111/j.1469-7793.1999.599ac.x

Cited by 70 publications

(57 citation statements)

References 37 publications

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“…For example H-reflexes evoked in ankle plantarflexors are depressed after fatigue (Garland and McComas, 1990;Garland, 1991;Loscher et al, 1996;Walton et al, 2002;Kuchinad et al, 2004). We suggested previously that the discrepancy between results based on the H-reflex and that for the CMEP in elbow flexors (Butler et al, 2003) could be attributable to presynaptic inhibition of group Ia afferent volleys by group III and IV muscle afferents (Pettorossi et al, 1999;Rossi et al, 1999;Rudomin and Schmidt, 1999). The current results suggest that differences in the behavior of flexors and extensors may also contribute.…”

Section: Discussionmentioning

confidence: 60%

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Fatigue-Sensitive Afferents Inhibit Extensor but Not Flexor Motoneurons in Humans

Martin¹,

Smith²,

Butler³

et al. 2006

J. Neurosci.

159

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The role of group III and IV muscle afferents in controlling the output from human muscles is poorly understood. We investigated the effects of these afferents from homonymous or antagonist muscles on motoneuron pools innervating extensor and flexor muscles of the elbow. In study 1, subjects (n ϭ 8) performed brief maximal voluntary contractions (MVCs) of elbow extensors before and after a 2 min MVC of the extensors. During MVCs, electromyographic responses from triceps were evoked by stimulation of the corticospinal tracts [cervicomedullary motor evoked potentials (CMEPs)]. The same subjects repeated the protocol, but input from fatigue-sensitive afferents was prolonged after the fatiguing contraction by maintained muscle ischemia. In study 2, CMEPs were evoked in triceps during brief extensor MVCs before and after a 2 min sustained flexor MVC (n ϭ 7) or in biceps during brief flexor MVCs before and after a sustained extensor MVC (n ϭ 7). Again, ischemia was maintained after the sustained contractions. During sustained MVCs of the extensors, CMEPs in triceps decreased by ϳ35%. Without muscle ischemia, CMEPs recovered within 15 s, but with maintained ischemia, they remained depressed (by ϳ28%; p Ͻ 0.001). CMEPs in triceps were also depressed (by ϳ20%; p Ͻ 0.001) after fatiguing flexor contractions, whereas CMEPs in biceps were facilitated (by ϳ25%; p Ͻ 0.001) after fatiguing extensor contractions. During fatigue, inputs from group III and IV muscle afferents from homonymous or antagonist muscles depress extensor motoneurons but facilitate flexor motoneurons. The more pronounced inhibitory influence of these afferents on extensors suggests that these muscles may require greater cortical drive to generate force during fatigue.

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Section: Discussionmentioning

confidence: 60%

“…First, they may inhibit group Ia terminals pre- synaptically and thus disfacilitate motoneurons (Pettorossi et al, 1999;Rossi et al, 1999). However, other factors could counteract such effects.…”

Section: Discussionmentioning

confidence: 99%

Fatigue-Sensitive Afferents Inhibit Extensor but Not Flexor Motoneurons in Humans

Martin¹,

Smith²,

Butler³

et al. 2006

J. Neurosci.

159

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show abstract

“…The strength of the stimulus was adjusted to three to five times the motor threshold (0.1-millisecond pulse duration). The gastrocnemius muscle was subjected to repetitive, fatiguing, tetanic stimulations with an increasing number of trains (1,3,6,12,30, and 60, for a total of 112 stimulations at 60-second intervals) at an 85-Hz fusion frequency (600-millisecond duration, 1-second intervals) in isometric conditions (28). The following measurements were made and compared between groups: peak tetanic force, isometric speed, and fatigability of the muscle (fatigue index).…”

Section: Animalsmentioning

confidence: 99%

Neuropeptide Y induces ischemic angiogenesis and restores function of ischemic skeletal muscles

Lee¹,

Michalkiewicz²,

Kitlińska³

et al. 2003

J. Clin. Invest.

122

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Previously we showed that neuropeptide Y (NPY), a sympathetic vasoconstrictor neurotransmitter, stimulates endothelial cell migration, proliferation, and differentiation in vitro. Here, we report on NPY’s actions, receptors, and mediators in ischemic angiogenesis. In rats, hindlimb ischemia stimulates sympathetic NPY release (attenuated by lumbar sympathectomy) and upregulates NPY-Y2 (Y2) receptor and a peptidase forming Y2/Y5-selective agonist. Exogenous NPY at physiological concentrations also induces Y5 receptor, stimulates neovascularization, and restores ischemic muscle blood flow and performance. NPY-mediated ischemic angiogenesis is not prevented by a selective Y1 receptor antagonist but is reduced in Y2–/– mice. Nonischemic muscle vascularity is also lower in Y2–/– mice, whereas it is increased in NPY-overexpressing rats compared with their WT controls. Ex vivo, NPY-induced aortic sprouting is markedly reduced in Y2–/– aortas and spontaneous sprouting is severely impaired in NPY–/– mice. NPY-mediated aortic sprouting, but not cell migration/proliferation, is blocked by an antifetal liver kinase 1 antibody and abolished in mice null for eNOS. Thus, NPY mediates neurogenic ischemic angiogenesis at physiological concentrations by activating Y2/Y5 receptors and eNOS, in part due to release of VEGF. NPY’s effectiveness in revascularization and restoring function of ischemic tissue suggests its therapeutic potential in ischemic conditions

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“…On the other hand, group III/IV afferents have inhibitory effects on spinal motoneurons during intense exercise and with prolonged fatiguing exercise they also inhibit corticospinal drive, a phenomenon known as central fatigue (reduction of motor output) [325]. In addition, capsaicin-sensitive afferents have an inhibitory effect on the monosynaptic reflex [326] which constitutes a substantial component of total neural drive to the muscle during walking. For the human soleus muscle, primary afferent feedback has been estimated to account for 30-60% of motoneuronal excitability [327].…”

Section: Consideration Of the Physiological Role Of Group III And Iv mentioning

confidence: 99%

“…The authors argue that the decrease in muscle spindle sensitivity is due to an increased compliance of the muscle (including the intrafusal fibers which are the end organs of the Ia afferents). Another possible explanation is that stretching resulted in the activation of nociceptive afferents which have been shown to reduce the excitability of the monosynaptic reflex through pre-synaptic inhibition of Ia afferent terminals within the spinal cord [326,356]. Stretching has been also reported to decrease H-reflex [357] or other reflex-based measures of motoneuronal excitability [110,358] in patients with spasticity, however, others found no effect on the excitability of H-reflex [359].…”

Section: Mechanism Of Stretch-induced Strength Loss and Its Relationsmentioning

confidence: 99%

Stretching adversely modulates locomotor capacity following spinal cord injury via activation of nociceptive afferents.

Keller¹

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The role of capsaicin‐sensitive muscle afferents in fatigue‐induced modulation of the monosynaptic reflex in the rat

Cited by 70 publications

References 37 publications

Fatigue-Sensitive Afferents Inhibit Extensor but Not Flexor Motoneurons in Humans

Fatigue-Sensitive Afferents Inhibit Extensor but Not Flexor Motoneurons in Humans

Neuropeptide Y induces ischemic angiogenesis and restores function of ischemic skeletal muscles

Stretching adversely modulates locomotor capacity following spinal cord injury via activation of nociceptive afferents.

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