scholarly journals Use of transcranial magnetic stimulation to assess relaxation rates in unfatigued and fatigued knee-extensor muscles

2020 ◽  
Author(s):  
Gianluca Vernillo ◽  
Arash Khassetarash ◽  
Guillaume Y. Millet ◽  
John Temesi
Keyword(s):  
Transcranial Magnetic Stimulation ◽  
Relaxation Rate ◽  
Nerve Stimulation ◽  
Magnetic Stimulation ◽  
Time Course ◽  
Muscle Relaxation ◽  
Femoral Nerve ◽  
Relaxation Rates ◽  
Repeatability Coefficient ◽  
Induced Changes

Abstract We examined whether transcranial magnetic stimulation (TMS) delivered to the motor cortex allows assessment of muscle relaxation rates in unfatigued and fatigued knee extensors (KE). We assessed the ability of this technique to measure time course of fatigue-induced changes in muscle relaxation rate and compared relaxation rate from resting twitches evoked by femoral nerve stimulation. Twelve healthy men performed maximal voluntary isometric contractions (MVC) twice before (PRE) and once at the end of a 2-min KE MVC and five more times within 8 min during recovery. Relative (intraclass correlation coefficient; ICC2,1) and absolute (repeatability coefficient) reliability and variability (coefficient of variation) were assessed. Time course of fatigue-induced changes in muscle relaxation rate was tested with generalized estimating equations. In unfatigued KE, peak relaxation rate coefficient of variation and repeatability coefficient were similar for both techniques. Mean (95% CI) ICC2,1 for peak relaxation rates were 0.933 (0.724–0.982) and 0.889 (0.603–0.968) for TMS and femoral nerve stimulation, respectively. TMS-induced normalized muscle relaxation rate was − 11.5 ± 2.5 s−1 at PRE, decreased to − 6.9 ± 1.2 s−1 (− 37 ± 17%, P < 0.001), and recovered by 2 min post-exercise. Normalized peak relaxation rate for resting twitch did not show a fatigue-induced change. During fatiguing KE exercise, the change in muscle relaxation rate as determined by the two techniques was different. TMS provides reliable values of muscle relaxation rates. Furthermore, it is sufficiently sensitive and more appropriate than the resting twitch evoked by femoral nerve stimulation to reveal fatigue-induced changes in KE.

Allergen-induced hyperresponsiveness to bradykinin is more pronounced than that to methacholine

1995 ◽  
Vol 78 (5) ◽  
pp. 1844-1852 ◽  
Author(s):  
A. R. Berman ◽  
A. G. Togias ◽  
G. Skloot ◽  
D. Proud
Keyword(s):  
Smooth Muscle ◽  
Vascular Permeability ◽  
Nerve Stimulation ◽  
Time Course ◽  
Sensory Nerve ◽  
Asthmatic Patients ◽  
Sensitive Index ◽  
Allergen Provocation ◽  
Allergen Inhalation ◽  
Induced Changes

Bradykinin reduces airflow in asthmatic patients via indirect mechanism(s), possibly involving sensory nerve stimulation and increased vascular permeability. We hypothesized that allergen inhalation, which affects reactivity of nerves and vessels, would differentially alter reactivity to bradykinin and the smooth muscle spasmogen methacholine. We compared reactivity to methacholine and bradykinin 1, 2, 4, 7, 11, and 14 days after allergen provocation in 12 atopic asthmatic patients with stable baseline reactivity to bradykinin. Maximal allergen-induced shifts from baseline in reactivity were 0.73 +/- 0.12 log unit for bradykinin compared with 0.27 +/- 0.13 log units for methacholine (P = 0.0005). Nine subjects showed significant increases in bradykinin reactivity, with four subjects increasing reactivity by > 1 log unit. Moreover, the maximal mean change in bradykinin reactivity occurred 2 days postallergen. Thus, allergen-induced changes in reactivity to bradykinin and methacholine differ in magnitude and time course. Bradykinin inhalational challenge provides a sensitive index of the airway's response to allergen.

scholarly journals Fatigue-induced changes in short-interval intracortical inhibition and the silent period with stimulus intensities evoking maximal versus submaximal responses

2020 ◽  
Vol 129 (2) ◽  
pp. 205-217
Author(s):  
Callum G. Brownstein ◽  
Loïc Espeit ◽  
Nicolas Royer ◽  
Thomas Lapole ◽  
Guillaume Y. Millet
Keyword(s):  
Transcranial Magnetic Stimulation ◽  
Magnetic Stimulation ◽  
Short Interval ◽  
Conditioning Stimulus ◽  
Silent Period ◽  
Single Pulse ◽  
Intracortical Inhibition ◽  
Fatiguing Exercise ◽  
Induced Changes

This study compared the change in silent period (SP) and short-interval intracortical inhibition (SICI) with conditioning stimulus and single-pulse transcranial magnetic stimulation (TMS) intensities (for SICI and SP, respectively) eliciting maximal and submaximal SICI and SP during fatiguing exercise. The results showed that changes in SICI were only detectable with intensities evoking maximal responses, with no difference between intensities for SP. These findings highlight the importance of maximizing SICI with appropriate intensities before measuring SICI during fatiguing exercise.

Transcranial Magnetic Stimulation in Different Current Directions Activates Separate Cortical Circuits

2011 ◽  
Vol 105 (2) ◽  
pp. 749-756 ◽  
Author(s):  
Zhen Ni ◽  
Samer Charab ◽  
Carolyn Gunraj ◽  
Aimee J. Nelson ◽  
Kaviraja Udupa ◽  
...  
Keyword(s):  
Transcranial Magnetic Stimulation ◽  
Median Nerve ◽  
Nerve Stimulation ◽  
Magnetic Stimulation ◽  
Primary Motor Cortex ◽  
Motor Units ◽  
Current Direction ◽  
Single Motor Units ◽  
Median Nerve Stimulation ◽  
Neuronal Mechanisms

Transcranial magnetic stimulation (TMS) to the primary motor cortex (M1) produces a series of corticospinal descending waves, with a direct (D) wave followed by several indirect (I) waves. TMS inducing posterior–anterior (PA) current in the brain predominantly recruits the early I1-wave, whereas anterior–posterior (AP) directed current preferentially recruits the late I3-wave. However, it is not known whether I-waves elicited by different current directions are mediated by the same neuronal populations. We studied the neuronal mechanisms mediating I-waves by examining the influence of short-latency afferent inhibition (SAI) on various I-waves. SAI was tested with electrical median nerve stimulation at the wrist followed by TMS to the contralateral M1 at different current directions. Surface electromyograms and single motor units were recorded from the first dorsal interosseous muscle. SAI was weaker for the AP compared with that for the PA current direction. With increasing median nerve stimulation intensities, SAI increased for the PA direction but showed a U-shaped relationship for the AP direction. SAI produced more inhibition of late I-waves generated by PA than those generated by AP current direction. We conclude that late I-waves generated by PA and AP current directions are mediated by different neuronal mechanisms.

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