Severe hypoxia affects exercise performance independently of afferent feedback and peripheral fatigue

2012 ◽  
Vol 112 (8) ◽  
pp. 1335-1344 ◽  
Author(s):  
Guillaume Y. Millet ◽  
Makii Muthalib ◽  
Marc Jubeau ◽  
Paul B. Laursen ◽  
Kazunori Nosaka

To test the hypothesis that hypoxia centrally affects performance independently of afferent feedback and peripheral fatigue, we conducted two experiments under complete vascular occlusion of the exercising muscle under different systemic O2 environmental conditions. In experiment 1, 12 subjects performed repeated submaximal isometric contractions of the elbow flexor to exhaustion (RCTE) with inspired O2 fraction fixed at 9% (severe hypoxia, SevHyp), 14% (moderate hypoxia, ModHyp), 21% (normoxia, Norm), or 30% (hyperoxia, Hyper). The number of contractions (performance), muscle (biceps brachii), and prefrontal near-infrared spectroscopy (NIRS) parameters and high-frequency paired-pulse (PS100) evoked responses to electrical muscle stimulation were monitored. In experiment 2, 10 subjects performed another RCTE in SevHyp and Norm conditions in which the number of contractions, biceps brachii electromyography responses to electrical nerve stimulation (M wave), and transcranial magnetic stimulation responses (motor-evoked potentials, MEP, and cortical silent period, CSP) were recorded. Performance during RCTE was significantly reduced by 10–15% in SevHyp (arterial O2 saturation, SpO2 = ∼75%) compared with ModHyp (SpO2 = ∼90%) or Norm/Hyper (SpO2 > 97%). Performance reduction in SevHyp occurred despite similar 1) metabolic (muscle NIRS parameters) and functional (changes in PS100 and M wave) muscle states and 2) MEP and CSP responses, suggesting comparable corticospinal excitability and spinal and cortical inhibition between SevHyp and Norm. It is concluded that, in SevHyp, performance and central drive can be altered independently of afferent feedback and peripheral fatigue. It is concluded that submaximal performance in SevHyp is partly reduced by a mechanism related directly to brain oxygenation.

2013 ◽  
Vol 38 (11) ◽  
pp. 1154-1161 ◽  
Author(s):  
Kevin E. Power ◽  
David B. Copithorne

Human studies have not assessed supraspinal or spinal motoneurone excitability in the quiescent state prior to a rhythmic and alternating cyclical motor output. The purpose of the current study was to determine whether supraspinal and (or) spinal motoneurone excitability was modulated in humans prior to arm cycling when compared with rest with no intention to move. We hypothesized that corticospinal excitability would be enhanced prior to arm cycling due, in part, to increased spinal motoneurone excitability. Supraspinal and spinal motoneurone excitability were assessed via transcranial magnetic stimulation (TMS) of the motor cortex and transmastoid stimulation of the corticospinal tract, respectively. Surface electromyography recordings of TMS motor evoked potentials (MEPs) and cervicomedullary MEPs (CMEPs) were made from the relaxed biceps brachii muscle prior to rhythmic arm cycling and at rest with no intention to move. The amplitude of the MEPs was greater (mean increase: +9.8% of maximal M wave; p = 0.006) and their onset latencies were shorter (mean decrease: –1.5 ms; p < 0.05) prior to cycling when compared with rest. The amplitudes of the CMEPs at any of 3 stimulation intensities were not different between conditions. We conclude that premovement enhancement of corticospinal excitability is greater prior to arm cycling than at rest because of increases in supraspinal but not spinal motoneurone excitability.


2020 ◽  
Vol 10 (4) ◽  
pp. 191 ◽  
Author(s):  
Amanda J. Morris ◽  
Anita D. Christie

The purpose of this study was to examine the effect of a mentally fatiguing task on neuromuscular function in young and older women. Neuromuscular measures were obtained prior to and following 20 min of a mentally fatiguing task. Maximal force output significantly decreased after the mental fatigue task (p = 0.02) and this was not different between age groups (p = 0.32). Increases in cortical silent period duration approached significance in both young and older groups (p = 0.06), suggesting that mental fatigue may cause increased cortical inhibition. Measures of peripheral neuromuscular function (contractile properties of the muscle, M-wave) did not change (p ≥ 0.09), suggesting that changes in force production with mental fatigue are more likely due to supraspinal than peripheral mechanisms. These findings provide further evidence of an interaction between mental fatigue and physical function.


2019 ◽  
Vol 9 (8) ◽  
pp. 205 ◽  
Author(s):  
Evan J. Lockyer ◽  
Katarina Hosel ◽  
Anna P. Nippard ◽  
Duane C. Button ◽  
Kevin E. Power

Background: We examined corticospinal and spinal excitability across multiple power outputs during arm cycling using a weak and strong stimulus intensity. Methods: We elicited motor evoked potentials (MEPs) and cervicomedullary motor evoked potentials (CMEPs) in the biceps brachii using magnetic stimulation over the motor cortex and electrical stimulation of corticospinal axons during arm cycling at six different power outputs (i.e., 25, 50, 100, 150, 200 and 250 W) and two stimulation intensities (i.e., weak vs. strong). Results: In general, biceps brachii MEP and CMEP amplitudes (normalized to maximal M-wave (Mmax)) followed a similar pattern of modulation with increases in cycling intensity at both stimulation strengths. Specifically, MEP and CMEP amplitudes increased up until ~150 W and ~100 W when the weak and strong stimulations were used, respectively. Further increases in cycling intensity revealed no changes on MEP or CMEP amplitudes for either stimulation strength. Conclusions: In general, MEPs and CMEPs changed in a similar manner, suggesting that increases and subsequent plateaus in overall excitability are likely mediated by spinal factors. Interestingly, however, MEP amplitudes were disproportionately larger than CMEP amplitudes as power output increased, despite being initially matched in amplitude, particularly with strong stimulation. This suggests that supraspinal excitability is enhanced to a larger degree than spinal excitability as the power output of arm cycling increases.


Author(s):  
Jacob R Thorstensen ◽  
Janet Louise Taylor ◽  
Justin J Kavanagh

Animal models indicate that serotonin (5-HT) release onto motoneurons facilitates motor output, particularly during strong motor activities. However, evidence for 5-HT effects during human movement are limited. This study examined how antagonism of the 5-HT2 receptor, which is a 5-HT receptor that promotes motoneuron excitability, affects human movement. Ten healthy participants (24.2 ± 1.9 yr) ingested 8 mg of cyproheptadine (competitive 5-HT2 antagonist) in a double-blinded, placebo-controlled, repeated-measures design. Transcranial magnetic stimulation (TMS) of the motor cortex was used to elicit motor evoked potentials (MEPs) from biceps brachii. First, stimulus-response curves (90-160% active motor threshold) were obtained during very weak elbow flexions (10% of maximal). Second, to determine if 5-HT effects are scaled to the intensity of muscle contraction, TMS at a fixed intensity was applied during elbow flexions of 20, 40, 60, 80 and 100% of maximal. Cyproheptadine reduced the size of MEPs across the stimulus-response curves (P = 0.045). Notably, MEP amplitude was 22.3% smaller for the cyproheptadine condition for the strongest TMS intensity. In addition, cyproheptadine reduced maximal torque (P = 0.045), lengthened the biceps silent period during maximal elbow flexions (P = 0.037), and reduced superimposed twitch amplitude during moderate-intensity elbow flexions (P = 0.035). This study presents novel evidence that 5-HT2 receptors influence corticospinal-motoneuronal output, which was particularly evident when a large number of descending inputs to motoneurons were active. While it is likely that antagonism of 5-HT2 receptors reduces motoneuron gain to ionotropic inputs, supraspinal mechanisms may have also contributed to the study findings.


2019 ◽  
Vol 127 (5) ◽  
pp. 1224-1237 ◽  
Author(s):  
Jakob Škarabot ◽  
Paul Ansdell ◽  
John Temesi ◽  
Glyn Howatson ◽  
Stuart Goodall ◽  
...  

A bout of maximal lengthening contractions is known to produce muscle damage, but confers protection against subsequent damaging bouts, with both tending to be lower in older adults. Neural factors contribute to this adaptation, but the role of the corticospinal pathway remains unclear. Twelve young (27 ± 5 yr) and 11 older adults (66 ± 4 yr) performed two bouts of 60 maximal lengthening dorsiflexions 2 weeks apart. Neuromuscular responses were measured preexercise, immediately postexercise, and at 24 and 72 h following both bouts. The initial bout resulted in prolonged reductions in maximal voluntary torque (MVC; immediately postexercise onward, P < 0.001) and increased creatine kinase (from 24 h onward, P = 0.001), with both responses being attenuated following the second bout ( P < 0.015), demonstrating adaptation. Smaller reductions in MVC following both bouts occurred in older adults ( P = 0.005). Intracortical facilitation showed no changes ( P ≥ 0.245). Motor-evoked potentials increased 24 and 72 h postexercise in young ( P ≤ 0.038). Torque variability ( P ≤ 0.041) and H-reflex size ( P = 0.024) increased, while short-interval intracortical inhibition (SICI; P = 0.019) and the silent period duration (SP) decreased ( P = 0.001) in both groups immediately postexercise. The SP decrease was smaller following the second bout ( P = 0.021), and there was an association between the change in SICI and reduction in MVC 24 h postexercise in young adults ( R = −0.47, P = 0.036). Changes in neurophysiological responses were mostly limited to immediately postexercise, suggesting a modest role in adaptation. In young adults, neural inhibitory changes are linked to the extent of MVC reduction, possibly mediated by the muscle damage–related afferent feedback. Older adults incurred less muscle damage, which has implications for exercise prescription. NEW & NOTEWORTHY This is the first study to have collectively assessed the role of corticospinal, spinal, and intracortical activity in muscle damage attenuation following repeated bouts of exercise in young and older adults. Lower levels of muscle damage in older adults are not related to their neurophysiological responses. Neural inhibition transiently changed, which might be related to the extent of muscle damage; however, the role of processes along the corticospinal pathway in the adaptive response is limited.


Author(s):  
Lavender A. Otieno ◽  
John G. Semmler ◽  
Ashleigh Elizabeth Smith ◽  
Simranjit K. Sidhu

Age-related changes in the neuromuscular system can result in differences in fatigability between young and older adults. Previous research has shown that single joint isometric fatiguing exercise of small muscle results in an age-related compensatory decrease in GABAB mediated inhibition. However, this has yet to be established in a larger muscle group. In 15 young (22 ± 4 years) and 15 older (65 ± 5 years) adults, long interval cortical inhibition (LICI; 100 ms ISI) and corticospinal silent period (SP) were measured in the biceps brachii during a 5% EMG contraction using transcranial magnetic stimulation (TMS) before, during and after a submaximal contraction (30% MVC force) held intermittently to task failure. Both age groups developed similar magnitude of fatigue (~24% decline in MVC; P = 0.001) and ~28% decline in LICI (P = 0.001) post fatiguing exercise. No change in SP duration was observed during and immediately following fatigue (P = 0.909) but ~ 6% decrease was seen at recovery in both age groups (P<0.001)." Contrary to previous work in a small muscle, these findings suggest no age-related differences in GABAB mediated inhibition following single joint isometric fatiguing exercise of the elbow flexors, indicating that GABAB modulation with ageing may be muscle group dependent. Furthermore, variations in SP duration and LICI modulation during and post fatigue in both groups suggest that these measures are likely mediated by divergent mechanisms.


Nutrients ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1530
Author(s):  
Francesco Fisicaro ◽  
Giuseppe Lanza ◽  
Carmela Cinzia D’Agate ◽  
Raffaele Ferri ◽  
Mariagiovanna Cantone ◽  
...  

Background: Celiac disease (CD) may present or be complicated by neurological and neuropsychiatric manifestations. Transcranial magnetic stimulation (TMS) probes brain excitability non-invasively, also preclinically. We previously demonstrated an intracortical motor disinhibition and hyperfacilitation in de novo CD patients, which revert back after a long-term gluten-free diet (GFD). In this cross-sectional study, we explored the interhemispheric excitability by transcallosal inhibition, which has never been investigated in CD. Methods: A total of 15 right-handed de novo, neurologically asymptomatic, CD patients and 15 age-matched healthy controls were screened for cognitive and depressive symptoms to the Montreal Cognitive Assessment (MoCA) and the 17-item Hamilton Depression Rating Scale (HDRS), respectively. TMS consisted of resting motor threshold, amplitude, latency, and duration of the motor evoked potentials, duration and latency of the contralateral silent period (cSP). Transcallosal inhibition was evaluated as duration and latency of the ipsilateral silent period (iSP). Results: MoCA and HDRS scored significantly worse in patients. The iSP and cSP were significantly shorter in duration in patients, with a positive correlation between the MoCA and iSP. Conclusions: An intracortical and interhemispheric motor disinhibition was observed in CD, suggesting the involvement of GABA-mediated cortical and callosal circuitries. Further studies correlating clinical, TMS, and neuroimaging data are needed.


2019 ◽  
Vol 122 (1) ◽  
pp. 413-423 ◽  
Author(s):  
Davis A. Forman ◽  
Daniel Abdel-Malek ◽  
Christopher M. F. Bunce ◽  
Michael W. R. Holmes

Forearm rotation (supination/pronation) alters corticospinal excitability to the biceps brachii, but it is unclear whether corticospinal excitability is influenced by joint angle, muscle length, or both. Thus the purpose of this study was to separately examine elbow joint angle and muscle length on corticospinal excitability. Corticospinal excitability to the biceps and triceps brachii was measured using motor evoked potentials (MEPs) elicited via transcranial magnetic stimulation. Spinal excitability was measured using cervicomedullary motor evoked potentials (CMEPs) elicited via transmastoid electrical stimulation. Elbow angles were manipulated with a fixed biceps brachii muscle length (and vice versa) across five unique postures: 1) forearm neutral, elbow flexion 90°; 2) forearm supinated, elbow flexion 90°; 3) forearm pronated, elbow flexion 90°; 4) forearm supinated, elbow flexion 78°; and 5) forearm pronated, elbow flexion 113°. A musculoskeletal model determined biceps brachii muscle length for postures 1–3, and elbow joint angles ( postures 4–5) were selected to maintain biceps length across forearm orientations. MEPs and CMEPs were elicited at rest and during an isometric contraction of 10% of maximal biceps muscle activity. At rest, MEP amplitudes to the biceps were largest during supination, which was independent of elbow joint angle. CMEP amplitudes were not different when the elbow was fixed at 90° but were largest in pronation when muscle length was controlled. During an isometric contraction, there were no significant differences across forearm postures for either MEP or CMEP amplitudes. These results highlight that elbow joint angle and biceps brachii muscle length can each independently influence spinal excitability. NEW & NOTEWORTHY Changes in upper limb posture can influence the responsiveness of the central nervous system to artificial stimulations. We established a novel approach integrating neurophysiology techniques with biomechanical modeling. Through this approach, the effects of elbow joint angle and biceps brachii muscle length on corticospinal and spinal excitability were assessed. We demonstrate that spinal excitability is uniquely influenced by joint angle and muscle length, and this highlights the importance of accounting for muscle length in neurophysiological studies.


2017 ◽  
Vol 118 (6) ◽  
pp. 3242-3251 ◽  
Author(s):  
Brandon Wayne Collins ◽  
Edward W. J. Cadigan ◽  
Lucas Stefanelli ◽  
Duane C. Button

The purpose of this study was to examine the effect of shoulder position on corticospinal excitability (CSE) of the biceps brachii during rest and a 10% maximal voluntary contraction (MVC). Participants ( n = 9) completed two experimental sessions with four conditions: 1) rest, 0° shoulder flexion; 2) 10% MVC, 0° shoulder flexion; 3) rest, 90° shoulder flexion; and 4) 10% MVC, 90° shoulder flexion. Transcranial magnetic, transmastoid electrical, and Erb’s point stimulation were used to induce motor-evoked potentials (MEPs), cervicomedullary MEPs (CMEPs), and maximal muscle compound potentials (Mmax), respectively, in the biceps brachii in each condition. At rest, MEP, CMEP, and Mmax amplitudes increased ( P < 0.01) by 509.7 ± 118.3%, 113.3 ± 28.3%, and 155.1 ± 47.9%, respectively, at 90° compared with 0°. At 10% MVC, MEP amplitudes did not differ ( P = 0.08), but CMEP and Mmax amplitudes increased ( P < 0.05) by 32.3 ± 10.5% and 127.9 ± 26.1%, respectively, at 90° compared with 0°. MEP/Mmax increased ( P < 0.01) by 224.0 ± 99.1% at rest and decreased ( P < 0.05) by 51.3 ± 6.7% at 10% MVC at 90° compared with 0°. CMEP/Mmax was not different ( P = 0.22) at rest but decreased ( P < 0.01) at 10% MVC by 33.6 ± 6.1% at 90° compared with 0°. EMG increased ( P < 0.001) by 8.3 ± 2.0% at rest and decreased ( P < 0.001) by 21.4 ± 4.4% at 10% MVC at 90° compared with 0°. In conclusion, CSE of the biceps brachii was dependent on shoulder position, and the pattern of change was altered within the state in which it was measured. The position-dependent changes in Mmax amplitude, EMG, and CSE itself all contribute to the overall change in CSE of the biceps brachii. NEW & NOTEWORTHY We demonstrate that when the shoulder is placed into two common positions for determining elbow flexor force and activation, corticospinal excitability (CSE) of the biceps brachii is both shoulder position and state dependent. At rest, when the shoulder is flexed from 0° to 90°, supraspinal factors predominantly alter CSE, whereas during a slight contraction, spinal factors predominantly alter CSE. Finally, the normalization techniques frequently used by researchers to investigate CSE may under- and overestimate CSE when shoulder position is changed.


2018 ◽  
Vol 119 (2) ◽  
pp. 652-661 ◽  
Author(s):  
Siobhan C. Dongés ◽  
Jessica M. D’Amico ◽  
Jane E. Butler ◽  
Janet L. Taylor

Plasticity can be induced at human corticospinal-motoneuronal synapses by delivery of repeated, paired stimuli to corticospinal axons and motoneurons in a technique called paired corticospinal-motoneuronal stimulation (PCMS). To date, the mechanisms of the induced plasticity are unknown. To determine whether PCMS-induced plasticity is dependent on N-methyl-d-aspartate receptors (NMDARs), the effect of the noncompetitive NMDAR antagonist dextromethorphan on PCMS-induced facilitation was assessed in a 2-day, double-blind, placebo-controlled experiment. PCMS consisted of 100 pairs of stimuli, delivered at an interstimulus interval that produces facilitation at corticospinal-motoneuronal synapses that excite biceps brachii motoneurons. Transcranial magnetic stimulation elicited corticospinal volleys, which were timed to arrive at corticospinal-motoneuronal synapses just before antidromic potentials elicited in motoneurons with electrical brachial plexus stimulation. To measure changes in the corticospinal pathway at a spinal level, biceps responses to cervicomedullary stimulation (cervicomedullary motor evoked potentials, CMEPs) were measured before and for 30 min after PCMS. Individuals who displayed a ≥10% increase in CMEP size after PCMS on screening were eligible to take part in the 2-day experiment. After PCMS, there was a significant difference in CMEP area between placebo and dextromethorphan days ( P = 0.014). On the placebo day PCMS increased average CMEP areas to 127 ± 46% of baseline, whereas on the dextromethorphan day CMEP area was decreased to 86 ± 33% of baseline (mean ± SD; placebo: n = 11, dextromethorphan: n = 10). Therefore, dextromethorphan suppressed the facilitation of CMEPs after PCMS. This indicates that plasticity induced at synapses in the human spinal cord by PCMS may be dependent on NMDARs. NEW & NOTEWORTHY Paired corticospinal-motoneuronal stimulation can strengthen the synaptic connections between corticospinal axons and motoneurons at a spinal level in humans. The mechanism of the induced plasticity is unknown. In our 2-day, double-blind, placebo-controlled study we show that the N-methyl-d-aspartate receptor (NMDAR) antagonist dextromethorphan suppressed plasticity induced by paired corticospinal-motoneuronal stimulation, suggesting that an NMDAR-dependent mechanism is involved.


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