ORCID Profile
0000-0002-4797-8298
Current Organisation
University of Adelaide
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Publisher: American Physiological Society
Date: 2012
Abstract: The purpose of the current study was to investigate corticospinal contributions to locomotor drive to leg muscles involved in cycling. We studied 1) if activation of inhibitory interneurons in the cortex via subthreshold transcranial magnetic stimulation (TMS) caused a suppression of EMG and 2) how the responses to stimulation of the motor cortex via TMS and cervicomedullary stimulation (CMS) were modulated across the locomotor cycle. TMS at intensities subthreshold for activation of the corticospinal tract elicited suppression of EMG for approximately one-half of the subjects and muscles during cycling, and in matched static contractions in vastus lateralis. There was also significant modulation in the size of motor-evoked potentials (MEPs) elicited by TMS across the locomotor cycle ( P 0.001) that was strongly related to variation in background EMG in all muscles ( r 0.86 P 0.05). When MEP and CMEP litudes were normalized to background EMG, they were relatively larger prior to the main EMG burst and smaller when background EMG was maximum. Since the pattern of modulation of normalized MEP and CMEP responses was similar, the data suggest that phase-dependent modulation of corticospinal responses during cycling in humans is driven mainly by spinal mechanisms. However, there were subtle differences in the degree to which normalized MEP and CMEP responses were facilitated prior to EMG burst, which might reflect small increases in cortical excitability prior to maximum muscle activation. The data demonstrate that the motor cortex contributes actively to locomotor drive, and that spinal factors dominate phase-dependent modulation of corticospinal excitability during cycling in humans.
Publisher: Cold Spring Harbor Laboratory
Date: 03-06-2019
DOI: 10.1101/653634
Abstract: The study aimed to examine the effect of a priming cathodal transcranial direct current stimulation (ctDCS) before subsequent anodal-tDCS (atDCS) was applied during low workload cycling exercise on the corticospinal responses in young healthy in iduals. Eleven young subjects participated in two sessions receiving either priming ctDCS or sham stimulation, followed by atDCS while cycling (i.e. ctDCS-atDCS, sham-atDCS) at 1.2 times their body weight (84 ± 20 W) in a counterbalanced double-blind design. Corticospinal excitability was measured with motor evoked potentials (MEPs) elicited via transcranial magnetic stimulation with the intensity set to produce an MEP litude of 1 mV in a resting hand muscle at baseline (PRE), following priming tDCS (POST-PRIMING) and post atDCS combined with cycling exercise (POST-TEST). There was a significant interaction between time and intervention ( P 0.01 ) on MEPs. MEPs increased from PRE (1.0 ± 0.06 mV) to POST-TEST (1.3 ± 0.06 mV) during ctDCS-atDCS ( P 0.001 ) but did not change across time during sham-atDCS (1.0 ± 0.06 mV, P 0.7 ). Furthermore, MEPs were higher in ctDCS-atDCS compared to sham-atDCS ( P 0.01 ) at both POST-PRIMING (ctDCS-atDCS: 1.1 ± 0.06, sham-atDCS: 1.0 ± 0.06) and POST-TEST (ctDCS-atDCS: 1.3 ± 0.06, sham-atDCS: 1.0 ± 0.06). These outcomes demonstrate that cathodal tDCS priming can enhance corticospinal excitability following anodal tDCS applied in combination with cycling exercise. The findings have implications for the application of tDCS in combination with cycling exercise in rehabilitation and sporting contexts.
Publisher: American Physiological Society
Date: 2021
DOI: 10.1152/JAPPLPHYSIOL.00288.2021
Abstract: Transcranial magnetic stimulation was used to examine GABA B -mediated inhibition during fatiguing exercise of large muscle group in older adults and young adults. We provide novel evidence to show that when older and young adults are faced with a similar magnitude of elbow flexor muscle fatigue, they have a similar decline in GABA B -mediated inhibition. This suggests that when measured in a large muscle group, older adults maintain the ability to modulate GABA B inhibition during fatiguing exercise.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 12-2019
DOI: 10.1161/HYPERTENSIONAHA.119.13366
Abstract: We investigated the impact of hypertension on circulatory responses to exercise and the role of the exercise pressor reflex in determining the cardiovascular abnormalities characterizing patients with hypertension. After a 7-day drug washout, 8 hypertensive (mean arterial pressure [MAP] 130±4 mm Hg 65±3 years) and 8 normotensive (MAP 117±2 mm Hg 65±2 years) in iduals performed single-leg knee-extensor exercise (7 W, 15 W, 50%, 80%-W peak ) under control conditions and with lumbar intrathecal fentanyl impairing feedback from µ-opioid receptor-sensitive leg muscle afferents. Femoral artery blood flow (Q L ), MAP (femoral artery), leg vascular conductance, and changes in cardiac output were continuously measured. While the increase in MAP from rest to control exercise was significantly greater in hypertension compared with normotension, the exercise-induced increase in cardiac output was comparable between groups, and Q L and leg vascular conductance responses were ≈18% and ≈32% lower in the hypertensive patients ( P .05). The blockade-induced decreases in MAP were significantly larger during exercise in hypertensive (≈11 mm Hg) compared with normotensive (≈6 mm Hg). Afferent blockade attenuated the central hemodynamic response to exercise similarly in both groups resulting in a ≈15% lower cardiac output at each workload. With no effect in normotensive, afferent blockade significantly raised the peripheral hemodynamic response to exercise in hypertensive, resulting in ≈14% and ≈23% higher Q L and leg vascular conductance during exercise. Finally, Q L and MAP during fentanyl-exercise in hypertensive were comparable to that of normotensive under control conditions ( P .2). These findings suggest that exercise pressor reflex abnormalities largely account for the exaggerated MAP response and the impaired peripheral hemodynamics during exercise in hypertension.
Publisher: American Physiological Society
Date: 10-2022
DOI: 10.1152/JAPPLPHYSIOL.00213.2022
Abstract: We use a novel form of repetitive transcranial magnetic stimulation to show that motor cortex plasticity is increased after acute exercise and that this effect is bolstered in endurance-trained cyclists. These findings indicate that participation in regular endurance exercise (involving lower limb muscles) has widespread effects on cortical plasticity (assessed in unexercised upper limb muscles) following acute lower-limb cycling exercise. It also highlights that exercise history is an important factor in exercise-induced cortical plasticity.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 04-2013
Publisher: Elsevier BV
Date: 2020
DOI: 10.1016/J.NEULET.2019.134597
Abstract: The study aimed to examine the effect of a pre-conditioning cathodal transcranial direct current stimulation (ctDCS) before subsequent anodal-tDCS (atDCS) was applied during low workload cycling exercise on the corticospinal responses in young healthy in iduals. Eleven young subjects participated in two sessions receiving either conditioning ctDCS or sham stimulation, followed by atDCS while cycling (i.e. ctDCS-atDCS, sham-atDCS) at 1.2 times their body weight (84 ± 20 W) in a counterbalanced double-blind design. Corticospinal excitability was measured with motor evoked potentials (MEPs) elicited via transcranial magnetic stimulation with the intensity set to produce an MEP litude of 1 mV in a resting hand muscle at baseline (PRE), following pre-conditioning tDCS (POST-COND) and post atDCS combined with cycling exercise (POST-TEST). There was a significant interaction between time and intervention (P < 0.01) on MEPs. MEPs increased from PRE (1.0 ± 0.06 mV) to POST-TEST (1.3 ± 0.06 mV) during ctDCS-atDCS (P 0.7). Furthermore, MEPs were higher in ctDCS-atDCS compared to sham-atDCS (both P < 0.01) at POST-COND (ctDCS-atDCS: 1.1 ± 0.06 mV, sham-atDCS: 1.0 ± 0.06 mV) and POST-TEST (ctDCS-atDCS: 1.3 ± 0.06 mV, sham-atDCS: 1.0 ± 0.06 mV). These outcomes demonstrate that pre-conditioning cathodal tDCS can enhance subsequent corticospinal excitability changes induced by anodal tDCS applied in combination with cycling exercise. The findings have implications for the application of tDCS in combination with cycling exercise in rehabilitation and sporting contexts.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 12-2018
DOI: 10.1249/MSS.0000000000001735
Abstract: The effect of an acute bout of exercise, especially high-intensity exercise, on the function of mitochondrial respiratory complexes is not well understood, with potential implications for both the healthy population and patients undergoing exercise-based rehabilitation. Therefore, this study sought to comprehensively examine respiratory flux through the different complexes of the electron transport chain in skeletal muscle mitochondria before and immediately after high-intensity aerobic exercise. Muscle biopsies of the vastus lateralis were obtained at baseline and immediately after a 5-km time trial performed on a cycle ergometer. Mitochondrial respiratory flux through the complexes of the electron transport chain was measured in permeabilized skeletal muscle fibers by high-resolution respirometry. Complex I + II state 3 (state 3 CI + CII ) respiration, a measure of oxidative phosphorylation capacity, was diminished immediately after the exercise (pre, 27 ± 3 ρm·mg −1 ·s −1 post, 17 ± 2 ρm·mg −1 ·s −1 P 0.05). This decreased oxidative phosphorylation capacity was predominantly the consequence of attenuated complex II–driven state 3 (state 3 CII ) respiration (pre, 17 ± 1 ρm·mg −1 ·s −1 post, 9 ± 2 ρm·mg −1 ·s −1 P 0.05). Although complex I–driven state 3 (3 CI ) respiration was also lower (pre, 20 ± 2 ρm·mg −1 ·s −1 post, 14 ± 4 ρm·mg −1 ·s −1 ), this did not reach statistical significance ( P = 0.27). In contrast, citrate synthase activity, proton leak (state 2 respiration), and complex IV capacity were not significantly altered immediately after the exercise. These findings reveal that acute high-intensity aerobic exercise significantly inhibits skeletal muscle state 3 CII and oxidative phosphorylation capacity. This, likely transient, mitochondrial defect might lify the exercise-induced development of fatigue and play an important role in initiating exercise-induced mitochondrial adaptations.
Publisher: Wiley
Date: 03-09-2018
DOI: 10.1113/JP276460
Publisher: Wiley
Date: 08-07-2016
DOI: 10.1113/JP272283
Publisher: American Physiological Society
Date: 02-2018
Abstract: Fatiguing intermittent single-joint exercise causes an increase in corticospinal excitability and a decrease in intracortical inhibition when measured with peripherally recorded motor evoked potentials (MEPs) after transcranial magnetic stimulation (TMS). Combined TMS and electroencephalography (TMS-EEG) allows for more direct recording of cortical responses through the TMS-evoked potential (TEP). The aim of this study was to investigate the changes in the excitatory and inhibitory components of the TEP during fatiguing single-joint exercise. Twenty-three young (22 ± 2 yr) healthy subjects performed intermittent 30-s maximum voluntary contractions of the right first dorsal interosseous muscle, followed by a 30-s relaxation period repeated for a total of 15 min. Six single-pulse TMSs and one peripheral nerve stimulation (PNS) to evoke maximal M wave (M max ) were applied during each relaxation period. A total of 90 TMS pulses and 5 PNSs were applied before and after fatiguing exercise to record MEP and TEP. The litude of the MEP (normalized to M max ) increased during fatiguing exercise ( P 0.001). There were no changes in local and global P30, N45, and P180 of TEPs during the development of intermittent single-joint exercise-induced fatigue. Global analysis, however, revealed a decrease in N100 peak of the TEP during fatiguing exercise compared with before fatiguing exercise ( P = 0.02). The decrease in N100 suggests a fatigue-related decrease in global intracortical GABA B -mediated inhibition. The increase in corticospinal excitability typically observed during single-joint fatiguing exercise may be mediated by a global decrease in intracortical inhibition. NEW & NOTEWORTHY Fatiguing intermittent single-joint exercise causes an increase in corticospinal excitability and a decrease in intracortical inhibition when measured with transcranial magnetic stimulation (TMS)-evoked potentials from the muscle. The present study provides new and direct cortical evidence, using TMS-EEG to demonstrate that during single-joint fatiguing exercise there is a global decrease in intracortical GABA B -mediated inhibition.
Publisher: Wiley
Date: 23-11-2022
DOI: 10.1113/JP282564
Abstract: Neural drive originating in higher brain areas reaches exercising limb muscles through the corticospinal‐motoneuronal pathway, which links the motor cortex and spinal motoneurones. The properties of this pathway have frequently been observed to change during fatiguing exercise in ways that could influence the development of central fatigue (i.e. the progressive reduction in voluntary muscle activation). However, based on differences in motor cortical and motoneuronal excitability between exercise modalities (e.g. single‐joint vs . locomotor exercise), there is no characteristic response that allows for a categorical conclusion about the effect of these changes on functional impairments and performance limitations. Despite the lack of uniformity in findings during fatigue, there is strong evidence for marked ‘inhibition’ of motoneurones as a direct result of voluntary drive. Endogenous forms of neuromodulation, such as via serotonin released from neurones, can directly affect motoneuronal output and central fatigue. Exogenous forms of neuromodulation, such as brain stimulation, may achieve a similar effect, although the evidence is weak. Non‐invasive transcranial direct current stimulation can cause transient or long‐lasting changes in cortical excitability however, variable results across studies cast doubt on its claimed capacity to enhance performance. Furthermore, with these studies, it is difficult to establish a cause‐and‐effect relationship between brain responsiveness and exercise performance. This review briefly summarizes changes in the corticomotoneuronal pathway during various types of exercise, and considers the relevance of these changes for the development of central fatigue, as well as the potential of non‐invasive brain stimulation to enhance motor cortical excitability, motoneuronal output and, ultimately, exercise performance. image
Publisher: Wiley
Date: 10-2013
DOI: 10.1111/APHA.12004
Abstract: Short-interval intracortical inhibition (SICI) can provide information on changes in cortical responsiveness during voluntary contractions. It is, however, unknown whether the magnitude of SICI changes throughout the cycle of rhythmic movements such as leg cycling. The effects of four conditioning stimulus (CS) intensities, 70, 80, 90 and 95% of active motor threshold (AMT), on the magnitude of SICI were tested during three conditions: (1) activation phase of the electromyography (EMG) burst, (2) deactivation phase of the EMG burst and (3) static contractions. The three conditions were matched for EMG litude and test motor-evoked potential (MEP) size with reference to the vastus lateralis muscle. Responses were also recorded from rectus femoris and vastus medialis. short-interval cortical inhibition was weak during static knee contractions (15% reduction in control MEP) relative to previous reports during contractions in other muscle groups. SICI was abolished during the activation phase of the knee extensor EMG burst (P > 0.05), but present (approx. 90% of control MEP size) during the deactivation phase of EMG (P < 0.05). Furthermore, inhibition was elicited at a lower CS intensity during the deactivation phase of EMG during cycling than during static contractions (70 AMT vs. 90% AMT). The results suggest that the efficacy of intracortical inhibitory projections to knee extensor corticomotoneurons is particularly weak during muscle activation. A lower threshold of activation for inhibitory cells during deactivation phase of cycling EMG was evident, and there was a phasic modulation of intracortical inhibition affecting corticospinal projections to the working muscles.
Publisher: Elsevier BV
Date: 05-2018
DOI: 10.1016/J.BRS.2017.12.013
Abstract: Alterations in inhibitory processes mediated by gamma-aminobutyric acid type B (GABA To utilise electroencephalography and TMS coregistration (TMS-EEG) to more directly assess age-related changes in GABA In 17 young (24.2 ± 1.1 years) and 17 older (71.4 ± 1.4 years) subjects, the TMS-evoked potential (TEP) was used to assess the global scalp response to single-pulse TMS and LICI applied at two interstimulus intervals of 100 ms (LICI For single-pulse stimulation, P30 litude was unaffected by age. Despite this, N45 litude was increased in older adults and both N100 and P180 showed altered spatial distributions. Furthermore, the latency of P30 was shorter, while the latency of P180 was longer, in the elderly. In addition, inhibition of the N100 and P180 was increased in older adults following both LICI These findings with TMS-EEG suggest that the ageing process is associated with a potentiation of GABAergic inhibition, particularly for the GABA
Publisher: Wiley
Date: 26-10-2017
DOI: 10.1111/EJN.13729
Abstract: The ability of priming non-invasive brain stimulation (NIBS) to modulate neuroplasticity induction (i.e. metaplasticity) within primary motor cortex (M1) may be altered in older adults. Previous studies in young subjects suggest that consecutive NIBS protocols interact in a time-dependent manner and involve homoeostatic metaplasticity mechanisms. This was investigated in older adults by assessing the response to consecutive blocks of paired-associative stimulation (PAS) separated by different inter-PAS intervals (IPIs). Fifteen older (62-82 years) subjects participated in four sessions, with each session involving two PAS blocks separated by IPIs of 10 (IPI
Publisher: American Physiological Society
Date: 15-06-2015
DOI: 10.1152/AJPREGU.00021.2015
Abstract: We investigated the role of exercise intensity and associated central motor drive in determining corticomotoneuronal excitability. Ten participants performed a series of nonfatiguing (3 s) isometric single-leg knee extensions (ISO 10–100% of maximal voluntary contractions, MVC) and cycling bouts (30–160% peak aerobic capacity, W peak ). At various exercise intensities, electrical potentials were evoked in the vastus lateralis (VL) and rectus femoris (RF) via transcranial magnetic stimulation (motor-evoked potentials, MEP), and electrical stimulation of both the cervicomedullary junction (cervicomedullary evoked potentials, CMEP) and the femoral nerve (maximal M-waves, M max ). Whereas M max remained unchanged in both muscles ( P 0.40), voluntary electromyographic activity (EMG) increased in an exercise intensity-dependent manner for ISO and cycling exercise in VL and RF (both P 0.001). During ISO exercise, MEPs and CMEPs progressively increased in VL and RF until a plateau was reached at ∼75% MVC further increases in contraction intensity did not cause additional changes ( P 0.35). During cycling exercise, VL-MEPs and CMEPs progressively increased by ∼65% until a plateau was reached at W peak . In contrast, RF MEPs and CMEPs progressively increased by ∼110% throughout the tested cycling intensities without the occurrence of a plateau. Furthermore, alterations in EMG below the plateau influenced corticomotoneuronal excitability similarly between exercise modalities. In both exercise modalities, the MEP-to-CMEP ratio did not change with exercise intensity ( P 0.22). In conclusion, increases in exercise intensity and EMG facilitates the corticomotoneuronal pathway similarly in isometric knee extension and locomotor exercise until a plateau occurs at a submaximal exercise intensity. This facilitation appears to be primarily mediated by increases in excitability of the motoneuron pool.
Publisher: American Physiological Society
Date: 11-2015
DOI: 10.1152/AJPHEART.00433.2015
Abstract: We investigated the influence of aging on the group III/IV muscle afferents in the exercise pressor reflex-mediated cardiovascular response to rhythmic exercise. Nine old (OLD 68 ± 2 yr) and nine young (YNG 24 ± 2 yr) males performed single-leg knee extensor exercise (15 W, 30 W, 80% max) under control conditions and with lumbar intrathecal fentanyl impairing feedback from group III/IV leg muscle afferents. Mean arterial pressure (MAP), cardiac output, leg blood flow (Q L ), systemic (SVC) and leg vascular conductance (LVC) were continuously determined. With no hemodynamic effect at rest, fentanyl blockade during exercise attenuated both cardiac output and Q L ∼17% in YNG, while the decrease in cardiac output in OLD (∼5%) was significantly smaller with no impact on Q L ( P = 0.8). Therefore, in the face of similar significant ∼7% reduction in MAP during exercise with fentanyl blockade in both groups, LVC significantly increased ∼11% in OLD, but decreased ∼8% in YNG. The opposing direction of change was reflected in SVC with a significant ∼5% increase in OLD and a ∼12% decrease in YNG. Thus while cardiac output seems to account for the majority of group III/IV-mediated MAP responses in YNG, the impact of neural feedback on the heart may decrease with age and alterations in SVC become more prominent in mediating the similar exercise pressor reflex in OLD. Interestingly, in terms of peripheral hemodynamics, while group III/IV-mediated feedback plays a clear role in increasing LVC during exercise in the YNG, these afferents seem to actually reduce LVC in OLD. These peripheral findings may help explain the limited exercise-induced peripheral vasodilation often associated with aging.
Publisher: Wiley
Date: 25-10-2013
Publisher: American Physiological Society
Date: 10-2018
DOI: 10.1152/AJPREGU.00156.2018
Abstract: To examine the impact of aging on neuromuscular fatigue following cycling (CYC large active muscle mass) and single-leg knee-extension (KE small active muscle mass) exercise, 8 young (25 ± 4 years) and older (72 ± 6 years) participants performed CYC and KE to task failure at a given relative intensity (80% of peak power output). The young also matched CYC and KE workload and duration of the old (iso-work comparison). Peripheral and central fatigue were quantified via pre- ostexercise decreases in quadriceps twitch torque (∆Q tw , electrical femoral nerve stimulation) and voluntary activation (∆VA). Although young performed 77% and 33% more work during CYC and KE, respectively, time to task failure in both modalities was similar to the old (~9.5 min P 0.2). The resulting ΔQ tw was also similar between groups (CYC ~40%, KE ~55% P 0.3) however, ∆VA was, in both modalities, approximately double in the young (CYC ~6%, KE ~9% P 0.05). While causing substantial peripheral and central fatigue in both exercise modalities in the old, ∆Q tw in the iso-work comparison was not significant (CYC P = 0.2), or ~50% lower (KE P 0.05) in the young, with no central fatigue in either modality ( P 0.4). Based on iso-work comparisons, healthy aging impairs fatigue resistance during aerobic exercise. Furthermore, comparisons of fatigue following exercise at a given relative intensity mask the age-related difference observed following exercise performed at the same workload. Finally, although active muscle mass has little influence on the age-related difference in the rate of fatigue at a given relative intensity, it substantially impacts the comparison during exercise at a given absolute intensity.
Publisher: Wiley
Date: 29-09-2014
DOI: 10.1113/JPHYSIOL.2014.275438
Abstract: We aimed to elucidate the role of group III/IV locomotor muscle afferents in the development of central fatigue and the responsiveness of the corticospinal tract in relation to an unexercised arm muscle. Intrathecal fentanyl, a μ‐opioid receptor agonist, was employed to attenuate afferent feedback from the leg muscles during intense cycling exercise characterized by either no or severe peripheral locomotor muscle fatigue. In the absence of locomotor muscle fatigue, group III/IV‐mediated leg afferent feedback facilitates the responsiveness of the motor pathway to upper limb flexor muscles. By contrast, in the presence of leg fatigue, group III/IV locomotor muscle afferents facilitate supraspinal fatigue in a remote muscle not involved in the exercise and disfacilitate the responsiveness of associated corticospinal projections. We investigated the influence of group III/IV lower limb muscle afferents on the development of supraspinal fatigue and the responsiveness of corticospinal projections to an arm muscle. Eight males performed constant‐load leg cycling exercise (80% peak power output) for 30 s (non‐fatiguing) and to exhaustion (∼9 min fatiguing) both under control conditions and with lumbar intrathecal fentanyl impairing feedback from μ‐opioid receptor‐sensitive lower limb muscle afferents. Voluntary activation (VA) of elbow flexors was assessed via transcranial magnetic stimulation (TMS) during maximum voluntary contraction (MVC) and corticospinal responsiveness was monitored via TMS‐evoked potentials (MEPs) during a 25% MVC. Accompanied by a significant 5 ± 1% reduction in VA from pre‐ to post‐exercise, elbow flexor MVC progressively decreased during the fatiguing trial ( P 0.05). By contrast, with attenuated feedback from locomotor muscle afferents, MVC and VA remained unchanged during fatiguing exercise ( P 0.3). MEPs decreased by 36 ± 6% ( P 0.05) from the start of exercise to exhaustion under control conditions, but this reduction was prevented with fentanyl blockade. Furthermore, fentanyl blockade prevented the significant increase in elbow flexor MEP observed from rest to non‐fatiguing exercise under control conditions and resulted in a 14% lower corticospinal responsiveness during this short bout ( P 0.05). Taken together, in the absence of locomotor muscle fatigue, group III/IV‐mediated leg muscle afferents facilitate responsiveness of the motor pathway to upper limb flexor muscles. By contrast, in the presence of cycling‐induced leg fatigue, group III/IV locomotor muscle afferents facilitate supraspinal fatigue in remote muscle not involved in the exercise and disfacilitate, or inhibit, the responsiveness of corticospinal projections to upper limb muscles.
Publisher: Wiley
Date: 07-10-2016
DOI: 10.1111/SMS.12754
Abstract: Carbohydrate (CHO) depletion is linked to neuromuscular fatigue during exercise. While its role at peripheral level is relatively well understood, less is known about its impact centrally. The aim of this systematic review was to critically analyze the effects of CHO on central fatigue (CF) assessed by various neurophysiological techniques. Four databases were searched using PRISMA guidelines through February 2016. The inclusion criteria were: CHO as intervention against a placebo control, fatigue induced by prolonged exercise and assessed using neurophysiological measures [voluntary activation (VA), superimposed twitch (SIT), M-wave, electromyography], alongside maximal voluntary contraction (MVC). Seven papers were reviewed, where exercise duration lasted between 115 and 180 min. CHO improved exercise performance in three studies, whereby two of them attributed it to CF via attenuation of VA and SIT reductions, while the other indicated peripheral involvement via attenuation of M-wave reduction. Although a few studies suggest that CHO attenuates CF, data on its direct effects on neurophysiological outcome measures are limited and mixed. Generally, measures employed in these studies were inadequate to conclude central contribution to fatigue. Factors including the techniques used and the lack of controls render additional confounding factors to make definitive deductions. Future studies should employ consistent techniques and appropriate neurophysiological controls to distinguish CHO effect at central level. The use of pharmacological intervention should be incorporated to elucidate involvement of central mechanisms.
Publisher: Springer Science and Business Media LLC
Date: 03-2013
DOI: 10.1007/S40279-013-0020-6
Abstract: There is substantial evidence that fatiguing exercise is accompanied by changes within the central nervous system that reduce the force that can be produced by working muscles. Here we review studies that used non-invasive neurophysiological techniques to show that sustained single-joint contractions have the capacity to increase corticospinal responsiveness and reduce motoneuronal responsiveness. We contrast these findings with new evidence from our laboratory regarding corticospinal responsiveness during sustained cycling exercise. There seems to be a similar increase in responsiveness of the intracortical inhibitory interneurons during sustained locomotor and single-joint exercise which might be due to acute exercise responses that are common to fatiguing exercise of any nature, such as local accumulation of fatigue metabolites. In contrast, the pattern of changes in corticospinal responsiveness is fundamentally different between the two modes of exercise which might be due to greater systemic fatigue responses to locomotor exercises.
Publisher: Elsevier BV
Date: 2017
Publisher: Elsevier BV
Date: 2019
DOI: 10.1016/J.NEUROSCIENCE.2019.11.022
Abstract: The effects of muscle fatigue are known to be altered in older adults, and age-related changes in the brain are likely to be a contributing factor. However, the neural mechanisms underlying these changes are not known. The aim of the current study was to use transcranial magnetic stimulation combined with electroencephalography (TMS-EEG) to investigate age-related changes in cortical excitability with muscle fatigue. In 23 young (mean age ± SD: 22 ± 2 years) and 17 older (mean age ± SD: 68.3 ± 5.6 years) adults, single-pulse TMS-EEG was applied before, during and after the performance of fatiguing, intermittent isometric abduction of the index finger. Motor-evoked potential (MEP) measures of cortical excitability were increased during (estimated mean difference, 123.3% P 0.5). For TMS-EEG, the litude of the P30 and P180 potentials were unaffected by fatigue in older participants (P > 0.05). In contrast, the litude of the N45 potential in older adults was significantly reduced both during (positive cluster: mean voltage difference = 0.7 µV, P < 0.005 negative cluster: mean voltage difference = 0.9 µV, P < 0.0005) and after (mean voltage difference = 0.5 µV, P < 0.005) fatiguing exercise, whereas this response was absent in young participants. These results suggest that performance of maximal intermittent isometric exercise in old but not young adults is associated with modulation of cortical inhibition likely mediated by activation of gamma-aminobutyric acid type A receptors.
Publisher: American Physiological Society
Date: 11-2021
DOI: 10.1152/AJPREGU.00158.2021
Abstract: Recently it was documented that fatiguing, high-intensity exercise resulted in a significant attenuation in maximal skeletal muscle mitochondrial respiratory capacity, potentially due to the intramuscular metabolic perturbation elicited by such intense exercise. With the utilization of intrathecal fentanyl to attenuate afferent feedback from group III/IV muscle afferents, permitting increased muscle activation and greater intramuscular metabolic disturbance, this study aimed to better elucidate the role of metabolic perturbation on mitochondrial respiratory function. Eight young, healthy males performed high-intensity cycle exercise in control (CTRL) and fentanyl-treated (FENT) conditions. Liquid chromatography-mass spectrometry and high-resolution respirometry were used to assess metabolites and mitochondrial respiratory function, respectively, pre- and postexercise in muscle biopsies from the vastus lateralis. Compared with CTRL, FENT yielded a significantly greater exercise-induced metabolic perturbation (PCr: −67% vs. −82%, Pi: 353% vs. 534%, pH: −0.22 vs. −0.31, lactate: 820% vs. 1,160%). Somewhat surprisingly, despite this greater metabolic perturbation in FENT compared with CTRL, with the only exception of respiratory control ratio (RCR) (−3% and −36%) for which the impact of FENT was significantly greater, the degree of attenuated mitochondrial respiratory capacity postexercise was not different between CTRL and FENT, respectively, as assessed by maximal respiratory flux through complex I (−15% and −33%), complex II (−36% and −23%), complex I + II (−31% and −20%), and state 3 CI+CII control ratio (−24% and −39%). Although a basement effect cannot be ruled out, this failure of an augmented metabolic perturbation to extensively further attenuate mitochondrial function questions the direct role of high-intensity exercise-induced metabolite accumulation in this postexercise response.
Publisher: Elsevier BV
Date: 03-2015
Publisher: American Physiological Society
Date: 08-2016
DOI: 10.1152/JAPPLPHYSIOL.00117.2016
Abstract: Recently, we documented age-related attenuation of efferent drive to contracting skeletal muscle. It remains elusive if this indication of reduced muscle strength is present with lifelong strength training. For this purpose, we examined evoked potentials in the calf muscles of 11 [71 ± 4 (SD) yr] strength-trained master athletes (MA) contrasted with 10 (71 ± 4 yr) sedentary (SO) and 11 (73 ± 6 yr) recreationally active (AO) old subjects, as well as 9 (22 ± 2 yr) young controls. As expected, MA had higher leg press maximal strength (MA, 185 ± 32 kg AO, 128 ± 15 kg SO, 106 ± 11 kg young, 147 ± 22 kg, P 0.01) and rate of force development (MA, 5,588 ± 2,488 N/s AO, 2,156 ± 1,100 N/s SO, 2,011 ± 825 N/s young, 3,663 ± 1,140 N/s, P 0.05) than the other groups. MA also exhibited higher musculus soleus normalized V waves during maximal voluntary contractions (MVC) [maximal V wave litude/maximal M wave during MVC (V sup /M sup ) 0.28 ± 0.15] than AO (0.13 ± 0.06, P 0.01) and SO (0.11 ± 0.05, P 0.01), yet lower than young (0.45 ± 0.12, P 0.01). No differences were apparent between the old groups in H reflex recorded at rest or during MVC [maximal H reflex litude/maximal M wave during rest (H max /M max ) maximal H reflex litude during MVC/maximal M wave during MVC (H sup /M sup )], and all were lower ( P 0.01) than young. MA (34.4 ± 2.1 ms) had shorter ( P 0.05) H reflex latency compared with AO (36.4 ± 3.7 ms) and SO (37.3 ± 3.2 ms), but longer ( P 0.01) than young (30.7 ± 2.0 ms). Using interpolated twitch analysis, MA (89 ± 7%) had plantar flexion voluntary activation similar to young (90 ± 6%), and this was higher ( P 0.05), or tended to be higher ( P = 0.06–0.09), than SO (83 ± 10%) and AO (84 ± 5%). These observations suggest that lifelong strength training has a protective effect against age-related attenuation of efferent drive. In contrast, no beneficial effect seems to derive from habitual recreational activity, indicating that strength training may be particularly beneficial for counteracting age-related loss of neuromuscular function.
Publisher: Wiley
Date: 12-01-2023
DOI: 10.1113/JP284271
Publisher: American Physiological Society
Date: 08-2012
DOI: 10.1152/JAPPLPHYSIOL.00486.2012
Abstract: The excitability of the motor cortex increases as fatigue develops during sustained single-joint contractions, but there are no previous reports on how corticospinal excitability is affected by sustained locomotor exercise. Here we addressed this issue by measuring spinal and cortical excitability changes during sustained cycling exercise. Vastus lateralis (VL) and rectus femoris (RF) muscle responses to transcranial magnetic stimulation of the motor cortex (motor evoked potentials, MEPs) and electrical stimulation of the descending tracts (cervicomedullary evoked potentials, CMEPs) were recorded every 3 min from nine subjects during 30 min of cycling at 75% of maximum workload (W max ), and every minute during subsequent exercise at 105% of W max until subjective task failure. Responses were also measured during nonfatiguing control bouts at 80% and 110% of W max prior to sustained exercise. There were no significant changes in MEPs or CMEPs ( P 0.05) during the sustained cycling exercise. These results suggest that, in contrast to sustained single-joint contractions, sustained cycling exercise does not increase the excitability of motor cortical neurons. The contrasting corticospinal responses to the two modes of exercise may be due to differences in their associated systemic physiological consequences.
Start Date: 2011
End Date: 2012
Funder: Sports Medicine Australia Research Foundation
View Funded ActivityStart Date: 2014
End Date: 2015
Funder: American Heart Association
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