ORCID Profile
0000-0002-2032-8498
Current Organisation
University of Utah
Does something not look right? The information on this page has been harvested from data sources that may not be up to date. We continue to work with information providers to improve coverage and quality. To report an issue, use the Feedback Form.
Publisher: Elsevier BV
Date: 2017
Publisher: American Physiological Society
Date: 12-05-0005
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: 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: 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: 10-2018
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: 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.
Location: United States of America
No related grants have been discovered for Joshua Weavil.