Dr. Kennedy is a US trained physiotherapist with 20yrs of clinical practice. Dr. Kennedy completed a PhD in neurophysiology at Neuroscience Research Australia through the University of New South Wales. His research examined the effects of nociceptive muscle afferents (think sensory nerve input that result in pain) on exercise performance during fatigue. Dr. Kennedy also holds three other degrees from the University of New Mexico, USA, including a Master’s of Science in Exercise Physiology, a Bachelor’s of Science in Physical Therapy, and a Bachelor’s of Arts in Psychology. He was a board-certified specialist in Cardiopulmonary Physical Therapy through the American Physical Therapy Association. He has worked in a variety of physiotherapy settings, including acute hospital care, intensive care units, and outpatient clinics, some in rural/underserved areas.
Currently, Dr. Kennedy is a Lecturer in Physiotherapy at the University of Technology, Sydney. Previously, he was a lecturer at the University of Sydney in the Discipline of Physiotherapy. He also holds an Honorary Post-Doctoral Fellowship at Neuroscience Research Australia, where he is conducting research in motor impairment, specifically central nervous system effects of fatigue, pain, and proprioception.
Can supervise: YES
Dr. Kennedy’s research interests are in how pain and fatigue alter central nervous system motor control. He currently working on improving proprioception assessments for people after stroke, particularly those with unilateral neglect and examining the effects of pain and fatigue on high level proprioception. He continues to examine how the central nervous system contributes to fatigue and what effects fatigue and pain have on proprioception and voluntary activation of muscles in healthy and clinical populations, specifically people with Multiple Sclerosis and Stroke.
Boyce, MJ, Kennedy, DS & McCambridge, AB 2020, 'Letter to the Editor, “A randomized study of botulinum toxin versus botulinum toxin plus physical therapy for treatment of cervical dystonia"', Parkinsonism & Related Disorders.View/Download from: Publisher's site
Finn, H, Rouffet, DM, Kennedy, DS, Green, S & Taylor, JL 2018, 'Motoneuron excitability of the quadriceps decreases during a fatiguing submaximal isometric contraction', Journal of Applied Physiology, vol. 124, no. 4, pp. 970-979.View/Download from: Publisher's site
Copyright © 2018 American Physiological Society. All rights reserved. During fatiguing voluntary contractions, the excitability of motoneurons innervating arm muscles decreases. However, the behavior of motoneurons innervating quadriceps muscles is unclear. Findings may be inconsistent because descending cortical input influences motoneuron excitability and confounds measures during exercise. To overcome this limitation, we examined effects of fatigue on quadriceps motoneuron excitability tested during brief pauses in descending cortical drive after transcranial magnetic stimulation (TMS). Participants (n = 14) performed brief (5-s) isometric knee extension contractions before and after a 10-min sustained contraction at 25% maximal electromyogram (EMG) of vastus medialis (VM) on one (n - 5) or two (n = 9) days. Electrical stimulation over thoracic spine elicited thoracic motor evoked potentials (TMEP) in quadriceps muscles during ongoing voluntary drive and 100 ms into the silent period following TMS (TMS-TMEP). Femoral nerve stimulation elicited maximal M-waves (Mmax). On the 2 days, either large (50% Mmax) or small (15% Mmax) TMS-TMEPs were elicited. During the 10-min contraction, VM EMG was maintained (P = 0.39), whereas force decreased by 52% (SD 13%) (P < 0.001). TMEP area remained unchanged (P = 0.9), whereas large TMS-TMEPs decreased by 49% (SD 28%) (P = 0.001) and small TMS-TMEPs by 71% (SD 22%) (P < 0.001). This decline was greater for small TMS-TMEPs (P = 0.019; n = 9). Therefore, without the influence of descending drive, quadriceps TMS-TMEPs decreased during fatigue. The greater reduction for smaller responses, which tested motoneurons that were most active during the contraction, suggests a mechanism related to repetitive activity contributes to reduced quadriceps motoneuron excitability during fatigue. By contrast, the unchanged TMEP suggests that ongoing drive compensates for altered motoneuron excitability. NEW & NOTEWORTHY We provide evidence tha...
Kennedy, DS, McNeil, CJ, Gandevia, SC & Taylor, JL 2016, 'Effects of fatigue on corticospinal excitability of the human knee extensors', EXPERIMENTAL PHYSIOLOGY, vol. 101, no. 12, pp. 1552-1564.View/Download from: Publisher's site
Kennedy, DS, Fitzpatrick, SC, Gandevia, SC & Taylor, JL 2015, 'Fatigue-related firing of muscle nociceptors reduces voluntary activation of ipsilateral but not contralateral lower limb muscles', JOURNAL OF APPLIED PHYSIOLOGY, vol. 118, no. 4, pp. 408-418.View/Download from: Publisher's site
Siegler, JC, Marshall, P, Pouslen, MK, Nielsen, N-PB, Kennedy, D & Green, S 2015, 'The effect of pH on fatigue during submaximal isometric contractions of the human calf muscle', EUROPEAN JOURNAL OF APPLIED PHYSIOLOGY, vol. 115, no. 3, pp. 565-577.View/Download from: Publisher's site
Kennedy, DS, McNeil, CJ, Gandevia, SC & Taylor, JL 2014, 'Fatigue-related firing of distal muscle nociceptors reduces voluntary activation of proximal muscles of the same limb', JOURNAL OF APPLIED PHYSIOLOGY, vol. 116, no. 4, pp. 385-394.View/Download from: Publisher's site
Robergs, RA & Kennedy, D 2011, 'Metabolic acidosis and fatigue: Where to from here?' in Regulation of Fatigue in Exercise, pp. 41-61.
For the last 35 years the central focus of acidosis has been on lactic acid or lactate as being the cause of acidosis and acidosis being the cause of fatigue during intense exercise. Unfortunately, causation has been implied from correlation. The organic chemistry of the lactate dehydrogenase reaction clearly demonstrates the error of the development of metabolic acidosis from lactate production. This is not to detract from the significant development of acidosis during intense exercise. However, the assumed negative effect of acidosis on contractile failure is also called into question. The purpose of this review and commentary is to reflect on past research that has investigated the role of acidosis in fatigue, provide extensive evidence from the record of prior and current 31P MRS research on muscle acidosis during exercise and recovery and provide further insight into proton balance during muscle energy catabolism based on computations of multiple competing cation and pH-dependent proton stoichiometry. Finally, we suggest the role of acidosis in fatigue may have a greater effect outside of the cell. © 2011 by Nova Science Publishers, Inc. All rights reserved.
Fisher, G, Kennedy, D, Quel De Oliveira, C & Gandevia, S 2019, 'Proprioception in unilateral neglect after stroke – A systematic review', Smart Strokes 2019, Hunter Valley NSW Australia.
McNeil, CJ, Kennedy, DS, Butler, JE, Gandevia, SC & Taylor, JL 2013, 'The responsiveness of knee extensor motoneurons to different fatigue tasks in humans', Neuroscience, San Diego CA.
Neuroscience Research Australia
University of Montreal
University of Manchester