Justin Kavanagh

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Associate Professor

Griffith University

Australia

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Dr. Justin Kavanagh is an Associate Professor at Griffith University, Australia. His research focuses on motor unit physiology, muscle activation, and the effects of hypoxia and serotonin on motoneurone excitability. Recent publications explore topics such as motor unit discharge rates in conditions like multiple sclerosis and the impact of cold-water immersion on neural circuits.

Recent Grants

Grant: Close

Is there an underlying neuromotor mechanism behind the development of sarcopenia in older adults?

Open Date: 2017-05-01

Close Date: 2019-05-01

Grant: Close

Competencies and Assessment tools for independent clinical measurements scientist practice in Queensland Health

Open Date: 2014-03-01

Close Date: 2016-03-01

Grant: Close

Can Resistance Training Improve Manual Dexterity, Postural and Force Tremor in Essential Tremor Patients? A Randomised Controlled Trial.

Open Date: 2012-06-01

Close Date: 2014-06-01

Grant: Close

Dynamic postural stability and falls prediction in older people during walking in real-world environments.

Open Date: 2007-01-01

Close Date: 2009-01-01

Articles (17)

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2025

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2022

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2022

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2022

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2022

Collaborators (6)

Benjamin Goodlich

Lecturer

University of the Sunshine Coast

AUSTRALIA

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Janet Taylor

Professor of Human Neurophysiology

Edith Cowan University

AUSTRALIA

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Surendran Sabapathy

Senior Lecturer / Researcher

Griffith University - Gold Coast Campus

AUSTRALIA

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Alessandro Del Vecchio

GERMANY

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Leanne Bisset

AUSTRALIA

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Tyler Henderson

Charles Darwin University

AUSTRALIA

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Justin Kavanagh

Research Interests

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About

Recent Grants

Articles (17)

5‐HT2 antagonism indirectly increases motor unit discharge rate and cervicomedullary motor evoked potential amplitude during submaximal elbow flexions

Motor unit discharge and torque steadiness are reduced in people with multiple sclerosis when performing voluntary muscle contractions

Short‐latency afferent inhibition is reduced with cold‐water immersion of a limb and remains reduced after removal from the cold stimulus

Oxygen deprivation is a muscle revelation: hypoxia enhances motor unit firing after spinal cord injury

Antagonism of 5‐HT2 receptors attenuates self‐sustained firing of human motor units

Excitatory drive to spinal motoneurones is necessary for serotonin to modulate motoneurone excitability via 5‐HT2 receptors in humans

The severity of acute hypoxaemia determines distinct changes in intracortical and spinal neural circuits

Motor unit tracking using blind source separation filters and waveform cross-correlations: reliability under physiological and pharmacological conditions

Muscarinic acetylcholine activity modulates cortical silent period, but not motor evoked potentials, during muscle contractions

Blockade of 5‐HT2 receptors suppresses motor unit firing and estimates of persistent inward currents during voluntary muscle contraction in humans

Voluntary muscle activation in people with multiple sclerosis is reduced across a wide range of forces following maximal effort-fatiguing contractions

Voluntary activation of muscle in humans: does serotonergic neuromodulation matter?

5‐HT2 receptor antagonism reduces human motoneuron output to antidromic activation but not to stimulation of corticospinal axons

People with multiple sclerosis have reduced TMS-evoked motor cortical output compared with healthy individuals during fatiguing submaximal contractions

Enhanced availability of serotonin limits muscle activation during high-intensity, but not low-intensity, fatiguing contractions

Post‐fatigue ability to activate muscle is compromised across a wide range of torques during acute hypoxic exposure

Blockade of 5-HT2 receptors suppresses rate of torque development and motor unit discharge rate during rapid contractions

Collaborators (6)

Benjamin Goodlich

Janet Taylor

Surendran Sabapathy

Alessandro Del Vecchio

Leanne Bisset

Tyler Henderson

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