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Dr Cedric Lamboley

Postdoctoral Research Fellow

School of Biomedical Sciences
Faculty of Medicine
c.lamboley@uq.edu.au

Overview

A life-long fascination in sciences provided me with the inspiration to graduate in exercise physiology (University of Sherbrooke, Canada, 2004), complete a PhD in physiology/biophysics (University of Sherbrooke, 2009) and continue in my current role as a postdoctoral researcher at the School of Biomedical Sciences (SBMS) of The University of Queensland. I am a physiologist first and foremost with a particular interest in understanding how skeletal muscle cell normally functions so as to try and elucidate what changes or factors contribute to various forms of muscle weakness with ageing, inactivity or various chronic diseases.

During my previous postdoctoral appointment at La Trobe University (Melbourne, 2010-2017), I have gained considerable experience using the "mechanically skinned muscle fibre" technique in animal muscle. Importantly, I have developed this technique for the first time in human muscle which allows the exciting opportunity to investigate cellular mechanisms of muscle weakness in different clinical population. This is vitally important since most of our existing knowledge on muscle function comes from studies on muscles obtained from animal models. This technical breakthrough has been recognized by editorials of different leading scientific journals in the field of Physiology. I’m now a world recognized expert of this technique which has immense potential for examining any number of physiological questions and even allows for biochemical analyses of any protein of interest in the same cell.

Research Interests

  • Skeletal muscle weakness with ageing and inactivity
    This research interest is central to any understanding of the mechanism(s) underlying abnormalities in protein expression and oxidation-induced dysfunction responsible for marked muscle weakness and fatigability occurring during ageing or inactivity. The aims of this study is to identify the specific mechanism and target protein responsible for the loss of muscle force in these populations. This is the first study to comprehensively investigate the effects of ageing and inactivity on the physiological and biochemical changes in human skeletal muscle at the single muscle cell level. Protecting muscle from exacerbated levels of oxidative stress represents a critical therapeutic approach to improve muscle function and quality of life of aged and inactive persons until a cure is developed. The identification in these populations of the precise molecular site and mechanisms involved in oxidative damage would be highly significant and make it realistic to design drugs to bind and protect this molecular site, and thereby aid muscle performance in disease states.
  • Ryanodine receptor mutations and skeletal muscle weakness
    Ryanodine receptors (RyR) are the Ca2+ release channels of skeletal muscle fibres that regulate muscle contraction. There are many known mutations in the RyR that can affect the function of this channel. In the event of mutated RyRs the outcome for an individual can be no obvious effect on muscle strength, or mild, through to very severe and life-shortening myopathy. As the severity of the mutation increases, so does the weakness of the muscle. The aim of this project is to apply the latest techniques established in our lab to assess how calcium moves in muscle with these mutations to find targets to improve muscle strength in this disease.

Research Impacts

My current postdoctoral research project within Brad Launikonis’ lab utilizes my unique abilities to perform comprehensive physiological examinations (skinned muscle fibre technique coupled with confocal microscopy) on single segments of individual fresh muscle cells, obtained from animal models or muscle biopsies of human subjects. No other research group other than ours is able to produce such results to date. This new and exciting development will open up enormous potential applications in physiotherapy, human physiology, understanding muscle fatigue and adaptability, as well as uncovering basic muscle defects in disease in humans.

I have made several important contributions to the field of human muscle physiology. Most notably, my research helped to debunk the commonly held misconception that the deficit in Ca2+ release from the sarcoplasmic reticulum (SR) observed in aged skeletal muscle was induced by a reduction in the number of voltage sensors coupled with the adjacent Ca2+ release channels (RyRs) (excitation-contraction uncoupling). Instead, my recent results demonstrated for the first time that there is an increased leakage of Ca2+ out of the SR through the RyRs in type I muscle fibres in aged humans as a result of the oxidative modification of the RyRs. This Ca2+ leakage is probably the primary cause of the decreased available SR Ca2+ content seen in such fibres and is a major contributing factor involved in muscle atrophy and weakness with ageing (Lamboley et al., J. Physiol. 2015, 2016). Such SR Ca2+ leakage and depletion in human fibres may arise from a self-reinforcing cycle in which Ca2+ leakage through the RyRs leads to increased reactive oxygen species production by the mitochondria, which in turn further exacerbates RyR leakage.

Qualifications

  • Doctor of Philosophy, Université de Sherbrooke

Publications

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Supervision

  • RyR1 Myopathy: A model of hypermetabolism

    Master Philosophy

  • Calcium handling in muscle: sarcoplasmic reticulum and mitochondria interplay

    Doctor Philosophy

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Publications

Journal Article

Conference Publication

PhD and MPhil Supervision

Note for students: Dr Cedric Lamboley is not currently available to take on new students.

Current Supervision

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Links

ResearcherID: H-7622-2018

ORCID: 0000-0002-4008-4929

Scopus ID: 16401935100

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