Cedric Lamboley

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.