About Professor David Allen
Understanding how muscle contracts has been a career-long aim. Diseases of muscle are a more recent development.
David Allen analyses heart and skeletal muscle function in both health and disease. His main focus is on the regulation and functional effects of intracellular calcium, sodium and pH.
Professor David Allen trained in Physiology and Medicine at University College in London. His PhD was on the contractility of cardiac muscle. He spent two years as a post-doc at the Mayo Clinic, Minnesota where he made the first ever measurements of intracellular calcium in the heart (1976-77). These studies established that changes in the intracellular Ca2+ were the principal means for regulating cardiac contractility. Later this approach was used to study how drugs, muscle length, pH, hypoxia and ischaemia affected cardiac function. In 1989 he was appointed to the Chair of Physiology at the University of Sydney. At Sydney he helped to develop the single isolated mouse muscle fibre as a model for studying muscle fatigue. An influential finding was that lactic acid was not the cause of muscle fatigue, instead Ca2+ transients failed after a few minutes causing reduced force by mechanisms which are still the focus of research. His laboratory also studies pacemaker mechanism and showed that changes in calcium release contributed to the pacemaker mechanisms. In recent years muscle damage caused by stretch and muscular dystrophy have become a new focus of interest. A key finding was that a stretch-activated channel is a major source of Ca2+ influx and, if blocked, the muscle pathology of muscular dystrophy is substantially improved. A current focus is to understand how these mechanosensitive Ca2+ channels are activated and why absence of dystrophin leads to the range of pathologies observed in dystrophic muscle.