Allen’s early work culminated in the demonstration that intracellular calcium was the central regulator of activation in the heart. From these fundamental findings, Allen elucidated the role of calcium in the cardiac length-tension relation, unravelled the role of calcium in cardiac ischaemia and identified a new pacemaker current that regulates the heart rate. These studies have become part of the mainstream of cardiac physiology and have been extensively utilised by the pharmaceutical industry in the design of drugs to increase cardiac output and to ameliorate the effects of ischaemia. In parallel studies of skeletal muscle, Allen established that muscle fatigue is primarily caused by failure of intracellular calcium release and the work has contributed to the demise of the lactic acid theory of fatigue. Most recently Allen has discovered that the muscle damage is a consequence of calcium entry through a stretch-activated channel. In a major development with possible therapeutic implications, he has shown that this channel is also important in muscular dystrophy and drugs that block this channel are able to reduce muscle damage.