Dr Al Benson

Profile

• BSc (Hons) Sports Science (2000-2003)
• PhD Computational Biology (2003-2006)
• Research Fellow (2006-2008)
• MRC Special Training Fellowship in Biomedical Informatics (2008-2011)
• BBSRC Research Fellow (2011-2013)
• Lecturer in Cardiovascular Science (2013-2021)
• Associate Professor in Systems Physiology (2021)

Responsibilities

• Director of Research and Innovation, School of Biomedical Sciences

Research interests

Computational modelling of cardiovascular physiology

I run the Leeds Systems Physiology Laboratory along with Dr Michael Colman, within the Cardiovascular and Exercise Sciences group. My research interests are in the use of computational models to study cardiovascular physiology in health and disease. Computational models allow us to examine the intricately integrated (and therefore non-intuitive) relationships that exist between the different components of complex physiological systems. A particular focus of my research has been the study of cardiac arrhythmias and exercise intolerance in heart failure.

Cardiac arrhythmias: Cardiac arrhythmias are a major cause of mortality and morbidity. Ventricular fibrillation is an often fatal arrhythmia in which the heart’s normal rhythm is disturbed when multiple electrical wavefronts continually re-excite the same tissue (re-entry); synchronous contraction of the ventricles is lost, circulation of the blood ceases and death occurs. Using magnetic resonance imaging, optical mapping and other experimental data, we develop biophysically-detailed computational models of the heart at the sub-cellular, cellular, tissue and organ levels. We use these models to examine the roles that structural (anatomical) and functional (electrophysiological and mechanical) changes seen with ageing, diseases and with certain drugs have on the initiation, maintenance and termination of cardiac arrhythmias such as ventricular fibrillation.

Exercise intolerance: The ability to initiate and sustain exercise is a key determinant of health, quality of life, and mortality. Exercise intolerance contributes to a downward spiral of inactivity, which is an “actual cause” of chronic disease, and is a hallmark of heart failure. However, the mechanisms underlying exercise intolerance remain poorly understood. We use experimental data – obtained using cardiopulmonary exercise testing, near-infrared spectroscopy, magnetic resonance spectroscopy and other techniques – to develop novel computational models describing how the pulmonary, circulatory and muscular systems integrate to effectively transport and utilise oxygen during exercise. These models help us understand how systems dynamics produce the rapid oxygen uptake (VO2) kinetics that are a major determinant of exercise tolerance, and thereby contribute to improving exercise performance, health, quality of life, and longevity.

• Remodelling of structure-function relationships underlying cardiac dysfunction in ageing and heart failure: A multi-scale systems approach

Qualifications

• BSc (Hons) Sports Science
• PhD Computational Biology

Student education

I manage the Faculty’s Cardiorespiratory Physiology modules that include options to study Exercise Rehabilitation and Cardiorespiratory Pharmacology. I run the Leeds Systems Physiology Laboratory along with Dr Michael Colman, within the Cardiovascular and Exercise Sciences group; our research-led teaching includes an introductory course on Computational Modelling in the Biomedical Sciences.

Research groups and institutes

• Cardiovascular
• Sport and Exercise Sciences