Philippe Lopes

Toxicologie, Pharmacologie et Signalisation céllulaire - UMR-S 1124
Université Paris Descartes
45 rue des Saints Pères
75270 Paris Cedex 06

Fax : +33 (0) 1 42 86 38 68

Philippe LOPES

Lecturer
Degeneration and neuromuscular plasticity

philippe.lopes@-Code a retirer pour éviter le SPAM-parisdescartes.fr
+33 1 42 86 21 53, room H330

Philippe Lopes is an Associate Professor in Exercise Physiology at the University of Evry. He has worked for several years on the effects of exercise on the autonomic nervous system in elite sports subjects and in primary and secondary prevention of cardiovascular disease. More recently, he has focused his activity on the effects of exercise on the cardiovascular and autonomic nervous systems in neurodegenerative diseases including spinal muscular atrophy (SMA) and amyotrophic lateral scoliosis (ALS) within the Neuromuscular Degeneration and Plasticity team at Paris Descartes University. He is also the head of the Sport and Exercise Science Department at the University of Evry.

After graduating with a BA Honours degree in Sports and Exercise Science from the University of Ulster in Belfast, Philippe Lopes obtained his Ph.D. in Exercise Physiology from the same University (1988). His research examined the influence of respiratory frequency and tidal volume on cardiac rhythm as well as the relationships between coronary heart disease risk factors, physical activity and cardiac vagal tone. After several teaching and research positions at universities in Wales (University of Aberystwyth) and England (University of Brighton and East London), he returned to France in 2004 as an Associate Professor and joined Frederic Charbonnier’s Neuromuscular Degeneration and Plasticity team.

His activity has focused on the effects of exercise on the cardiovascular and autonomic nervous systems in neurodegenerative diseases including spinal muscular atrophy (SMA) and amyotrophic lateral scoliosis (ALS). Some of his work in association with Olivier Biondi has demonstrated severe cardiac defects in type 2 SMA-like mice including (1) a dramatic alteration of intrinsic cardiac conduction associated with bradycardia; (2) a severe cardiomyopathy associated with extensive ventricular fibrosis; and (3) a delay in cardiac muscle maturation associated with contractile protein expression defects. Interestingly, physical exercise provided many benefits, including the reduction of the cardiac protein expression defect, the reduction of fibrosis, the increase in cardiac electrical conduction velocity, and the drastic reduction in bradycardia and arrhythmias which resulted in the partial restoration of the cardiac function in SMA-like mice.

Recent Publications

Articles