Fifth Annual Peter A. Rechnitzer Lecture


SaltinBengt Saltin, M.D.

The Copenhagen Muscle Research Centre
August Krogh Institute
University of Copenhagen

Wednesday, May 12, 1999

Dr. Saltin graduated from the Medical School, Karolinska Institute (KI), Stockholm. He completed his thesis in physiology at KI. Dr. Saltin became a professor of applied physiology in the Department of Physiology III, KI, Stockholm. Then he became a professor of human physiology, August Krogh Institute, University of Copenhagen (UC). He became a professor of physiology in the Department of Physiology and Pharmacology, KI, Stockholm and then a professor of human physiology, August Krogh Institute. Now he is the Director of the Copenhagen Muscle Research Centre at Rigshospitalet and UC, founded by the Danish National Research Foundation. He is also an adjunct professor, August Krogh Institute (UC). He has received many major awards and has participated in several field expeditions (Nomadic Lapps, Mt. Evans, Mexico City, The Andes, The Himalayas and Kenya). He is the author of 250 original articles and reviews or chapters in books. He is the editor of several scientific books and texts for pre- and post-graduate students, including a textbook in physiology for medical students. He is the keynote speaker at the ALCOA National Forum on Active Living and Older Adults. This forum, hosted by the Canadian Centre for Activity and Aging, will be held at the University of Western Ontario, May 13 to 16th.


ABSTRACT: The energy turnover in skeletal muscle is a direct function of the work performed. Accordingly oxygen uptake and power are linearly related up to peak oxygen uptake of the muscle and the body. The signal interaction in this regulation in humans is slowly being unravelled. For one thing it appears as if oxygen delivery is the regulated variable as both at the systemic and at the local muscle level the delivery of oxygen is a close function of power output with variations in blood flow adjusting for variability in the arterial oxygen content. Moreover, it is indeed the arterial oxygen content rather than oxygen tension that is critical for this regulation. Lately, several hypotheses have been put forward as to how the haemoglobin molecule and its binding of O2 or NO could play a role in this regulation.

A special problem in humans with a low cardiac capacity in relation to muscle mass is that if a large fraction of the muscles is engaged in the exercise, all capillary beds in the active skeletal muscle cannot be fully vasodilated. Thus, at some stage there has to be an overriding control mechanism that causes vasocontriction in active limbs in order to maintain blood pressure. The sympathetic nervous system acting on the resistance vessels serves this role, but it is unclear by which mechanisms it is activated and how it overcomes the so-called "functional sympatolysis" that secures optimal vasodilation in small muscle group exercise.

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Don Paterson
Research Director

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