Rechnitzer Lecture
Eleventh Annual Peter A. Rechnitzer Lecture
Age, Exercise and Adaptation: The Mitochondria Link
KE Conley,
PhD
Professor of Physiology and Biophysics
in the Muscle
Metabolism & Systems Biology Laboratory,
Department
of Radiology, University of Washington Medical Center.
Monday May 16, 2005
4:00PM
Rm 35 South Valley Building
KE Conley, PhD
Professor of Physiology and Biophysics
in the Muscle Metabolism & Systems Biology Laboratory,
Department of Radiology, University of Washington Medical Center.
Dr Conley is currently Professor of Physiology and Biophysics in the Muscle Metabolism & Systems Biology Laboratory, Department of Radiology, University of Washington Medical Center. Dr. Conley’s research group examines the relationship between muscle contractile properties and the metabolic organization within muscle across species, including humans. A recent research focus and the focus of this lecture titled “Age, Exercise and Adaptation: The Mitochondria Link” presents evidence to suggest that the age-related decline in performance and aerobic energy production is a result of age-associated changes occurring in the mitochondria that affect the efficiency of energy production and its effect on work and exercise performance in older adults. In addition, his research team is now examining how endurance exercise training can slow or improve exercise performance and the ability or efficiency of the mitochondria to provide energy for daily activity.
Lecture Abstract:
"Age, Exercise and Adaptation: The Mitochondria
Link”
Mitochondria are central to energy supply in muscle.
The mitochondrial theory of aging proposes that this
organelle is also at the center of aging processes
in the cell. My presentation will focus on how mitochondria
link aging, loss of muscle performance and improvement
of function with exercise training. Our new data point
to mitochondrial dysfunction – specifically,
the energetic uncoupling of ATP supply from O2 uptake – as
a critical factor in the loss of aerobic muscle function
in elderly humans. This insight was made possible by
innovative optical and magnetic resonance spectroscopic
methods that non-invasively measure energy coupling
(ATP/O2) in vivo. We also found reduced exercise efficiency – the
uncoupling of work per VO2 – in these elderly
subjects that paralleled the mitochondrial dysfunction.
We present evidence that the reduced exercise efficiency
likely reflects mitochondrial uncoupling rather than
a shift of fiber type properties with age. Finally,
the link between mitochondria and adaptation is demonstrated
by results of an endurance training program. Trained
elderly subjects showed improved mitochondrial coupling
, greater exercise efficiency and no change in muscle
fiber type. Thus, mitochondria may be a key factor
in the loss of muscle performance with age but may
also be the key to the reversal of these functional
losses with training in elderly muscle. Top
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Don Paterson
Research Director
Candian Centre for Activity and Aging
Phone: 519.661.1606 x81606
Email: dpaterso@uwo.ca
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