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Articles in PresS, published online ahead of print May 24, 2002
J Appl Physiol, 10.1152/jap.00231.2002
Submitted on March 18, 2002
Accepted on May 17, 2002
1 Department of Physiology and Biomedical Engineering, Norwegian University of Science and Technology, Trondheim, Norway
2 Department of Physiology and Biomedical Engineering, Norwegian University of Science and Technology, Trondheim, Norway; Department of Cardiology, St. Olavs Hospital HF, Trondheim, Norway
* To whom correspondence should be addressed. E-mail: ole.kemi{at}medisin.ntnu.no.
Whereas novel pathways of pathological heart enlargement have been unveiled by thoracic aorta constriction in genetically modified mice, the molecular mechanisms of adaptive cardiac hypertrophy remain virtually unexplored, and call for an effective and well-characterized model of physiological mechanical loading. Experimental procedures of maximal oxygen consumption (VO2max) and intensity-controlled treadmill running were established in 40 female and 36 male C57BL/6J mice. An inclination-dependent VO2max with 0.98 test-retest correlation was found at 25°-treadmill grade. Two-hour daily interval running, 5 days.week-1, with 8-minutes at 85-90% of VO2max and 2-minutes at 50% (adjusted to weekly VO2max-testing) increased VO2max to a plateau 49% above sedentary females and 29% in males. Running economy improved in both genders, and echocardiography indicated significantly increased left ventricle posterior wall thickness. Ventricular weights increased 19-29% and 12-17% in females and males, whereas cardiomyocyte dimensions increased 20-32%, and 17-23% in females and males; skeletal muscle mass increased by 12-18%. Thus, the model mimics human responses to exercise, and can be used in future studies of molecular mechanisms underlying these adaptations.
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