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1 Department of Physiology and Biomedical Engineering, Norwegian University of Science and Technology, N-7489 Trondheim; and 2 Department of Cardiology, St. Olavs Hospital HF, N-7006 Trondheim, Norway
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
(
O2 max) and intensity-controlled treadmill running were established in 40 female and 36 male C57BL/6J mice. An inclination-dependent
O2 max
with 0.98 test-retest correlation was found at 25° treadmill grade.
Running for 2 h/day, 5 days/wk, in intervals of 8 min at 85-90%
of
O2 max and 2 min at 50% (adjusted
to weekly
O2 max testing) increased
O2 max to a plateau 49% above
sedentary females and 29% in males. Running economy improved in both
sexes, and echocardiography indicated significantly increased left
ventricle posterior wall thickness. Ventricular weights
increased by 19-29 and 12-17% in females and males,
respectively, whereas cardiomyocyte dimensions increased by 20-32,
and 17-23% in females and males, respectively; 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.
maximal oxygen uptake; work economy; respiratory exchange ratio; cardiomyocyte; allometric scaling
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