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Exercise and Isoproterenol‐Induced Cardiac Hypertrophy in Aged Mice
Author(s) -
Luckey Stephen,
McLaughlin Nathan,
Soo Sherilynn
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.1239.5
Subject(s) - ventricle , medicine , muscle hypertrophy , heart failure , cardiology , heart rate , cardiac hypertrophy , stimulation , cardiac function curve , pathological , body weight , endocrinology , blood pressure
Approximately half of the people with heart failure are older than 75 year of age. Despite this statistic, and the fact that the aged heart undergoes changes that impact its structure and function, the vast majority of heart failure research is conducted using young animal models. Therefore, the objective of this study was to investigate how age‐related changes affect the ability of the heart to adapt to physiological (e.g. exercise) and pathological (e.g. heart failure induced by beta adrenergic stimulation) stimuli. CB6F1 male mice at 22 months of age were used for this investigation. Mice were divided into four groups: sedentary, voluntary exercise, vehicle, and isoproterenol. We assessed exercise capacity and found that these mice voluntarily ran on a cage wheel and, on average, ran 2.4 ± 0.3 km and spent 2.9 ± 0.4 hours per day on the wheel. Wheel running speed was 0.8 ± 0.1 km/hr when averaged over the 3‐week period. Although mice had a slight, but insignificant increase in heart weight‐to‐tibial length ratio (HW/TL), exercise induced a 13% increase in left ventricle‐to‐tibial length ratio (LV/TL). Mini‐osmotic pumps delivered vehicle or isoproterenol (30mg/kg/day) for 14 days. Isoproterenol treatment resulted in a 10% and 13% increase in HW/TL ratio and LV/TL ratio, respectively. In conclusion, these investigations suggest that the aged left ventricle has the ability to undergo cardiac hypertrophy following physiological or pathological stimuli. We are currently investigating the underlying molecular and cellular mechanisms that play a role in the observed cardiac adaptations. Support or Funding Information M.J. Murdock Charitable Trust (S.W.L.)