Physiological cardiac hypertrophy of exercise training is absent in mice deficient in adiponectin

Adiponectin is known to exert protective effects in the post‐ischemic myocardium; however, its role in physiological cardiac hypertrophy induced by exercise training remains unknown. We tested the hypothesis that adiponectin is necessary in exercise training‐induced physiological cardiac hypertrophy. Adult C57BL/6 wild‐type (WT) or homozygous adiponectin knockout (AdipoKO) mice were obtained at 10 wks of age and underwent treadmill exercise training (12 m/min, 5° incline, 1 hr/day, 5 days/wk for 8 wks) or remained sedentary in cages. At the beginning and end of the exercise training or cage confinement period, echocardiographic assessment of cardiac function was performed with the Vevo 2100 high‐resolution imaging system. M‐mode imaging was used to evaluate systolic and diastolic dimensions, posterior and anterior wall thickness, fractional shortening and ejection fraction. Pulsed‐wave doppler was used to measure early (E wave) and late (A wave) mitral valve inflow, and to calculate isovolumic relaxation time. In WT mice, exercise training increased left ventricular (LV) mass, and anterior and posterior wall thickness, without a change in chamber diameter. End‐systolic volume decreased with exercise training, contributing to increased ejection fraction. Fractional shortening also increased with exercise training in WT mice. In contrast, in WT and KO sedentary mice, LV mass and anterior and posterior wall thickness did not change over the 8‐wk period. In sedentary WT mice, chamber diameter did not change, but in sedentary Adipo KO mice, chamber diameter increased over 8 wks. In Adipo KO mice, 8 weeks of exercise training did not produce the adaptations that occurred in WT mice. As in sedentary KO mice, LV mass and anterior and posterior wall thickness did not change over the 8‐wk period of training. Ejection fraction and fractional shortening decreased and end‐systolic volume increased during the 8‐wk training period in Adipo Ko mice. Similar to sedentary Adipo KO mice, chamber diameter increased in exercise trained Adipo KO mice. These data indicate that the outward hypertrophy and increased systolic function that occurs with exercise training in young adult mice is absent in age‐matched adiponectin‐deficient mice. Thus, these results suggest that adiponectin is required for the physiological hypertrophy that is induced by exercise training in the healthy, adult heart. Support or Funding Information NIH R21 AG044858