Treadmill exercise prevents reduction of bone mineral density after myocardial infarction in apolipoprotein E-deficient mice

Abstract

Aims Recent clinical studies demonstrated the association between myocardial infarction (MI) and osteoporotic fractures. We examined whether MI causes bone loss and the effects of exercise training on bone in mice after MI. Methods We created a MI model in 16-week-old male apolipoprotein E-deficient mice ( n = 42), which were randomly assigned to exercise group (MI-Ex) and sedentary group (MI-Sed). We also performed sham operations in other mice ( n = 10). Treadmill exercise training was performed from one week after operation to eight weeks. At eight weeks, the bone parameters of the femur were measured by quantitative computed tomography, followed by histological analysis ( n = 10–17). Results Bone mineral density (BMD) of the femur was significantly decreased in the MI-Sed group as compared with the sham group ( P < 0.001), whereas the BMD was significantly increased in the MI-Ex group as compared with the MI-Sed group ( P < 0.05). In histological analysis, Rho-associated coiled-coil kinase 2 and tartrate-resistant acid phosphate positive (bone resorptive) area in distal femur were significantly increased in the MI-Sed group as compared with the sham group ( P < 0.05), whereas those parameters were significantly decreased in the MI-Ex group as compared with the MI-Sed group ( P < 0.05). In contrast, alkaline phosphatase (ALP)-positive (bone-forming) area was significantly decreased in the MI-Sed group as compared with the sham group ( P < 0.05), whereas ALP-positive area was significantly increased in the MI-Ex group as compared with the MI-Sed group ( P < 0.05). Conclusions The present study demonstrates that MI reduces BMD and treadmill exercise training prevents the reduction of BMD in apolipoprotein E-deficient mice.