The influence of exercise training on collagen accretion and mature crosslinking were assessed in viable left ventricle free wall (LVFW) and skeletal muscle of infarcted rats. Infarcts (11% of heart weight) were surgically induced in two groups of 4 mo-old rats (sedentary and exercise trained). The exercise trained group performed 10 wk of treadmill running (6× 60 min per wk). Treadmill speed was increased from 10 m·min-1 to 22 m·min-1 over the 10 wk program. Rats were sacrificed at 8 mo of age, heart and soleus muscle were excised, and entire left ventricle dissected from the rest of the myocardium and separated into the LVFW and scar. LVFW and soleus muscle were analyzed for concentrations of collagen ([coll]) and the nonreducible collagen crosslink hydroxylysylpyridinoline ([HP]). Maximal treadmill running speeds were significantly greater (p≤0.05) in the trained rats (40.5±14.2 m·min-1) as compared to the sedentary group (25.4±3.7 m·min-1). [Coll] was unaltered by training in either the LVFW or soleus muscle. [HP] decreased significantly (p≤0.05) in both the LVFW(0.29±0.03 vs 0.41±0.02 mol HP·mol collagen-1) and soleus (0.32±0.03 vs 0.52±0.07 mol HP·mol collagen-1) with training. These results mirror those seen for normal animals exposed to exercise training. Furthermore, exercise training seems to normalize crosslinking values in infarcted LVFW to those seen in in young healthy hearts. Attenuated collagen crosslinking associated with exercise training in infarcted myocardium and corresponding soleus muscle may have resulted from accretion of less mature collagen due to increased turnover. Diminished crosslinking in both heart and soleus muscle imply reduced stiffness and may account for improved heart function and exercise capacity noted in trained humans and animals post-infarction.
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