Scott D. Zimmerman

The avian low score normal muscle weakness alters decorin expression and collagen crosslinking.

Extracellular matrix development of chicken pectoral muscle was examined in the Low Score Normal (LSN) genetic muscle weakness and compared to both normal and avian muscular dystrophy (MD). At 20 days of embryonic development significant elevations were noted in LSN total glycosaminoglycan concentration and decorin, while at 14 days, LSN glycosaminoglycan and decorin levels were indistinguishable from the controls. Levels of a large skeletal muscle chondroitin sulfate proteoglycan (M-CSPG) appear to be unaffected. Morphologically, at 20 days, the extracellular matrix space between muscle fibers increased to a level characteristic to that observed in avian muscular dystrophy. At six weeks posthatch a marked increase in LSN collagen crosslinking relative to MD or control tissues was observed, while collagen concentration was not altered. By one year posthatch LSN collagen crosslink levels did not significantly differ from normal tissue. These data support the concept that the LSN muscle weakness is associated with changes in both proteoglycan and collagen characteristics.

Exercise training post-MI favorably modifies heart extracellular matrix in the rat.

PURPOSE In order to assess the effect of daily exercise on extracellular matrix remodeling in the heart after myocardial infarction (MI), we measured collagen concentration (%COL) and nonreducible collagen cross-linking (hydroxylysylpyridinoline, HP) in the right ventricle (RV), and regionally within the infarcted (INF) and viable left ventricular free wall (LVF) and septum (LVS), using a rodent MI training model. METHODS Infarcts (19%-24% of LV) were surgically induced in adult rats that were assigned to either trained (MI-TR) or sedentary (MI-SED) groups and compared to sham-surgery sedentary controls (SHAM). RESULTS In LVF, 10 wk of treadmill running had no effect on the increase (P < 0.001) in %COL seen with MI (MI-SED = 7.14% ± 0.15%, MI-TR = 7.61% ± 0.19%, SHAM = 3.55% ± 0.19%). However, it normalized the increase (P < 0.05) in HP cross-linking (MI-SED = 0.43 ± 0.02, MI-TR = 0.27 ± 0.03, SHAM = 0.30 ± 0.04 mol HP·mol(-1) collagen). The INF scar in MI-SED rats showed a sevenfold increase in %COL (P < 0.001) compared to SHAM LVF myocardium, an increase that was attenuated by training (MI-SED = 26% ± 1% vs MI-TR = 21% ± 2%; P < 0.05). However, training had no effect on MI-induced increases in cross-linking in the INF scar (1.01 ± 0.22 vs 0.84 ± 0.14 mol HP·mol(-1) collagen). In LVS, although a small but significant increase in %COL was seen in both MI groups, HP cross-linking was unaltered compared to SHAM rats. Training also normalized the increase observed in cross-linking in RV after MI. CONCLUSIONS Because increased HP cross-linking in the heart is associated with decreased chamber compliance, these findings may help to explain the improved heart function seen after daily exercise in cardiac rehabilitation patients.