Five myofibrillar lesion types in eccentrically challenged, unloaded rat adductor longus muscle - A test model

Sarcomere disruptions are observed in the adductor longus (AL) muscles foll owing voluntary reloading of spaceflown and hindlimb suspension unloaded (H SU) rat, which resemble lesions in eccentrically challenged muscle. We devi sed and tested an eccentric contraction (ECCON) test system for the 14-day HSU rat AL. Six to 7 hours following ECCON, ALs were fixed to allow immunos taining and electron microscopy (EM). Toluidine blue-stained histology semi thin sections were screened for lesion density (#/mm(2)). Serial semithin s ections from the ECCON group were characterized for myosin immunointensity of lesions. Five myofibrillar lesion types were identified in histological semithin sections: focal contractions; wide A-bands; opaque areas; missing A-bands; and hyperstretched sarcomeres. Lesion density by type was greater for ECCON than NonECCON ALs (P less than or equal to 0.05; focal contractio ns and opaque regions). Lesion density (#-of-all-five-types/mm(2)) was sign ificantly different (ECCON: 23.91 +/- 10.58 vs. NonECCON: 5.48 +/- 1.28, P less than or equal to 0.05; ECCON vs. SHAM: 0.00 +/- 0.00; P less than or e qual to 0.025). PostECCON optimal tension decreased (Poi-drop, 17.84 +/- 4. 22%) and was correlated to lesion density (R-2 = 0.596), but prestretch ten sion demonstrated the highest correlation with lesion density (R-2 = 0.994) . In lesions, the darkly staining A-band lost the normally organized thick filament alignment to differing degrees across the different lesion types. Ranking the five lesion types by a measure of lesion length deformation (hy percontracted to hyperstretched) at the light microscopy level, related to the severity of thick filament registry loss across the lesion types at the electron microscopic level. This ranking suggested that the five lesion ty pes seen in semithin sections at the light level represented a lesion progr ession sequence and paralleled myosin immunostaining loss as the distorted A-band filaments spread across the hyperlengthening lesion types. Lesion ul trastructure indicated damage involved calcium homeostasis loss (focal cont raction lesions) and "thick-filament-centering" failure of titin (wide A-ba nd lesions) in the early stages of lesion development. Anat Rec 254:39-52, 1999. (C) 1999 Wiley-Liss, Inc.