Damage to the turkey pectoralis major muscle was studied in a randombred control line (RBC2), a subline (F) from the RBC2 line selected long-term for increased 16-wk BW only, and a commercial sire line (B) at 25 d of incubation and at 1, 4, 8, 16, and 20 wk posthatch. Pectoralis major muscle samples were obtained from three females and three males from each line in a manner to avoid contraction. After being fixed and sectioned, the muscle samples were stained with hematoxylin and eosin to view muscle fiber and muscle fiber bundle morphology. Beginning at 8 wk posthatch, differences in muscle fiber morphology were observed among the different lines. The RBC2 line throughout the duration of the study maintained well-organized muscle fibers and muscle fiber bundles with large capillary networks. In contrast, the growth-selected F line began to show muscle fiber degeneration at 8 wk posthatch, and limited capillary beds were observed as development proceeded. The B line had intermediate muscle morphology between the RBC2 and F lines, but by 20 wk posthatch significant muscle fiber degeneration was present with limited capillary supply. The degenerative muscle fiber changes were predominant in the growth-selected F-line, suggesting that growth selection for just BW may be associated with posthatch muscle damage.

The inheritance of, and effect of selection for increased BW on, measurements of muscle fibers and extracellular space in turkeys were studied using a randombred control line (RBC2), a subline (F) of RBC2 selected long-term only for increased 16 wk BW, a commercial sire line (B), and reciprocal crosses of the F and B lines. Measures of additive genetic variation were obtained by comparing all of the pure lines or just the large-bodied F and B lines. Estimates of nonadditive genetic variation were obtained by contrasting the average of the reciprocal crosses with the average of the parental lines. A contrast of the reciprocal crosses provided estimates of sex linkage or maternal effects. Samples of pectoralis major muscle were obtained from three males and three females of each genetic group at 1, 4, 8, and 16 wk of age in a manner to avoid muscle contraction. After fixing and cross sectioning, the muscle samples were stained with hematoxylin and eosin to view muscle morphology. The stained sections were analyzed for muscle fiber width, muscle fiber bundle width (except at 16 wk of age), number of fibers within a 136-microm2 area, and extracellular matrix perimysial (PW) and endomysial (EW) width. Additive genetic variation, as measured by line differences, of measures of muscle fibers and extracellular matrix was a more important source of variation when the RBC2 line was included in the comparison. When all of the pure lines were compared, line differences were significant for fiber bundle width at 4 wk of age; individual fiber width and number of fibers in a given area at 4, 8, and 16 wk of age; PW at all ages; and EW at 1, 8, and 16 wk of age. With the possible exception of PW, nonadditive genetic variation was not an important source of variation for muscle measurements. For PW, the estimates of heterosis were -14.6, 26.4, 14.5, and 17.3% at 1, 4, 8, and 16 wk of age, respectively, but none of the values was significant (P > 0.05). Genetic increases in BW were associated with an increase in muscle fiber width, a smaller number of fibers in a given area, and less extracellular space at older ages. Apparent differences in growth patterns among the genetic groups may have been responsible for the different patterns of change in muscle measurements in the various genetic groups over ages.

Muscle development at 20 and 25 d of incubation was studied in a randombred control line (RBC2), a subline (F) of RBC2 selected only for increased 16-wk BW, a commercial sire line (B), and reciprocal crosses of the F and B lines. Muscle samples from three males and three females of each genetic group were collected in such a manner to avoid contraction. After fixing, the muscles were stained with hematoxylin and eosin, measurements of muscle fiber width, muscle fiber bundle length and width, number of fibers within a 15.6 microm2 area, and extracellular matrix perimysial (PW) and endomysial (EW) width were taken with an Olympus XI 70 microscope equipped with an Olympus Magna Fire digital camera linked to Image Pro software. From each slide, 20 measurements were taken for each characteristic analyzed. In most of the muscle traits measured, additive genetic variation, as indicated by line differences, occurred when the RBC2 line was included in the comparison of pure lines. However, when only the B and F lines were compared, line differences were less frequent. In comparisons of the B and F lines and their reciprocal crosses, heterosis, as measured by contrasts of the average of the pure lines and the average of the reciprocal crosses, was an important source of variation for individual fiber measurements (negative) and extracellular space (positive) at 20 d of incubation but was less important at 25 d of incubation. No significant interactions between genetic group and sex were noted at 20 d of incubation, but such interactions were frequent at 25 d of incubation. These results suggest that muscle organizational differences between the two sexes begin to occur between these two ages and are not the same for different genetic groups.

The avian Low Score Normal (LSN) genetic muscle weakness is phenotypically characterized by a reduction in the ability of the birds to right themselves from a supine position. Compared to normal skeletal muscle, LSN muscle has normal myosin isoform switching and cell-cell recognition, elevated glycosaminoglycan and decorin levels at embryonic Day 20, and a large increase in collagen crosslinking at 6 wk posthatch. To begin to determine the biological mechanism involved in the elevated decorin protein concentration at embryonic Day 20, the steady-state levels of transcripts encoding both decorin and collagen Type I at embryonic Days 14, 19, and 20, and at 1 d and 6 wk posthatch were measured. On embryonic Day 20, collagen Type I transcripts were not different from the control but there was a significant elevation in decorin transcript levels. At 1 d and 6 wk posthatch, transcript levels of decorin and collagen Type I were not different between LSN and controls. The change in decorin transcript steady-state levels is limited to late embryonic development and suggests an alteration in a signal transduction pathway regulating decorin transcription.