Onset of spermatozoal degeneration in low-fertility Delaware roosters and test for autoimmune basis.

The objectives of this study were 1) to determine the onset of a heritable reproductive disorder in the rooster that is characterized by extensive spermatozoal degeneration within the ductus deferens, and 2) to determine if autoimmunity was associated with spermatozoal degeneration. Seventy-five percent of the affected roosters did not ejaculate large percentages of degenerate spermatozoa at 20 wk of age, approximately the age of sexual maturity. Rather, seminal quality gradually declined over the next 6 wk, as both ejaculate volume and number of spermatozoa ejaculated increased. The evaluation of testicular and excurrent duct tissues via immunofluorescence failed to reveal either IgY or IgA associated with spermatozoa. While histological examination revealed greater lymphocyte numbers (P less than .05) in the proximal ductus deferens, these cells were not associated with spermatozoa nor spermatozoal clumping. While spermatozoal degeneration tends to be latent at the onset of semen production, it does not appear to be due to spermatozoal autoimmunity.

Effects of glucose or fructose feeding on glycogen repletion in muscle and liver after exercise or fasting.

In athletics, muscle and liver glycogen content is critical to endurance. This study compared the effectiveness of glucose and fructose feeding on restoring glycogen content after glycogen was decreased by exercise (90-min swim) or fasting (24 h). After 2 h of recovery from either exercise or fasting there was no measurable glycogen repletion in red vastus lateralis muscle in response to fructose. In contrast, glucose feeding induced a similar and significant carbohydrate storage after both depletion treatments (8.44 mumol X g-1 X 2 h-1). In the liver, following 2 h of recovery, the rates of glycogen storage were similar after either glucose or fructose ingestion, but fasting caused a greater rate of repletion (83 mumol X g-1 X 2 h-1) than exercise (50 mumol X g-1 X 2 h-1). After 4 h of recovery fructose-fed exercised animals had the highest glycogen concentration (165 mumol X g-1) followed by the glucose-fed exercised group (119 mumol X g-1). These values were 50 and 36%, respectively, of that measured in the normal-fed liver (327 mumol X g-1). In contrast, liver glycogen values in the fasted group decreased between the 2nd and 4th hour of recovery in response to both feeding regimens. From these results we conclude that fructose is a poor nutritional precursor for rapid glycogen restoration in muscle after exercise, but that both glucose and fructose promote rapid accumulation of glycogen in the liver.