Submitted to: Journal of Nutrition
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: March 3, 1999
Publication Date: N/A
Interpretive Summary: Skeletal muscle glycogen is important in the chicken not only as a source of energy for contracting muscle, but also as an important component influencing the quality of poultry meat. Glycogen is important as a glucose storage molecule. Meat- type chickens are subjected to feed withdrawal prior to processing, therefore the effect of prolonged feed withdrawal on muscle glycogen and meat quality characteristics is of importance. This study was conducted to determine the difference in muscle versus liver glycogen in response to feed deprivation. It was found that feed withdrawal results in dramatic drops in liver glycogen while muscle glycogen stores remained unchanged. Feed deprivation does not have a sustained effect on muscle glycogen levels. The results of this study illustrate the similarities between avian and mammalian muscle glycogen regulation in that muscle glycogen is resilient to metabolic changes that occur. This information will be of interest to other scientists.
Using cervical dislocation to collect issues, a method which involves extensive strenuous muscle contraction, previous studies have reported time dependent losses in muscle glycogen with prolonged feed withdrawal. Cervical dislocation results in a 23% decrease in muscle glycogen levels compared to birds sacrificed using barbituate overdose. This study examined the effects of feed deprivation and refeeding on tissue glycogen using barbituate overdose to block all muscle contraction. Plasma and tissues samples were analyzed for various metabolites, hormones and tissue glycogen concentrations. Plasma glucose was decreased while glucagon was elevated following a 24 hour feed withdrawal. Liver glycogen was decreased, while muscle glycogen was only slightly decreased and then returned to control levels. Feed deprivation followed by refeeding resulted in increased circulating insulin and glucose levels when compared to controls. Muscle glycogen levels were unaffected following refeeding, while liver glycogen was increased 380%. In conclusion, using methods of tissue collection which ensure that muscle glycogen determinations are not confounded by artifactual degradation, feed deprivation resulted in a significant decrease in liver glycogen where as muscle glycogen was found to be relatively resilient to depletion induced by feed deprivation. These results verify that regulation of avian muscle glycogen stores is similar to that in mammals.