Glycogen

Human liver - 50 g/kg wet wt. Skeletal muscle - 15 g/kg wet wt. Glycogenin = protein core Glycosome ~ ~

 1-4 bonds  1-6 bonds Glycoside bonds

Proglycogen (acid insoluble) Macroglycogen (acid soluble) Size = glycogenin – Proglycogen – Macroglycogen 12 tiers is the maximum – branches too dense to allow GS Tier 8

Lomako, et al., FASAB J. 9, , 1995 Macroglycogen Proglycogen Glygogenin Two Forms of Muscle Glycogen 75% proglycogen/25% macroglycogen

Glycogen Synthesis Glycogen Synthase  1-4 bonds Glycosyl 4:6 transferase Branching enzyme (at least 11) ( leave at least 4) (move at least 7)

1-4 Bond1-6 Bond Glycogenolysis (Glucose-1-PGlucose-6-P) (phosphoglucomutase) phosphorylase Glucose -6-P to glycolysis glycosyl 4:4 transferase (breaks a 1-4, makes a 1-4) (NEXT) abc fed abc

abcfed Glycogenolysis (cont.) abc to another chain free glucose Amylo 1:6 glucosidase abc fed glycosyl 4:4 transferase abc free glucose

Glycogen Synthesis- the storage of glucose via glycogen formation -Glycogen Synthase- enzyme responsible for making  1-4 bonds between glucose molecules -Glycosyl 4:6 transferase- enzyme that breaks  1-4 bonds, and makes  1-6 bonds to allow for branching Glycogenolysis- the break down of glycogen into glucose Summary

Skeletal Muscle Epi/N-Epi (beta receptor)  C-AMP  Ca++ (actives phosphorylase kinase These will increase activity of phosphorylase and decrease glycogen synthase Insulin  PDE activity which will decrease C-AMP  PP-1 which will increase the activity of GS and decrease the activity of phosphorylase

HOW CAN WE AVOID THIS EVENT?

VERY GENERALIZED SCHEME of SUBSTRATE USE vs TIME Liver depleting Muscle depleting Reliance on fats

Three CHO-Loading Protocols: Two Depletion & One Taper Saltin and Hermansen, Nut. Physical Activity, pp.32-46, 1967

Phosphorylates glycogen synthase

CA ++ actives Phosphorylase Kinase at the start of exercise by 20x. Ca ++ binds to gamma subunit of PK. Phosphorylase Kinase activated via C-AMP and PKA. Phosphorylase kinase phosphorylates Phosphorylase at serine 14. AMP allosterically actives Phosphorylase.

Active Inactive - P Insulin activates PP-1 and PDE (phosphodiesterase). This will decrease C-AMP and dephosphorylate proteins that were phosphorylated by PKA

Lomako, et. al.,FASAB 7: Order of Glycogen Resynthesis

Glycogen Storage Diseases Type I: Von Gierke Disease; Glucose-6-phosphatase Defect  Hypoglycemia occurs due to defect of the final step of gluconeogenesis.  This disease, affects only liver and renal tubule cells  Decreased mobilization of glycogen produces hepatomegaly. Type V: McArdle Disease; Skeletal Muscle Glycogen Phosphorylase Defect  Skeletal muscle is affected, whereas the liver enzyme is normal.  Exercise capacity is greatly reduced, hypoglycemia during exercise  There is no rise in blood lactate during strenuous exercise.  Muscle contains a high level of glycogen with normal structure Type VI: Hers Disease; Liver Glycogen Phosphorylase Defect  Liver is affected, whereas the skeletal muscle enzyme is normal.  Marked hepatomegaly occurs due to a high level of glycogen with normal structure..  Following administration of glucagon, there is no increase in blood glucose.

Casey, et al., J.Physiol. 48(1): , Rapid Phase – increased insulin sensitivity GLUT 4 from exercise Slow Phase- dependent on insulin concentration

EFFECT of DETRAINING on MUSCLE GLYCOGEN CONCENTRATIONS Costill, et., al., Med. Sci. Sports Exerc., 17(3): , %80%72%100%

Costill, et. al., J.A.P. 31(6): , Muscle Glycogen During 3 days of Endurance Training and al Low-CHO vs High-CHO Diet