Scholarly
    Communications Project


Document Type:Master's Thesis
Name:Timothy Wayne Batts
Email address:twbatts@vt.edu
URN:1998/00027
Title:The Effect of Glycogen Depletion on Sarcoplasmic Reticulum Function
Degree:M.S.
Department:HNFE
Committee Chair: JAy H. Williams
Chair's email:jhwms@vt.edu
Committee Members:Laurence D. Moore
Elizabeth A. Thomas
Keywords:skeletal muscle, fatigue, exercise, calcium
Date of defense:December 4, 1997
Availability:Release the entire work for Virginia Tech access only.
After one year release worldwide only with written permission of the student and the advisory committee chair.

Abstract:

The role of glycogen in endurance performance has been accepted in theory. It has been shown that higher resting muscle glycogen levels prolong endurance performance. On the other hand, low glycogen levels have been associated with fatigue. Ultimately, a person’s muscle glycogen level dictates the duration in which an activity can be maintained at a maximal effort, after which time, performance will decrease. As of yet, there has been no evidence as to what happens to the fatigued muscle. Force production in skeletal muscle is dictated by the release and uptake of Ca2+ from the sarcoplasmic reticulum (SR). Force production is proportional to [Ca2+], as [Ca2+] increases so does force. At the point of fatigue, there is a decrease in force production. Since fatigue has been associated with glycogen depletion, it is likely that SR function has been altered causing this decrease in force. The purpose of this study was to determine the effect of glycogen depletion on the SR. Twenty male Sprague-Dawley (Harlan Sprague-Dawley, Indianapolis, IN) rats weighing, 345 ± 70 gm were housed two per cage in the Virginia Tech Lab Animal Resources facility. They were fed ad libitum (Purina Rodent Laboratory Chow and water) until time of experiment. Ten of the rats were used as control animals and the other ten were assigned to the experimental group. Rats were allowed a minimum of 5 days to acclimate to their housing. On the morning of the day of testing, rats were selected in pairs according to the housing cage in an effort to decrease variations in food consumption. To reduce muscle glycogen levels, experimental rats were given an initial injection of either epinephrine (1mg/g: ip) while control rats were injected with saline (equal volume) at 0 hr. Thirty minutes later they received another injection of epinephrine or saline (0.5 mg/g: ip). At the end of the hour the rats were anesthetized with pentobarbital sodium (60 mg/kg:ip) for tissue harvesting. Upon reaching a surgical plane of anesthesia one gastrocnemious muscle was extracted for the muscle glycogen assay and the other removed for SR vesicle preparation. Rats were then euthanized with an overdose of pentobarbital sodium. The tissue was assayed for glycogen and glucose levels as well as for Ca2+ uptake and release and ATPase activity. It was found that epinephrine animals had 23% less glycogen than did the control animals and almost twice the amount of glucose (control – 2.9 nmol/g and epinephrine – 5.9 nmol/g). Ca2+ uptake rates in epinephrine animals were significantly decreased by 19.7% (p < .05). Control animals had a release rate of 77.15 ± 1.26 nmol/mg/min and epinephrine animals had a release rate of 75.01 ± 1.86 nmol/mg/min. Ca2+ release rates were decreased but not significantly. Ca2+ stimulated ATPase activity was significanlty decreased by 17.7% in epinephrine animals (p < .05). This is one of the first studies that demonstrate that glycogen reduction in a rested muscle causes altered SR function similar to those caused by exercise. This study shows that low glycogen levels are associated with decreased SR function, which is the primary reason for causing the loss of force in muscle. Ultimately, this study suggests that glycogen loading will enhance endurance performance.

List of Attached Files

TWBATTS.PDF

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