Semester

Summer

Date of Graduation

2014

Document Type

Thesis

Degree Type

MS

College

School of Medicine

Department

Exercise Physiology

Committee Chair

Randy W. Bryner

Committee Co-Chair

Stephen E. Alway

Committee Member

Emidio Pistilli

Abstract

Chronic stress has been implicated as a possible contributing factor to the onset of Type 2 Diabetes Mellitus through its negative effects on peripheral insulin sensitivity and the insulin producing beta cells of the pancreas. Exercise could serve as a possible countermeasure to the damaging effects of chronic stress due to its proven ability to increase insulin sensitivity at the level of the muscle and improve or maintain beta cell function and mass. To date, no published research has examined the effects of chronic stress in combination with voluntary wheel running on murine islet morphology and skeletal muscle atrophy. The purpose of this study was to evaluate the effects of chronic stress and voluntary wheel running on murine beta cell number per Islet, insulin positive area in the pancreas, hind limb skeletal muscle morphometrics, autophagy protein expression, and muscle atrophy gene expression. 40 Male Balb/c mice were randomized into 4 groups; sedentary (N=10: Sed), sedentary stressed (N=10: SedSt), exercise (N=10: EX), and exercise stressed (N=10: EXSt). 20 mice were given free access to running wheels over 4 weeks after which, 10 were randomized to 7 hrs/d, 5 d/wk. of stress for 8 wks. 20 mice remained sedentary with no access to running wheels; after 4 weeks 10 of these mice were randomized to 7hrs/d, 5d/wk. of stress for 8 wks. The average islet area was significantly increased in ExSt (24223.810 +/- 2670) when compared to Ex mice (16811.00 +/- 2704) (P < .05). Average beta cell number per islet was significantly higher in ExSt (93.21+/- 5.69) and SedSt (90.99+/- 5.22) mice when compared to Ex (68.64+/- 3.73) or Sed (70.73 +/- 4.77) (P < .05). Muscle wet weight was increased in EXSt mice vs. SedSt mice (P < .05). These results indicate that 8 weeks of chronic stress caused beta cell proliferation and an increase in islet area, but did not result in an increase in muscle ubiquitin associated atrophy gene mRNA levels. Exercise coupled with stress appeared to improve muscle protein accumulation and therefore, could be a potential means to reduce muscle losses under conditions of high stress or beta cell dysfunction.

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