title: Short-term treadmill running in the rat: what kind of stressor is it?
abstract: The use of short-term (1-5 days) treadmill running is becoming increasingly common as a model to study physiological adaptations following the exercise. Although the beneficial effects of acute exercise seem clear, a paucity of data exist describing potential markers of stress in response to forced running. We subjected male and female Sprague-Dawley rats to 0, 1, 2, 5, or 10 days of treadmill running. Twenty-four to 32 h after the last bout of exercise animals were killed and examined for training-induced changes in several physiological variables. No effect of skeletal citrate synthase activity was observed in the male animals after any duration, and only at 10 days of running did females show a significant increase in citrate synthase. Myocardial heat shock protein 72 (HSP72) content was higher in male rats than female rats, and exercise led to increased HSP72 in both sexes, although the time course was different between males and females. Animals displayed several markers of systemic stress in response to the treadmill running, and this was done in a sex-dependent manner. Serum corticosterone was significantly elevated in both sexes 24 h after exercise in three of four exercise groups. Corticosterone-binding globulin was higher in females, and decreased after running in female rats. Body and spleen weights decreased in males (but not females) in response to the exercise training, and running did not alter adrenal gland weights in either sex. These data indicate that in response to short-term treadmill running both male and female rats show signs of systemic stress, but that the pattern of changes occurs in a sex-specific manner.
authors.affiliation: Department of Integrative Physiology, University of Colorado at Boulder, Boulder, CO 80309-0354, USA.
authors.forename: David A
authors.initials: DA
authors.lastname: Brown
authors.forename: Micah S
authors.initials: MS
authors.lastname: Johnson
authors.forename: Casey J
authors.initials: CJ
authors.lastname: Armstrong
authors.forename: Joshua M
authors.initials: JM
authors.lastname: Lynch
authors.forename: Nicholas M
authors.initials: NM
authors.lastname: Caruso
authors.forename: Lindsay B
authors.initials: LB
authors.lastname: Ehlers
authors.forename: Monika
authors.initials: M
authors.lastname: Fleshner
authors.forename: Robert L
authors.initials: RL
authors.lastname: Spencer
authors.forename: Russell L
authors.initials: RL
authors.lastname: Moore
mesh_terms: D000222:Adaptation, Physiological; D000311:Adrenal Glands / Q000473:pathology; D000818:Animals; D001284:Atrophy; D001835:Body Weight; D002950:Citrate (si)-Synthase / Q000378:metabolism; D003345:Corticosterone / Q000097:blood; D005080:Exercise Test; D005260:Female; D050884:HSP72 Heat-Shock Proteins / Q000378:metabolism; D006984:Hypertrophy; D008297:Male; D023421:Models, Animal; D018482:Muscle, Skeletal / Q000201:enzymology; D009206:Myocardium / Q000378:metabolism; D005082:Physical Exertion; D051381:Rats; D017207:Rats, Sprague-Dawley; D012737:Sex Factors; D013154:Spleen / Q000473:pathology; D013312:Stress, Physiological / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D013997:Time Factors; D014156:Transcortin / Q000378:metabolism; D015854:Up-Regulation
chemical_list: D050884:HSP72 Heat-Shock Proteins; D014156:Transcortin; D002950:Citrate (si)-Synthase; D003345:Corticosterone