by the American College of Sports Medicine. Unauthorized reproduction of this article is prohibited. Copyright @ 2010 373 1711 Board #148 June 2 2:00 PM - 3:30 PM IGF-1 and VEGF Expression In Response To Therapeutic Ultrasound In Human Skeletal Muscle. Diana C. Delgado Diaz, Brad Gordon, Matthew C. Kostek. University Of South Carolina, Columbia, Sc. (Sponsor: James A. Carson, FACSM) Email: dianakarolibna@yahoo.es (No disclosure reported) Therapeutic ultrasound treatment (TUS) has been widely used in sports medicine and physical therapy. Although US has historically been used for its thermal properties, current theories suggest that its effects are non-thermal; US may affect protein signaling cascades via conformational changes in signaling proteins, affecting gene expression. In-vitro and animal models have shown that US can affect vascular remodeling, cell proliferation, and inflammation; specific increases in VEGF and IGF1 gene expression have been reported. PURPOSE: To examine changes in VEGF and IGF1 expression levels in induced muscle damage, treated with TUS. METHODS: Six healthy and moderately physically active, aged 18 to 25 years, were randomly assigned to either control (CON) or experimental group (EXP). EXP group was subjected to 200 eccentric contractions of the quadriceps of both legs, 48h before the TUS. Both groups received TUS in one leg. Continuous TUS was delivered for 10min on a standardized area of the vastus lateralis, frequency of 1.0 MHz and intensity of 1.5W/cm2. Muscle biopsies were taken from both legs of all subjects 6h after the TUS. Total RNA was extracted and reverse transcribed for IGF1 and VEFG gene expression analysis by qRT-PCR. RESULTS: Muscle damage was confirmed by 26.54 and 21.45% decrease in the isometric peak torque immediately after damage protocol and 48h after damage, respectively. Blood CK activity levels increased 48h after the muscle damage protocol from 674 ± 337 to 3559 ± 1652 U/L (p < 0.05). IGF-1 gene expression as compared to the control limb, was 6.90± 4.75 fold higher in the TUS treated limb after damage (n=4, p= 0.28). TUS did not substantially alter IGF1 gene expression in the CON group (0.4 fold). Yet, compared to the control IGF-1 was 17.2 fold higher. Our damage protocol alone induced an increase of 1.7±1.6 fold in IGF-1. Due to TUS, VEGF gene expression increased 4.15 ± 3.11 fold in the EXP group (treated to untreated leg, p=0.17); no change was detected in the CON group, 0.44 fold. Our damage protocol accounted for a 3.5 fold increase. CONCLUSION: TUS in human skeletal muscle may increase IGF1 and VEGF gene expression in response to muscle damage though due to small sample size we were not able to detect a statistically significant change. Our laboratory is currently collecting additional samples for analysis. 1712 Board #149 June 2 2:00 PM - 3:30 PM The Effects of Creatine and Chronic Low Frequency Stimulation on Muscle Fiber Cross-Sectional Area. Joel R. Krentz, Maria Gallo, Karen J.B. Martins, Gordon Murdoch, Walter T. Dixon, Daniel G. Syrotuik, Charles T. Putman. University of Alberta, Edmonton, AB, Canada. Email: joel.krentz@ualberta.ca (No disclosure reported) We have shown that creatine (Cr) loading of rat muscle attenuates fast-to-slow fiber type transformations in plantaris after wheel running and in tibiailis anterior (TA) after chronic low frequency stimulation (CLFS). A model of muscle endurance training, CLFS alone also induces decreases in fiber cross-sectional areas (CSA’s). PURPOSE: To test the hypothesis that attenuated fast-to-slow fiber type transformations in Cr loaded rat TA after 10-days(d) of CLFS will correspond to larger CSA of type II fibers. METHODS: Sprague-Dawley rats were randomly assigned to one of four groups: Cr + CLFS (Cr-Stim), CLFS (Con-Stim), Cr + sham (Cr-Sham) or sham (Con-Sham). CLFS (10 Hz, 10 h daily, impulse width 380 s) was applied to the left TA via electrodes implanted across the common peroneal nerve; the right contralateral TA served as an internal control. Animals in the Cr groups consumed a solution of 1% Cr in 5% dextrose for 10-d before CLFS began and during 10-d of CLFS; control groups received 5% dextrose. Standardized regions of serial sections of left and right TA’s were immunohistochemically stained for adult myosin heavy chain (MyHC) isoforms and CSA’s were quantified. Group differences were assessed using multi-factorial ANOVA and Tukey HSD post hoc. RESULTS: The CSA of pooled type-II fibers was 18% lower (p< 0.05) in stimulated TA’s (i.e., Con-Stim), compared with contralateral controls. Importantly, this effect was absent in the Cr-Stim group. Further analysis revealed the effect was greatest within the type-IID/X fiber population, where a 24% decrease (p< 0.05) in CSA was noted in Con-Stim, while no difference was detected between stimulated and unstimulated TA’s within the Cr-Stim group. Our morphological findings are consistent with measured 6% (p< 0.05) and 30% (p< 0.05) increases in whole muscle MyHC-IId/x protein and mRNA contents, respectively. CONCLUSION: Cr loading of fast-twitch muscle during endurance training exerts a protective effect on IID/X fibers. Funded by NSERC and AHFMR. 1713 Board #150 June 2 2:00 PM - 3:30 PM An Evaluation of Two Experimental Models for Acute Glucocorticoid-Induced Skeletal Muscle Atrophy in Rats Humberto Nicastro, Nelo E. Zanchi, Vitor Felitti, Fabio M. Lorenzeti, Mário A. de Siqueira Filho, Antonio H. Lancha, Jr. University of São Paulo, São Paulo, Brazil. Email: nicastro@usp.br (No disclosure reported) Glucorcorticoids are well known for its therapeutic anti-inflammatory effects when used acutely and in low doses. However, it is already known that chronic and/or acute high doses promote several side effects, such as skeletal muscle atrophy. Furthermore, experimental models in order to induce glucocorticoid- induced skeletal muscle atrophy with high doses fail, according to the mode and dose of administration, in promoting a significant atrophic response with low death tool. PURPOSE: To evaluate the magnitude of two experimental models of acute glucocorticoid-induced skeletal muscle atrophy based on different modes of administration. METHODS: The study was conducted in accordance with the National Institute of Health Guidelines. Adult male Wistar rats (400g) were randomly divided into a dexamethasone-treated via intraperitoneal injection (IP; n=6) and via drinking water (DW; n=6). Both groups received 5 mg/kg-1 of DEXA per day during 7 days. Control group was pair-fed (PF; n=6) to dexamethasone-treated groups. Blood samples were collected for measuring plasma glucose levels. Soleus, plantaris and EDL muscles were used for protein content measurement. Statistical analyses consisted of a one-way ANOVA with Tukeys post hoc testing. RESULTS: IP, DW, and PF groups showed a 23%, 25% and 4% decrease in body weight, respectively. Soleus muscle mass and total protein content showed no statistical difference among groups. Plantaris muscle mass and total protein content were significantly decreased in DW compared with IP and PF (274±27 vs. 337±32 vs. 405±27mg, p<0.05; 8.6±1.4 vs. 9.8±1.0 vs. 11.1±2.3μg/μl, p<0.05). The same result pattern was observed for EDL muscle for DW, IP, and PF (160±17 vs. 184±23 vs. 206±15mg, p<0.05; 5.9±0.5 vs. 7.3±0.6 vs. 9.6±0.8μg/μl, p<0.05). Blood glucose level was significantly increased in DEXA-treated groups but did not differ between them (140±11 in DW and 139±66 in IP vs. 93±9mg/dl in PF, p<0.05).