Abstract

Application of intermittent pneumatic compressions (IPC) has been successfully employed to treat conditions such as peripheral artery disease and and soft-tissue injuries, but the mechanisms by which this therapy works remain unknown. We have previously reported in rodents that IPC acutely up-regulates the expression of genes involved in vascular remodeling in the compressed muscle. In humans, however, the gene expression responses to this therapy in skeletal muscle have not been characterized. PURPOSE: To determine the impact of a single session of IPC on the expression (mRNA) of genes involved in angiogenesis, matrix remodeling and inflammation in skeletal muscle (VEGF, eNOS, MCP-1, CXCL1, CXCL12, CYR61, CTGF and PGC1α). METHODS: Healthy young male subjects (26±2 yrs) were randomly assigned to one of three intervention groups: high frequency IPC (12 compressions/min) (n=5), low-frequency IPC (3 compressions/min) (n=5) and control (no compression) (n=3). With the subjects in the seated position, IPC was applied at a pressure of 120 mmHg for one hour in the foot and calf using a commercially available unit. Muscle biopsies were taken from the lateral portion of the calf using the percutaneous needle biopsy technique prior to (baseline) and after IPC (30 and 150min). Gene expression responses were studied using real-time RT-PCR. Changes in mRNA levels with time were compared using ANOVA for repeated measures. RESULTS: In the high frequency group (12 comp/min) IPC evoked a significant increase from baseline in the expression of CXCL1 at 150 min (2.3 fold increase, p=0.01) and a decrease in the levels of CYR61 at both 30 min (3.8 fold, p<0.01) and 150 min (2.8 fold, p<0.01). In contrast no changes in the expression of these factors were seen in the low frequency and control groups. VEGF, eNOS, MCP-1, CXCL12, CTGF and PGC1α mRNA expression was not significantly altered in any of the three groups. CONCLUSIONS: Preliminary results indicate that when applied at a high frequency (12 comp/min) foot and calf IPC acutely alters the expression of genes involved in inflammation and matrix remodeling in skeletal muscle in humans. Support: ACSM Research Endowment (S.C.N)

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