School of Public Health

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The collections in this community comprise faculty research works, as well as graduate theses and dissertations.

Note: Prior to July 1, 2007, the School of Public Health was named the College of Health & Human Performance.

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    EFFECTS OF CARDIOVASCULAR DISEASE AND PHYSICAL INACTIVITY ON THE PARACRINE FUNCTION OF CIRCULATING ANGIOGENIC CELLS
    (2015) Landers-Ramos, Rian Quinn; Hagberg, James M; Kinesiology; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)
    Cardiovascular disease (CVD) is the leading cause of death in developed countries. Traditional cardiovascular risk factors account for only a fraction of events related to CVDs, emphasizing the need for investigations into more novel risk factors. Circulating angiogenic cells (CACs) are involved in the repair and maintenance of the vascular endothelium and function mainly through paracrine mechanisms. The studies presented in this dissertation provide new insight into differences in the paracrine actions of CACs as a function of habitual physical activity and CVD. The first study presented identifies, for the first time, that secreted factors from CD34+ and CD34-/CD31+ CACs affect HUVEC tube formation as a function of habitual physical activity. Study #1 identifies inflammatory proteins S100A8 and S100A9 as major factors contributing to the depressed tube formation observed when using CD34-/CD31+ conditioned media (CM) from inactive younger adults compared to endurance-trained athletes. The second study aimed to confirm the effects of S100A8 and S100A9 in CD34-/CD31+ CM on HUVEC tube formation in CVD patient populations compared to endurance-trained athletes. Study #2 found that the CM from non-ST- segment elevation myocardial infarction (NSTEMI) patient CD34-/CD31+ CACs impaired tube formation compared to athletes’ CM, and that pretreatment of HUVECs with an inhibitor for TLR4, a major receptor for S100A8 and S100A9, rescued tube formation to the levels observed when using CD34-/CD31+ CM from athletes. Higher S100A8 and S100A9 content was found in the CM of NSTEMIs compared to athletes. Finally, the study #2 mechanistically demonstrated the direct role of S100A8 and S100A9 on tube formation using recombinant S100A8 and S100A9 and confirmed that these actions were mediated by TLR4. Preliminary data in study #2 suggest that cell surface markers on selected CD34-/CD31+ CACs are inherently different between NSTEMI patients and endurance-trained athletes with lower presence of T-cell and monocyte markers on the CD34-/CD31+ CACs of NSTEMI patients. Collectively, the two studies presented in this dissertation demonstrate that both physical inactivity and CVD alter the paracrine actions of CD34-/CD31+ CACs which in turn impair HUVEC tube formation. These findings are of particular importance as new methods to improve CAC function for therapeutic purposes are being developed.
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    Insulin-like Growth Factor 1 Genotype Influences Muscle Strength Response to Sterngth Training in Older Adults
    (2004-11-03) kostek, matt; Hurley, Ben F; Kinesiology; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)
    Strength training (ST) is considered an intervention of choice for the prevention and treatment of sarcopenia. The insulin-like growth factor 1 protein (IGF-I) plays a major role in ST-induced skeletal muscle hypertrophy and strength improvements. A microsatellite repeat in the promoter region of the IGF1 gene has been associated with IGF-I blood levels and phenotypes related to IGF-I in adult men and women. To examine the influence of this polymorphism on muscle hypertrophic and strength responses to strength training (ST), we studied 67 Caucasian men and women before and after a 10-week single leg knee extension ST program. One repetition maximum (1RM) strength, muscle volume (MV) via computed tomography (CT), and muscle quality (MQ) were assessed at baseline and after 10 weeks of training. The IGF1 repeat promoter polymorphism and three single nucleotide polymorphisms (SNP) were genotyped. For the promoter polymorphism, subjects were grouped as homozygous for the 192 allele, heterozygous, or non-carriers of the 192 allele. After 10 weeks of training, 1RM, MV, and MQ increased significantly for all groups combined (P < 0.001). However, carriers of the 192 allele gained significantly more strength with ST than non-carriers of the 192 allele (P = 0.02). There was also a non-significant trend for a greater increase in MV in 192 carriers than non-carriers (P = 0.08). No significant associations were observed for the other polymorphisms studied. Thus, these data suggest that the IGF1 promoter polymorphism may influence the strength response to ST. Larger sample sizes should be used in future studies to verify these results