## LSU Historical Dissertations and Theses

1996

Dissertation

#### Degree Name

Doctor of Philosophy (PhD)

Kinesiology

B. Don Franks

David B. West

#### Abstract

This study investigated postexercise hypotension (PEH) in five normotensive dogs testing these hypotheses: (1) PEH is present in the dog model; (2) high intensity exercise of 85% HR$\rm\sb{max}$ as compared to moderate intensity exercise of 60% HR$\rm\sb{max}$ induces a greater PEH; and (3) IL-1 and its activation of PGE$\sb2$ are associated with PEH. In experiment I, it was found that 85% HR$\rm\sb{max}$ exercise decreased systolic blood pressure (SBP) and mean arterial blood pressure (MABP) at 30 and 60 minutes postexercise (p $<$ 0.05). Both IL-1 and PGE$\sb2$ increased immediately following intense exercise, although temporal patterns were dissimilar. During non-exercise infusion of ibuprofen or dexamethasone (experiment II), blood pressure was not affected, but ibuprofen led to an overall inhibition of PGE$\sb2$. However, dexamethasone infusion led to a significant increase in PGE$\sb2$ at 180 and 210 minutes postinfusion. In experiment IIIA, after intense exercise following ibuprofen or saline infusion, PGE$\sb2$ increased at 120 to 180 minutes postexercise. Similar results were noted after exercise during dexamethasone treatment (experiment IIIB). In experiment IIIA & B, neither ibuprofen nor dexamethasone significantly affected PEH, although non-significant reductions in PEH was observed in dexamethasone treated animals. However, PGE$\sb2$ significantly increased after exercise at time points when PEH was not observed. These data indicate that (1) the intensity of exercise may have an effect on PEH, (2) there is partial support for the involvement of IL-1 and PGE$\sb2$ in PEH due to their immediate increase after exercise although a direct relationship was not observed, and (3) IL-1 still remains a possible mechanism responsible for PEH because of trends for attenuated PEH and PGE$\sb2$ responses following dexamethasone treatment.

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