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Histamine is a molecular transducer of physical activity responses in humans, namely endurance exercise. Research shows that H1/H2-receptors mediate exercise responses, such as post-exercise vasodilation and hypotension. Histamine is produced and released within skeletal muscle in response to exercise; however, the intramuscular trigger of histamine release that mediates this response to dynamic exercise has not been identified. Exercise factors, such as an acidic pH, could favor increased histadine decarboxylase enzyme activity and mast cell degranulation and thus heightened de novo histamine formation as a response to exercise. Using sodium bicarbonate (SB) to buffer the acidosis in the skeletal muscle may help clarify the relationship, if any, between histamine release and blood pH. The overall goal of the project was to determine if histamine-mediated vasodilation in skeletal muscle is mediated by a decrease in pH that occurs in response to exercise. This was a double-blind placebo-controlled study to access the concentration of histamine release before and after an exercise bout. The experiment included three subjects participated in three separate sessions. An hour prior to exercise, the subject blindly ingested either 0.3g/kg body mass of NaCl (control) or 0.3 g/kg body mass of sodium bicarbonate to prevent acidosis. The subject then performed 60-minutes of one-legged knee extension exercise at 60% of their maximum resistance determined prior. Blood flow velocity and diameter in the femoral artery were bilaterally measured via ultrasound at the end of the rest period, and at minutes 0, 30 and 60 of the post-exercise period. I hypothesized that bicarbonate would decrease the post-exercise histamine-mediated vasodilation. Results demonstrated femoral blood flow at minute 0 post-exercise was significantly increased compared to resting conditions within both placebo and bicarbonate conditions. There was a significant increase in vascular conductance as well as blood flow within the active leg from pre-exercise to minute 0 post-exercise compared to resting in both placebo and bicarbonate groups. The acute increase in blood flow and vascular conductance in the active leg were unexpectedly not significantly sustained at minutes 30 and 60 post-exercise. There were no group differences in femoral blood flow and vascular conductance within the active or inactive leg, suggesting that the given concentration of sodium bicarbonate may not have a significant effect on post-exercise vasodilation. Further studies should be done with an appropriate tool to ascertain the efficacy of sodium bicarbonate as a buffer, such as a near-infrared spectroscopy tool. |
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