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1. Introduction
A common technique in measuring blood flow in the human forearm is by venous occlusion plethysmography. The fundamental principle is that if the venous return from the arm is blocked, the forearm will swell at a rate relative to the rate of the arterial inflow (Whitney, 1953). However, the rate of increase in volume of the forearm and its relationship with the arterial flow can be true only if the veins in the forearm are not completely distended because when the veins are full, a rise in the pressure and the blood will run off under the congesting cuff and …show more content…
Evaluation of the t-test between pre and post occlusion yielded a significant relationship with P < 0.05.
Figure 2: Comparison of the mean (n = 33) of the relative changes in the slope between forearm perfusion immediately after strenuous physical exercise and blood flow occlusion. Measurements were taken at 30 second intervals for 4 minutes. Trend shows a gradual return to baseline perfusion post exercise and an initial sharp decline and then a gradual levelling off post occlusion. A t-test (paired and equal variance) between post exercise post occlusion yielded a significant P value (P<0.05). The error bars comprise SEM.
Greatest increase in blood flow to the forearm was observed post exercise, while minimal deviation in the slope was observed post mental stress. A t-test between mental stress and exercise and occlusion yielded significant P values (P= 0.000003 and 0.000913 respectively), no significant relationship was observed between exercise and occlusion (P> 0.05) (figure …show more content…
The metabolic demand for O2 would have increased drastically during exercise and remained high for some time after as can be seen in Figure 2, where the slope increased by a factor of 5 ± 0.8 mV/s from an average baseline value of 32.7 ±8.1mV/s immediately after exercise ceased. The active hyperemia observed here may be due to a combination of tissue hypoxia and the generation of local vasodilator metabolites such as potassium ions, carbon dioxide, nitric oxide, and adenosine. More recently, ideas have emerged that NO bound to haemoglobin may be released as oxygen is removed from the red blood cells, thus evoking vasodilatation in the active muscles. This is an attractive hypothesis because blood flow to areas where oxygen demand is high, would be elevated (Stamler et al. 1997). Unless there is another source of NO for the red blood cells or some other mechanism for NO production, it seems unlikely that this mechanism is a major and/or obligatory role in exercise hyperemia (Joyner & Wilkins 2007). The explanation of exercise hyperemia, until proven otherwise, must be due to a combination of