Master of Science (MS)



Document Type



Excess post-exercise oxygen consumption (EPOC) has been attributed to metabolic, hemodynamic, neuroendocrine, and pulmonary factors. In one particular study, Barclay (J Appl Physiol 1986;61(3):1084-90) suggested that a lower rate of fatigue and hyperperfusion following a bout of exercise was due to a mechanism other than increased oxygen and substrate delivery. Interestingly, few studies have examined the influence of venous function on EPOC. The purpose of this study was to examine the relationship between measures of vascular function and EPOC. Measures of vascular function and VO2 recovery kinetics were examined in 20 individuals [age=22+2.41 yrs]. Nondominant forearm arterial inflow, venous capacitance and venous outflow were evaluated at rest and after 5 minutes of upper arm occlusion, using strain gauge plethysmography. VO2 recovery kinetics was assessed using gas exchange analysis following a six-minute constant work rate protocol at 60 percent of VO2peak, on a cycle ergometer. The average VO2peak was 33.48+8.22 ml/kg/min (Range: 18.7 to 46.1 ml/kg/min). Recovery half-time (T1/2VO2) and Tao were 17.01+3.51 seconds and 54.45+11.28 seconds, respectively. Resting inflow was 2.77+1.51 ml/100ml/min, reactive hyperemic blood flow was 17.72+3.65 ml/100ml/min, venous capacitance was 2.86+0.72 percent, and venous outflow was 34.19+10.03 ml/100ml/min. Bivariate correlations revealed significant associations between T1/2VO2 and the reactive hyperemic response (r=-0.48, p=0.03) and T1/2VO2 and venous outflow post-occlusion (r=-0.50, p=0.02). In conclusion, these findings suggest an important role of both the arterial and venous circulation on EPOC.



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Committee Chair

Michael Welsch



Included in

Kinesiology Commons