Submitted on October 26, 2004
Accepted on December 12, 2004
Is postexercise hypotension related to excess postexercise oxygen consumption through changes in leg blood flow?
Jay T Williams1, Mollie P Pricher1, and John R Halliwill1*
1 Department of Human Physiology, University of Oregon, Eugene, OR, USA
* To whom correspondence should be addressed. E-mail: halliwil{at}uoregon.edu.
After a single bout of aerobic exercise, oxygen consumption remains elevated above preexercise levels (Excess Postexercise Oxygen Consumption; EPOC). Likewise, skeletal muscle blood flow remains elevated for an extended period of time. This results in a postexercise hypotension. The purpose of this study was to explore the possibility of a causal link between EPOC, postexercise hypotension, and postexercise elevations in skeletal muscle blood flow by comparing the magnitude and duration of these postexercise phenomena. Sixteen healthy, normotensive, moderately active subjects (7 men and 9 woman, 20-31 years) were studied before and through 135 min after a 60 min bout of upright cycling at 60% of VO2 peak. Resting and recovery VO2 were measured with a custom dilution hood and mass spectrometer-based metabolic system. Mean arterial pressure was measured via an automated blood pressure cuff and femoral blood flow was measured using ultrasound. During the first hour postexercise, VO2 was increased 11 ± 2 %, leg blood flow was increased 51 ± 18 %, leg vascular conductance was increased 56 ± 19 %, and mean arterial pressure was decreased 2.2 ± 1.0 mmHg (all P < 0.05 vs preexercise). At the end of the protocol, VO2 remained elevated 4 ± 2 % (P < 0.05) while leg blood flow, leg vascular conductance, and mean arterial pressure returned to preexercise levels (all P > 0.7 vs preexercise). Taken together, these data demonstrate that EPOC and the elevations in skeletal muscle blood flow underlying postexercise hypotension do not share a common time-course. This suggests that there is no causal link between these two postexercise phenomena.
