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Excerpt
After a single bout of aerobic exercise, oxygen consumption remains elevated above pre-exercise levels for up to 30 hours in humans (Excess Postexercise Oxygen Consumption; EPOC). Likewise, skeletal muscle blood flow remains elevated above pre-exercise levels for an extended period of time resulting in a postexercise hypotension. PURPOSE: To explore the possibility of a causal link between EPOC and postexercise hypotension by comparing the magnitude and duration of these postexercise phenomenon. METHODS: Eight healthy, normotensive, moderately active subjects (seven men and one woman, 20–32 years) were studied before and through 180 min after a 60 min bout of upright cycling at 60% of VO2 peak. Oxygen consumption was measured with a custom dilution hood and mass spectrometer-based metabolic system. Mean arterial pressure was measured via an automated blood pressure cuff (Dinamap) and femoral blood flow was measured using ultrasound (Vingmed). RESULTS: Oxygen consumption was stable from 30 min postexercise (3.8 ± 0.2 l/min) to 180 min postexercise (3.8 ± 0.2 l/min; p = 0.6). In contrast, mean arterial pressure returned from 75.7 ± 2.1 mmHg at 30 min postexercise to 83.5 ± 0.2 mmHg at 180 min postexercise (p<0.01) and femoral blood flow returned from 169 ± 34 ml/min at 30 min postexercise to 115 ± 19 ml/min at 180 min postexercise (p<0.05). CONCLUSIONS: Taken together, these data demonstrate that excess postexercise oxygen consumption and the elevation 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 phenomenon. Supported by AHA grant 30403Z.
