A single bout of exercise lowers blood pressure (BP) for up to 24 h afterwards. The magnitude of this post-exercise hypotension (PEH) has been reported to be correlated most strongly to pre-exercise BP, and this apparent relationship has influenced position statements about the value of exercise in arterial hypertension. Nevertheless, this correlation could be adversely affected by mathematical coupling and regression-to-the-mean artefacts. Therefore, we aimed to examine the degree to which BP status moderates PEH while, for the first time, controlling for these statistical artefacts. A total of 32 participants, with preexercise mean arterial pressures of 65-110 mm Hg, cycled for 30 min at 70% peak oxygen uptake. Systolic BP and diastolic BP were measured (Portapres) before exercise and for 20 min after exercise. Changes in BP were regressed against pre-exercise values, and against the mean of pre-and post-exercise BP, among other indices that are also known not to be prone to artefacts. Correlations between pre-exercise BP and the exercisemediated reductions were typical of those previously reported (r ¼ 0.37-0.62, Po0.05), but not large enough to rule out spuriousness (P40.05). Artefact-free indices of BP status (pre-and post-exercise mean as well as an earlier independent measurement) did not correlate with reductions in BP (P40.05), which were moderated more by peak oxygen uptake and time of day (Po0.05). These data indicate that, if statistical artefacts are not controlled for, the influence of BP status on the degree of PEH can be spuriously exaggerated to the extent that other more important moderators of BP change are masked.

The siesta habit is associated with a 37% reduction in coronary mortality, possibly because of reduced cardiovascular stress associated with daytime sleep. Whether the most important behavior is the daytime nap itself, a supine posture, or the expectancy of a nap is unknown. We present the first detailed description on healthy individuals of the acute changes in cardiovascular function during defined phases of the daytime sleep-onset period. These responses were compared with lying awake and standing. Following a night of restricted (4 h) sleep, nine healthy participants (aged 34 +/- 5 yr) were allowed to sleep at 1400 for up to 1 h. Polysomnography was used to calculate three phases of daytime sleep onset: phase 1, a baseline period of relaxed wakefulness before lights out; phase 2, the period between lights out and onset of stage 1 sleep; and phase 3, the period between onsets of stages 1 and 2 sleep. Differences (means +/- SD) in blood pressure, heart rate, and forearm cutaneous vascular conductance (CVC) between phases were analyzed. During the 9.7 +/- 13.8 min of phase 2, systolic and diastolic blood pressure was 4.7 +/- 4.5 and 3.6 +/- 2.8 mmHg lower than baseline, whereas CVC was 9.5 +/- 4.3% higher than baseline (P < 0.05). Subsequent changes in cardiovascular function during the sleep itself were trivial (P > 0.05). The above changes were not observed when subjects stood or laid supine in relaxed wakefulness for 1 h (P > 0.05). Our findings suggest that the period between lights out and sleep onset is associated with the largest acute reduction in blood pressure during one afternoon siesta.