Does body temperature mediate anxiolytic effects of acute exercise?

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Abstract
We tested the thermogenic hypothesis that reductions in blood pressure and self-reported state anxiety and altered brain electrocortical (electroencephalographic, EEG) activity after acute exercise are due to increased body temperature. Eleven fit [cycle peak O2 consumption (VO2peak) = 57 +/- 5.8 ml.kg-1 x min-1] males (26 +/- 5.8 yr) were randomly assigned to four 20-min conditions in a within-subjects counterbalanced design: 1) thermoneutral (32–35 degrees C) or 2) cold (18–23 degrees C) cycling at 70% VO2peak, 3) passive warm water exposure (39–41 degrees C), and 4) quiet rest (60 dB below ambient; 22 +/- 1 degrees C). All exercise testing was conducted in shoulder-deep water. Esophageal temperature increased equally during thermoneutral cycling (+1.45 +/- 0.05 degrees C) and passive heating (+1.51 +/- 0.06 degrees C), was blunted during cold cycling (+0.40 +/- 0.12 degrees C), and was unchanged at rest. Mean radial arterial pressure (MAP), self-reported state anxiety (State-Trait Anxiety Inventory, STAI), and spontaneous occipital (O1 + O2) and photostimulated temporal (T5 + T6) surface EEG activity (10–20 system) in theta (4–8 Hz), alpha (9–13 Hz), and beta (14–40 Hz) frequency bands were assessed 5 min pre- and 10–15 and 20–25 min postcondition and analyzed in 4- (condition) by-3 (time) repeated-measures analysis of variance (P < 0.05). Results showed a condition-by-time interaction for MAP, which decreased from pre- to 15 min postcondition for thermoneutral cycling (81 +/- 2 to 73 +/- 2.7 mmHg) and passive heating (86 +/- 2.5 to 74 +/- 1.4 mmHg) and persisted at 25 min postcondition.(ABSTRACT TRUNCATED AT 250 WORDS)

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