Does body temperature mediate anxiolytic effects of acute exercise?

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 (V̇O(2 peak)) = 57 ± 5.8 ml · kg^-1 · 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°C) or 2) cold (18-23°C) cycling at 70% V̇O(2 peak), 3) passive warm water exposure (39-41°C), and 4) quiet rest (60 dB below ambient; 22 ± 1°C). All exercise testing was conducted in shoulder-deep water. Esophageal temperature increased equally during thermoneutral cycling (+1.45 ± 0.05°C) and passive heating (+1.51 ± 0.06°C), was blunted during cold cycling (+0.40 ± 0.12°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 θ (4-8 Hz), α (9-13 Hz), and β (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. There was a significant time effect for absolute (μV²) and relative (% of total μV²) spontaneous EEG activity: θ frequencies decreased, while α and β frequencies increased from pre- to 15 and 25 min posttreatment. STAI was reduced only at 1 min after quiet rest. Changes in MAP were the only responses consistent with the thermogenic hypothesis. Acute cycling and passive heating at equivalent body temperatures elicited similar reductions in MAP. Because reduced MAP occurred independently of changes in STAI and EEG, these responses cannot be viewed as concomitant indexes of reduced anxiety after acute exercise. Our results do not provide compelling support for the thermogenic hypothesis.