| Cycling exercise (CE) and warm-water immersion (WW) both acutely alter anxiety, implying an association through the underlying thermal stress (TS). Endogenous Benzodiazepine (BZD) inverse agonists also increase anxiety and raise body temperature. We hypothesized that blocking endogenous BZD inverse agonists with the BZD-receptor antagonist Flumazenil (FLU) would attenuate the anxiety reduction associated with the recovery from TS. Eight male subjects with anxiety (44.4 +/- 9.0 STAI) were studied during and after 25 minutes of TS by CE and by WW. WW was performed in a manner so as to increase body temperature to that achieved during CE after 25 minutes. FLU or placebo was given intravenously immediately post-CE or post-WW. Rectal temperature (T) was measured every 5 minutes, and state anxiety questionnaire (STAI) and venous BZD levels were measured at baseline, after 25 minutes of TS, and at 20 and 40 minutes after TS. CE and WW similarly increased T (1.0 +/- 0.3 vs 1.1 +/- 0.2, ns) and STAI (5.1 +/- 3.8 vs 3.1 +/- 2.9, ns). FLU blocked the latent rise in T during the 5 minutes immediately after TS by CE (slope: mpla = +10.0 mK · min-1, mflu = -8.8 mK · min-1, p < 0.05), but not by WW. Lastly, the observed difference between post-exercise FLU and PLA cooling was due to the first 5 minutes of recovery. STAI was decreased at 40 minutes after TS by CE (-10.1 +/- 6.4, p < 0.05) and by WW (-5.8 +/- 6.0, p < 0.05). FLU had no effect on STAI at 40 minutes after TS by either CE or WW. Plasma Diazepam Binding Inhibitor (ODN fragment)-like immunoreactivity was decreased 28% at 40 minutes post-CE (p < 0.05), which correlated with the post-exercise reduction in STAI (r 2 = 0.56). The data suggest the anxiolytic effect following acute exercise is related to endogenous BZD. Furthermore, since FLU blocked the post-exercise increase in rectal temperature but did not block this temperature increase after passive warming, the data suggest some unique role for endogenous BZD in thermoregulation during exercise. |
