The physiological and cognitive performance of acclimatized soldiers undertaking routine patrol and reconnaissance activities in the tropics was investigated. Data were obtained during a patrol and a reconnaissance exercise followed by a short assault. Ambient conditions were characterized by temperatures of 30 to 33 degrees C, low humidity (52-59%), and moderate to high solar radiation. Maximum metabolic rates during patrol were high, although the equipment carried was modest and the terrain was not severe. Rectal temperatures peaked at 38.2 and 38.4 degrees C for patrol and assault activities, respectively; peak heart rates were 160 beats min-1 for each activity. Sweat rates of approximately 9 and 14 g kg-1 body weight h-1 were recorded for patrol and assault activities, respectively. The soldiers maintained adequate hydration levels and displayed no evidence of deterioration in cognitive performance. The data show that routine operational activities in tropical conditions induced physiological strain in acclimatized soldiers. However, this strain was not maintained at hazardous levels for lengthy periods.

Tacrine (THA) selectively modulates binding of M₁ ligands in an allosteric fashion causing positive cooperativity. The binding affinity of THA to M₁ and M₂ cholinoceptors is similar. It is therefore proposed that the allosteric selectivity of THA is a function of the binding site and not of THA itself. Its interaction of M₁ and M₂ cholinoceptors was examined in guinea pig brain homogenates using the selective M₁ and M₂ antagonists [³H]-pirenzepine ([³H]PZ) and [³H]AF-DX 384. The dissociation constants were 0.36 nmol/l for the M₁ receptor and 0.23 nmol/l for the M₂ receptor. We also compared the binding of THA and methoctramine (MTA) at M₂ receptors. Tacrine displayed similar binding affinity for both M₁ and M₂ receptor subtypes. MTA was 100 times more potent an inhibitor of [³H]AF-DX 384 binding at M₂ receptors than THA. In addition, THA was found to slow the dissociation of [³H]PZ from the M₁ receptor. In contrast, the dissociation of [³H]AF-DX 384 from M₂ receptor subtypes was unaffected. We conclude that THA acts as an agonist at M₁ cholinoceptors because it slowed the dissociation of [³H]PZ. At M₂ cholinoceptors its nature is that of an antagonist because it had no effect on [³H]AF-DX 384 dissociation.

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