A fluid response: Alpha-amylase reactions to acute laboratory stress are related to sample timing and saliva flow rate

•sAA increase to a common laboratory stressor was only seen immediately post-task.•No sAA increase was observed during the acute stress tasks, unlike cardiovascular indices.•Direction and magnitude of the sAA response during mental stress varied with sample timing.•Adjustment for saliva flow rate robustly altered the magnitude of sAA responses.•sAA release appears co-determined by parasympathetic and sympathetic activity. Salivary alpha-amylase (sAA) is used as a sympathetic (SNS) stress marker, though its release is likely co-determined by SNS and parasympathetic (PNS) activation. The SNS and PNS show asynchronous changes during acute stressors, and sAA responses may thus vary with sample timing. Thirty-four participants underwent an eight-minute memory task (MT) and cold pressor task (CPT). Cardiovascular SNS (pre-ejection period, blood pressure) and PNS (heart rate variability) activity were monitored continuously. Unstimulated saliva was collected repeatedly during and after each laboratory stressor, and sAA concentration (U/ml) and secretion (U/minute) determined. Both stressors increased anxiety. The MT caused an immediate and continued cardiac SNS activation, but sAA concentration increased at task cessation only (+54%); i.e., when there was SNS–PNS co-activation. During the MT sAA secretion even decreased (−35%) in conjunction with flow rate and vagal tone. The CPT robustly increased blood pressure but not sAA. In summary, sAA fluctuations did not parallel changes in cardiac SNS activity or anxiety. sAA responses seem contingent on sample timing and flow rate, likely involving both SNS and PNS influences. Verification using other stressors and contexts seems warranted.