Influence of acute fasting on cerebrovascular reactivity during mental stress

Document Type


Publication Date



Department of Kinesiology and Integrative Physiology


Acute fasting has been adopted in fitness communities, and has been practiced for religious purposes. Short‐term fasting does not affect cognitive function, and therefore may not affect cerebrovascular responsiveness. Cerebral blood flow velocity increases with mental stress, however the combined influences of an acute fast and mental stress on cerebrovascular responses are unknown. The purpose of this study was to describe the effects of a 24‐hour, water‐only fast on cerebral blood flow velocity responses to mental stress in a small cohort of research volunteers. Eight young healthy participants (7 males, average age of 25 yrs) completed the protocol in a fed state (4 hours post‐prandial) and in a fasted state (24–25 hours post‐prandial). Whole blood was collected and analyzed before experimentation for β‐Ketones, total cholesterol, HDL, LDL, triglycerides (TRG), and glucose. With participants in a supine position, we recorded the electrocardiogram, beat‐to‐beat arterial pressure (finger plethysmography), and cerebral artery blood flow velocity (transcranial Doppler). After a 5‐min baseline, participants performed 5‐min of mental stress via mental arithmetic (rapid continuous subtraction). Mental stress reactivity was calculated as the mean stress response for each minute of mental stress minus the corresponding 5‐min baseline. The minute‐by‐minute reactivity was analyzed with repeated measures ANOVA. Blood variables were analyzed with paired t‐tests. Data were expressed as mean ± SE. Baseline blood variables were different in the fasted compared with the fed state: TRG (112±14 fed vs. 68±13 mg/dL fasted; p<.01) Glucose (101±5 fed vs. 79±6 mg/dL fasted; p<.01) and β‐Ketone (.1±.01 fed vs. .5±.2 mmol/L fasted; p<.05). Mean arterial pressures and heart rate reactivities to mental stress were not affected by fasting. Mean cerebral blood flow velocity reactivity to mental stress was reduced in the fasted compared with the fed condition (condition × time, p<.01), with a particular divergent responsiveness during the third minute of mental stress. The results we present are new, but preliminary. We did not attempt to ascribe mechanisms to fasting and cerebral blood flow velocity reactivity during mental stress. The changes we observed with our preliminary data set suggest that fasting, and associated changes of plasma glucose, β‐Ketone and TRG may be associated with reductions of cerebral blood flow velocity during mental stress.

Publication Title

The FASEB Journal