(747.4) Acute Fasting Decreases Tolerance to Lower Body Negative Pressure

Poster Board Number: E393

Joshua Gonzalez (Oregon Health amp; Science University, Michigan Technological University), William Cooke (Michigan Technological University)

Potential health benefits of an acute fast include reductions in blood pressure and increases in vagal cardiac control. These purported health benefits could put fasted humans at risk for cardiovascular collapse when exposed to central hypovolemia. Intense lower body negative pressure (LBNP) induces reproducible and reversible central hypovolemia. The purpose of this study was to investigate the influence of an acute 24-hour fast on tolerance to severe LBNP. We tested the hypothesis that fasting would reduce tolerance to severe LBNP. Ours was a randomized, crossover design with an LBNP tolerance test occurring 3-hrs postprandial (fed) and 24-hrs postprandial (fast). A standardized meal was provided for both conditions. Criteria for termination of LBNP was; 1) a drop in systolic pressure of 15 mmHg or greater for 10 s and/or 2) sudden bradycardia. Eighteen young (23±0.7 yrs), normotensive, non-obese (25±0.8 BMI), participants were brought to presyncope. We measured blood glucose (GLU), ketones (β-OHB), and triglycerides (TRG) to confirm a successful fast. With subjects in a supine position, we recorded the ECG, beat-to-beat arterial pressure (finger plethysmography), muscle sympathetic nerve activity (MSNA; N=7), and forearm blood flow via venous occlusion plethysmography (VOP; N=12). Following a 5-min baseline, LBNP was increased in 15 mmHg increments every 5 min in a stepwise manner until onset of presyncope. LBNP levels eliciting presyncope were denoted as 100% tolerance, data were assessed relative to this normalized maximal tolerance by expressing LBNP as 80, 40, and 0% (baseline) of maximal tolerance. Data are expressed as means ± SE. P-values ≤ 0.05 were considered statistically significant and indicated by an (*). Changes in TRG, GLU and β-OHB with fasting were consistent with expectations: TRG and GLU decreased (TRG; 130±16 fed vs. 78±9* mg/dL fast) (GLU; 100±3 fed vs. 81±2* mg/dL fast), and β-OHB increased (β-OHB; 0.12±.04 fed vs. 0.47±.11* mmol/L fast). Our participants were similarly hydrated, measured via urine specific gravity, (1.0168±.002 fed vs. 1.0122±.003 a.u. fast) and weight stable (77.8±3.6 fed vs. 76.9±3.4 kg fast) between conditions. Tolerance to central hypovolemia was decreased by ~10% in the fasted condition measured via total duration of negative pressure (1370±89 fed vs. 1229±94* s fast). At each normalized time point, heart rate and MSNA increased similarly in both conditions. Additionally, systolic blood pressure and stroke volume decreased similarly in both conditions. Both forearm blood flow (FBF) and forearm vascular resistance (FVR) are expressed as a percent change from 0 to 100%. ΔFBF significantly decreased in the fed condition at 100% (-45.8±4.8 fed vs. -23.5±8.1* % fast) and ΔFVR increased in the fed condition at 100% (141.6±34.5 fed vs. 67.1±24.8* % fast). Our results suggest that acute fasting reduces tolerance to central hypovolemia by blunting increases in peripheral vascular resistance, and could lead to earlier decompensation when compared to the normal, fed state.

This work was supported by a grant from the Michigan Space Grant Consortium, an endowment from the Portage Health Foundation (Houghton, Michigan), and by an Oregon Health amp;amp; Science University Fellowship for Diversity in Research.