Fast-food meal reduces peripheral artery endothelial function but not cerebral vascular hypercapnic reactivity in healthy young men

Abstract

Consumption of a representative fast-food meal (FFMeal) acutely impairs peripheral conduit artery vascular function; however, the effect on cerebral vascular function remains unknown. This study tested the hypothesis that a FFMeal would impair cerebral vascular function as indexed by an attenuated increase in cerebral vascular conductance (CVCI) in the middle cerebral artery (MCA) during a hypercapnic challenge. Ten healthy men (age: 24 ± 3 years, BMI: 24.3 ± 3.8 kg/m² ) were studied under two conditions; a standardized FFMeal (990 kcals, 50% fat, 36% carbohydrate, 14% protein, and 2120 mg sodium) and a fasting control condition. Basal hemodynamics, cerebral vasomotor reactivity (CVMR), and brachial artery flow-mediated dilation (BA FMD) were completed after an overnight fast (Pre) and again 2 h and 4 h later both days. To assess CVMR, subjects rebreathed from a 5-L bag while MCA velocity (MCAV_mean ) was measured using transcranial Doppler (TCD) ultrasound and converted into CVCI (MCAV_mean /mean arterial pressure). Peripheral artery endothelial function was assessed via BA FMD following a standard 5-min occlusion protocol. As expected, BA FMD was reduced at 2 h (Pre: 6.6 ± 1.7% vs. 5.2 ± 1.8%, P = 0.01). However, despite significant impairment in BA FMD, neither peak CVCI_%baseline nor CVMR was affected by the FFMeal (Control-Pre: 1.9 ± 1.1, 2 h: 2.1 ± 1.1, 4 h: 1.7 ± 1.1 ∆CVCI%·∆P_ET CO₂^-1 vs. FFMeal-Pre: 2.1 ± 1.1, 2 h: 2.2 ± 0.7, 4 h: 1.9 ± 0.9 ∆CVCI%·∆P_ET CO₂^-1 , time × condition P = 0.88). These results suggest that cerebral vascular reactivity to hypercapnia in healthy young men is not altered by an acute FFMeal.

Keywords: Atherosclerosis; Western diet; endothelial function; human; postprandial.

Figure 1

(A) Peak CVCI (% Baseline) at Pre, 2 h, and 4 h in control (open bars) and FFMeal (solid bars) conditions. No significant differences were detected across time or condition (interaction: P = 0.33). (B) ∆P_ETCO ₂ from resting levels at peak CVCI indicating that peak CVCI occurs at a consistent ∆P_ETCO ₂ (time x condition: P = 0.10). (C) There was no difference in reactivity (∆CVCI·∆P_ETCO ₂ ⁻¹) across time or condition (P = 0.88). All data are expressed as Mean ± SD.

Figure 2

(A) The change in BA FMD from Pre at 2 h and 4 h in control (open bars) and FFMeal (solid bars) conditions. Following FFMeal, BA FMD was reduced at 2 h compared to control. All data are expressed as Mean ± SD. (B) The relationship between the change in serum [TG] and BA FMD from Pre to 2 h indicating a reduction in BA FMD with an increase in serum [TG].

Figure 3

(A) Peak reactive hyperemia blood velocity in the brachial artery following 5 min of occlusion in control (open bars) and FFmeal (solid bars). (B) Reactive hyperemia AUC (i.e., total blood flow) during the first 120 sec post cuff release. All data are expressed as Mean ± SD. Neither time nor condition significantly affected either index of peripheral microvascular function.