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The combined influence of fat consumption and repeated mental stress on brachial artery flow‐mediated dilatation: a preliminary study
Author(s) -
Poitras Veronica J.,
Slattery David J.,
Levac Brendan M.,
Fergus Stevenson,
Gurd Brendon J.,
Pyke Kyra E.
Publication year - 2014
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/expphysiol.2013.077131
Subject(s) - postprandial , brachial artery , mental stress , meal , calorie , medicine , endothelial dysfunction , endothelium , supine position , cardiology , endocrinology , blood pressure , insulin
New FindingsWhat is the central question of this study? Both a high‐fat meal and acute mental stress can impair conduit artery endothelial function. The objective of this study was to determine whether the combination of a high‐fat meal and repeated postprandial stressful tasks would exacerbate dysfunction versus either stimulus alone.What is the main finding and its importance? Endothelial function was modestly greater when the postprandial state was accompanied by mental stress. Thus, in healthy subjects acute stress may confer protection from a negative impact of food consumption, possibly due in part to a stress‐induced reduction in plasma phosphorus levels. These findings challenge the position of acute mental stress as universally detrimental to endothelial function.Experienced separately, both acute mental stress and high‐fat meal consumption can transiently impair endothelial function, and the purpose of the present study was to investigate their combined impact. On four separate days, 10 healthy men (23 years old) underwent brachial artery flow‐mediated dilatation (FMD) tests, before and hourly for 4 h post‐consumption of a high‐fat (HFM; 54 g fat) or low‐fat meal (LFM; 0 g fat; each meal ∼1000 calories), with hourly mental stress (mental arithmetic, speech) or control (counting) tasks (conditions HFM+S, LFM+S, HFM and LFM). Data are presented as means ± SD. Plasma triglycerides increased and remained elevated after the high‐fat but not the low‐fat meal ( P = 0.004) and were not affected by mental stress ( P = 0.329). Indices of stress reactivity increased during mental stress tasks (mean arterial pressure, ∼∆20 mmHg; heart rate, ∼∆22 beats min −1 ; salivary cortisol, ∼∆2.37 nmol l −1 ; and plasma noradrenaline, ∼∆0.17 ng ml −1 ) and were not influenced by meal ( P > 0.05). There was no effect of the type of meal on FMD ( P = 0.562); however, FMD was 4.5 ± 0.5% in the control conditions and 5.8 ± 0.6% in the mental stress conditions ( P = 0.087), and this difference was significant when normalized for the shear stress stimulus (FMD/area under the curve of shear stress, P = 0.045). Overall, these preliminary data suggest that postprandial FMD was augmented with mental stress irrespective of meal type. These results are contrary to previous reports of impaired endothelial function after mental stress or fat consumption independently and highlight the need to further investigate the mechanisms underlying the interactions between these factors.