The combined influence of fat consumption and repeated mental stress on brachial artery flow-mediated dilatation: a preliminary study.

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.

The impact of handgrip exercise duty cycle on brachial artery flow-mediated dilation.

Endothelial function is essential for vasoprotection and regulation of vascular tone. Using handgrip exercise (HGEX) to increase blood flow-associated shear stress is an increasingly popular method for assessing brachial artery endothelial function via flow-mediated dilation (FMD). However, different exercise duty cycles [ratio of handgrip relaxation: contraction (seconds)] produce different patterns of brachial artery shear stress with distinct antegrade/retrograde magnitudes. To determine the impact of HGEX duty cycle on brachial artery %FMD, three distinct duty cycles were employed while maintaining a uniform mean shear stress. Brachial artery diameter and mean blood velocity were assessed via echo and Doppler ultrasound in 16 healthy male subjects. Shear stress was estimated as shear rate (SR = blood velocity/brachial artery diameter) and the target mean SR during HGEX was 75 s(-1). Subjects performed three 6-min HGEX trials on each of 2 days (like trials averaged). In each trial, subjects performed one of the three randomly ordered HGEX duty cycles (1:1, 3:1, 5:1). %FMD was calculated from baseline to the end of HGEX and (subset N = 10) during each minute of HGEX. Data are mean ± SD. As intended, mean SR was uniform across duty cycles (6 min HGEX average: 72.9 ± 4.9s(-1), 72.6 ± 3.6s(-1), 72.8 ± 3.5 s(-1), p = 0.835), despite differences in antegrade/retrograde SR (p < 0.001). End-exercise %FMD (4.0 ± 1.3 %, 4.1 ± 2.2 %, 4.2 ± 1.4 %, p = 0.860) and %FMD during exercise (p = 0.939) were not different between duty cycles. These data indicate that the endothelium responds to the mean shear stress and is not specifically sensitive to the contraction/relaxation or retrograde shear stress created by a range of HGEX protocols.

Impaired handgrip exercise-induced brachial artery flow-mediated dilation in young obese males.

Flow mediated dilation (FMD) stimulated by different shear stress stimulus profiles may recruit distinct transduction mechanisms, and provide distinct information regarding endothelial function. The purpose of this study was to determine whether obesity influences brachial artery FMD differently depending on the shear stress profile used for FMD assessment. The FMD response to a brief, intermediate, and sustained shear stress profile was assessed in obese (n = 9) and lean (n = 19) young men as follows: brief stimulus, standard reactive hyperemia (RH) following a 5 min forearm occlusion (5 min RH); intermediate stimulus, RH following a 15 min forearm occlusion (15 min RH); sustained stimulus, 10 min of handgrip exercise (HGEX). Brachial artery diameter and mean shear stress were assessed using echo and Doppler ultrasound, respectively, during each FMD test. There was no group difference in HGEX shear stress (p = 0.390); however, the obese group had a lower HGEX-FMD (5.2 ± 3.0% versus 11.5 ± 4.4%, p < 0.001). There was no group difference in 5 min RH-FMD (p = 0.466) or 15 min RH-FMD (p = 0.181); however, the shear stress stimulus was larger in the obese group. After normalization to the stimulus the 15 min RH-FMD (p = 0.002), but not the 5 min RH-FMD (p = 0.118) was lower in the obese group. These data suggest that obesity may have a more pronounced impact on the endothelium's ability to respond to prolonged increases in shear stress.

Evidence that meal fat content does not impact hemodynamic reactivity to or recovery from repeated mental stress tasks.

The magnitude (reactivity) and duration (recovery) of hemodynamic stress responses are predictive of cardiovascular risk, and fat intake has been shown to enhance hemodynamic reactivity to psychological stress tasks. The objective of this study was to determine the impact of a high-fat meal (HFM) on the magnitude and stability of hemodynamic stress reactivity and recovery. This was assessed by: (i) the peak changes from baseline to during stress for heart rate (HR); mean, systolic, and diastolic blood pressure; cardiac output; and total peripheral resistance; and (ii) the residual arousal in hemodynamic parameters at 2 points post-stress ("early" and "late" recovery). On different days, 10 healthy males (aged 23.2 ± 3.3 years) consumed either a HFM (54 g fat) or low-fat meal (LFM; 0 g fat) (∼1000 calories each), followed by 4 hourly 10-min stress tasks (mental arithmetic and speech tasks). Pre-stress (baseline) parameters did not differ between HFM and LFM conditions (all P > 0.05). Plasma triglycerides were greater following the HFM versus the LFM (P = 0.023). No reactivity or recovery parameters differed between meals (all P > 0.05). Stress reactivity and recovery parameters were stable over the 4 stress tasks (main effects of time, all P > 0.05), with the exception of HR (P < 0.05). Contrary to previous reports, meal fat content did not impact hemodynamic reactivity to laboratory stressors. These data also provide the first evidence that meal fat content does not impact hemodynamic recovery from repeated mental stress tasks.