It is widely accepted that there is a positive relationship between the fat content of a meal and the resultant lipaemia , inflammation , coagulation and oxidative stress [30, 31]. The current study demonstrated a significant increase in arterial stiffness measured as PWV with a significant decrease in wave reflection measured as AIx compared to baseline in the four hour period in response to a high fat meal. No differential effect was seen on either PWV or AIx when some of the SFA in the SFA-meal was substituted for MUFA.
Effect of the test-meal fat quantity on postprandial arterial stiffness and wave reflection
A significant increase from baseline of 0.3 m/s in PWV following the high-fat meal was seen in the current study although this was not significant when the data were adjusted for the increase in MAP. The meal provided 56 g dietary fat and data from a number of other studies of lean healthy men [32, 33] demonstrate an increase in serum triacylglycerol rich lipoproteins (TRLs) in response to a similar amount of dietary fat. It has been suggested that this hypertriglyceridaemic state may affect non-serum risk factors for CVD such as vascular function . A number of studies have examined the acute effect of fat quantity on postprandial vascular function in healthy participants [12–24, 35, 36] and although there were methodological differences between the studies, results concluded an impairment in vascular function following a meal rich in fat . The majority of these studies used flow mediated dilation (FMD) or forearm blood flow (FBF) as their measure of vascular function. Only three studies have examined the acute effect of fat ingestion where arterial stiffness was the primary outcome measure but suffer from methodological differences [25–27]. The measurement of carotid-femoral PWV that was used in the current study is widely recognised as the gold-standard method of assessing arterial stiffness. The first of these three studies demonstrated an impairment in systemic arterial compliance in response to 50 g fat . The second showed no change in PWV, pulse wave analysis (PWA) or digital volume pulse (DVP) in response to 60 g fat  although carotid-radial PWV was used which has not been shown to be of prognostic value and is not recommended for assessing arterial stiffness. The third study by Phillips and colleagues (2010) showed an acute decrease in AIx after 58 g fat was consumed . Two of the studies were carried out in lean and obese men [25, 26] with no differential effect of body mass index (BMI). The third study  was carried out in both men and women although BMI was not reported. While one may argue that the increase in PWV shown in the current study was BP dependent and therefore not significant, we believe that this unfavourable acute haemodynamic effect of a high-fat meal does support a view of a pro-atherogenic postprandial milieu.
The mechanism proposed by Nestel and colleagues  is that postprandial serum TRLs contribute to arterial stiffening, a hypothesis that is put forward by the authors of the current study. Others have observed this association and have postulated that an increase in lipolysis may increase the production of reactive oxygen species (ROS) and increase the possibility that circulating fatty acids may become oxidised . In addition, the ROS can decrease the bioavailability of nitric oxide (NO) [18, 20], either through decreased synthesis and/or enhanced degradation . Through effects on coagulation and inflammatory signalling pathways in the endothelium, circulating TRL remnants which result from a high-fat meal may increase the breakdown of NO [39, 40]. Serum TRLs were not measured in the current study although it is hypothesised that significant hypertriglyceridaemia occurred in response to the 56 g fat consumed which had either a direct or indirect effect on vascular health.
Most published work shows a reduction in wave reflection following a high-fat meal. In the current study, there was a significant decrease in AIx compared to baseline in response to the high-fat meal, although this disappeared when adjusted for the increase in heart rate and MAP. However, AIx75, which is corrected for heart rate, significantly decreased following the high-fat meal, independent of a change in MAP. This reduction is counter intuitive when we consider data showing impaired endothelial function following the acute ingestion of dietary fat and larger studies are required to improve our understanding. One of the hypotheses put forward to explain this paradox includes the proposal that the ingestion of any type of food causing a reduction in wave reflection from the splanchnic bed  which may be related to the release of insulin, a known vasodilator .
Effect of the test-meal fatty acid quality on postprandial arterial stiffness and wave reflection
The second aim of the current study was to assess whether replacement of dietary SFA with MUFA would affect postprandial arterial stiffness measured as PWV and wave reflection measured as AIx, and results indicated that no differential effect was seen over the 4 hour intervention period. When serum markers of CVD risk are measured, it is well accepted that an MUFA-rich diet results in a less atherogenic profile compared to a SFA-rich diet . A number of studies have investigated the effect of isoenergetic meals of different fatty acid composition on measures of vascular function and substantial differences in study design has led to difficulties in drawing conclusions . In addition, some studies tested healthy subjects [38, 44–48] whilst other investigated hyercholesterolaemic patients , type two diabetics [50, 51] or adults with the metabolic syndrome . The overall evidence suggests a moderate decrease in vascular function following a SFA-rich meal  but the data are less consistent when SFA is replaced by MUFA. Importantly, the majority of studies used FMD, FBF or ischaemic reactive hyperaemia  as measures of vascular function and only one study  examined the effect on arterial stiffness measured as PVW and/or PWA. Berry and colleagues  tested the postprandial effect of a stearic acid rich meal (50 g fat) versus an oleic-acid rich meal (50 g fat) and showed a decrease in PWV and PWA after both meals when compared with baseline. Such results should be interpreted with caution however because although stearic acid is correctly classified as a SFA, it can result in an uncharacteristically low postprandial lipaemic and oxidative stress response  when compared to a meal rich in the MUFA oleic acid. In the current study, the main sources of SFA in the SFA-meal were palmitic acid and myristic acid and therefore this issue was avoided.
The current study showed a significant increase in both brachial and aortic SBP in response to the high-fat meal but no differential effect of fatty acid quality on either measure. It is unknown however whether the increased systolic blood pressure was caused by the increase in PWV or vice versa. Increased blood pressure in response to a high-fat meal has been seen elsewhere  and it is hypothesised that the fat-load-induced increase in circulating free fatty acids and TRLs stimulate production of ROS [53, 54], and contribute to endothelial dysfunction , hypothesised to contribute to hypertension. In the current study, whether the meal was rich in MUFA or SFA had no differential effect on either brachial or aortic systolic blood pressure.
It could be argued that the changes in vascular function observed over the 4 hour postprandial period in the current study may be as a result of eating per se rather than dietary fat intake. Studies have shown that dietary intake, regardless of the composition, can cause a change in arterial stiffness [56–58]. Eating is known to cause changes in a number of hemodynamic responses  although these tend to lead to vasodilation rather than vasoconstriction , as previously discussed. Studies where carbohydrate has replaced fat have resulted in improved endothelial function . Whilst the current study allowed us to test the postprandial effect of a fat rich meal compared to baseline, it was not specifically designed with this in mind and as such did not use a control isoenergetic low-fat/high carbohydrate meal. The other components of any test-meal can make the interpretation of the resultant data somewhat complex. The protein , anti-oxidant [61, 62] and fibre content  of test-meals can complicate the interpretation of data and make it difficult for conclusions to be drawn on the effect of fats of differing quality. The test-meals used in the current study were identical in volume, taste, appearance and in macronutrient composition other than a difference in MUFA and SFA content. One limitation in the current study however, is that the MUFA-meal contained olive oil which is known to contain phenolic compounds. Ruano and colleagues (2005) showed that a meal containing high-phenolic virgin olive oil improves ischemic reactive hyperaemia during the postprandial state, a phenomenon which might be mediated via a reduction in oxidative stress and the increase of nitric oxide metabolites . The phenolic content of the olive oil used in the current study was not measured and therefore could have been a confounding factor. In addition, it would have been preferable if the intervention period was longer than 240 minutes since studies and a recently published expert panel statement suggest that many serum markers take greater than 240 minutes to return to baseline after a high-fat meal [26, 65].
Another limitation of the current study is that chronic or habitual dietary intake was not measured. In a review published by Lopez-Miranda and colleagues in 2007 , it was suggested that the habitual diet of an individual may influence the postprandial response  Williams  suggested that background diets rich in monounsaturated fat or omega-3 polyunsaturated fatty acids tend to lower the postprandial lipid response compared with diets rich in saturated fatty acids [68–70]. The key limitation of the current study however is the lack of simultaneous collection of venous blood samples. This would have allowed the measurement of circulating TRLs, insulin, markers of oxidative stress and other parameters which would facilitate a greater understanding of the mechanism behind the relationship between dietary fat and arterial stiffness.