Results from the present investigation support the theory that ingesting a multiflavonoid plus fish oil supplement in combination with aerobic exercise significantly reduces SBP and AIx at 30 minutes after exercise and significantly increases resting levels of FRAP in postsupplementation levels compared with presupplementation.
The attenuation of AIx, a measure linked to aortic arterial stiffness, was likely due to the significant increase in FRAP which may have led to greater bioavailability of NO within the elastic modulus of the aortic vessel. Since the amount of reflected wave was decreased, the amount of elastic “cushion” had to be augmented to absorb the pulsatile bolus of blood being ejected from the left ventricle. The increased expression of NO following flavonoid and fish oil supplementation has been shown in many studies [7
]. Interestingly, despite the decrease in AIx, there was no decrease in PWV as both are considered to be indicators or measures of arterial stiffness. This finding is not surprising since it has been shown on several occasions that AIx is not proportional to PWV in systolic hypertension, but instead has been shown to be inversely related [20
]. In one study by Vyas et al. [21
], AIx was inversely related to aortic PWV and weakly related to aortic compliance and an increase in AIx is not a reliable replacement for increased aortic stiffness. However, it did show that higher stiffness (increased PWV and lower compliance) was associated with a lower AIx [21
]. The increased distensibility that resulted in a more favorable augmentation index could be due to the composition of the matrix of the vessel. The aorta has been shown to have the largest amount of eNOS potential and the supplement may have the greatest potential to upregulate this synthase pool.
Although the antioxidant supplementation did not have any effect on vascular distensibility (PWV) or resting SBP, the magnitude of PEH was significantly decreased in the 30-minute postexercise period after supplementation for the treatment condition when compared to the placebo without showing a correlating decrease in HR or PWV. Although resting SBP did not change with supplementation, there was a significant decrease in the systolic component of PEH. Because there was no change in PWV, one can only postulate that arterial distensibility was not the cause of this reduction in blood pressure. One possible explanation is that supplementation caused a decrease in oxidative stress, potentially due to an increase in antioxidant power (an increase in FRAP). A reduction in ROS would increase the bioavailability of NO, stimulating vasodilation. A second theory would be a change in sympathovagal regulation in which the supplement may induce a sympatholytic effect on sympathetic tone, thereby increasing the vagal tone.
The results of the present investigation support research done by Edwards et al. [22
] who demonstrated a reduction in resting blood pressure in hypertensive versus pre-hypertensive patients following an antioxidant supplementation regimen of quercetin. Many studies have shown a beneficial decrease in resting blood pressure in hypertensives, indicating the possibility that this decrease in blood pressure can affect the hypertensive patient but not a normotensive or pre-hypertensive patient. To those authors' knowledge, this is the first investigation to support the premise that prehypertensives may also benefit from an antioxidant and n-3 fatty acid supplement. This also supports research demonstrating that antioxidants (like quercetin and Vitamin C) increased plasma quercetin levels but had no influence on oxidative stress or antioxidant capacity measures [23
] and that chronic quercetin ingestion does not protect against exercise-induced oxidative stress or inflammation [24
]. Without this protective mechanism against oxidative stress, it is possible that NO was not increased. Much of the research concerning antioxidant use has been shown to have beneficial effects in animal models [25
], but there is a lack of benefits shown in human models. Speculatively, this could be due to the dosages ingested by humans being too large to be absorbed and simply excreted.
The significant increase in FRAP in the treatment group demonstrates that the total plasma antioxidant capacity increased following supplementation which may be related to the further decrease in systolic blood pressure during the postexercise period. This increase in antioxidant capacity could lead to an increase of free radical scavenging by antioxidants, thereby decreasing oxidative stress and potentially increasing NO levels. An increase of NO in the vasculature would lead to vasodilation and a further decrease of the systolic blood pressure after exercise. Interestingly, resting blood pressure following two weeks of supplementation was unchanged, demonstrating that a decrease in blood pressure in the 30-minute postexercise period from antioxidant supplementation occurred in conjunction with postexercise vasodilation.
The favorable effects of the supplement could be due to the multiflavonoid plus fish oil approach, unlike the single antioxidant approach that many previous research investigations have experimented with. The ingestion of many of the elements in the supplement has not shown consistent vascular benefits in humans. Chronic quercetin ingestion has not been proven to protect against exercise-induced oxidative stress or inflammation [24
]. EGCG was shown to decrease stroke and mortality in stroke-prone, spontaneously hypertensive rats [11
]. In relation to blood pressure, EGCG has been shown to decrease systolic blood pressure and enhances endothelial function and insulin sensitivity of spontaneous hypertensive rats, yet there is a paucity of the literature regarding the cardiovascular benefits of EGCG in humans.
People with a high risk of ischemic heart disease and/or hypertension could benefit from eating fish as clinical trials have shown that undergoing supplementation of fatty acids like fish oil can improve arterial elasticity in subjects with diabetes or dyslipidemia and even improved large arterial elasticity in overweight hypertensive patients [12
]. A combination of fish oil and aerobic exercise has been shown to be more effective than individual components in decreasing triglycerides, increasing high-density lipoprotein (HDL), and improving endothelium dependent arterial vasodilation [33
]. However, results from fish oil studies are equivocal. A 12-week double-blind crossover designed study by Lofgren et al. [34
] found no change from pre-supplementation in systolic or diastolic blood pressure in middle-aged normotensive men [34
In conclusion, we have found that a novel multiflavonoid plus fish oil supplement decreases augmentation index and systolic blood pressure with concomitant increases in FRAP, suggesting that cardiovascular benefits may be realized from this course of supplementation.