Cardiac disease is the primary cause of death in the United States of America (CDC, 2017). Despite ongoing efforts and investments to improve cardiac health in the United States, most of the population will suffer from cardiovascular diseases. There is a multitude of research supporting that diet can contribute to cardiac disease, but it is less known that diet can greatly contribute to regulation and reversal of cardiovascular disease processes (Huang et al., 2012; Satija et al., 2017; Kim et al., 2019). Existing research supports the efficacy of plant-based diets to manage and reverse certain cardiac diseases (Tuso et al., 2015; Esselstyn, 1999; Ornish 1998; Campbell et al., 1998). Plant-based diets have the potential to save many lives and drastically reduce healthcare costs. The purpose of this literature review is to evaluate current research on plant-based diets as interventions for cardiac disease and to identify the reasoning for underutilization of plant-based diets as intervention with cardiac health within the United States population. A database search of CINAHL Plus, MEDLINE, BIOSIS, Cochrane, Google Scholar, and PubMED was conducted and university librarians were utilized. Inclusive criteria and keyword searches were comprised of coronary artery disease and plant-based diets, cardiac disease and diet interventions, intensive lifestyle changes for reversal of coronary heart disease, plant-based diets and cardiac disease and inflammation, and plant-based diets reducing cardiac inflammation.

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African Americans have the highest prevalence of hypertension in the world which may emanate from their predisposition to heightened endothelial inflammation. The purpose of this study was to evaluate the in vivo influence of aerobic exercise training (AEXT) on the anti-inflammatory biomarker interleukin-10 (IL-10), the inflammatory biomarkers interleukin-6 (IL-6) and C-reactive protein (CRP), the endothelial activation marker CD62E+ endothelial microparticle (EMP), and the vasodilatory biomarker nitric oxide (NO) in an African American cohort. A secondary purpose was to conduct a complementary in vitro study on the influence of IL-10 and laminar shear stress (LSS) on African American endothelial cells. In Vivo Methods: The subjects were sedentary, putatively healthy, 45-71 y/o African American men and women. A pre-post study design was employed with baseline and post-intervention evaluations of office blood pressure, fasting blood sampling, and graded exercise testing. Subjects engaged in AEXT three times per week for six months at an intensity equivalent to 65% of their VO2max. Plasma concentrations of IL-10 and IL-6 were determined using an enzyme-linked immunosorbent assay. Levels of nitric oxide metabolites (NOx) were determined using a modified Griess assay. Plasma samples for CRP were sent to Quest Diagnostics Inc. for analysis. Circulating CD62E+ EMPs were quantified using a flow cytometer. In Vitro Methods: Human umbilical vein endothelial cells (HUVEC) from an African American donor were cultured and exposed to four experimental conditions: Static, Static with IL-10 Incubation, LSS at 20 dynes/cm2, and LSS at 20 dynes/cm2 with IL-10 Incubation. Western blotting experiments were conducted to measure endothelial nitric oxide synthase (eNOS) protein expression and its phosphorylated form (p-eNOS) at Serine 1177 in the cells in all four conditions. A modified Griess assay was used to measure NOx in the cell culture supernatant. In Vivo Results: There was a significant increase in NO (n=24; p=0.002), a significant decrease in IL-6 (n=32; p=0.04), a significant decrease in CRP (n=37; p=0.01), and a significant decrease in CD62E+ EMPs (n=28; pIn Vitro Results: Protein expression levels of both eNOS and p-eNOS were significantly increased in the LSS at 20 dynes/cm2 and LSS at 20 dynes/cm2 with IL-10 Incubation experimental conditions when compared to the Static experimental condition. NO concentration levels were significantly increased in the LSS at 20 dynes/cm2 and LSS at 20 dynes/cm2 with IL-10 Incubation experimental conditions when compared to the Static experimental condition. Conclusion: Based on these results, AEXT may be a viable, non-pharmacologic method to improve vascular inflammation status and vasodilation, and thereby contribute to reduced hypertension and cardiovascular disease risk in African Americans. / Kinesiology

<p> Physical inactivity or deconditioning has been shown to be an independent risk factor for cardiovascular disease. Contrary to the previously demonstrated effects of exercise training on the cardiovascular system, the vascular adaptations that occur with a deconditioned state have not been adequately characterized within a young, healthy population. Thus, it was the interest of the present study to examine vascular adaptations to 12 days of unilateral lower limb immobilization (ULI) in young, healthy humans. Previous studies have used other models to mimic a deconditioned state such as paraplegia, simulated micro gravity and bed rest; however, such models are also associated with factors that are not physiologically applicable to normal deconditioning in the able-bodied population. Fifteen young, healthy participants [age: 20.6±0.51 (mean ± SEM)] participated in the 12-day knee-braced immobilization period that consisted of PRE and 12-DAY time point testing sessions. Measurements of supine common carotid, popliteal and common femoral artery cross sectional compliance as well as popliteal artery endothelial function (using flow mediated vasodilation (FMD)) were acquired prior to the 12-day immobilization (PRE) and on the 12th day of the immobilization (12-DAY). Arterial characteristics of the Immobilized legs (IMM) and NON-Immobilized (NIM) legs were assessed by echo Doppler ultrasound and applanation tonometry.</p> <p> Resting carotid artery cross sectional compliance and blood flow showed no change throughout the 12-day time period, (Compliance: PRE = 0.001209 ± 0.000067 mm^2/mmHg, 12-DAY= 0.001230 ± 0.00085 mm^2/mmHg; Blood Flow: PRE = 242.8±14.2 mL/min, 12-DAY = 226.0±14.27 mL/min). Popliteal artery cross sectional compliance decreased significantly over the 12 day time period in both legs (p<0.05) (IMM PRE = 5.7±0.4 10^-4mm^2/mmHg, IMM 12-DAY = 3.8±0.4 10^-4mm^2/mmHg; NIM PRE= 6.7±0.9 10^-4mm^2/mmHg, NIM 12-DAY = 5.5±0.6 10^-4mm^2/mmHg). Common femoral artery cross sectional compliance decreased in the immobilized leg but not in the non-immobilized leg (p<0.05) over 12 days of immobilization (PRE= 1.2±0.1 10^-4mm^2 /mmHg, 12-DA Y =: 0. 79±0.1 10^-4mm^2/mmHg). Neither popliteal nor common femoral artery mean blood flow changed throughout the 12 days of immobilization. Popliteal arterial mean diameter decreased significantly over time in both the IMM and NIM legs showing greater decreases in the IMM leg, while common femoral arterial mean diameter decreased in both the IMM and NIM legs through the 12 days (Popliteal: IMM PRE = 0.57±0.02 cm, IMM 12-DAY = 0.50±0.02 cm; NIM PRE = 0.59±0.02 cm, NIM 12-DAY = 0.55±0.02 cm; Common Femoral IMM PRE = 0.83±0.04 cm, IMM 12-DAY = 0.77±0.03 cm; NIM PRE = 0.81±0.03 cm, NIM 12-DAY = 0.77±0.03 cm). Popliteal artery endothelial function, calculated as both relative FMD and FMD normalized to shear stress, increased (p<0.05) throughout the 12 days in the immobilized leg while showing no change in the non-immobilized leg (Relative FMD: IMM PRE 6.0 ± 1.4%, IMM 12-DAY = 12.6 ± 2.7%; NIM PRE = 5.8 ± 1.4%, NIM 12-DAY = 8.3 ± 1.6 %; Normalized FMD: IMM PRE = 0.023 ± 0.007%/^sec-1, IMM 12-DAY = 0.037 ± 0.008%/^sec-1; NIM PRE = 0.016 ± 0.003%/^sec-1, NIM 12-DAY = 0.022 ± 0.004%/^sec-1).</p> <p> In conclusion, 12 days of deconditioning by ULI was able to cause structural and functional changes in the arteries of the immobilized leg, but not the central elastic artery in the neck in healthy young humans. Specifically in the legs, a decrease in arterial compliance, increases in mean blood velocity and increases in endothelial function were noted, with no change in volumetric blood flow. Surprisingly, our results suggest, with regards to endothelial function, that the vascular effects of deconditioning are not simply the inverse of exercise training which also shows increases in endothelial function. Thus the present study concludes that there exists a very short time course to arterial adaptations in healthy young humans with significant changes within the vasculature occurring within 12 days of deconditioning.</p> / Thesis / Master of Science (MSc)

<p> Increased arterial stiffness and vascular endothelial dysfunction have been identified as independent risk factors for the development and progression of cardiovascular disease. Traditional endurance training has been associated with elevated levels of central arterial compliance and an attenuation of cardiovascular events. As well, the positive benefits of aerobic-based training have been acknowledged as effective modulators of vascular endothelial function. To date, the impact of sprint interval training on cardiovascular health has not been evaluated. Furthermore, the mechanisms responsible for previously observed enhancements in endurance (750 kJ) performance following two weeks of sprint interval training remain unclear, but may be related to changes in vascular structure and function.</p> <p> Nine young healthy males [age: 22 ± 0.5 (mean± SEM)] participated in a two week sprint interval training program consisting of 4-6 30 second maximum effort exercise bouts performed every other day on a cycle ergometer. In addition, each participant was required to complete a 750 kJ time trial on a cycle ergometer as a measure of aerobic exercise performance before (PRE) and after (POST) training. Measurements of supine, resting carotid pulse pressure, carotid cross-sectional compliance, and brachial vascular endothelial function (using flow mediated dilation) were also acquired PRE and POST training.</p> <p> Resting pulse pressure did not show any significant changes with exercise training (PRE= 48.6±1.6, POST= 52.4±2.5 mmHg, p>0.05). Mean brachial artery diameter was not changed with sprint interval training (PRE= 4.29±0.17, POST= 4.38±0.18 mm, p>0.05); however, mean carotid artery diameter increased significantly PRE to POST (PRE= 6.40±0.15, POST= 6.49±0.14 mm, p=0.008). Carotid cross-sectional compliance did not change PRE to POST training (PRE= 0.164±0.010, POST= 0.162±0.007 mm^2/mmHg, p>0.05). Brachial vascular endothelial function measured using flow-mediated dilation did not show a significant change with sprint interval training, however a trend towards improvement was noted (PRE= 4.6±1.8, POST= 6.4±1.0 %, p=0.296). When normalized for shear rate (which was also unaltered with sprint interval training) there were no changes in endothelial function (PRE = 0.158±0.068, POST= 0.198 ± 0.034 %/S^-1, p>0.05). Average brachial post-occlusion blood flow was significantly enhanced following training possibly revealing enhanced resistance vessel function (PRE= 296.0±37.4, POST= 324.8±38.8 ml/min, p=0.04), despite no change in peak brachial blood flow (PRE= 332.0±42.3, POST= 362.6±45.7 ml/min, p>0.05). 750 kJ time trial performance was significantly enhanced with training (PRE = 62.8±4.9; POST= 55.84±3.55 min; p=0.006).</p> <p> In conclusion, sprint interval training did not change resting carotid compliance or brachial endothelial function, despite significant improvements in aerobic performance (750 kJ). However, carotid resting diameters and brachial post occlusion blood flow were significantly increased PRE to POST and a trend towards improvement was seen for brachial flow mediated dilation. The exact mechanisms responsible for such changes remain unknown and require further investigation.</p> / Thesis / Master of Science (MSc)

Endothelial function is influenced by a variety of factors, including shear stress direction and magnitude. Whereas improvements in endothelial function have mostly been attributed to increased anterograde flow, the results of many interventional models in humans suggest that enhancing blood flow in both anterograde and retrograde directions to create a high shear stress oscillatory stimulus may be optimal for improving endothelial function. Well-controlled studies are necessary to further this theory. The purposes of this study were to determine the brachial artery acute shear stress and endothelial function responses to (1) passive heat stress (HEAT), (2) ECG-gated cuff compressions (CUFF), and (3) ECG-gated rhythmic handgrip exercise (HGEX); and (4) to determine if there is a relationship between the degree of shear stress oscillation and endothelial function, regardless of the stimulus applied. We hypothesized that (1) HEAT would increase anterograde shear stress and decrease retrograde shear stress, leading to an unpredictable change in endothelial function; (2) CUFF would increase both anterograde and retrograde shear stress, leading to an increase in endothelial function; (3) HGEX would increase anterograde and retrograde shear stress and exercise metabolites, leading to an increase in endothelial function; and (4) the change in oscillatory shear index would be positively associated with the change in flow-mediated dilation, such that an increment increase in the degree of shear stress oscillation would be accompanied by a proportional improvement in endothelial function. In separate visits, 10 young healthy males (22±3 years) underwent 10 minutes of unilateral HEAT, CUFF, or HGEX on the left arm (EXP), while the right arm served as a within-subject time control (CON). Non-invasive finger plethysmography was used to measure heart rate (HR) and blood pressure (BP) throughout the testing sessions. Ultrasonography was used to obtain measures of blood velocity and arterial diameter from the brachial artery of both limbs throughout the interventions. Anterograde and retrograde shear stress (SS) and oscillatory shear index (OSI) were calculated at baseline and during each intervention to assess the blood flow pattern changes. Endothelial function was assessed before and after each intervention, in both limbs simultaneously using a flow-mediated dilation (FMD) test. HEAT increased HR during the intervention (P < 0.05), mean BP and diastolic BP after the intervention (P < 0.05), anterograde SS in EXP (rest: 15.2 ± 2.9 vs. HEAT: 29.8 ± 8.5 dynes/cm2, P < 0.05), and FMD% in both limbs (P = 0.000). CUFF did not change HR or BP, increased anterograde (rest: 17.9 ± 4.1 vs. CUFF: 43.0 ± 12.4 dynes/cm2, P < 0.05) and retrograde (rest: -3.1 ± 2.5 vs. CUFF: -22.7 ± 6.0 dynes/cm2, P < 0.05) SS in EXP, but did not change FMD% in either limb (P = 0.248). HGEX increased HR during the intervention (P < 0.05), mean BP during and after the intervention (P < 0.05), anterograde SS in EXP (rest: 18.7 ± 5.9 vs. HGEX: 56.4 ± 11.5 dynes/cm2, P < 0.05), and FMD% in both limbs (P = 0.001). These findings suggest that an anterograde-dominant shear stress stimulus may be effective at improving endothelial function, but the confounding effect of sympathetic nervous system activation may play a more dominant role in the acute control response for shorter duration interventions such as the ones explored in this study. / Thesis / Master of Science (MSc) / It has been well established that the pattern of blood flow can impact arterial function, but the nuances of this relationship remain unclear. Through the use of heating, cuff compression, and exercise, this study sought to determine the optimal shear stress pattern to see beneficial changes in arterial function in the arm of young healthy males. Our results show many real life interventions alter not only the shear stress pattern in the artery, but also involve other systems like the brain and muscle that are crucial to maintaining the body’s physiological balance. It is clear that arterial function is regulated through a variety of different mechanisms, and that the changes we observe will depend on the parameters (e.g. duration, intensity, timing of assessment) of the applied stimulus. More specifically, isolating study designs should be constructed to determine the individual contributions of different human body systems to the arterial regulatory response.

Endothelium-dependent vasodilation is an important marker of vascular function. Brachial artery flow-mediated dilation (FMD) is a noninvasive assessment of peripheral artery endothelial function that is associated with coronary artery endothelial function and is an index of cardiovascular health. This thesis sought to investigate factors that may influence the brachial artery FMD response in humans, particularly the sex hormone estrogen and low-volume sprint interval training (SIT). We first demonstrated the intra-individual consistency of the FMD response pattern in healthy young adults and introduced visual data screening as a tool for improving data accuracy. Having established best practices for FMD data analysis, we investigated the brachial artery FMD response in adults with different estrogen profiles: men, premenopausal women with a natural menstrual cycle (NAT), and premenopausal women using combined oral contraceptive pills (OCP). Our findings suggest that estrogen does not augment FMD during high-estrogen phases of a NAT or OCP cycle compared to low-estrogen phases or to men. We also investigated the acute and chronic brachial artery FMD response to a 3x20-s low-volume SIT model. Following a single SIT session, FMD was unchanged in men or women. These findings demonstrate that estrogen does not influence endothelium-dependent dilation at rest or following intense intermittent exercise, but also suggest that low-volume SIT may be an insufficient stimulus for eliciting changes in endothelial function. This stimulus magnitude postulation was further supported by a 12-wk exercise training study, whereby vascular changes were evident following moderate-intensity continuous training but not SIT. Taken together, this work suggests that controlling for menstrual cycle phase and/or OCP use in premenopausal women may not be necessary, making it more feasible to include women as research participants, and highlights the need for future characterization of the minimum low-volume interval stimulus that evokes improvements in endothelial function in healthy young adults. / Thesis / Doctor of Philosophy (PhD) / The endothelium is the inner lining of an artery that separates it from the flowing blood. A healthy endothelium responds to increases in blood flow by producing substances that enable an artery to widen. The projects in this thesis examined whether the responsiveness, and overall function, of the endothelium in healthy young adults is enhanced by the sex hormone estrogen or by “all-out” cycling sprints, an exercise protocol that has gained appeal for its time-efficiency. We demonstrated that estrogen does not enhance endothelial function in women, compared to men, at any phase of a menstrual or birth control pill cycle. A single session or 12-weeks of the intense but brief interval exercise also does not enhance endothelial function. This work suggests it may be easier to include women in future research assessing this measure and that this particular interval exercise protocol may not enhance endothelial function in healthy adults.