Dietary Sodium, Oxidative Stress, and Pulsatile Hemodynamics

The Role of Oxidative Stress and Endothelial Dysfunction in High Sodium-Induced Changes in Pulsatile Hemodynamics

High sodium diets impair vascular function, which may influence the work of the heart. This investigation is designed to determine if this change in vascular function results in a greater workload in the heart and if people who regularly exercise are protected from these effects.

Excess dietary sodium is associated with cardiac hypertrophy independent of changes in blood pressure. Importantly, increased arterial pulsatile load predicts left ventricular hypertrophy, and thus presents a potential mechanism through which high dietary sodium augments cardiovascular disease risk.

While high sodium diets impair vascular function via an increase in oxidative stress, how high sodium influences central pulsatile hemodynamics is not known. This project aims to a) determine how impaired vascular function affects pulsatile hemodynamics and thus influences the work of the heart during periods of high sodium consumption and b) examine whether regular aerobic exercise and/or fitness protects against the deleterious effects of excess sodium.

Inclusion Criteria:

• Healthy individuals (age 21-45) who are either sedentary (1 or less days of exercise per week during past year) or habitually active (4 or more days of aerobic exercise per week for a minimum of 1 year)

Exclusion Criteria:

• Body mass index <18 or >35
• Systolic blood pressure ≥140 mmHg and/or diastolic blood pressure ≥90
• Blood donation within past 8 weeks,
• Glucose 6 phosphate dehydrogenase (G6PD) deficiency
• A history of cancer, diabetes, or any other chronic disease
• A history of any heart disease
• A history of hormone therapy
• Use of nicotine products
• Pregnancy
• Nursing mothers
• Participation in regular physical activity greater than 1 day/week- but less than 4 days/week