Exercise is probably the most effective approach to reduce blood pressure. In fact, a single bout of exercise induces a physiological response known as Post-Exercise Hypotension (PEH) where a prolonged decrease in resting blood pressure occurs in the minutes and hours after exercise. However, it is not fully understood how this response triggers. Recent evidence suggests that oral bacteria may play a key role in blood pressure control by enhancing nitrite, and then nitric oxide (NO) bioavailability under resting conditions in humans. However, no previous study has investigated whether this is a key mechanism involve in PEH. Thus, the main aim of this study was to investigate if the oral nitrate/nitrite pathway is a key regulator of PEH and vasodilation in healthy humans.
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
BASIC_SCIENCE
Masking
DOUBLE
Enrollment
23
Four sets of 7 minutes at 65% of VO2peak interspersed with 3 min of passive recovery
Laboratory of Nutrition, Exercise & Health
Plymouth, Devon, United Kingdom
Change in blood pressure after exercise
Blood pressure was measured before and at 1 hour and 2hours after exercise using an electronic sphygmomanometer (ProBP 3400, Welch Allyn). The second and third readings will be averaged to determine mean blood pressure.
Time frame: Baseline and 1 hour and 2 hours after exercise
Change in reactive hyperaemia
Tissue oxygenation index (TOI) were recorded on the left forearm (extensor digitorum) using a NIRS system (NIRO-200NX, Hamamatsu) before exercise and 2 hours after exercise. After baseline measurements (2 minutes), an automatic pneumatic cuff (Hokanson E-20 AG101) was inflated \~5cm above the elbow for 5 minutes to an occlusion pressure of 200 mmHg. Then, inflation of the cuff was rapidly released (\< 1 second) and the NIRS measurements were continuously monitored for 5 minutes.
Time frame: Baseline and 1 hour and 2 hours after exercise
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