Suboptimal blood pressure, defined as \>115/75 mmHg by meta-analysis, exhibits a positive relationship with cardiovascular disease, and is the leading attributable risk factor for death. Research has illustrated that even blood pressure (BP) below the hypertensive levels can contribute to increased vascular mortality. It has been demonstrated that for incremental increases in blood pressure (every 20 mmHg systolic or 10 mmHg diastolic) there is a twofold increase in cardiovascular disease risk. However, mounting evidence suggests that increased fitness and physical activity4 may attenuate the typical age related increase in BP to hypertensive levels. Exercise has been recommended as the first line of treatment in prehypertension and suboptimal BP, and a single bout of exercise (as short at 10 min) has been shown to lower BP for up to 12 hours post. It is this extended bout of postexercise hypotension (PEH) that is thought to contribute to the anti-hypertensive effects of exercise.
PEH is well documented in lean and overweight individuals, but there is limited data on PEH in obese populations of both genders. Well characterized for lean and overweight individuals matched for BP, how obese men and women react postexercise is largely unknown and undefined. Only a few published studies exist. A recent meta-analysis examined PEH, but only included subjects with a body mass index of \< 31 kg/m2. Only one study to date included exclusively obese subjects (all women), but the authors only demonstrated a PEH 10 min postexercise. To date, we are aware of no published data examining BP matched PEH in centrally obese men and women to that of non-obese men and women.
Exercise intensity has been shown to play a role in PEH as well. Data from this lab has demonstrated that short duration, high intensity exercise (aerobic interval exercise -AIE) was able to stimulate a greater duration of PEH when compared to that of a longer duration, moderate intensity exercise (continuous exercise- CE) or even sprint like training. One recently published study examines the effects on AIE training of young, obese women. No significant PEH was found after one hour, however, this time period may not have been long enough to see a significant change in PEH, hence why we are proposing a longer postexercise measurement period.
The mechanism for which PEH occurs is unclear. It is thought to be from structural, neurohormonal, and vascular effects of exercise, however, how these variables effect PEH in obese vs non-obese populations has not been studied directly. Using non-invasive methods such as heart rate variability (HRV), cardiac output (CO), and systemic vascular resistance (SRV) will assist us in creating a better idea of the mechanism that which PEH occurs, and any clinical difference central obesity has on these factors. A prior study from this lab found that obese subjects had a heterogeneous response in CO and SVR (increased cardiac output and augmented SVR) when compared to that of non-obese matched subjects, but once more these subjects were only evaluated for 1 hour postexercise.
