The objective of this systematic review was to provide insight into the controversy that still abounds as to the impact of acute aerobic exercise on immediate changes in arterial stiffness. Electronic databases were searched to identify articles assessing the effects of acute aerobic exercise on parameters of arterial stiffness. Eligible studies included arterial stiffness measurements before and after acute aerobic exercise in healthy human subjects. Forty-three studies were included. The effect of acute aerobic exercise on arterial stiffness was found to be dependent on the anatomical segment assessed, and on the timing of the measurement post-exercise. Arterial stiffness of the central and upper body peripheral arterial segments was found to be increased relative to resting values immediately post-exercise (0-5 min), whereas, thereafter (>5 min), decreased to a level at or below resting values. In the lower limbs, proximal to the primary working muscles, arterial stiffness decreased immediately post-exercise (0-5 min), which persisted into the recovery period post-exercise (>5 min). This systematic review reveals a differential response to acute exercise in the lower and upper/central arterial segments in healthy adult subjects. We further showed that the effect of acute aerobic exercise on arterial stiffness is dependent on the timing of the measurements post-exercise. Therefore, when assessing the overall impact of exercise on arterial stiffness, it is important to consider the arterial segment being analyzed and measurement time point, as failure to contextualize the measurement can lead to conflicting results and misleading clinical inferences.
Rationale:Previous studies suggest an association between obstructive sleep apnea (OSA) and resistant hypertension. Continuous positive airway pressure (CPAP) treatment may improve blood pressure (BP) in such patients. However it has not been established whether fixed CPAP (FCPAP) versus auto-titrating CPAP (APAP) lower BP and cardiovascular risk comparably. Our objective was to compare the effects of FCPAP versus APAP on OSA control, BP and arterial stiffness in patients with resistant hypertension and OSA. Methods: In this randomized blinded cross-over trial, adults with resistant hypertension (BP above target on ≥3 anti-hypertensive medications or target BP requiring ≥4 medications) diagnosed with OSA (AHI > 15 events/h) on polysomnography (PSG) underwent manual CPAP titration and were then randomized to 6 weeks of either FCPAP or APAP followed immediately by 6 weeks of the alternate modality. Objective CPAP compliance data and PSG on treatment were obtained at 6 and 12 weeks. 24-hour ambulatory BP monitoring, arterial stiffness measurements (carotid-femoral pulse wave velocity -cfPWV) were performed at baseline, 6 and 12 weeks. We report results of a blinded interim analysis using SAS for random-effect models with order, time and treatment as fixed effects. The two forms of CPAP are labeled as Tx1 and Tx2. Results: For 9 subjects to date (7 male) on 4.1±1.3 (SD) anti-hypertensive medications, mean age was 57±13y, baseline AHI was 52.8±25.9/h and 4% ODI was 33.1±25.5/h. For Tx1 vs. Tx2, CPAP compliance was comparable (5.1±0.7 vs. 5.4±0.7 h/night, p = 0.61), as were measures of sleep quality and residual OSA on PSG (AHI: 9.7±3.7 vs. 12.4±3.7/h, p=0.16; 4% ODI: 4.9±2.0 for both). Values for 24h and nighttime BP were comparable for Tx1 and Tx2. However, Tx1 was associated with significantly lower daytime diastolic BP 75.6±2.6 mmHg vs. Tx2 79.3±2.6 mmHg, p=0.03) and a tendency to lower daytime mean arterial pressure (p=0.08). cfPWV values did not differ significantly for Tx1 vs. Tx2. Conclusion: To date, FCPAP and APAP produced similar suppression of OSA, and were associated with comparable 24h BP and arterial stiffness values, although one CPAP modality (Tx1) seems to be associated with a greater beneficial effect on daytime BP values.
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