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Post‐Exercise Central Hypotension is Associated with Changes in Forward Pulse Wave Amplitude and Reflected Pulse Wave Timing in Young, Healthy Individuals
Author(s) -
Patik Jordan C.,
Stock Joseph M.,
Chouramanis Nicholas V.,
Mehrer Justin D.,
Chirinos Julio A.,
Edwards David G.
Publication year - 2020
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2020.34.s1.03448
Subject(s) - cardiology , blood pressure , medicine , pulsatile flow , hemodynamics , pulse pressure , pulse wave velocity , vasodilation , pulse (music) , blood flow , pulse wave analysis , aortic pressure , physics , detector , optics
In the hours following moderate intensity aerobic exercise (AE), persistent dilation of the arterial circulation supplying previously exercised muscle decreases total peripheral resistance (TPR) and contributes to post‐exercise hypotension. In addition to the effect of vasodilation on TPR, the diameter and tone of arterial vessels also influences central blood pressures via changes in the amplitude of forward (Pf) and backward (Pb) pulse waves, as well as the apparent wave reflection return timing (i.e. reflected wave transit time, RWTT). Prior research has assessed these parameters over a limited timeframe (e.g. 15 min) and relied on synthesized aortic flow waves rather than measured left ventricular outflow. As such, the prolonged post exercise effects of AE on pulse wave characteristics and central blood pressure are unclear. Purpose This study aimed to characterize changes in pulsatile hemodynamics in the two hours following AE. We hypothesized that Pf and Pb would be reduced, and RWTT would be increased post‐AE relative to baseline (BL). Methods Twelve young, recreationally active participants (8M/4F, 26±3 years, VO 2 max: 50.8±14.3 ml·kg −1 ·min −1 ) were studied at BL and then every 20 min after completing 60 min of upright cycling at 60% VO 2 max. At each timepoint, central pressure waveforms were derived from radial artery applanation tonometry and aortic inflow waves were acquired via echocardiographic pulsed‐Doppler assessment of blood velocity in the left ventricular outflow tract. Pressure and flow waves were averaged over 10 cardiac cycles and pressure‐flow relations were determined offline via wave separation analysis. Results As expected, brachial systolic blood pressure (SBP) was decreased across the 120 min period post‐AE relative to BL (time effect P<0.001) while TPR was only reduced at 20 min (Δ−15±5%, P<0.05 vs BL) and cardiac output (CO) was maintained at all timepoints (time effect P=0.12). The nadir in central SBP occurred at 60 min post‐AE (Δ−11±2%, P<0.001 vs BL). At 60 min post‐AE, Pf and Pb were reduced by Δ−14.3±2.5% and Δ−24.2±3.3%, respectively (each P<0.001 vs BL) and RWTT was increased (Δ19.5±5.3% P<0.02 vs BL). The percent change in central SBP from BL to 60 min was related to changes in RWTT (r=−0.79, P=0.02) and Pf (r=0.65, P=0.02) but not Pb (r=0.38, P=0.22), CO (r=0.27, P=0.40) or TPR (r=0.14, P=0.66). Conclusions These data highlight the contribution of changes in pulsatile hemodynamic parameters, in contrast to changes in non‐pulsatile parameters (CO and TPR), to reductions in central BP following moderate intensity AE. Support or Funding Information Supported by NIH grants R01‐HL104106 and P20‐GM113125