Haemodynamic and cerebrovascular effects of intermittent lower-leg compression as countermeasure to orthostatic stress.

NEW FINDINGS: What is the central question of this study? Does smartly timed intermittent compression of the lower legs alter cerebral blood velocity and oxygenation during acute orthostatic challenges? What is the main finding and its importance? Intermittent compression timed to the local diastolic phase increased the blood flux through the legs and heart after two different orthostatic stress tests. Cerebral blood velocity improved during the first minute of recovery, and indices of cerebral tissue oxygenation remained elevated for 2 min. These results provide promise for the use of lower-leg active compression as a therapeutic tool for individuals vulnerable to initial orthostatic hypotension and orthostatic stress. ABSTRACT: Intermittent compression of the lower legs provides the possibility of improving orthostatic tolerance by actively promoting venous return and improving central haemodynamics. We tested the hypothesis that intermittent compression of 65 mmHg timed to occur only within the local diastolic phase of each cardiac cycle would attenuate the decrease in blood pressure and improve cerebral haemodynamics during the first minute of recovery from two different orthostatic stress tests. Fourteen subjects (seven female) performed four squat-to-stand transitions and four repeats of standing bilateral thigh-cuff occlusion and release (TCR), with intermittent compression of the lower legs applied in half of the trials. Blood flow in the superficial femoral artery, mean arterial pressure, Doppler ultrasound cardiac output, total peripheral resistance, middle cerebral artery blood velocity (MCAv) and cerebral tissue saturation index (TSI%) were monitored. With both orthostatic stress tests, there was a significant compression × time interaction for superficial femoral artery flow (P < 0.001). The hypotensive state was attenuated with intermittent compression despite decreased total peripheral resistance (squat-to-stand, compression × time interaction, P < 0.001; TCR, compression × time interaction, P = 0.002) as a consequence of elevated cardiac output in both tests (P < 0.001). Intermittent compression also increased MCAv (P = 0.001) and TSI% (P < 0.001) during the squat-to-stand transition and during TCR (MCAv and TSI%, compression × time interaction, P < 0.001). Intermittent compression of the lower legs during quiet standing after an active orthostatic challenge augmented local, central and cerebral haemodynamics, providing potential as a therapeutic tool for individuals vulnerable to orthostatic stress.

Superficial femoral artery blood flow with intermittent pneumatic compression of the lower leg applied during walking exercise and recovery.

The purpose of this study was to determine if muscle blood flow during walking exercise and postexercise recovery can be augmented through the application of intermittent compression of the lower legs applied during the diastolic phase of the cardiac cycle. Results from four conditions were assessed: no compression (NoComp), compression during walking (ExComp), compression during postexercise recovery (RecComp), and compression applied throughout (AllComp). Superficial femoral artery (SFA) blood flow was measured (Doppler ultrasound) during rest and postexercise recovery. Mean arterial blood pressure (MAP, finger photoplethysmography) was used to calculate vascular conductance as VC = SFA flow/MAP. Near infrared spectroscopy measured changes in oxygenated (O2Hb) and deoxygenated hemoglobin concentration throughout the test. Compression during exercise increased SFA blood flow measured over the first 15 s of postexercise recovery (AllComp: 532.2 ± 123.1 mL/min; ExComp: 529.8 ± 99.2 mL/min) compared with NoComp (462.3 ± 87.3 mL/min P < 0.05) and corresponded to increased VC (NoComp: 4.7 ± 0.9 mL·min-1·mmHg-1 versus ExComp: 5.5 ± 1.0 mL·min-1·mmHg-1, P < 0.05). Similarly, compression throughout postexercise recovery also resulted in increased SFA flow (AllComp: 190.5 ± 57.1 mL/min; RecComp: 158.7 ± 49.1 mL/min versus NoComp: 108.8 ± 28.5 mL/min, P < 0.05) and vascular conductance. Muscle contractions during exercise reduced total hemoglobin with O2Hb comprising ~57% of the observed reduction. Compression during exercise augmented this reduction (P < 0.05) with O2HB again comprising ~55% of the reduction. Total hemoglobin was reduced with compression during postexercise recovery (P < 0.05) with O2Hb accounting for ~40% of this reduction. Results from this study indicate that intermittent compression applied during walking and during postexercise recovery enhanced vascular conductance during exercise and elevated postexercise SFA blood flow and tissue oxygenation during recovery.NEW & NOTEWORTHY Intermittent compression mimics the mechanical actions of voluntary muscle contraction on venous volume. This study demonstrates that compression applied during the diastolic phase of the cardiac cycle while walking accentuates the actions of the muscle pump resulting in increased immediate postexercise muscle blood flow and vascular conductance. Similarly, compression applied during the recovery period independently increased arterial flow and tissue oxygenation, potentially providing conditions conducive to faster recovery.

Investigating the impact of passive external lower limb compression on central and peripheral hemodynamics during exercise.

PURPOSE: The objective of this study was to assess the effectiveness of graduated compression socks (GCS) on enhancing muscle blood flow and oxygenation during exercise and recovery in healthy subjects. METHODS: Twelve healthy volunteers completed a protocol involving baseline, exercise, and recovery periods with and without GCS. Each test was repeated twice to assess repeatability of the results. The applied sock pressure was measured prior to experimentation using a custom pressure sensing system, and modified as necessary using tensor bandages to control the applied load. During each of the experimental phases, blood velocity in the popliteal artery, calf muscle tissue oxygenation, muscle activity, heart rate, blood pressure, cardiac output, and applied pressure from the sock were measured. Popliteal artery diameter was measured during baseline and recovery periods. RESULTS: The GCS significantly reduced deoxyhemoglobin (HHb) in the leg during baseline (HHb, p = 0.001) and total blood volume and HHb in the leg during exercise (total hemoglobin, p = 0.01; HHb, p = 0.02). However, there were no differences in leg muscle blood flow velocity or any other variables with and without GCS at baseline, exercise, or recovery. Interestingly, it was found that the local applied sock pressure was very sensitive to the sock application process and, furthermore, the pressure varied considerably during exercise. CONCLUSIONS: No significant changes were observed in measures reflecting oxygen delivery for healthy subjects using GCS during exercise and recovery. Applied sock pressure was carefully controlled, thus eliminating the sock application process as a variable.