Vascular function is related to blood flow during high-intensity, but not low-intensity, knee extension exercise

2020 ◽  
Vol 128 (3) ◽  
pp. 698-708 ◽  
Author(s):  
Brady E. Hanson ◽  
Meagan Proffit ◽  
Jayson R. Gifford

While vascular function, assessed as the ability of the vasculature to dilate in response to a stimulus, is related to cardiovascular health, its relationship to exercise hyperemia is unclear. This study sought to determine if blood flow during submaximal and maximal exercise is related to vascular function. Nineteen healthy adults completed multiple assessments of vascular function specific to the leg, including passive leg movement (PLM), rapid onset vasodilation (ROV), reactive hyperemia (RH), and flow-mediated dilation (FMD). On a separate day, exercise blood flow (Doppler ultrasound) was assessed in the same leg during various intensities of single-leg, knee-extension (KE) exercise. Vascular function, determined by PLM, ROV, and RH, was related to exercise blood flow at high intensities, including maximum work rate (WRmax) ( r = 0.58–0.77, P < 0.001), but not low intensities, like ~21% WRmax ( r = 0.12–0.34, P = 0.12–0.62). Relationships between multiple indices of vascular function and peak exercise blood flow persisted when controlling for quadriceps mass and exercise work rate ( P < 0.05), indicating vascular function is independently related to the blood flow response to intense exercise. When divided into two groups based upon the magnitude of the PLM response, subjects with a lower PLM response exhibited lower exercise flow at several absolute work rates, as well as lower peak flow ( P < 0.05). In conclusion, leg flow during dynamic exercise is independently correlated with multiple different indices of microvascular function. Thus microvascular function appears to modulate the hyperemic response to high-intensity, but not low-intensity, exercise. NEW & NOTEWORTHY While substantial evidence indicates that individuals with lower vascular function are at greater risk for cardiovascular disease, with many redundant vasodilator pathways present during exercise, it has been unclear if low vascular function actually impacts blood flow during exercise. This study provides evidence that vascular function, assessed by multiple noninvasive methods, is related to the blood flow response to high-intensity leg exercise in healthy young adults. Importantly, healthy young adults with lower levels of vascular function, particularly microvascular function, exhibit lower blood flow during high-intensity, and maximal knee extension exercise. Thus it appears that in addition to increasing one’s risk of cardiovascular disease, lower vascular function is also related to a blunted blood flow response during high-intensity exercise.

2005 ◽  
Vol 98 (4) ◽  
pp. 1575-1583 ◽  
Author(s):  
Barbara J. Lutjemeier ◽  
Akira Miura ◽  
Barry W. Scheuermann ◽  
Shunsaku Koga ◽  
Dana K. Townsend ◽  
...  

To test for evidence of a muscle pump effect during steady-state upright submaximal knee extension exercise, seven male subjects performed seven discontinuous, incremental exercise stages (3 min/stage) at 40 contractions/min, at work rates ranging to 60–75% peak aerobic work rate. Cardiac cycle-averaged muscle blood flow (MBF) responses and contraction-averaged blood flow responses were calculated from continuous Doppler sonography of the femoral artery. Net contribution of the muscle pump was estimated by the difference between mean exercise blood flow (MBFM) and early recovery blood flow (MBFR). MBFM rose in proportion with increases in power output with no significant difference between the two methods of calculating MBF. For stages 1 and 5, MBFM was greater than MBFR; for all others, MBFM was similar to MBFR. For the lighter work rates ( stages 1–4), there was no significant difference between exercise and early recovery mean arterial pressure (MAP). During stages 5–7, MAP was significantly higher during exercise and fell significantly early in recovery. From these results we conclude that 1) at the lightest work rate, the muscle pump had a net positive effect on MBFM, 2) during steady-state moderate exercise ( stages 2–4) the net effect of rhythmic muscle contraction was neutral (i.e., the impedance due to muscle contraction was exactly offset by the potential enhancement during relaxation), and 3) at the three higher work rates tested ( stages 5–7), any enhancement to flow during relaxation was insufficient to fully compensate for the contraction-induced impedance to muscle perfusion. This necessitated a higher MAP to achieve the MBFM.


2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S198-S198
Author(s):  
Joseph R Meno ◽  
Thien-son K Nguyen ◽  
Elise M Jensen ◽  
G Alexander West ◽  
Leonid Groysman ◽  
...  

Circulation ◽  
1995 ◽  
Vol 92 (4) ◽  
pp. 796-804 ◽  
Author(s):  
Danilo Neglia ◽  
Oberdan Parodi ◽  
Michela Gallopin ◽  
Gianmario Sambuceti ◽  
Assuero Giorgetti ◽  
...  

Hypertension ◽  
1995 ◽  
Vol 26 (3) ◽  
pp. 497-502 ◽  
Author(s):  
Daniel Hayoz ◽  
Roger Weber ◽  
Blaise Rutschmann ◽  
Roger Darioli ◽  
Michel Burnier ◽  
...  

Author(s):  
Goncalo V. Mendonca ◽  
Carolina Vila-Chã ◽  
Carolina Teodósio ◽  
André D. Goncalves ◽  
Sandro R. Freitas ◽  
...  

2008 ◽  
Vol 28 (7) ◽  
pp. 1369-1376 ◽  
Author(s):  
Inna Sukhotinsky ◽  
Ergin Dilekoz ◽  
Michael A Moskowitz ◽  
Cenk Ayata

Cortical spreading depression (CSD) evokes a large cerebral blood flow (CBF) increase in normal rat brain. In contrast, in focal ischemic penumbra, CSD-like periinfarct depolarizations (PID) are mainly associated with hypoperfusion. Because PIDs electrophysiologically closely resemble CSD, we tested whether conditions present in ischemic penumbra, such as tissue hypoxia or reduced perfusion pressure, transform the CSD-induced CBF response in nonischemic rat cortex. Cerebral blood flow changes were recorded using laser Doppler flowmetry in rats subjected to hypoxia, hypotension, or both. Under normoxic normotensive conditions, CSD caused a characteristic transient CBF increase (74 ± 7%) occasionally preceded by a small hypoperfusion (−4 ± 2%). Both hypoxia ( pO2 45 ± 3 mm Hg) and hypotension (blood pressure 42 ± 2 mm Hg) independently augmented this initial hypoperfusion (−14 ± 2% normoxic hypotension; −16 ± 6% hypoxic normotension; −21 ± 5% hypoxic hypotension) and diminished the magnitude of hyperemia (44 ± 10% normoxic hypotension; 43 ± 9% hypoxic normotension; 27 ± 6% hypoxic hypotension). Hypotension and, to a much lesser extent, hypoxia increased the duration of hypoperfusion and the DC shift, whereas CSD amplitude remained unchanged. These results suggest that hypoxia and/or hypotension unmask a vasoconstrictive response during CSD in the rat such that, under nonphysiologic conditions (i.e., mimicking ischemic penumbra), the hyperemic response to CSD becomes attenuated resembling the blood flow response during PIDs.


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