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HIITing the Brain after Stroke: An Investigation of the Cerebrovascular System
Whitaker-Hilbig, Alicen
Whitaker-Hilbig, Alicen
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Abstract
High intensity interval exercise (HIIT) is currently being implemented within stroke rehabilitation, despite insufficient randomized controlled trials. The primary driver for performing HIIT in individuals post-stroke is the shorter amount of total exercise time needed to match or further improve rehabilitation outcomes and aerobic fitness compared to moderate intensity continuous exercise. However, no studies have examined the effects of HIIT on the cerebrovascular system in individuals with an underlying cerebrovascular injury such as a stroke. The cerebrovascular system ensures the crucial delivery of oxygen and nutrients to neuron cells, which are needed for motor function and cognition. Our laboratory uses transcranial doppler ultrasound (TCD) to indirectly measure 1) cerebral blood flow during exercise using the middle cerebral artery blood velocity (MCAv) and 2) the ability of the cerebrovascular system to react independently to changes in peripheral mean arterial pressure (MAP), called dynamic cerebral autoregulation (dCA). Many narrative reviews have suggested an attenuated cerebrovascular response to HIIT in individuals post-stroke due to the rapid and repetitive hemodynamic changes that may challenge the cerebrovascular system, especially in individuals post-stroke who have a reduced cerebrovascular response to aerobic exercise. Despite the paucity of research on the effects of HIIT on the cerebrovascular system in individuals post-stroke, clinical practice guideline for locomotor training have included HIIT as a potential exercise to improve walking outcomes. This body of work aimed to address this critical gap in knowledge and study the cerebrovascular response to HIIT, via the MCAv and dCA response, in individuals post-stroke compared to their age- and sex-matched controls.We developed a protocol to examine the cerebrovascular response 1) during an acute bout of low-volume HIIT, 2) immediately following HIIT, and 3) 30-minutes after HIIT, and characterized 25 healthy young adults prior to implementation in individuals post-stroke. The cerebrovascular response to a single bout of low-volume HIIT was first characterized in healthy young adults to determine the “typical” cerebrovascular response. The total body recumbent stepper (TBRS) submaximal exercise test determined the workload for the HIIT bout. The 10-minute HIIT bout consisted of 1-minute high-intensity at ~70% estimated maximal watts followed by active recovery at ~10% estimated maximal watts. We found that in healthy young adults, MCAv during HIIT followed the pattern of end-tidal carbon dioxide (PETCO2), potentially due to the ability of the downstream arterioles to vasoconstrict and vasodilate with changes in arterial carbon dioxide. During HIIT, MCAv peaked at minute 3 and then decreased during high-intensity bouts, potentially due to hyperventilation-induced decreases in PETCO2 causing arteriole vasoconstriction. During active recovery, MCAv “rebounded” and began to increase when individuals were able to recover their breathing and PETCO2 increased. Immediately following HIIT, MCAv was decreased below baseline (BL) values, similar to PETCO2, but MCAv returned to BL values by 30-minutes after HIIT. Therefore, the “typical” MCAv response to HIIT may follow the pattern of PETCO2, potentially due to the vasomotor ability and reactivity to PETCO2 in the downstream cerebrovascular vessels.Following characterization of a “typical” cerebrovascular response to HIIT in healthy young adults, we tested our hypotheses in individuals with chronic stroke (n = 25) and age- and sex-matched adult controls (CON, n = 25). We found that individuals post-stroke had lower MCAv at BL, during HIIT, immediately following HIIT, and 30-minutes after HIIT compared to CON. However, when controlling for BL differences between groups, MCAv was no longer significantly different at all time points. MCAv during HIIT in individuals post-stroke and CON also did not follow the pattern of PETCO2 but rather the pattern of MAP and heart rate. Previous studies have shown individuals post-stroke have reduced arteriole vasomotor activity, due to increased arterial stiffness as well as an inability to react to changes in PETCO2, which could have contributed to the attenuated MCAv response to HIIT. We also found that individuals post-stroke had reduced MCAv “responsiveness”, measured as the coefficient of variation of MCAv between high-intensity and active recovery bouts during HIIT, compared to CON. Peripheral arterial stiffness, collected via pulse wave velocity, was also higher in individuals post-stroke and associated with reduced MCAv responsiveness during HIIT. Therefore, individuals post-stroke may have reduced arteriole vasomotor ability to react to physiological changes during HIIT. They may also have a protective mechanism against large fluctuations in MCAv when switching between high-intensity and active-recovery during HIIT.This body of work led to the development of a new technique for the dCA sit-to-stand maneuver. The current standard is to examine the cerebrovascular response 60 seconds after verbal command to stand. However, we questioned whether this would be accurate for older adults and people with stroke. We developed a custom force sensor that interfaced with the physiological recording of dCA and marked the exact moment someone lifted off the chair for stance, as the timing of stance is critical. During a sit-to-stand, MAP transiently drops due to peripheral vasodilation and gravity. Therefore, dCA must react independently to the peripheral vascular system and increase the cerebrovascular conductance index (CVCi). One of the metrics examining dCA during a sit-to-stand is called the time delay (TD) before the onset of the regulation response, which is measured as the time from stance until an increase in CVCi. Traditionally, TD was calculated from the estimated stance time, or the time participants were verbally asked to stand. However, in individuals post-stroke with hemiparesis and longer sit-to-stand times, we identified a need to mark the exact time of stance rather than estimating from when they were verbally asked to stand. We then tested whether the development of the custom force sensor would significantly improve the calculation of the TD response in healthy young adults (n = 25), individuals post-stroke (n = 20), and CON (n = 20). We found that the custom force sensor significantly improved the calculation of the TD response and reduced measurement error for all groups. Due to the relatively quick TD response (on average ~3 seconds), the custom force sensor was able to account for a slower sit-to-stand of ~0.5 seconds and a measurement error of ~17%.Next, we examined the effects of HIIT on the dCA response following HIIT and at a follow up 30-minutes after HIIT in individuals post-stroke compared to CON. dCA was measured during spontaneous fluctuations at rest using transfer function analysis as well as during a sit-to-stand. We found individuals post-stroke had lower transfer function analysis phase immediately following HIIT compared to CON, meaning dCA was less efficient at regulating the shift between spontaneous fluctuations in MAP and MCAv waveforms following HIIT. Individuals post-stroke also had greater drops in MCAv during a sit-to-stand following HIIT compared to baseline, despite no change from BL in the drop in MAP during a sit-to-stand. Therefore, dCA in individuals post-stroke may have become more pressure passive following HIIT and allowed greater concordant changes between MAP and MCAv compared to at BL. The attenuated dCA response following HIIT could be driven by the decrease in MAP below BL found only in individuals post-stroke. dCA is directional sensitive and has a less efficient response during decreases in MAP. Therefore, MAP decreased below BL values may be the driving factor for an attenuated dCA response following HIIT in individuals post-stroke. At the 30-minute follow up after HIIT, dCA returned to resting BL values in individuals post-stroke. However, the exact recovery time of dCA following HIIT (between 5-minutes and 35-minutes) in individuals post-stroke is still unknown.Together our results show that individuals post-stroke had an attenuated cerebrovascular response during HIIT and immediately following HIIT compared to their age- and sex-matched peers. Individuals post-stroke may need a longer recovery period following an acute bout of HIIT to return MCAv and dCA back to resting baseline values. Clinically, the hemodynamic response to exercise is often measured via peripheral blood pressure. However, our study shows that the cerebrovascular system responds independently to peripheral blood pressure during HIIT. Measures of hemodynamic stability following HIIT should include measures of the cerebrovascular system. Our foundational characterization of the cerebrovascular response to HIIT in individuals post-stroke provides the knowledge and rationale for future studies to examine underlying mechanisms contributing to the attenuated cerebrovascular response to exercise as well as therapeutic interventions to improve cerebrovascular health. Further research should include individuals across the stages of stroke recovery and determine the association between the cerebrovascular response to HIIT and stroke rehabilitation outcomes.
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2023-05-31
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University of Kansas
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This item contains archived web content.
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Keywords
Physical therapy, Aging, Medical imaging, Aging, Cerebral Hemodynamics, Dynamic Cerebral Autoregulation, High Intensity Interval Exercise, Middle Cerebral Artery Blood Velocity, Stroke