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Fluctuating arterial blood pressure during high-intensity interval exercise (HIIE) may challenge dynamic cerebral autoregulation (dCA), specifically after stroke after an injury to the cerebrovasculature. We hypothesized that dCA would be attenuated at rest and during a sit-to-stand transition immediately after and 30 min after HIIE in individuals poststroke compared with age- and sex-matched control subjects (CON). HIIE switched every minute between 70% and 10% estimated maximal watts for 10 min. Mean arterial pressure (MAP) and middle cerebral artery blood velocity (MCAv) were recorded. dCA was quantified during spontaneous fluctuations in MAP and MCAv via transfer function analysis. For sit-to-stand, time delay before an increase in cerebrovascular conductance index (CVCi = MCAv/MAP), rate of regulation, and % change in MCAv and MAP were measured. Twenty-two individuals poststroke (age 60 ± 12 yr, 31 ± 16 mo) and twenty-four CON (age 60 ± 13 yr) completed the study. Very low frequency (VLF) gain ( P = 0.02, η 2 = 0.18) and normalized gain ( P = 0.01, η 2 = 0.43) had a group × time interaction, with CON improving after HIIE whereas individuals poststroke did not. Individuals poststroke had lower VLF phase ( P = 0.03, η 2 = 0.22) after HIIE compared with CON. We found no differences in the sit-to-stand measurement of dCA. Our study showed lower dCA during spontaneous fluctuations in MCAv and MAP following HIIE in individuals poststroke compared with CON, whereas the sit-to-stand response was maintained. NEW & NOTEWORTHY This study provides novel insights into poststroke dynamic cerebral autoregulation (dCA) following an acute bout of high-intensity interval exercise (HIIE). In people after stroke, dCA appears attenuated during spontaneous fluctuations in mean arterial pressure (MAP) and middle cerebral artery blood velocity (MCAv) following HIIE. However, the dCA response during a single sit-to-stand transition after HIIE showed no significant difference from controls. These findings suggest that HIIE may temporarily challenge dCA after exercise in individuals with stroke.

Background The primary aim of this study was to characterize the middle cerebral artery blood velocity (MCAv) dynamic response to an acute bout of exercise in humans at 3- and 6-months poststroke. As a secondary objective, we grouped individuals according to the MCAv dynamic response to the exercise bout as responder or nonresponder. We tested whether physical activity, aerobic fitness, and exercise mean arterial blood pressure differed between groups. Methods and Results Transcranial Doppler ultrasound measured MCAv during a 90-second baseline followed by a 6-minute moderate intensity exercise bout. Heart rate, mean arterial blood pressure, and end-tidal CO 2 were additional variables of interest. The MCAv dynamic response variables included the following: baseline, time delay, amplitude, and time constant. Linear mixed model revealed no significant differences in our selected outcomes between 3- and 6-months poststroke. Individuals characterized as responders demonstrated a faster time delay, higher amplitude, and reported higher levels of physical activity and aerobic fitness when compared with the nonresponders. No between-group differences were identified for baseline, time constant, or exercise mean arterial blood pressure. In the nonresponders, we observed an immediate rise in MCAv following exercise onset followed by an immediate decline to near baseline values, while the responders showed an exponential rise until steady state was reached. Conclusions The MCAv dynamic response profile has the potential to provide valuable information during an acute exercise bout following stroke. Individuals with a greater MCAv response to the exercise stimulus reported statin use and regular participation in exercise.

Background : Lung function is compromised in stroke survivors, which may cause fatigue and exercise intolerance. Furthermore, past studies of aerobic exercise have involved only stroke survivors who could walk independently. Stroke survivors who were unable to walk were not included in the previous research-investigating changes in lung function from walking exercise interventions. In this pilot study, the feasibility and the effect of aerobic walking exercise on lung function was examined in non-ambulatory stroke survivors using a treadmill, bodyweight support system, and a gait training device. Methods : This study was a single group trial. Eight non-ambulatory stroke survivors (five males, mean age 63.3 ± 13.7 years, seven with ischemic stroke) completed a low intensity walking exercise program (30 min/session; three sessions/week for 8 weeks) and lung function test. Before and after the intervention, vital capacity (VC) and forced vital capacity (FVC) using a spirometer were measured according to the guideline from American Thoracic Society/European Respiratory Society. Results : The rates of compliance and attrition were 100% and 10%; respectively, and no adverse events were reported. There were significant differences between pre- and post-intervention assessments in FVC ( p = .09), percentage of predicted VC ( p = .08), and percentage of predicted FVC ( p = .08). Conclusions : In non-ambulatory stroke survivors, aerobic walking exercise is feasible and safe. Also, the results are promising and suggest that aerobic walking exercise may improve lung function; more data are needed.

Blood flow regulation is impaired in people with stroke. However, the time course of change in middle cerebral artery velocity (MCAv) following repeated stroke at rest and during exercise remains unknown. In this case study, we provide novel characterization of the dynamic kinetic MCAv response profile to moderate-intensity exercise before and after repeated ischemic MCA stroke. The initial stroke occurred in the left MCA. At 3 months poststroke, left MCAv amplitude (Amp) was ~50% lower than the right. At the 6-month follow-up visit, MCAv Amp declined in both MCA with the left MCAv Amp ~50% lower than the right MCAv Amp. Following a second right MCA stroke, we report further decline in Amp for the left MCA. At the 3- and 6-month visit following the second stroke, the left MCAv Amp declined further (~10%). The right MCAv Amp dramatically decreased by 81.3% when compared to the initial study visit. The MCAv kinetic analysis revealed a marked impairment in the cerebrovascular response to exercise following stroke. We discuss potential pathophysiological mechanisms contributing to poststroke cerebrovascular dysfunction and the need to test therapeutic interventions (such as exercise) that might attenuate cerebrovascular decline in people following stroke., (© 2019 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society.)

Improvements in cancer screening, diagnosis, and treatment have resulted in an increasing population of cancer survivors with impairments in physical function, cancer-related symptoms, and reduced quality of life. Exercise and physical activity have therapeutic value at multiple points along the cancer disease continuum, spanning disease prevention, treatment, survivorship, prognostic outcomes, and end-of-life issues. Molecular mechanisms for the influence of exercise in persons with cancer include altering tumor initiation pathways and affecting hormonal, inflammatory, immune, and insulin pathways. Physical activity has been found to play a role in the prevention of certain malignancies, including breast, colon, and other cancers. An increasing amount of evidence indicates that physical activity may affect prognostic outcomes in certain cancer diagnoses, especially breast cancer. Structured exercise and physical activity interventions can be helpful in addressing specific survivorship issues, including overall quality of life, cardiorespiratory impairment, cancer-related fatigue, and lymphedema. Exercise also may be helpful during the palliative care phase to alleviate symptoms and increase physical well-being. This article will familiarize physiatrists with the current state of evidence regarding the role and efficacy of exercise in persons with cancer., (Copyright © 2012 American Academy of Physical Medicine and Rehabilitation. Published by Elsevier Inc. All rights reserved.)

Background and Purpose: Chronic hyperglycemia contributes to cerebrovascular dysfunction by damaging blood vessels. Poor glucose control has been tied to impairments in cerebral blood flow, which may be particularly detrimental for people recovering from major cerebrovascular events such as acute ischemic stroke. In this secondary analysis, we explore for the first time the connection between chronic hyperglycemia before acute stroke and the cerebrovascular response (CVR) to exercise 3 and 6 month into the subacute recovery period. Methods: We recorded middle cerebral artery velocity (MCAv) using transcranial Doppler ultrasound bilaterally at rest and during moderate‐intensity exercise in stroke patients at 3 (n = 19) and 6 (n = 12) months post‐stroke. We calculated CVR as the difference between MCAv during steady‐state exercise and resting MCAv. We obtained hemoglobin A1c levels (HbA1c; a measure of blood glucose over the prior 3 months) from the electronic medical record (EMR) and divided participants by HbA1c greater or less than 7%. Results: Participants with high HbA1c (>7%) at the time of acute stroke had significantly lower CVR to exercise for both the stroke‐affected (p =.009) and non‐affected (p =.007) hemispheres at 3 months post‐stroke. These differences remained significant at 6 months post‐stroke (stroke‐affected, p =.008; non‐affected, p =.016). Conclusions: Patients with chronic hyperglycemia before acute ischemic stroke demonstrated impaired cerebrovascular function during exercise months into the subacute recovery period. These findings highlight the importance of maintaining tight glucose control to reduce morbidity and improve recovery post‐stroke and could have implications for understanding cerebrovascular pathophysiology. [ABSTRACT FROM AUTHOR]