The exaggerated blood pressure response to exercise in the sub‐acute phase after stroke is not affected by aerobic exercise

Wijkman, Magnus; Sandberg, Klas; Kleist, Marie; Falk, Lars; Enthoven, Paul

doi:10.1111/jch.13157

Cited by 6 publications

(3 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In paper 2 we obtained baseline SBP data during a symptom-limited ergometer exercise test from 53 patients. 135 Resting blood pressure (ICF code b420) was well controlled at baseline on average (mean resting blood pressure 139.8±21.8/77.6±10.2 mmHg). The overall prevalence of an exaggerated blood pressure response was 35/53 (66%) during work.…”

Section: Study Amentioning

confidence: 95%

See 1 more Smart Citation

Effects of exercise in different phases after stroke

Sandberg

2023

Linköping University Medical Dissertations

View full text Add to dashboard Cite

Background: Stroke is a complex disease that can vary in severity. After a stroke, patients often have long-term disabilities that require major rehabilitation efforts. Evaluation of treatment and methods are important for development of effective rehabilitation after stroke. Various forms of physiotherapy interventions have been tested in different phases after stroke, but there are still questions about timing and forms of exercise. In this work, aerobic exercise with an ergometer cycle and an in-bed cycle were used as models for intervention in subacute and acute phase after stroke. Exercise has been evaluated both after discharge from hospital and in hospital care. Aim: The overall aim of the dissertation was to study the effects of exercise in different phases after stroke of varying severity. Method: Two studies were performed in Swedish stroke units during 2013-2018. Both studies were randomized controlled trials focusing on the effects of exercise in different phases after stroke. Study A included 56 patients with mild stroke from one hospital. Patients were discharged from the hospital and enrolled to intervention in median 22.5 days after stroke onset. All patients received usual care in a stroke unit according to national guidelines, and the intervention group received additionally aerobic exercise for 1 hour 2 times per week for 12 weeks post-discharge. The session included 2x8 minutes of intense aerobic exercise on an ergometer cycle. In study A, the effects of exercise were evaluated by aerobic exercise, walking distance and hemodynamic responses and compared to usual care. Study B included 52 patients in the acute phase of moderate to severe stroke from two hospitals. Patients were enrolled to intervention 2 days after onset, and all patients received usual care. In addition to usual care, one group received in-bed cycle exercise 20 minutes daily, 5 days per week for 3 weeks. In study B, the effects of exercise were evaluated by walking distance and hemodynamic responses and compared to usual care. Results: Study A showed that intensive aerobic exercise twice weekly for 12 weeks during the subacute phase of mild stroke improved the patient's aerobic capacity and walking distance after the intervention period. The study also showed that exaggerated blood pressure reactions associated with exercise were common in the subacute phase but not significantly affected by participation in a 12-week exercise period. Study B showed that the addition of in-bed cycle exercise in the acute phase after more severe stroke was not superior to usual care with regards to walking distance after 3 months. From baseline to post-intervention, systolic blood pressure decreased significantly to a similar extent in both groups, but the exercise group seemed to normalize their blood pressure response to exercise to a greater extent than patients in the control group. Conclusion:For patients with mild symptoms, aerobic exercise initiated 3 weeks after stroke onset was beneficial for aerobic capacity and walking distance. In t...

show abstract

Section: Study Amentioning

confidence: 95%

“…The overall prevalence of an exaggerated blood pressure response was 35/53 (66%) during work. 135 Table 7 provides an overview of the results in paper 2. Abbreviations: DBP, diastolic blood pressure; SBP, systolic blood pressure.…”

Section: Study Amentioning

confidence: 99%

Effects of exercise in different phases after stroke

Sandberg

2023

Linköping University Medical Dissertations

View full text Add to dashboard Cite

show abstract

“…This protection is marked by the attenuation of A Review on the Mechanisms of Stroke-Induced Muscle Atrophy DOI: http://dx.doi.org/10.5772/intechopen.114989 TNF-α and IL-1 expression, in conjunction with the inhibition of apoptosis in cases of focal cerebral ischemia [45]. Additionally, administration of the β-blocker propranolol or antibiotic enrofloxacin demonstrated similar results [46,47].…”

Section: Autonomic Dysregulation Inflammation and Their Widespread Ef...mentioning

confidence: 97%

A Review on the Mechanisms of Stroke-Induced Muscle Atrophy

Bovio,

M. Abd,

C. Ku

et al. 2024

Physiology

View full text Add to dashboard Cite

This comprehensive review elucidates the intricate, multifactorial pathophysiology underpinning post-stroke skeletal muscle atrophy, a detrimental complication impacting patient outcomes. Post-stroke complications including dysphagia, malabsorption, and inadequate protein intake precipitate a catabolic state, exacerbating muscle wasting. The dearth of essential amino acids perpetuates proteolysis over protein synthesis, highlighting the importance of nutritional interventions. Immobility-induced disuse atrophy and dysregulation of anabolic pathways, notably IGF/Akt/PI3K, favor proteolysis, disrupting muscle protein homeostasis. Proteolytic systems including the ubiquitin-proteasome pathway and autophagy play central roles. Moreover, transcriptomic alterations, insulin resistance, autonomic dysregulation, inflammation, oxidative stress, and dysregulated microRNAs contribute to reduced muscle mass post-stroke. Notably, matrix metalloproteinases’ (MMPs) implication unveils potential therapeutic avenues via MMP inhibition. Unraveling this complex pathophysiological interplay is crucial for developing multi-modal interventions to manage post-stroke muscle atrophy effectively.

show abstract