Effects of Exercise Intensity on Acute Circulating Molecular Responses Poststroke

Abstract

Background. Exercise intensity can influence functional recovery after stroke, but the mechanisms remain poorly understood. Objective. In chronic stroke, an intensity-dependent increase in circulating brain-derived neurotrophic factor (BDNF) was previously found during vigorous exercise. Using the same serum samples, this study tested acute effects of exercise intensity on other circulating molecules related to neuroplasticity, including vascular-endothelial growth factor (VEGF), insulin-like growth factor-1 (IGF1), and cortisol, with some updated analyses involving BDNF. Methods. Using a repeated-measures design, 16 participants with chronic stroke performed 3 exercise protocols in random order: treadmill high-intensity interval training (HIT-treadmill), seated-stepper HIT (HIT-stepper), and treadmill moderate-intensity continuous exercise (MCT-treadmill). Serum molecular changes were compared between protocols. Mediation and effect modification analyses were also performed. Results. VEGF significantly increased during HIT-treadmill, IGF1 increased during both HIT protocols and cortisol nonsignificantly decreased during each protocol. VEGF response was significantly greater for HIT-treadmill versus MCT-treadmill when controlling for baseline. Blood lactate positively mediated the effect of HIT on BDNF and cortisol. Peak treadmill speed positively mediated effects on BDNF and VEGF. Participants with comfortable gait speed ≥0.4 m/s had significantly lower VEGF and higher IGF1 responses, with a lower cortisol response during MCT-treadmill. Conclusions. BDNF and VEGF are promising serum molecules to include in future studies testing intensity-dependent mechanisms of exercise on neurologic recovery. Fast training speed and anaerobic intensity appear to be critical ingredients for eliciting these molecular responses. Serum molecular response differences between gait speed subgroups provide a possible biologic basis for previously observed differences in training responsiveness.

Effects of Combined Interventions with Aerobic Physical Exercise and Cognitive Training on Cognitive Function in Stroke Patients: A Systematic Review

“…Moreover, some of the molecular effects of exercise are intensity-dependent. For example, a bout of exercise on a treadmill produced intensity-dependent increases in brain-derived neurotrophic factor (BDNF) and vascular endothelial growth factor (VEGF) in serum, and, to a lesser extent, insulin-like growth factor 1 (IGF-1), in stroke patients [ 58 ]. The exercise intensities used in the revised studies were not very different and can be all be classified as moderate or moderate-to-vigorous.…”

Is High-Intensity Interval Training Suitable to Promote Neuroplasticity and Cognitive Functions after Stroke?

“…Figure 1 also illustrates the effects of HIIT on neuroplasticity processes and cognitive functions after stroke. A single bout of HIIT just as a 4-week HIIT program increase serum VEGF and IGF1 levels as well as BDNF levels that are correlated with higher blood lactate concentrations compared to MICT, without a concomitant cortisol stress response (known to limit neuroplasticity processes) [ 24 , 35 , 77 , 129 , 130 ]. In the ipsilesional hemisphere, HIIT induces higher deoxyhemoglobin concentrations compared to MICT, reflecting greater improvements in systemic and cerebral O 2 consumption, but no cognitive recovery is found [ 35 ].…”

“…Exercise regimens with higher intensities, such as high-intensity interval training (HIIT), emerge as encouraging alternatives to improve cardiovascular and brain health following stroke [ 24 , 25 , 26 , 27 ]. HIIT, the most popular trend of 2018 [ 28 ], involves repeated short-to-long bouts of high-intensity exercise interspersed with active or passive recovery periods [ 29 ].…”

“…Moreover, HIIT is considered to be enjoyable and a time-efficient strategy to improve wellbeing and cardiovascular and muscular functions [ 28 , 32 , 33 , 34 , 35 , 36 ]. In individuals with stroke, recent evidence indicates a potential role of HIIT by measuring circulating molecular markers of neuroplasticity that might improve cognition functions [ 24 , 25 , 37 , 38 ]. In rodents with cerebral ischemia, HIIT, which induced strong improvements in aerobic parameters, also upregulated neuroplasticity markers in the hippocampus and the cortex when initiated during the therapeutic window (the 2 first weeks poststroke) [ 37 , 38 , 39 ].…”

Are Sarcopenia and Cognitive Dysfunction Comorbid after Stroke in the Context of Brain–Muscle Crosstalk?

“…This study found that HIIT was more effective, because increased BDNF promoted neuronal activity and induced better health outcomes. Future studies that focus on neurologic recovery using intensity-dependent exercise should consider BDNF as a marker [ 51 ].…”