The Impact of Voluntary Exercise on Stroke Recovery.
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ABSTRACT:
SUBMITTER: Lohkamp KJ
PROVIDER: S-EPMC8311567 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Previous treadmill exercise studies showing neuroprotective effects have raised questions as to whether exercise or the stress related to it may be key etiologic factors. In this study, we examined different exercise regimens (forced and voluntary exercise) and compared them with the effect of stress-only on stroke protection. Adult male Sprague-Dawley rats (n = 65) were randomly assigned to treatment groups for 3 weeks. These groups included control, treadmill exercise, voluntary running wheel exercise, restraint, and electric shock. Levels of the stress hormone, corticosterone, were measured in the different groups using ELISA. Animals from each group were then subjected to stroke induced by a 2-h middle cerebral artery (MCA) occlusion followed by 48-h reperfusion. Infarct volume was determined in each group, while changes in gene expression of stress-induced heat shock proteins (Hsp) 27 and 70 were compared using real-time PCR between voluntary and treadmill exercise groups. The level of corticosterone was significantly higher in both stress (P < 0.05) and treadmill exercise (P < 0.05) groups, but not in the voluntary exercise group. Infarct volume was significantly reduced (P < 0.01) following stroke in rats exercised on a treadmill. However, the amelioration of damage was not duplicated in voluntary exercise, even though running distance in the voluntary exercise group was significantly (P < 0.01) longer than that of the forced exercise group (4,828 vs. 900 m). Furthermore, rats in the electric shock group displayed a significantly increased (P < 0.01) infarct volume. Expression of both Hsp 27 and Hsp 70 mRNA was significantly increased (P < 0.01) in the treadmill exercise group as compared with that in the voluntary exercise group. These results suggest that exercise with a stressful component, rather than either voluntary exercise or stress alone, is better able to reduce infarct volume. This exercise-induced neuroprotection may be attributable to up-regulation of stress-induced heat shock proteins 27 and 70.
| S-EPMC2668645 | biostudies-other
Project description:Colon cancer is the second most cancer type in Europe. Its development is highly influenced by life style factors such as nutrition and physical inactivity. Detailed biological mechanisms are so far unclear. The purpose of this study was to investigate the effects of chronic wheel running on gene expression in rat colon mucosa. Therefore six-week-old male Wistar rats (exercise (EX) group, n=20) completed a stress free voluntary running exercise period of 12 weeks. Sedentary rats served as a control (CO, n=9) group. In the colon mucosa, steady-state mRNA expression levels of approximately 10,000 genes were compared between both groups by micro-array analysis (MWG rat 10k array). 8,846 mRNAs were detected above background level. Chronic exercise led to a decreased expression of 47 genes at a threshold-factor of 2.0. 3 genes were found to be up-regulated in the EX group. The identified genes encode proteins involved in signal transduction (n=11), transport (n=8), immune system (n=7), cytoskeleton (n=6), protein targeting (n=6) and metabolism (n=5). Among the genes regulated by chronic exercise, the betaine-homocysteine methyltransferase 2 (BHMT2) seems to be of particular interest. Physical activity may protect against aberrant methylation by repressing the BHMT2 gene and thus contribute to a decreased risk of developing colon cancer. In summary, our experiment presents the first gene expression pattern in rat colon mucosa following chronic wheel running and therefore represents an important step in understanding the molecular mechanisms responsible for the preventive effect of physical activity on the development of colon cancer. Keywords: voluntary running exercise, animal model
2007-05-30 | GSE3342 | GEO
Project description:Muscle hypertrophy occurs following increased protein synthesis, which requires activation of the ribosomal complex. Additionally, increased translational capacity via elevated ribosomal RNA (rRNA) synthesis has also been implicated in resistance training-induced skeletal muscle hypertrophy. The time course of ribosome biogenesis following resistance exercise (RE) and the impact exerted by differing recovery strategies remains unknown. In the present study, the activation of transcriptional regulators, the expression levels of pre-rRNA, and mature rRNA components were measured through 48 h after a single-bout RE. In addition, the effects of either low-intensity cycling (active recovery, ACT) or a cold-water immersion (CWI) recovery strategy were compared. Nine male subjects performed two bouts of high-load RE randomized to be followed by 10 min of either ACT or CWI. Muscle biopsies were collected before RE and at 2, 24, and 48 h after RE. RE increased the phosphorylation of the p38-MNK1-eIF4E axis, an effect only evident with ACT recovery. Downstream, cyclin D1 protein, total eIF4E, upstream binding factor 1 (UBF1), and c-Myc proteins were all increased only after RE with ACT. This corresponded with elevated abundance of the pre-rRNAs (45S, ITS-28S, ITS-5.8S, and ETS-18S) from 24 h after RE with ACT. In conclusion, coordinated upstream signaling and activation of transcriptional factors stimulated pre-rRNA expression after RE. CWI, as a recovery strategy, markedly blunted these events, suggesting that suppressed ribosome biogenesis may be one factor contributing to the impaired hypertrophic response observed when CWI is used regularly after exercise.
| S-EPMC4760384 | biostudies-other
Project description:ObjectivePreviously, we demonstrated that forced aerobic exercise (FE) increases the pattern of neural activation in Parkinson's disease. We sought to evaluate whether FE, when coupled with repetitive task practice, could promote motor recovery poststroke.MethodA 46-yr-old man with ischemic stroke exhibited chronic residual upper-extremity deficits, scoring 35/66 on the Fugl-Meyer Assessment (FMA) at baseline. He completed 24 training sessions comprising 45 min of FE on a motorized stationary bicycle followed by 45 min of upper-extremity repetitive task practice.ResultsFrom baseline to end of treatment, the FMA score improved by 20 points, perceived level of recovery on the Stroke Impact Scale increased by 20 percentage points, and cardiovascular function measured by peak oxygen uptake improved 30%. These improvements persisted 4 wk after the intervention ceased.ConclusionFE may be a safe and feasible rehabilitation approach to augment recovery of motor and nonmotor function while improving aerobic fitness in people with chronic stroke.
| S-EPMC4482578 | biostudies-literature
Project description:Background and objectivePrediction of voluntary upper extremity (UE) movement recovery is largely unknown in patients with little voluntary UE movement at admission. The present study aimed to investigate (1) the extent and variation of voluntary UE movement recovery, and (2) the best predictive model of the recovery of voluntary UE movement by clinical variables in patients with severe UE paresis.DesignProspective cohort study.Methods140 (out of 590) stroke patients with severe UE paresis completed all assessments. Voluntary UE movement was assessed using the UE subscale of the Stroke Rehabilitation Assessment of Movement (STREAM-UE). Two outcome measures, STREAM-UE scores at discharge (DC(STREAM-UE)) and changes between admission and discharge (Δ(STREAM-UE)), were investigated to represent the final states and improvement of the recovery of voluntary UE movement. Stepwise regression analyses were used to investigate 19 clinical variables and to find the best predictive models of the two outcome measures.ResultsThe participants showed wide variation in both DC(STREAM-UE) and Δ(STREAM-UE). 3.6% of the participants almost fully recovered at discharge (DC(STREAM-UE) > 15). A large improvement (Δ(STREAM-UE) >= 10) occurred in 16.4% of the participants, while 32.9% of the participants did not have any improvement. The four predictors for the DC(STREAM-UE) (R(2) = 35.0%) were 'baseline STREAM-UE score', 'hemorrhagic stroke', 'baseline National Institutes of Health Stroke Scale (NIHSS) score', and 'cortical lesion excluding primary motor cortex'. The three predictors for the Δ(STREAM-UE) (R(2) = 22.0%) were 'hemorrhagic stroke', 'baseline NIHSS score', and 'cortical lesion excluding primary motor cortex'.ConclusionsRecovery of voluntary UE movement varied widely in patients with severe UE paresis after stroke. The predictive power of clinical variables was poor. Both results indicate the complex nature of voluntary UE movement recovery in patients with severe UE paresis after stroke.
| S-EPMC4431803 | biostudies-literature
Project description:Effects of voluntary exercise in rat aorta. Spontaneously hypertensive rats (SHR) performed 5 weeks of voluntary exercise (wheel-cage running). Aortic tissue was collected and samples were pooled (3 aortae/chip). Aortae from running rats were compared to aortae from non-running rats. Keywords: parallel sample
2005-03-22 | GSE2418 | GEO
Project description:Although physical exercise is an effective strategy for treatment of ischemic stroke, the underlying protective mechanisms are still not well understood. It has been recently demonstrated that neural progenitor cells play a vital role in the recovery of neurological function (NF) through differentiation into mature neurons. In the current study, we observed that physical exercise significantly reduced the infarct size and improved damaged neural functional recovery after an ischemic stroke. Furthermore, we found that the treatment not only exhibited a significant increase in the number of neural progenitor cells and neurons but also decreased the apoptotic cells in the peri-infarct region, compared to a control in the absence of exercise. Importantly, the insulin-like growth factor-1 (IGF-1)/Akt signaling pathway was dramatically activated in the peri-infarct region of rats after physical exercise training. Therefore, our findings suggest that physical exercise directly influences the NF recovery process by increasing neural progenitor cell count via activation of the IGF-1/Akt signaling pathway.
| S-EPMC4100192 | biostudies-literature
Project description:Evidence supports early rehabilitation after stroke to limit disability. However, stroke survivors are typically sedentary and experience significant cardiovascular and muscular deconditioning. Despite growing consensus that preclinical and clinical stroke recovery research should be aligned, there have been few attempts to incorporate cardiovascular and skeletal muscle deconditioning into animal models of stroke. Here, we demonstrate in rats that a hindlimb sensorimotor cortex stroke results in both cardiovascular and skeletal muscle deconditioning and impairments in gait akin to those observed in humans. To reduce poststroke behavioral, cardiovascular, and skeletal muscle perturbations, we then used a combinatorial intervention consisting of aerobic and resistance exercise in conjunction with administration of resveratrol (RESV), a drug with exercise mimetic properties. A combination of aerobic and resistance exercise mitigated decreases in cardiovascular fitness and attenuated skeletal muscle abnormalities. RESV, beginning 24 hours poststroke, reduced acute hindlimb impairments, improved recovery in hindlimb function, increased vascular density in the perilesional cortex, and attenuated skeletal muscle fiber changes. Early RESV treatment and aerobic and resistance exercise independently provided poststroke benefits, at a time when individuals are rapidly becoming deconditioned as a result of inactivity. Although no additive effects were observed in these experiments, this approach represents a promising strategy to reduce poststroke behavioral impairments and minimize deconditioning. As such, this treatment regime has potential for enabling patients to engage in more intensive rehabilitation at an earlier time following stroke when mechanisms of neuroplasticity are most prevalent.
| S-EPMC8135250 | biostudies-literature
Project description:Improved stroke care has resulted in greater survival, but >50% of patients have chronic disabilities and 33% are institutionalized. While stroke rehabilitation is helpful, recovery is limited and the most significant gains occur in the first 2-3 months. Stroke triggers an early wave of gene and protein changes, many of which are potentially beneficial for recovery. It is likely that these molecular changes are what subserve spontaneous recovery. Two interventions, aerobic exercise and environmental enrichment, have pleiotropic actions that influence many of the same molecular changes associated with stroke injury and subsequent spontaneous recovery. Enrichment paradigms have been used for decades in adult and neonatal animal models of brain injury and are now being adapted for use in the clinic. Aerobic exercise enhances motor recovery and helps reduce depression after stroke. While exercise attenuates many of the signs associated with normal aging (e.g., hippocampal atrophy), its ability to reverse cognitive impairments subsequent to stroke is less evident. It may be that stroke, like other diseases such as cancer, needs to use multimodal treatments that augment complimentary neurorestorative processes.
| S-EPMC4824016 | biostudies-literature
Project description:Aphasic deficits are usually only interpreted in terms of domain-specific language processes. However, effective human communication and tests that probe this complex cognitive skill are also dependent on domain-general processes. In the clinical context, it is a pragmatic observation that impaired attention and executive functions interfere with the rehabilitation of aphasia. One system that is important in cognitive control is the salience network, which includes dorsal anterior cingulate cortex and adjacent cortex in the superior frontal gyrus (midline frontal cortex). This functional imaging study assessed domain-general activity in the midline frontal cortex, which was remote from the infarct, in relation to performance on a standard test of spoken language in 16 chronic aphasic patients both before and after a rehabilitation programme. During scanning, participants heard simple sentences, with each listening trial followed immediately by a trial in which they repeated back the previous sentence. Listening to sentences in the context of a listen-repeat task was expected to activate regions involved in both language-specific processes (speech perception and comprehension, verbal working memory and pre-articulatory rehearsal) and a number of task-specific processes (including attention to utterances and attempts to overcome pre-response conflict and decision uncertainty during impaired speech perception). To visualize the same system in healthy participants, sentences were presented to them as three-channel noise-vocoded speech, thereby impairing speech perception and assessing whether this evokes domain general cognitive systems. As expected, contrasting the more difficult task of perceiving and preparing to repeat noise-vocoded speech with the same task on clear speech demonstrated increased activity in the midline frontal cortex in the healthy participants. The same region was activated in the aphasic patients as they listened to standard (undistorted) sentences. Using a region of interest defined from the data on the healthy participants, data from the midline frontal cortex was obtained from the patients. Across the group and across different scanning sessions, activity correlated significantly with the patients' communicative abilities. This correlation was not influenced by the sizes of the lesion or the patients' chronological ages. This is the first study that has directly correlated activity in a domain general system, specifically the salience network, with residual language performance in post-stroke aphasia. It provides direct evidence in support of the clinical intuition that domain-general cognitive control is an essential factor contributing to the potential for recovery from aphasic stroke.
| S-EPMC3891442 | biostudies-literature