Muscle activation changes during body weight support treadmill training after focal cortical ischemia: A rat hindlimb model

Le, Li; Wei, Rong; Zheng, Ke; Hu, Xiao; Yip, Shea Ping; Tong, Kai-Yu

doi:10.1016/j.jelekin.2010.09.008

Cited by 14 publications

(12 citation statements)

References 43 publications

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“…Animal and human studies reported that acute exercise could reveal changes in muscle activation regulation after cerebral ischemia. More precisely, the electromyographic (EMG) activity was lower in affected hindlimb muscles during a single bout of treadmill exercise compared to unaffected muscles, reflecting a strong decrease of the motoneuronal recruitment from spinal and/or supraspinal motor pathways [ 4 , 20 ]. A reduced corticospinal excitability to the paretic quadriceps was also observed by showing strong decrease of the motor evoked potential (MEP) amplitude during a running exercise [ 4 ].…”

Section: Acute Exercise-induced Neural Adjustments After Strokementioning

confidence: 99%

“…More precisely, the electromyographic (EMG) activity was lower in affected hindlimb muscles during a single bout of treadmill exercise compared to unaffected muscles, reflecting a strong decrease of the motoneuronal recruitment from spinal and/or supraspinal motor pathways [ 4 , 20 ]. A reduced corticospinal excitability to the paretic quadriceps was also observed by showing strong decrease of the motor evoked potential (MEP) amplitude during a running exercise [ 4 ]. In addition, cortical activation increased in the unaffected side while it decreased in the affected side after ankle dorsiflexion movements that suggested compensatory neural mechanisms [ 21 – 26 ].…”

Section: Acute Exercise-induced Neural Adjustments After Strokementioning

confidence: 99%

“…Indeed, the asymmetry of muscle activation pattern between affected and unaffected hindlimbs was restored because the EMG burst duration was increased at the affected side [ 83 ]. Muscle fatigue observed during locomotion was reduced as indicated by the increase of MPF at the unaffected side (see Section 2 ) [ 4 ].…”

Section: Effects Of Poststroke Physical Training On Neuroplasticitmentioning

confidence: 99%

“…First, acute fatiguing exercise is used in preclinical experiments as a diagnostic tool to detect sensorimotor dysfunctions and/or reveal treatment effectiveness that cannot be observed in resting condition. Indeed, alteration of motor unit activation in both affected and unaffected sides or changes of the motor reflex regulation were highlighted during/after acute exercise [ 4 , 5 ]. Moreover, a higher corticospinal tract activity was found only after acute treadmill exercise in trained patients contrary to untrained patients [ 6 ].…”

Section: Introductionmentioning

confidence: 99%

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Physical Exercise as a Diagnostic, Rehabilitation, and Preventive Tool: Influence on Neuroplasticity and Motor Recovery after Stroke

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Laurin

2015

Neural Plasticity

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Stroke remains a leading cause of adult motor disabilities in the world and accounts for the greatest number of hospitalizations for neurological disease. Stroke treatments/therapies need to promote neuroplasticity to improve motor function. Physical exercise is considered as a major candidate for ultimately promoting neural plasticity and could be used for different purposes in human and animal experiments. First, acute exercise could be used as a diagnostic tool to understand new neural mechanisms underlying stroke physiopathology. Indeed, better knowledge of stroke mechanisms that affect movements is crucial for enhancing treatment/rehabilitation effectiveness. Secondly, it is well established that physical exercise training is advised as an effective rehabilitation tool. Indeed, it reduces inflammatory processes and apoptotic marker expression, promotes brain angiogenesis and expression of some growth factors, and improves the activation of affected muscles during exercise. Nevertheless, exercise training might also aggravate sensorimotor deficits and brain injury depending on the chosen exercise parameters. For the last few years, physical training has been combined with pharmacological treatments to accentuate and/or accelerate beneficial neural and motor effects. Finally, physical exercise might also be considered as a major nonpharmacological preventive strategy that provides neuroprotective effects reducing adverse effects of brain ischemia. Therefore, prestroke regular physical activity may also decrease the motor outcome severity of stroke.

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Section: Acute Exercise-induced Neural Adjustments After Strokementioning

confidence: 99%

Section: Acute Exercise-induced Neural Adjustments After Strokementioning

confidence: 99%

Section: Effects Of Poststroke Physical Training On Neuroplasticitmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Physical Exercise as a Diagnostic, Rehabilitation, and Preventive Tool: Influence on Neuroplasticity and Motor Recovery after Stroke

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Laurin

2015

Neural Plasticity

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show abstract

“…Moreover, it was shown that aerobic treadmill training (20min/day, during 21 days) improved cholinergic system regulation/homeostasis and it was suggested that such adaptation allowing better limb motor function [36]. The muscle electromyographic activity returned to normal activity only after 10 days of treadmill training, optimizing balance and motor coordination during locomotion [37]. Unfortunately, the underlying neuromuscular adaptations at the spinal and supraspinal levels remain poorly understood in animal as well as in human models and deserves more attention.…”

Section: Beneficial Effects and Physiological Adaptationsmentioning

confidence: 99%

Physiological Adaptations Following Endurance Exercises after Stroke: Focus on the Plausible Role of High-Intensity Interval Training

Laurin

Pin-Barre²

2014

Int J Phys Med Rehabil

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The endurance training is considered as an integral part of stroke rehabilitation. However, medical institutions did not systematically include aerobic exercises because of the lack of scientific evidence. It is mainly the case for highintensity interval training (HIT) for which very few experiments were focused on after stroke. This review was designed to examine and compare the neurophysiological and physiological adaptations associated with two effective modalities of endurance training after stroke: the continuous low-intensity endurance training and the HIT. Based on the beneficial adaptations induced by HIT in healthy people and in patients with cardiovascular disorders, we postulate that this training modality might be involved in endurance program as complement or alternate of the traditional low intensity training in stroke patient. Therefore, including HIT in stroke rehabilitation may improve functional recovery by inducing rapid and significant beneficial physiological adaptations. Moreover, no clear recommendations were found on the appropriate timing for using HIT and other endurance training after stroke despite that the intervention timing is one of the major determinant of an effective recovery. The optimal time to initiate endurance program rehabilitation is thus discussed. Further studies are required to investigate the physiological adaptations to HIT compared to traditional endurance training as well as the combination of these two training modalities.

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Mechanical and microstructural changes of skeletal muscle following immobilization and/or stroke

Jalal

Zidi

2019

Biomech Model Mechanobiol

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Muscle activation changes during body weight support treadmill training after focal cortical ischemia: A rat hindlimb model

Cited by 14 publications

References 43 publications

Physical Exercise as a Diagnostic, Rehabilitation, and Preventive Tool: Influence on Neuroplasticity and Motor Recovery after Stroke

Physical Exercise as a Diagnostic, Rehabilitation, and Preventive Tool: Influence on Neuroplasticity and Motor Recovery after Stroke

Physiological Adaptations Following Endurance Exercises after Stroke: Focus on the Plausible Role of High-Intensity Interval Training

Mechanical and microstructural changes of skeletal muscle following immobilization and/or stroke

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