From Mechanisms to Recovery: A Review on the Impact of Aerobic Exercise Modality and Intensity on Brain Function and Cognitive Rehabilitation

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Aerobic exercise offers a cost-effective approach to mitigate cognitive decline. However, clinical application is hindered by inconsistencies in exercise protocols, assessment tools, and mechanistic interpretations. This review synthesizes evidence on structural, functional, and molecular mechanisms underlying the cognitive benefits of exercise. These mechanisms include hippocampal neurogenesis and cortical thickening (structural), enhanced network connectivity and cerebral blood flow (functional), and upregulation of BDNF, VEGF, and irisin (molecular). We systematically evaluate how exercise intensity and modality affect different cognitive domains. Moderate-intensity regimens (40–69% VO 2 max) are consistently shown to improve executive function. The effects on memory, attention, and visuospatial processing are found to vary, likely due to methodological heterogeneity. This work advances evidence-based guidelines for optimizing aerobic exercise prescriptions to enhance cognitive function, with relevance for age-related decline and neurological rehabilitation.
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Data may be preliminary. 29 December 2025 V1 Latest version Share on From Mechanisms to Recovery: A Review on the Impact of Aerobic Exercise Modality and Intensity on Brain Function and Cognitive Rehabilitation Authors : Lili Qin , Tianqi Liu 0009-0009-9059-4829 , Dengyun Xu , Lanqing Ling , Tianfeng Lu [email protected] , and Hong Li Authors Info & Affiliations https://doi.org/10.22541/au.176700444.44876411/v1 288 views 73 downloads Contents Abstract Information & Authors Metrics & Citations View Options References Figures Tables Media Share Abstract Aerobic exercise offers a cost-effective approach to mitigate cognitive decline. However, clinical application is hindered by inconsistencies in exercise protocols, assessment tools, and mechanistic interpretations. This review synthesizes evidence on structural, functional, and molecular mechanisms underlying the cognitive benefits of exercise. These mechanisms include hippocampal neurogenesis and cortical thickening (structural), enhanced network connectivity and cerebral blood flow (functional), and upregulation of BDNF, VEGF, and irisin (molecular). We systematically evaluate how exercise intensity and modality affect different cognitive domains. Moderate-intensity regimens (40–69% VO 2 max) are consistently shown to improve executive function. The effects on memory, attention, and visuospatial processing are found to vary, likely due to methodological heterogeneity. This work advances evidence-based guidelines for optimizing aerobic exercise prescriptions to enhance cognitive function, with relevance for age-related decline and neurological rehabilitation. Type of contribution: Review paper From Mechanisms to Recovery: A Review on the Impact of Aerobic Exercise Modality and Intensity on Brain Function and Cognitive Rehabilitation Lili Qin a , Tianqi Liu a , Dengyun Xu a , Lanqing Ling a , Tianfeng Lu a* and Hong Li b a 11* Corresponding author. Tel: 86 (021) 65985242 E-mail address: [email protected] .; [email protected] a Sports and Health Research Center, Department of Physical Education, Tongji University, Shanghai 200092, People’s Republic of China b School of Humanities, Tongji University, Shanghai 200092, People’s Republic of China Lili Qin Siping Road No.1239 China Email: [email protected] Corresponding author: Tianfeng Lu Siping Road No.1239 Shanghai China Email: [email protected] Hong Li Siping Road No.1239 Shanghai China Email: [email protected] From Mechanisms to Recovery: A Review on the Impact of Aerobic Exercise Modality and Intensity on Brain Function and Cognitive Rehabilitation Lili Qin a , Tianqi Liu a , Dengyun Xu a , Lanqing Ling a , Tianfeng Lu a* and Hong Li b a 11* Corresponding author. Tel: 86 (021) 65985242 E-mail address: [email protected] .; [email protected] a Sports and Health Research Center, Department of Physical Education, Tongji University, Shanghai 200092, People’s Republic of China b School of Humanities, Tongji University, Shanghai 200092, People’s Republic of China Abstract Aerobic exercise offers a cost-effective approach to mitigate cognitive decline. However, clinical application is hindered by inconsistencies in exercise protocols, assessment tools, and mechanistic interpretations. This review synthesizes evidence on structural, functional, and molecular mechanisms underlying the cognitive benefits of exercise. These mechanisms include hippocampal neurogenesis and cortical thickening (structural), enhanced network connectivity and cerebral blood flow (functional), and upregulation of BDNF, VEGF, and irisin (molecular). We systematically evaluate how exercise intensity and modality affect different cognitive domains. Moderate-intensity regimens (40–69% VO₂max) are consistently shown to improve executive function. The effects on memory, attention, and visuospatial processing are found to vary, likely due to methodological heterogeneity. This work advances evidence-based guidelines for optimizing aerobic exercise prescriptions to enhance cognitive function, with relevance for age-related decline and neurological rehabilitation. Keywords: Aerobic exercise; Cognition; Mechanism research; Functional research; Aerobic exercise intensity; Introduction Numerous studies show that regular physical activity and improved physical fitness, including cardiorespiratory capacity, muscular strength, and endurance—benefit cognitive domains like attention, executive function, and long-term memory [1-3]. Understanding the neural mechanisms behind exercise-induced cognitive improvements has become a key focus in psychology, neuroscience, and sports medicine in recent decades. Neuroimaging techniques like functional magnetic resonance imaging (fMRI), functional near-infrared spectroscopy (fNIRS), and electroencephalography (EEG) have advanced our knowledge of exercise-brain interactions [4-6]. Newer methods such as retinal microcirculation analysis, pupillometry, and saccadic eye movement tracking are also increasingly used to study cognitive neuroscience in exercise [7]. Among non-drug interventions, aerobic exercise represents a cost-effective, accessible, and low-risk strategy for cognitive health preservation, demonstrating significant promise for populations with chronic conditions such as mild cognitive impairment, stroke survivorship, and neurodegenerative disorders [8]. Characterized by sustained, rhythmic moderate-to-vigorous intensity activities (e.g., walking, cycling, swimming), this modality promotes cognitive enhancement through synergistic multiscale pathways spanning molecular, structural, and functional adaptations. At the molecular level, exercise-induced upregulation of neurotrophic factors (BDNF, VEGF) and myokines (e.g., irisin) orchestrates synaptic plasticity while suppressing pro-inflammatory cytokines (e.g., IL-12p40) [9-11,38-39]. These molecular cascades drive macroscopic neuroplastic changes, including hippocampal neurogenesis to counteract age-related atrophy and cortical thickening within prefrontal-parietal networks [12,15,18]. Concurrently, functional reorganization optimizes brain connectivity—enhancing neural efficiency in attentional circuits, augmenting cerebral blood flow in hippocampal-prefrontal pathways, and strengthening default mode network coherence [17,23,25].Critically, these interconnected mechanisms translate to domain-specific cognitive improvements: Executive function gains correlate with BDNF-mediated prefrontal cortex efficiency [34,47]; working memory enhancements link to hippocampal vascularization and neurogenesis [14,45]; and accelerated processing speed arises from improved white matter integrity and frontoparietal synchronization [22,49]. Both human and animal studies consistently validate these cognitive benefits, underscoring clinical utility for cognitive function recovery [13-15,21,44]. Despite progress, critical gaps remain. First, differences in exercise protocols—such as intensity thresholds (%VO₂max, heart rate zones), modalities (continuous vs. interval training), and durations—hinder cross-study comparisons [16-18]. Second, inconsistencies in cognitive assessment tools such as task-specific and domain-general measures, and mechanistic interpretations limit clinical use [19]. Third, while moderate-intensity aerobic exercise reliably improves executive function, its effects on memory, visuospatial processing, and attention vary across populations, especially older adults and those with neurological conditions [20-22]. These issues highlight the need for standardized exercise guidelines to optimize cognitive function. This review synthesizes evidence on the structural, functional, and molecular mechanisms through which aerobic exercise enhances cognition. We systematically evaluate how exercise intensity and modality impact different cognitive domains, focusing on reconciling methodological differences. By integrating findings from healthy adults, older populations, and clinical groups, we aim to advance evidence-based recommendations for prescribing aerobic exercise, bridging the gap between research and practical cognitive health promotion. Mechanisms of Aerobic Exercise on Cognitive Function Brain Structural and Functional Adaptations Stroke-induced neuroanatomical injury leads to post-stroke cognitive impairment. Brain modularity, a key aspect of cognitive plasticity, enables functional specialization across regions [9]. Key brain areas have distinct roles: • Dorsolateral prefrontal cortex: Executive function • Precuneus: Episodic memory integration, visuospatial processing, self-awareness • Inferior parietal lobe: Attention, language, visuospatial coordination [15-16] • Hippocampus: Spatial memory Aerobic exercise counteracts structural brain decline, particularly attenuating age-related hippocampal volume loss and improving spatial memory as demonstrated by longitudinal neuroimaging studies [10-13]. This protective effect is evidenced in sedentary older adults through 6-month aerobic interventions that significantly increase hippocampal volume via high-resolution MRI, concurrently enhancing cognitive performance [14]. Notably, exercise-induced benefits extend beyond local neuroanatomical changes: translational research indicates that plasma transfer from exercised rodents reduces neuroinflammation and improves cognition in sedentary recipients, highlighting circulating factors (e.g., clusterin) as potential mediators [17]. Structural adaptations also manifest as cortical thickening in cognition-critical regions including the bilateral dorsolateral prefrontal cortex, precuneus, and inferior parietal cortex across healthy adults [15,17]. Critically, gray matter volume increases in frontal, parietal, and cingulate cortices have been documented in mild cognitive impairment (MCI) patients following combined aerobic exercise and nutraceutical interventions, with MRI confirming consistent volumetric gains in hippocampal, prefrontal, and cingulate regions regardless of cognitive status [18]. These structural enhancements collectively promote neural function and validate exercise as a potent inducer of brain plasticity.Beyond the changes in volume and thickness of local brain regions, the effects of aerobic exercise on brain structure involve broader physiological processes—including cellular and molecular alterations such as angiogenesis, neurogenesis, and inflammation regulation, as well as coordinated adjustments at the behavioral and systemic levels (e.g., sleep and stress pathways), as depicted in Fig. 2. This figure systematically outlines the key pathways through which aerobic exercise impacts brain structure from the cellular-molecular level to the behavioral and socioemotional level, further confirming that structural adaptation is the result of the combined action of multiple factors. Neuroimaging evidence supports a bidirectional brain-exercise relationship wherein physical activity remodels functional networks. fMRI studies reveal intensity-dependent activation patterns: spatial tasks elicit augmented parietal-hippocampal engagement [19], while working memory paradigms variably modulate frontal lobe activity [20]. In subcortical ischemic vascular cognitive impairment, moderate-intensity aerobic training reorganizes functional connectivity, with reduced activation in occipitotemporal regions correlating with improved executive function—indicating heightened neural efficiency [21]. Exercise intensity differentially engages motor-cognitive networks. Low-intensity exercise primarily activates motor-cerebellar circuits, whereas high-intensity exertion recruits broader sensorimotor regions (somatosensory cortex, insula) while suppressing prefrontal-hippocampal activity—suggesting a shift toward cardiovascular-motor prioritization [22]. Crucially, aerobic exercise strengthens hippocampal-left superior frontal connectivity, optimizing memory consolidation through enhanced inter-regional communication [23]. Age-related cerebrovascular decline, characterized by endothelial dysfunction and reduced nitric oxide bioavailability, impairs cerebral perfusion. Since higher cerebral blood flow (CBF) correlates with superior executive function and memory [24], exercise-induced CBF augmentation represents a key neuroprotective mechanism. Transcranial Doppler studies confirm that 6-month aerobic interventions reduce cerebrovascular resistance and increase CBF in middle-aged/older adults, concomitantly improving executive function [25]. Perfusion MRI further demonstrates exercise-mediated CBF elevation in frontal lobes (callosal sulcus, anterior cingulate) and hippocampus, enhancing verbal-spatial memory [14,26]. Hemodynamic monitoring reveals intensity-specific oxygenation patterns: moderate-intensity exercise decreases oxyhemoglobin in right dorsolateral prefrontal cortex (indicating elevated metabolic demand), while high-intensity exertion increases left prefrontal oxygenation—directly linking hemodynamic responses to functional optimization [27]. In summary, aerobic exercise improves corresponding cognitive functions by enhancing blood flow in the prefrontal lobe, corpus callosum inferior gyrus, anterior cingulate gyrus, and hippocampus. Ultrasound Doppler, functional magnetic resonance perfusion imaging, and high-density functional near-infrared spectroscopy can assess hemodynamic changes in functional brain areas. Neuroplasticity and Molecular Pathways The cognitive benefits of aerobic exercise are not driven by a single-dimensional effect but by coordinated regulation across multiple levels and systems. From fundamental cellular and molecular changes to macroscopic remodeling of brain structure and function, and ultimately to observable alterations in behavioral and socioemotional outcomes, a complete functional chain is formed, as shown in Fig. 1. This framework clearly illustrates the key links from aerobic exercise input to cognitive output, providing a systematic perspective for subsequent analysis of specific mechanisms.Aerobic exercise also promotes neuronal function and synaptic growth. It encourages synaptic growth, neurogenesis, and increased dendrite spine density, all of which aid nerve function recovery [28]. Fig. 1 Effect of aerobic exercise on cognitive processes Fig. 2 Effect of aerobic exercise on brain structure Neuroplasticity impairment contributes to neurological disease progression, driving interest in non-pharmacological interventions to restore neural adaptability. Aerobic exercise emerges as a potent modulator of neuroplasticity through molecular and cellular neurotrophic mechanisms. Substantial evidence [28-29] demonstrates its ability to enhance synaptic plasticity, stimulate adult hippocampal neurogenesis, and increase dendritic spine density. The aerobic metabolic system plays a critical role in triggering exercise-induced neural remodeling, including new neuron formation [30]. Rodent studies specifically highlight improved hippocampal synaptic plasticity following aerobic training [31], correlating with enhanced learning and memory. Additionally, astrocytes, the predominant glial cells of the central nervous system (CNS), exert their influence on exercise-induced via vascular modulation and metabolic sustenance. Aerobic exercise enhances cognitive function through systemic regulation of neurotrophic factors, cytokines, and inflammatory mediators [32]. Central to this process is brain-derived neurotrophic factor (BDNF), which drives cortical synaptic remodeling and hippocampal plasticity. Both human and animal studies demonstrate exercise-induced increases in serum and cerebral BDNF levels, with older adults showing immediate post-exercise elevations correlated with working memory improvements [34-36]. Recent systematic reviews highlight that high-intensity interval exercise (e.g., sprint cycling) induces more rapid and pronounced BDNF elevation compared to moderate continuous training, particularly in sedentary individuals (Hedge’s g = 0.49 for high-intensity vs. 0.18 for moderate-intensity) [56]. Sex-specific responses are also observed, with women exhibiting greater BDNF upregulation during aerobic exercise, potentially mediated by ovarian hormone interactions [57]. Parallel mechanisms involve vascular endothelial growth factor (VEGF) and insulin-like growth factor-1 (IGF-1). In rodent models of cerebral infarction, moderate-intensity aerobic swimming upregulated hippocampal BDNF/VEGF expression, accelerating spatial learning in Morris water maze tests [33]. Human trials mirror these findings, showing elevated serum IGF-1 and VEGF levels alongside enhanced executive function in amnestic mild cognitive impairment (aMCI) patients [36]. Peripheral signaling pathways further amplify these effects. Muscle-derived cathepsin B (CTSB) increases during sustained running, enhancing hippocampal BDNF and doublecortin (DCX) expression in neural progenitor cells through P11-dependent mechanisms [37]. Concurrently, exercise activates peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α) in skeletal muscle, stimulating fibronectin type III domain-containing protein 5 (FNDC5) cleavage into irisin. This exercise-responsive myokine crosses the blood-brain barrier to boost hippocampal BDNF levels and spatial memory [38]. Aerobic training also modulates neuroinflammation by reducing pro-aging cytokines like IL-12p40. Both genetic ablation studies and exercise interventions show that IL-12p40 suppression decreases amyloid accumulation and synaptic loss while improving spatial memory [39-40]. Clinical studies in depression highlight the synergistic effects of exercise and pharmacological treatments, where high-intensity cycling (70% max HR) elevates serum BDNF more effectively than low-intensity exercise (6.91 vs. 3.24 ng/mL, p < 0.01), paralleling improvements in executive function [57]. Collectively, these multi-target effects on BDNF, VEGF, CTSB, irisin, and inflammatory pathways establish aerobic exercise as a potent regulator of cognitive plasticity across species [28-40]. The effects of form and intensity of aerobic exercise on cognitive function recovery Aerobic exercise encompasses various forms such as walking, running, cycling, swimming, and ball sports. The appropriate exercise modality depends on individual fitness levels, with walking typically suitable for frail individuals and higher-intensity activities like running better suited for trained individuals [21,33]. Clinical selection of aerobic exercise modalities for elderly and patient populations requires consideration of exercise accessibility and functional capacity. Evidence indicates that diverse exercise forms—including walking and swimming—can effectively enhance cognitive function when appropriately prescribed. In subcortical ischemic vascular cognitive impairment cohorts, walking interventions significantly improved executive function reaction times compared to controls [21]. Similarly, longitudinal swimming regimens demonstrate cognitive enhancement through moderate-intensity protocols [33]. Fig. 3 Effect of aerobic exercise on concrete cognitive performance Different forms of aerobic exercise all exert an influence on cognitive function. Cycling has been extensively studied due to its safety and adjustable intensity features, consistently showing positive effects on cognition, especially for the elderly and patients [18,36,43,47,50]. The form of aerobic exercise is not associated with the recovery of cognitive function, while the intensity of aerobic exercise does have an impact. The intensity of aerobic exercise can be divided into low intensity aerobic exercise, moderate intensity aerobic exercise, high intensity aerobic exercise and higher intensity aerobic exercise. Aerobic exercise intensity can be classified into four categories based on physiological parameters: The oxygen intake of low-intensity aerobic exercise is below 40% of VO2max, the heart rate is below 55% of HRmax, and the HRR is below 40%, and the fatigue degree is scored 10-11 points on the RPE scale. The oxygen intake of moderate intensity aerobic exercise is between 40% and 69% of VO2max, the heart rate is between 55% and 74% of HRmax, and the HRR is between 40% and 69%, and the fatigue level is scored 12-13 points on the RPE scale. For higher intensity aerobic exercise, oxygen uptake is between 70% and 85% of VO2max, heart rate is between 75% and 90% of HRmax, and HRR is between 70% and 85%, and fatigue is scored at 14-16 points on the RPE scale. The oxygen uptake of higher intensity aerobic exercise is greater than 85% of VO2max, the heart rate is greater than 90% of HRmax, greater than 85% of HRR, and the fatigue degree is scored 17-19 points on the RPE scale.Moderate-intensity regimens (30–60 minutes/session, including warm-up) demonstrate the most robust cognitive improvements, particularly in executive function and processing speed [21,33,47,51,52]. This intensity optimizes the balance between physiological stress and neural adaptation. A functional study on improving cognitive impairment by aerobic exercise Aerobic exercise enhances executive function and memory function Executive function represents higher-order cognitive processes governed by frontal brain regions, encompassing impulse control (selective attention/cognitive inhibition), information integration, and cognitive flexibility. Clinical evidence demonstrates that sustained aerobic training improves executive control abilities. In healthy adults, structured aerobic interventions enhanced performance on the Groton Maze Learning Test, multitask paradigms (MTT), and spatial span tasks (SSP), confirming exercise-induced executive optimization [17,26,41]. Similar benefits extend to older adults with mild cognitive impairment (MCI), where aerobic training shortened reaction times in Erikson Flanker tasks and improved scores on MMTM-A/B assessments [21,36,42]. Notably, disease-specific studies corroborate these findings. Multiple sclerosis patients undergoing high-intensity interval training showed improved processing speed and task-switching accuracy via MMT-A/B testing [43]. Parkinson’s disease cohorts exhibited enhanced Stroop Test performance (word-color conflict resolution) following moderate aerobic regimens [44]. Standardized evaluation tools—including Groton Maze tests, Flanker paradigms, and multitask batteries—collectively validate aerobic exercise as a robust modulator of executive function. This collective evidence substantiates aerobic exercise as an effective intervention for executive function enhancement across diverse populations [17,21,26,36,41-44]. Memory function is the ability to remember, maintain, re-recognize and reproduce the content and experience reflected by objective things. It is related to the hippocampus in the brain. Studies have shown that aerobic exercise increases the volume of the hippocampus and increases blood flow to the hippocampus, thus improving memory function. Studies have found that aerobic exercise can improve memory in older adults. High intensity aerobic exercise can improve memory in younger people [45] . High-intensity interval aerobic training resulted in the best memory performance [43,46] . Table. 1 systematically summarizes the effects of varying aerobic exercise intensities on memory function across distinct populations, clarifying how factors such as participant characteristics and assessment tools influence outcome variability. Table. 1 Effects of Aerobic Exercise Intensity on Memory Function Across Populations Study (Author, Year) Population Exercise Intensity Memory Assessment Method Key Findings Maass et al. [14] (2015) Sedentary older adults Moderate-intensity Verbal Learning & Memory Test (VLMT) Increased hippocampal volume linked to improved spatial memory. Kleinloog et al. [26] (2019) Sedentary older men Moderate-intensity Delayed Matching to Sample (DMS) No significant change in visual memory performance. Zimmer et al. [43] (2018) Multiple sclerosis patients High-intensity interval Brief Visuospatial Memory Test (BVMT) High-intensity interval training improved verbal memory more than moderate. Kovacevic et al. [46] (2020) Older adults Low/Moderate/High Rey Auditory Verbal Learning Test Moderate intensity showed optimal episodic memory improvement. Kamijo et al. [47] (2019) Healthy young adults Acute moderate 2-back task (working memory) Reduced reaction time and increased hit rate post-exercise. Lefferts et al. [48] (2019) Adults with hypertension Moderate-intensity Word recognition task Faster reaction time, but no change in recognition accuracy. Silveira et al. [44] (2018) Parkinson’s patients Moderate-intensity California Verbal Learning Test (CVLT) Improved recall in cognitively normal subjects, no effect in impaired. Research on aerobic exercise-induced memory enhancement in healthy adults reveals divergent outcomes depending on assessment methodologies. When evaluated with standardized Verbal Learning and Memory Tests (VLMT), significant improvements in verbal-spatial memory have been consistently documented [14]. However, working memory assessments yield mixed results: 2-back task paradigms demonstrate enhanced processing speed and accuracy [47], whereas modified Rey Auditory Verbal Learning Tests and paired associate learning tasks show negligible effects [17,26]. Similarly, delayed matching-to-sample and paired associate learning evaluations detect no exercise-related memory changes in healthy elderly populations [26]. In clinical populations, the cognitive benefits of aerobic exercise exhibit disease-specific patterns. Multiple sclerosis patients undergoing high-intensity interval training show greater verbal memory improvement on VLMT compared to moderate-intensity protocols [43]. Parkinson’s disease studies using California Verbal Learning Tests (CVLT) reveal differential effects based on cognitive status, with intact patients demonstrating enhanced recall but impaired patients showing no significant change [44]. Middle-aged hypertensive individuals exhibit faster reaction times in recognition memory tasks without accuracy alterations following moderate-intensity training [48]. These findings collectively underscore three key determinants of exercise-induced memory effects: (1) domain-specific assessment tool sensitivity (e.g., VLMT for verbal memory vs. 2-back for working memory), (2) clinical population characteristics (e.g., MS vs. PD vs. hypertension), and (3) exercise protocol parameters (intensity/duration). The current lack of standardized evaluation protocols contributes substantially to observed outcome variability across studies. Fig. 4 The possible effects of different lifestyle habits on brain structure Effects of aerobic exercise on processing speed and attention function The improvements in cognitive function induced by aerobic exercise can be quantified through assessments of specific cognitive performance. Its effects not only involve core cognitive domains such as attention and processing speed but also are closely associated with functional changes in the autonomic nervous system and cerebrovascular system, as presented in Fig. 3. This figure clearly demonstrates the pathways by which aerobic exercise modulates physiological processes (e.g., the noradrenergic system, retinal vascular dynamics) to ultimately influence specific cognitive performances including executive function and saccadic eye movements, providing a physiological-cognitive association framework for subsequent analysis of changes in processing speed and attention function.Visuospatial function encompasses the cognitive capacity to perceive, integrate, and analyze multidimensional spatial relationships through visual content and structural details. This ability underpins critical judgments of object characteristics (size, shape, position) and motion perception, primarily regulated by parieto-occipital and inferior temporal regions [43,44].Current evidence suggests limited aerobic exercise benefits for visuospatial processing. In multiple sclerosis patients, neither high-intensity interval training (HIIT) nor moderate-intensity regimens improved spatial memory scores on the Brief Visuospatial Memory Test-Revised (BVMT-R) [43]. Parkinson’s disease cohorts similarly showed no visuospatial enhancement on cross-pentagon or Benton Line Orientation tests post-exercise, though aerobic training may attenuate functional decline [44]. These null findings contrast with exercise benefits observed in other cognitive domains. Attention and processing speed constitute critical cognitive domains essential for efficient task execution in daily activities. While sustained aerobic exercise demonstrates potential to improve concentration and dual-task performance [48-49], empirical evidence regarding its efficacy remains inconsistent across populations. In multiple sclerosis cohorts, both high-intensity interval and moderate-intensity aerobic training progressively enhance attentional performance as measured by the Test of Attentional Performance (TAP), with significant reductions in reaction time observed over intervention periods [43]. Notwithstanding this acute benefit pattern, a single bout of vigorous aerobic exercise significantly improves attentional processing in adults with attention-deficit/hyperactivity disorder (ADHD) [49]. Contrasting findings emerge in other populations. Aerobic interventions show no significant effects on psychomotor speed or reaction time in healthy elderly individuals when assessed through Motor Screening Task (MOT) and Reaction Time Index (RTI) [26]. Similarly, Parkinson’s disease patients exhibit negligible changes in attentional metrics measured by digit span and Corsi Block tests following training [44]. These discrepancies align with the perceptual load theory, which posits that exercise-induced cognitive benefits may be more detectable under low cognitive demand conditions where attentional resources are not maximally engaged [17]. Collectively, the heterogeneous outcomes—ranging from significant improvements in clinical populations (MS, ADHD) to null effects in healthy aging and neurodegenerative disorders—highlight the influence of methodological factors including participant characteristics, task complexity, and assessment tools (e.g., TAP vs. Corsi Block). This variability underscores the need for population-specific exercise prescriptions optimized for attentional enhancement. Clinical Implications The current evidence demonstrates that aerobic exercise interventions should be incorporated into standard rehabilitation protocols for cognitive impairment. Findings from the reviewed studies indicate that structured aerobic exercise programs produce measurable improvements in executive function, memory, and processing speed across multiple patient populations. For older adults with age-related cognitive decline, moderate-intensity aerobic exercise (40-69% VO₂max) administered 3-5 times per week appears most effective for enhancing hippocampal volume and prefrontal cortex function [58,60]. This intensity range optimizes cerebral blood flow while minimizing cardiovascular stress in elderly populations. In neurological rehabilitation, the combination of aerobic exercise with targeted cognitive training yields superior outcomes compared to either intervention alone. Patients with first-episode schizophrenia showed significantly greater cognitive gains when aerobic exercise was added to computerized cognitive training, particularly in working memory and processing speed domains [59]. The synergistic effect appears mediated by exercise-induced increases in BDNF levels, which facilitate neuroplasticity during subsequent cognitive training sessions. This suggests that aerobic exercise may prime the brain for enhanced learning capacity.For concussion management, subsymptom threshold aerobic exercise accelerates recovery of autonomic nervous system function and reduces persistent post-concussion symptoms [61,62]. The Buffalo Concussion Treadmill Test provides a safe, objective method to establish individualized exercise intensity thresholds. Early implementation of controlled aerobic activity (beginning within 2 weeks post-injury) appears crucial for optimal outcomes, contrasting with traditional rest-based approaches.Practical implementation requires consideration of patient-specific factors. Frail elderly patients may benefit from supervised cycling or aquatic exercise to minimize injury risk, while younger patients can tolerate higher-intensity interval training. Adherence strategies should incorporate remote monitoring technologies and behavioral incentives, as demonstrated in recent trials [59,62]. Standardized cognitive assessments (e.g., MATRICS battery for schizophrenia, ImPACT for concussion) should guide treatment progression. Future research directions include investigating dose-response relationships across different neurological conditions and developing biomarkers to predict individual treatment responses. The integration of neuroimaging with physiological monitoring may further optimize exercise prescription parameters. These advances will facilitate the transition from empirical to precision medicine approaches in exercise-based cognitive rehabilitation. Summary Aerobic exercise exerts heterogeneous effects on cognitive function across populations. While it consistently improves executive function, its efficacy on other cognitive subdomains remains inconsistent. This variability may stem from three factors: (1) lack of standardized intensity thresholds, (2) insufficient reliability of assessment tools, and (3) methodological heterogeneity in study designs. In China, stroke exhibits a trend toward younger onset and higher severity, characterized by high incidence, disability, and mortality rates. Approximately 30% of stroke patients develop post-stroke cognitive impairment (PSCI), severely compromising quality of life. As a low-cost and accessible intervention, aerobic exercise holds promise for stroke rehabilitation. Therefore, how much intensity of aerobic training is suitable for stroke patients, how to formulate the prescription of aerobic exercise, and whether the formulation of aerobic exercise prescription combined with cardiopulmonary exercise test can more effectively improve the cognitive function and cardiopulmonary function of stroke patients, these issues still need to be further discussed and studied. It is important to note that the cognitive benefits of aerobic exercise do not act in isolation; instead, they interact with overall lifestyle habits (e.g., diet, daily routine) to collectively shape brain health. Different lifestyle habits—such as intake of healthy fats versus unhealthy fats, and low cardiometabolic risk versus high cardiometabolic risk—exert distinct effects on brain structure, which may either exacerbate or alleviate brain aging and neurodegenerative diseases, thereby influencing cognitive function and quality of life, as illustrated in Fig. 4. This figure suggests that future development of cognitive rehabilitation programs should integrate aerobic exercise with other healthy lifestyle practices to form multi-dimensional intervention strategies, rather than relying solely on exercise interventions. However, critical question persist: Do differences between exercise modalities (e.g., continuous vs. interval training) yield clinically meaningful outcomes? 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Journal of Athletic Training, 58(7/8), 602–610. https://doi.org/10.4085/1062-6050-0186.22 Information & Authors Information Version history V1 Version 1 29 December 2025 Copyright This work is licensed under a Non Exclusive No Reuse License. Authors Affiliations Lili Qin Tongji University Department of Physical Education View all articles by this author Tianqi Liu 0009-0009-9059-4829 Tongji University Department of Physical Education View all articles by this author Dengyun Xu Tongji University Department of Physical Education View all articles by this author Lanqing Ling Tongji University Department of Physical Education View all articles by this author Tianfeng Lu [email protected] Tongji University Department of Physical Education View all articles by this author Hong Li Tongji University Department of Physical Education View all articles by this author Metrics & Citations Metrics Article Usage 288 views 73 downloads .FvxKWukQNSOunydq8rnd { width: 100px; } Citations Download citation Lili Qin, Tianqi Liu, Dengyun Xu, et al. From Mechanisms to Recovery: A Review on the Impact of Aerobic Exercise Modality and Intensity on Brain Function and Cognitive Rehabilitation. Authorea . 29 December 2025. 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