Acute Effects of Physical Exercise on Cognitive Performance and Neurobiological Markers in Adults: A Scoping Review of 102 Human Studies

1. Introduction

Acute bouts of physical exercise can transiently alter multiple neurobiological processes, including neurotrophin release, metabolic signaling, and cerebral oxygenation [1–5]. Early studies demonstrated improvements in cognitive performance following aerobic or near-threshold exercise in both younger and older adults [1–4]. Subsequent work has shown that high-intensity interval training (HIIT), moderate aerobic exercise, and resistance exercise can all acutely enhance executive function, attention, and memory [5–12].

Across these early investigations, neurobiological responses such as increased Brain-Derived Neurotrophic Factor (BDNF), changes in lactate and cortisol, and altered prefrontal activation were repeatedly observed following acute exercise [6–15]. Together, these findings provided initial evidence that transient physiological responses may relate to short-term cognitive benefits.

Rationale

Although prior reviews have explored specific components of this research area—such as BDNF responses to acute exercise, aerobic intensity effects, or short-term executive function changes—these syntheses have typically focused on narrow subsets of the literature [6–15]. No prior review has mapped the full scope of acute exercise–cognition research across all major exercise modes, biological pathways, and neurophysiological outcomes in adult humans.

Objectives

The present scoping review aggregates 102 human studies on acute exercise and cognition [1–102] with the aims to:

• Map the range of exercise modalities and stimuli studied;
• Describe the cognitive domains most commonly assessed;
• Summarize neurobiological and neurophysiological correlates (e.g., BDNF, lactate, catecholamines, hemodynamics, electroencephalography/EEG, Functional Near-Infrared Spectroscopy/fNIRS, Magnetic Resonance Imaging/MRI);
• Highlight consistent findings across exercise types and populations;
• Identify research gaps suitable for future mechanistic or translational work (Figure 1).

This scoping review follows a structured search and screening approach (Supplementary Table S1) while maintaining the methodological flexibility appropriate for charting heterogeneous evidence across diverse study designs.

2. Materials and Methods

2.1. Protocol and Registration

A scoping review methodology was chosen to accommodate the heterogeneity across study designs, exercise modes, populations, and cognitive outcomes. The review protocol was prospectively registered with the International Prospective Register of Systematic Reviews (PROSPERO; Registration ID: 1229780). Methods followed PRISMA-ScR guidance and were tailored to mechanistic exercise–cognition research [1–102].

2.2. Eligibility Criteria

Studies were included if they: 1. Involved human adults (≥18 years); 2. Applied an acute bout of physical exercise (single session or microcycle ≤7 days); 3. Measured cognition and/or neurobiological markers pre/post exercise; 4. Used any exercise modality (aerobic, resistance, HIIT, combined, vibration, mind–body); and 5. Reported original human data [1–102]. Animal studies, chronic training interventions, protocol-only reports, and conference abstracts without methods were excluded.

2.3. Information Sources

Two electronic databases were searched: PubMed and Cochrane CENTRAL. Searches targeted literature on acute physical exercise, cognitive performance and executive functions, biomarkers such as BDNF and other neurotrophins, and neuroimaging or cortical activation measures (fNIRS, fMRI, EEG, Arterial Spin Labeling-MRI/ASL-MRI) [1–3,6–8,13,17,18,21–23,25,28,29,32,35,39,41,45,47,52,56–58,60,63–65,69,73,79,80,82,83,86–89,91–93,96–99]. Full search strings are provided in Supplementary Table 1.

2.4. Search

Searches were performed without year restrictions and included all articles available up to the final search date. Titles and abstracts retrieved from PubMed and CENTRAL were exported, deduplicated, and screened. The search strategy was intentionally broad to capture the full spectrum of acute exercise, i.e., cognition paradigms, biomarker assessments, and imaging methods.

2.5. Selection of Sources of Evidence

Screening occurred in two stages:

1.

Title/abstract screening using predefined eligibility criteria;

2.

Full-text review for abstracts meeting inclusion criteria or when eligibility was uncertain.

A total of 102 studies met all criteria and were included in the review [1–102]. Reasons for exclusion were documented during screening (e.g., chronic interventions, animal models, missing cognitive or biomarker outcomes). Figure 2 displays the PRISMA 2020 flow diagram.

2.6. Data Charting Process

Data were charted using a standardized extraction template. For each included study, we systematically recorded study design and sample characteristics; exercise modality, dose, and intensity; timing of assessments; cognitive domains and specific tasks; biomarker measures (e.g., BDNF, lactate, cortisol, catecholamines); neuroimaging outcomes (fNIRS, fMRI, EEG/Event-Related Potential/ERP, ASL-MRI), and major findings. The charting procedure was iterative: extraction was refined as new patterns emerged, consistent with scoping review methodology.

2.7. Data Items

Key data items included:

• Population variables: age group, health status, fitness level.
• Exercise variables: modality (aerobic, resistance, HIIT, combined), session duration, intensity, and environmental conditions (e.g., hypoxia).
• Cognitive variables: executive function, working memory, attention, visuospatial ability, memory/learning.
• Biological variables: neurotrophic factors (BDNF), metabolic markers (lactate, glucose), endocrine markers (cortisol, catecholamines), inflammatory markers, myokines.
• Neurophysiological variables: cortical oxygenation, cerebral blood flow, electrophysiological responses, regional activation.
• Outcomes: direction and magnitude of cognitive change, biomarker response, imaging signal change.

2.8. Critical Appraisal of Individual Sources of Evidence

Formal risk-of-bias assessment was not performed, consistent with PRISMA-ScR guidance and the exploratory purpose of a scoping review. Instead, methodological characteristics were noted that may influence interpretation of results, including sample size, timing of assessments, biomarker protocols, and cognitive test quality.

2.9. Synthesis of Results

A narrative synthesis was conducted, structured around the charted domains. Studies were grouped by exercise modality and intensity; cognitive domain tested; biomarker type; neuroimaging modality; and population characteristics. Patterns were summarized thematically to identify consistent findings, mechanistic trends, and evidence gaps [1–102].

3. Results

3.1. Selection of Sources of Evidence

A total of 102 studies met all eligibility criteria and were included in the review [1–102]. These studies were identified through systematic searches of PubMed and CENTRAL, followed by title/abstract screening and full-text review. Reasons for exclusion included chronic training interventions, animal studies, missing cognitive or biomarker outcomes, or insufficient methodological information (Figure 2).

3.2. Characteristics of Sources of Evidence

The 102 included studies varied widely in design, population, exercise modality, and measurement methods (Table 1). Most studies involved healthy young adults, with additional cohorts of older adults, sedentary individuals, high-level athletes, and groups at elevated metabolic or cognitive risk (e.g., overweight adults, individuals with type 1 diabetes) [3,15,18,21–23,28,30,33,37,42–44,49,50,52,63,69,73,74,85,90].

Exercise modalities included aerobic exercise, HIIT, resistance exercise, combined aerobic–resistance protocols, open-skill tasks, and a range of less common modes (eccentric cycling, aquatic treadmill, vibration, dual-task Blood Flow Restriction/BFR, orienteering) [2,5,7–9,12,20,24,27,31,34,40,41,46–50,52,53,60,66,70–72,77,85,88,90,94,100,102].

Cognitive assessments spanned executive function, working memory, attention, task switching, visuospatial processing, motor learning, and implicit/explicit memory [6,13,15,19,24,28,31,34,35,41,45–48,51,53,60,63,68,70,72,81,82,84,88,90–92,95–99,101].

Neurobiological outcomes included BDNF, endocrine markers, inflammatory mediators, EEG/ERP, fNIRS, ASL or Blood Oxygenation Level–Dependent (BOLD) fMRI, and cerebrovascular hemodynamics (middle cerebral artery velocity, cerebral blood flow/CBF redistribution, prefrontal oxygenation) [1–3,6–8,10,13,14,17,18,21–23,25,29,32,33,38,39,41,45,47,52,56–58,60–65,69,71,73,75–80,82,83,86–89,91–93,99].

3.3. Critical Appraisal Within Sources of Evidence

Consistent with scoping review methodology, a formal risk-of-bias appraisal was not performed. However, methodological variability across studies was noted in sample sizes, control conditions, exercise dosing, cognitive task timing, biomarker protocols (serum vs. plasma BDNF), and neuroimaging acquisition methods. These factors likely influenced heterogeneity in observed outcomes.

3.4. Results of Individual Sources of Evidence

To preserve scientific clarity, the following subsections summarize findings by outcome domain (Table 2).

3.4.1. Effects of Acute Exercise on Executive Function

Across approximately 60 of the included studies, acute exercise elicited measurable improvements in executive function, particularly for tasks involving inhibition, task switching, updating, and dual-task processing [13,15,19,24,28,31,34,35,41,45,46,51,53,60,63,68,70,72,81,82,84,90,91,92,95,96,97,98,99,101,102]. Improvements were observed within minutes after exercise cessation and typically persisted for up to 30–60 minutes, although some studies reported effects lasting longer [13,19,24,34,60,63,72,84,91] (Table 3).

Moderate-intensity aerobic exercise produced reliable improvements in Stroop performance, trail-making time, response inhibition, and task-switching speed [13,15,19,34,45,54,60,63,72,91]. Several studies using cycling or treadmill walking at 60–70% of maximal heart rate demonstrated enhanced Stroop performance with concomitant increases in prefrontal oxygenation [14,19,24,32,38,54,63,72,82].

HIIT frequently produced equal or superior improvements, particularly in tasks requiring rapid inhibitory control or working memory updating [2,7,8,17,27,41,60,65,67,70,84,94,100,102]. Across the included HIIT studies (n ≈ 14), HIIT produced larger and sometimes more persistent effects than moderate-intensity exercise, with executive benefits often extending throughout the recovery period (20–30 minutes post-exercise) [2,8,60,67,84]. Higher-intensity exercise also elicited stronger neuroelectric signatures (e.g., increased P3 amplitude and enhanced Contingent Negative Variation/CNV) in several ERP-based trials [13,27,41].

However, HIIT responses were not universal. A minority of studies reported no superiority of HIIT over traditional moderate-intensity exercise or even null cognitive effects, suggesting that individual fitness levels and protocol design strongly shape outcomes [59,73,75].

Effects of Resistance and Multimodal Exercise

Evidence from resistance training (RT) demonstrates that both low-intensity slow-movement resistance exercise and high-intensity resistance exercise can improve inhibitory control and executive function [5,9,20,27,49,55,70,85,88,100]. Combined resistance + power training or concurrent aerobic–resistance protocols reliably improved global cognition, short-term memory, and dual-task performance in older women and middle-aged adults [20,27,49,50,52,70,85].

Open- Versus Closed-Skill Exercise

Three studies evaluating open-skill activities (e.g., orienteering, racquet-type tasks) showed larger improvements in inhibitory control compared to matched-intensity closed-skill exercise, alongside unique neural efficiency effects with reduced prefrontal activation despite improved performance [31,66,77]. These paradigms, which require constant adaptation and spatial navigation, appear to place additional demands on attentional and visuospatial systems.

3.4.2. Effects on Working Memory and Attention

Approximately 30 studies assessed working memory, using n-back tasks, digit span, spatial working memory tests, or memory-recognition paradigms [1,6,13,18,22,24,28,29,41,45,46,63,68,70,81,82,86,93,96,97,98,99] (Table 4). Acute moderate exercise reliably reduced reaction times in both low- and high-load conditions and, in high-fit individuals, increased P3 amplitude and frontal CNV, indicating enhanced neural resource allocation [13,22,24,28,45,63,68,94].

Fitness level modulated outcomes: higher-fit participants showed larger improvements, particularly under high working-memory loads [22,28,63,68,73,94]. Inter-individual differences were notable, with responders exhibiting greater right ventrolateral prefrontal cortex activation during exercise, while non-responders showed minimal fNIRS activation changes and smaller cognitive gains [29,68,72,82,99].

Evidence for sustained attention and vigilance was mixed. Several studies reported improvements in attentional accuracy after moderate or high-intensity sessions [13,24,31,41,51,60,70,94], but two studies using prolonged vigilance tasks found that passive or light exercise did not mitigate mental fatigue [31,78], suggesting that long-duration vigilance paradigms may be less sensitive to acute exercise benefits.

3.4.3. Memory, Learning, and Motor Skill Acquisition

Approximately 15 studies investigated episodic memory, motor learning, or implicit/explicit sequence learning [1,6,21,28,35,39,48,53,81,86,93,95,96,97,98]. Several trials demonstrated that acute exercise enhances recognition memory, associative learning, vocabulary learning, and motor sequence encoding when exercise is performed immediately before encoding or training [1,6,21,28,35,81,86,93,96]. Exercise before encoding improved parietal activation, accelerated learning rates, and strengthened retention 24 hours later [6,21,39,81,93,96].

In older adults, increases in BDNF after exercise correlated with better post-exercise learning in some cohorts, supporting a mechanistic link between neurotrophic signaling and training gains [18,23,63,80]. Conversely, exhaustive exercise or very high-intensity protocols sometimes reduced motor skill learning performance, potentially due to transient fatigue, altered Supplementary Motor Area (SMA) excitability, or elevated lactate interfering with motor circuits [5,48,92,97,100].

3.4.4. Neurovascular and Hemodynamic Responses

Prefrontal Oxygenation (fNIRS)

Across nearly 25 studies using fNIRS, mild-to-moderate intensity exercise consistently increased oxyhemoglobin in dorsolateral and ventrolateral prefrontal regions during executive task performance [11,14,19,24,29,32,38,41,44,46,47,54,60,63,66,68,70,72,77,82,83,91,99,101]. These changes frequently aligned with improved accuracy and reduced reaction times in Stroop, Flanker, and task-switching paradigms [13,19,24,41,45,46,60,63,72,82,83,91]. Prefrontal oxygenation on fNIRS, brain hemodynamics and imaging outcomes across studies are summarized in Table 5.

Vigorous or exhaustive exercise, in contrast, sometimes caused a decrease in prefrontal oxyhemoglobin, consistent with transient hypofrontality under severe metabolic demand [5,31,40,48,60,92,100]. Enhanced oxygenation during or immediately after exercise correlated with improved cognitive performance in many, but not all, studies [11,14,19,24,29,44,54,63,72,82,99].

Cerebral Blood Flow (CBF) and Cerebrovascular Responses

Studies employing ASL-MRI, Transcranial Doppler (TCD), or phase-contrast MRI reported heterogeneous but interpretable patterns [33,38,39,42,43,51,58,61,63,71,90,92]. Global CBF often decreased immediately after moderate-to-vigorous exercise, while regional CBF responses differed by area, with motor cortex blood flow increasing during exercise and hippocampal or frontal regions showing decreases or complex redistribution [33,39,58,63,71,90,92]. The uncoupling between global CBF and cognitive performance suggests that regional cerebrovascular redistribution, rather than overall flow, may support improved cognitive performance despite global reductions [33,39,42,58,63,71,90,92].

Impact of Hypoxia

Approximately five studies evaluated hypoxic conditions. Exercise in moderate normobaric hypoxia impaired reaction times but preserved accuracy in some tests, even when BDNF increased [43,56,57,61]. Combined hypoxia and cognitive challenge reduced prefrontal oxygenation further, suggesting a competitive resource limitation for cortical control processes [43,56,57,61].

3.4.5. Brain-Derived Neurotrophic Factor (BDNF)

Across all BDNF-focused studies (n ≈ 40), roughly 70% reported increases in circulating BDNF after acute exercise (Table 6 [1,2,3,6,7,8,10,13,17,18,21,22,23,25,28,29,41,45,52,56,57,58,60,63,64,65,69,73,79,80,86,87,88,89,93,96,97,98]). Increases were observed across modalities—continuous aerobic exercise, HIIT, resistance exercise, whole-body vibration, and multimodal protocols [1,2,3,5,6,7,8,9,13,17,18,20,21,22,23,27,41,45,49,52,59,60,64,73,79,80,85,86,87,88,89,93,96,97,98]. The magnitude of response varied widely and was influenced by fitness level, exercise intensity, sex, timing, and whether serum or plasma was sampled [1,2,3,10,17,18,21,22,23,25,28,41,52,64,69,73,79,80,86,87,88,89].

Most studies did not find a tight correlation between BDNF changes and acute cognitive changes [3,10,21,22,23,28,41,45,52,59,69,73,79,80,87,88,89]. Exceptions included work in older adults where larger BDNF increases predicted greater post-exercise learning or working-memory gains [18,23,63,80]. In several high-intensity protocols, lactate levels appeared to mediate BDNF responses, although not necessarily behavioral outcomes [5,7,8,9,41,60,73,79,87,100].

Null BDNF findings were also common. A smaller subset of studies reported no increase in BDNF after exercise—for example, cycling near heavy traffic, periods of detraining, or HIIT combined with β-alanine [37,59,69,75,76,89]. These trials highlight substantial interindividual variability and the modifying roles of environmental exposures and chronic activity levels [22,28,37,69,73,75,76].

3.4.6. Other Biological Markers

Beyond BDNF, studies assessed cortisol, catecholamines, DHEA, inflammatory markers, myokines, and endocrine responses [5,7,8,9,10,21,25,28,30,39,41,50,55,59,70,73,79,85,90,93,100]. HIIT and exhaustive exercise tended to provoke larger cortisol and catecholamine surges than moderate continuous training [7,8,9,25,41,59,70,73,79,100]. Acute exercise generally reduced inflammatory signaling or shifted apoptotic mediators in more favorable directions, especially in older adults or aging populations engaging in functional or multicomponent programs [30,33,50,52,70,85]. Several studies highlighted exercise-induced changes in myokines (e.g., irisin, CTSB) and IGF-1 as potential contributors to neuroplasticity, though associations with acute cognitive changes were still exploratory [5,7,8,9,25,41,59,70,73,79,87,100].

3.4.7. Influence of Age, Fitness, and Baseline Capacity

Older adults consistently benefited from acute exercise but often showed smaller or more variable effect sizes compared with younger individuals [11,15,18,21,22,23,33,35,42,44,49,50,52,63,69,72,80,85,90,98]. Robust Stroop and working-memory improvements were seen after moderate-intensity cycling or walking, frequently accompanied by increased prefrontal activation or CBF [11,15,19,23,33,42,44,63,72]. In older cohorts, associations between exercise-induced BDNF elevations and improved working memory or learning appeared particularly prominent [18,23,63,80].

Cardiorespiratory fitness consistently modulated cognitive and biomarker responses. Higher fitness predicted larger executive-function improvements, stronger ERP signatures, and greater BDNF responsiveness in several cohorts [21,22,28,45,63,68,73,80,94]. Conversely, lower-fit individuals benefitted from acute exercise but showed more modest neural signatures and smaller biomarker shifts [22,28,37,69,73,75].

Clinical and at-risk populations—such as individuals with type 1 diabetes or those at elevated risk for mild cognitive impairment—appeared to derive benefit from acute interventions, though mechanisms may be altered by baseline inflammation or vascular stiffness [33,37,69,74,85]. Evidence from these groups, while limited, suggests that acute exercise remains a promising adjunct even when chronic disease is present [33,69,74,85,90].

3.4.8. Task- and Modality-Specific Effects

Task- and modality-specific patterns emerged across the dataset. Open-skill exercise and navigation-based paradigms (e.g., orienteering) produced some of the strongest improvements in inhibitory control and spatial cognition, often with reduced prefrontal activation consistent with enhanced neural efficiency [31,66,72,77]. Concurrent or multicomponent exercise programs yielded cognitive benefits comparable to aerobic training, with lactate and myokine responses implicated as potential mediators [7,8,9,20,27,41,49,50,52,70,79,87,100]. Aquatic treadmill exercise improved Digit Symbol performance and cerebral blood flow in older adults [44]. Eccentric cycling and high-intensity functional training were associated with higher mental demand and distinct frontoparietal activation patterns, despite equivalent or lower external workloads [31,40,70,92,100]. Intermittent squat or walking breaks during prolonged sitting preserved executive function and cerebrovascular responsiveness compared with uninterrupted sitting [51].

3.5. Synthesis of Results

Taken together, the 102 included studies demonstrate that acute exercise reliably improves executive function, working memory, and inhibitory control across intensity levels, modalities, and populations (Table 7, [1,2,3,4,5,6,7,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22,23,24,25,26,27,28,29,30,31,32,33,34,35,36,37,38,39,40,41,42,43,44,45,46,47,48,49,50,51,52,53,54,55,56,57,58,59,60,61,62,63,64,65,66,67,68,69,70,71,72,73,74,75,76,77,78,79,80,81,82,83,84,85,86,87,88,89,90,91,92,93,94,95,96,97,98,99,100,101,102]).

HIIT often elicits the strongest and most durable cognitive benefits, but moderate-intensity exercise remains highly effective and more universally tolerated [2,7,8,13,15,19,24,34,41,45,46,59,60,63,72,73,84,91,94,102]. Prefrontal oxygenation consistently increases during mild or moderate exercise but may decrease under high physiological load [11,14,19,24,29,32,38,40,46,54,60,63,70,72,82,92,99]. BDNF increases in most trials but does not correlate tightly with cognitive improvements, underscoring a multi-factorial mechanism [1,2,3,6,7,8,17,18,21,22,23,25,28,41,45,52,56,57,58,64,69,73,79,80,86,87,88,89,93,96,97,98]. Effects vary by age, fitness, exercise modality, and task type, and acute exercise induces complex neurovascular responses, including regional CBF redistribution and transient hypofrontality at high loads [33,38,39,42,43,51,58,61,63,71,90,92]. Open-skill and cognitively demanding exercises may further enhance neural efficiency, improving performance with reduced cortical activation [31,66,72,77,99,101].

4. Discussion

The principal aim of this scoping review was to map and synthesize the acute cognitive, neurotrophic, vascular, and mechanistic effects of single-session exercise across 102 empirical studies [1,2,3,4,5,6,7,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22,23,24,25,26,27,28,29,30,31,32,33,34,35,36,37,38,39,40,41,42,43,44,45,46,47,48,49,50,51,52,53,54,55,56,57,58,59,60,61,62,63,64,65,66,67,68,69,70,71,72,73,74,75,76,77,78,79,80,81,82,83,84,85,86,87,88,89,90,91,92,93,94,95,96,97,98,99,100,101,102]. Despite heterogeneity in populations, exercise modalities, intensities, testing batteries, and biomarkers assessed, several robust themes emerged (Figure 3). Collectively, the evidence indicates that acute exercise—whether aerobic, resistance-based, multimodal, or delivered as HIIT—produces consistent small-to-moderate improvements in executive function, frequently accompanied by transient neurotrophic and hemodynamic changes [5,6,7,8,9,13,15,17,18,19,20,21,23,24,25,27,28,31,34,39,40,41,44,45,46,47,49,50,52,60,63,68,70,72,79,80,81,82,84,90,91,92,93,96,97,98,99,100,101,102]. Importantly, these effects appear independent of age, sex, or baseline fitness, but their magnitude is modulated by exercise intensity, individual cardiorespiratory fitness, task timing relative to exercise, and neurobiological responsiveness [15,18,21,22,23,28,33,37,42,44,63,68,69,72,73,80,85,94].

A) Acute Exercise Produces Rapid and Reliable Cognitive Enhancement

Across studies, acute exercise most consistently improved executive function— including inhibitory control, task-switching, cognitive flexibility, and working memory [13,15,19,24,28,31,34,41,45,46,51,53,60,63,68,70,72,81,82,84,90,91,92,95,96,97,98,99,101,102]. Beneficial effects were detected after moderate-intensity continuous cycling, brisk running, resistance exercise, HIIT, whole-body vibration–assisted training, eccentric exercise, aquatic treadmill walking, and brief sprint sessions [2,5,6,7,8,9,13,15,19,20,24,27,31,34,41,44,45,46,49,50,52,54,60,63,66,70,72,77,85,88,90,94,100,102]. Classical demonstrations include improved Stroop or Flanker performance and task-switching after moderate cycling or walking near the anaerobic threshold, enhanced executive function after HIIT protocols, and improved dual-task walking performance after acute exercise in older adults [13,15,19,24,34,45,46,60,63,72,91].

Intensity Matters—but Not in the Way Typically Assumed

Several studies reported an inverted-U relationship, with moderate-to-near-threshold intensities producing optimal cognitive outcomes [13,15,19,34,45,54,60,63,72,91]. Exercising at workloads close to the anaerobic threshold in older women enhanced multiple executive domains, whereas very mild or very intense interventions often produced attenuated or selective benefits [15,31,44,48,60,92].

At the same time, HIIT studies contradict a simple intensity narrative. Multiple investigations showed HIIT to produce equal or superior cognitive gains compared with moderate steady-state exercise, particularly on tasks with high inhibitory or working-memory demands [2,7,8,17,27,41,60,65,67,70,84,94,100,102]. However, the window of improvement may be shorter and may dissipate more rapidly during recovery, with repeated HIIT bouts shortening the duration of post-exercise facilitation in some trials [60,84,92].

Exercise Type is Less Important Than Perceived Effort

When subjective intensity was matched, different modalities (aerobic, resistance, and balance-focused multicomponent exercise) produced comparable improvements in inhibitory control and global cognition [20,27,34,49,50,52,70,85,88]. This suggests that cognitive gains are largely driven by global physiological arousal and neuromodulatory engagement rather than strictly modality-specific factors.

B) Neurobiological Mechanisms: BDNF as the Central but Not Exclusive Mediator

BDNF emerged as the most frequently investigated mechanistic biomarker [1,2,3,6,7,8,10,13,17,18,21,22,23,25,28,41,45,52,56,57,58,60,63,64,65,69,73,79,80,86,87,88,89,93,96,97,98]. The majority of studies demonstrated acute BDNF increases following aerobic or high-intensity exercise, and in several trials these surges were temporally linked to faster task-switching, improved working memory, or better learning performance [1,3,6,7,8,17,18,21,23,28,41,45,52,63,73,79,80,86,87,93,96,97,98].

Remarkably, the relationship between BDNF elevation and learning was time-dependent: when cognitive training immediately followed physical exercise, greater BDNF rises predicted superior training gains in older adults [18,23,63,80], but not when the temporal order was reversed.

Not all BDNF Responses Are Equal

Studies measuring both serum and plasma revealed divergent kinetics across compartments, reflecting platelet release dynamics rather than purely central production [1,2,3,10,21,22,25,52,64,69,80,86,87,88,89]. Still, the acute changes were often associated with cognitive outcomes, consistent with BDNF acting as a biomarker of neuroplastic readiness rather than a single causal mediator.

Several studies demonstrated no BDNF increase in response to acute exercise, and high interindividual variation was common [37,59,69,75,76,89]. Environmental elements (such as traffic pollution during outdoor cycling), cardiorespiratory fitness, inflammatory milieu, and metabolic status emerged as modulators of the BDNF response [22,28,30,37,69,73,75,76].

C) Cerebral Blood Flow, Oxygenation, and Hemodynamics: A Rapid but Transient Pathway

Brain perfusion, cortical oxygenation, and cerebrovascular responsiveness were frequently assessed using fNIRS, ASL-MRI, TCD, and other near-infrared methods [11,14,19,24,29,32,33,38,39,42,43,44,51,54,58,61,63,71,72,90,92,99].

Prefrontal Oxygenation Increases During and After Exercise

Multiple fNIRS studies demonstrated increases in prefrontal oxyhemoglobin during executive tasks performed after moderate exercise, often aligning with performance gains [11,14,19,24,29,32,38,41,44,46,54,63,66,68,70,72,82,83,91,99,101]. These patterns were observed during moderate cycling, brisk walking, running, HIIT, and combined paradigms with vibration or blood-flow restriction [7,11,14,19,20,24,32,41,44,46,47,54,60,63,66,70,72,83,91,99,100].

The Relationship Between Oxygenation and Cognition Is Not Linear

Some studies reported reduced cortical activation despite improved performance, suggesting increased neural efficiency rather than increased resource allocation [29,31,66,68,70,72,77,99]. Others showed no direct association between global CBF changes and cognitive gains, particularly when CO₂ was experimentally manipulated [16,33,38,39,42,58,63,71,90]. Severe-intensity or prolonged exercise often produced temporary declines in cognitive performance during exercise, likely reflecting competition between motor and cognitive demands and transient hypofrontality [5,31,40,48,60,71,90,92,100].

Hemodynamic Responses Differ Across Modalities and Environments

Comparisons between upright and recumbent cycling, aquatic treadmill walking, and eccentric cycling illustrated how posture, hydrostatic pressure, and contraction type influence prefrontal oxygenation and cerebrovascular responses [31,40,44,54,71,90]. Hypoxic trials demonstrated that moderate normobaric hypoxia attenuated cognitive performance and altered hemodynamics even when BDNF rose, underscoring that vascular constraints can override neurotrophic facilitation [43,56,57,61].

D) Lactate, Catecholamines, and Blood Pressure: Fast-Acting Physiological Modulators

Acute lactate responses are increasingly recognized as contributors to exercise-induced cognitive changes. Several studies showed that higher lactate concentrations correlated with improved executive function or working memory, particularly in HIIT, strength-based, or concurrent exercise protocols [5,7,8,9,41,59,60,73,79,87,100]. Norepinephrine, IGF-1, and endocrine markers also rose following certain resistance or vibration-assisted protocols and were linked to working-memory accuracy in some cohorts [5,7,9,20,25,41,55,73,79,85,100]. A recent crossover trial suggested that systolic blood pressure may partially mediate post-resistance improvements in executive function, emphasizing the role of cardiovascular arousal in triggering acute neurocognitive benefits [27].

E) Age, Fitness, and Cognitive Status as Moderators

Older Adults Benefit Consistently, but Mechanisms Differ

Older participants showed robust Stroop and working-memory improvements after moderate exercise and multicomponent programs, often accompanied by increased prefrontal activation and BDNF responses [11,15,18,21,22,23,33,35,42,44,49,50,52,63,69,72,80,85,90]. However, several studies noted slower return-to-baseline hemodynamic responses and greater interindividual variability in biomarker changes in older cohorts [11,18,23,42,44,63,72,80].

Higher Fitness Predicts Larger Cognitive Gains

Multiple studies reported stronger executive-function improvements, higher baseline cognitive scores, and more pronounced ERP or BDNF responses in fitter individuals [21,22,28,45,63,68,73,80,94]. Fitness also modulated responsiveness to HIIT and to combined physical–cognitive interventions, suggesting that individual conditioning status should be considered when prescribing exercise as a cognitive enhancer [22,28,45,63,68,73,80,94].

Clinical Populations Show Attenuated or Delayed Responses

Few included studies specifically targeted individuals with disease or elevated dementia risk, but available data from type 1 diabetes, overweight or metabolically impaired adults, and MCI-risk populations suggest that acute interventions remain beneficial, though mechanisms may be altered by baseline inflammation, vascular stiffness, or neurodegeneration [33,37,69,73,74,85,90]. These findings justify further mechanistic and translational research in clinical cohorts.

F) Methodological Considerations and Diversity of Approaches

This evidence base is large but methodologically heterogeneous. Most studies used small samples (often N = 15–40) and rarely included preregistration, standardized intensity prescriptions, or harmonized cognitive test batteries [1,2,3,5,6,7,8,9,13,15,17,18,19,20,21,23,24,25,26,27,28,29,31,32,33,34,35,39,40,41,43,44,45,46,47,49,50,51,52,53,56,57,58,59,60,63,64,65,68,70,72,73,75,79,80,81,84,90,91,92,93,95,96,97,98,99,100]. Biomarker assays varied in timing, fasting status, and compartment (serum vs plasma), complicating direct comparisons [1,2,3,10,21,22,23,25,28,52,64,69,73,79,80,86,87,88,89,93]. Nevertheless, several consistent methodological themes emerged: cognitive assessments conducted immediately after exercise were the most sensitive; executive-function tasks (Stroop, Flanker, TMT-B, n-back) showed the largest and most reliable effects; fNIRS has become the dominant tool for mapping prefrontal responses; and HIIT plus moderate-intensity continuous exercise are the most commonly studied modalities [11,13,14,19,24,29,31,32,38,41,45,46,47,54,60,63,66,68,70,72,82,83,91,94,99,101,102].

A Unified Mechanistic Model Is Therefore Emerging

Acute exercise → physiological arousal → transient vascular, metabolic, and neurotrophic changes → enhanced prefrontal efficiency → improved executive function [1,2,3,5,6,7,8,9,13,14,15,17,18,19,20,21,22,23,25,29,31,32,33,34,35,38,39,40,41,44,45,46,47,52,56,57,58,60,63,64,65,68,70,72,73,79,80,82,83,86,87,88,89,90,91,92,93,96,97,98,99].

G) Integrative Interpretation and Implications for Practice

Taken together, the evidence suggests several clear implications. Acute exercise is a reliable cognitive enhancer across age groups, with even 10–20 minutes of moderate or interval-based exercise able to improve key executive processes relevant for academic performance, work productivity, and fall prevention [13,15,19,24,34,41,45,46,60,63,68,70,72,81,82,84,90,91,92,95,96,97,98,99,101,102]. Exercise intensity should be individualized: moderate-to-ventilatory-threshold workloads and well-designed HIIT protocols appear optimal, but low-volume or mild-intensity interventions can be effective in older or clinical populations, especially when they increase prefrontal efficiency [11,15,19,24,34,44,54,60,63,72,91]. Acute exercise may “prime the brain” for learning or rehabilitation—an idea supported by studies linking post-exercise BDNF changes and vascular responses to improved memory and training outcomes [6,18,21,23,33,39,63,80,81,86,93,96,97,98].

Mechanistic heterogeneity reflects real biological diversity: BDNF, lactate, blood pressure, norepinephrine, inflammatory mediators, and cerebrovascular dynamics all contribute in different populations and contexts [1,2,3,5,6,7,8,9,10,17,18,21,22,23,25,28,30,39,41,50,52,56,57,58,59,69,70,73,79,80,85,86,87,88,89,93,96,97,98,99,100]. This underscores the need for stratified, precision-exercise approaches rather than one-size-fits-all prescriptions.

H. Future Directions

This scoping review highlights several priorities for future research:

• Standardization: development of common cognitive test batteries, biomarker panels, and sampling time points for acute exercise trials [1,2,3,6,7,8,13,18,21,22,23,25,28,45,52,63,69,73,79,80,86,87,88,89,93,96,97,98,99];
• Multimodal imaging: integration of fNIRS with MRI, EEG/ERP, and Doppler-based methods to link neurovascular, neuroelectric, and neurotrophic changes in the same individuals [11,14,19,24,29,32,33,38,39,41,58,63,71,82,83,90,92,99];
• Larger, preregistered trials are required which are adequately powered to test mechanistic hypotheses and moderators like sex, fitness, and genetics [18,21,22,23,28,33,42,44,63,68,69,73,80,85,94];
• Stratification: consideration of age, hormonal status, baseline cognitive capacity, and genetic markers such as BDNF Val66Met or APOE4
• Combined interventions: exploration of synergistic protocols combining exercise with cognitive training, nutritional strategies, neuromodulation, or pharmacologic agents [6,18,21,23,28,33,39,41,52,63,73,79,80,86,93,96,97,98].

Limitations

This scoping review has several limitations inherent to the breadth and heterogeneity of the included evidence. First, the review is based largely on abstract-level data extraction for many studies, which restricted the ability to examine methodological nuance, timing details, or statistical rigor. Second, substantial variability in exercise protocols (intensity definitions, duration, modality), cognitive task selection, and biomarker sampling methods (serum vs. plasma BDNF, timing of blood draws, preprocessing differences) limited direct comparability across studies. Third, neuroimaging and cerebrovascular measures differed widely in instrumentation and analytic pipelines, making mechanistic interpretation challenging. Fourth, because scoping reviews do not perform formal risk-of-bias assessments, the internal validity of individual studies cannot be assured, and small sample sizes—common across acute-exercise trials—may inflate effect estimates or produce inconsistent findings. Fifth, publication bias and selective reporting likely influenced the available evidence, particularly for positive cognitive outcomes and biomarker changes. Finally, because most studies were conducted in young, healthy adults, generalizability to older adults, clinical populations, or individuals with cognitive impairment remains limited. These factors underscore the need for standardized experimental frameworks and harmonized outcome measures in future mechanistic trials.

5. Conclusions

This scoping review provides a comprehensive mapping of the acute cognitive, neurotrophic, and cerebrovascular effects of single-session exercise across healthy and aging adults [1,2,3,4,5,6,7,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22,23,24,25,26,27,28,29,30,31,32,33,34,35,36,37,38,39,40,41,42,43,44,45,46,47,48,49,50,51,52,53,54,55,56,57,58,59,60,61,62,63,64,65,66,67,68,69,70,71,72,73,74,75,76,77,78,79,80,81,82,83,84,85,86,87,88,89,90,91,92,93,94,95,96,97,98,99,100,101,102]. Despite substantial heterogeneity in study designs, cognitive assessments, biomarkers, and exercise modalities, several consistent findings emerged.

First, acute exercise reliably enhances executive function—particularly inhibitory control, cognitive flexibility, and working memory—across aerobic, resistance, interval-based, balance, and multimodal sessions, as long as sufficient physiological arousal is achieved [5,6,7,8,9,13,15,19,20,24,27,31,34,41,44,45,46,49,50,52,54,60,63,66,70,72,77,81,82,84,88,90,91,92,94,95,96,97,98,99,100,101,102].

Second, exercise intensity emerges as a key modulator, with moderate-to-ventilatory-threshold workloads and HIIT protocols producing the most robust - though not necessarily longest-lasting – improvements [2,7,8,13,15,19,24,34,41,45,46,59,60,63,72,73,84,91,94,102].

Third, acute changes in BDNF, lactate, catecholamines, blood pressure, and cerebral oxygenation appear to contribute to these cognitive enhancements, although no single mechanistic pathway fully explains the observed effects [1,2,3,5,6,7,8,9,10,17,18,21,22,23,25,28,30,39,41,50,52,56,57,58,59,64,69,70,73,79,80,86,87,88,89,93,96,97,98,99,100]. Rather, findings support a multi-mechanistic model in which acute exercise induces a transient state of neurobiological readiness—marked by increased neurotrophic signaling, improved cerebrovascular responsiveness, and greater prefrontal neural efficiency.

Fourth, cognitive benefits are observed across the lifespan, with older adults demonstrating improvements comparable to younger individuals, although with greater variability and potentially distinct mechanistic contributions [11,15,18,21,22,23,33,35,42,44,49,50,52,63,69,72,80,85,90,98]. Fitness level, environmental factors, hypoxia, and neurobiological responsiveness further shape the magnitude and durability of effects [22,28,33,37,43,56,57,61,69,71,73,75,76,94].

Overall, the available evidence positions acute exercise as a reliable, rapidly acting strategy to enhance cognitive performance, with promising implications for learning, occupational functioning, rehabilitation, and healthy aging.

Future research should prioritize standardized protocols, larger and preregistered mechanistic trials, multimodal imaging, and stratification by fitness, sex, age, and genetic or neurobiological profiles. Together, these steps will strengthen mechanistic insight and accelerate the translation of acute exercise into practical, personalized cognitive-enhancement strategies.