Low intrinsic capacity is associated with a blunted exercise‐induced cognitive enhancement in physically active middle‐aged and older adults

Abstract

INTRODUCTION

The World Health Organization supports intrinsic capacity (IC) as a framework for assessing and monitoring an older person's cognitive health. Low IC is associated with higher dementia risk. Regular exercise participation improves cognitive health, reduces dementia risk, and may increase IC. However, the long‐term chronic brain benefits of regular exercise training are dependent upon the effectiveness of single exercise bouts to augment cognition. Yet, how IC influences the magnitude of improvement following a single exercise bout has not been elucidated.

METHODS

A convenience sampling of 40 physically active adults (55 ± 6 years; mean ± SD) with a body mass index ≥ 24.9 kg/m² (range: 24.9 to 36.3) were included in this study. IC domains were operationally defined as follows: cognitive (Mini Cog and Trail Making Test Parts A and B [TMT A+B] performance), vitality (body composition and exercise performance), and locomotor function (habitual gait speed). Participants were stratified by locomotor function into a slow group (≤1.0 m/s; LOW‐IC) and a normal group (>1.0 m/s; NORM‐IC). Immediately prior to and following the exercise session (161‐km cycling event) participants completed the executive function task (TMT A+B). An analysis of covariance, controlling for baseline TMT A+B performance, was used to detect a significant improvement in TMT A+B (p < 0.05).

RESULTS

Participants had similar cognitive abilities and vitality, but groups significantly differed by locomotor function. A significant interaction (p = 0.004) was revealed where improvement for NORM‐IC (−13 s [−18 to −8]; p < 0.001; partial η² = 0.47; adjusted mean [95% confidence interval]) was greater than for LOW‐IC (−3 s [−9 to 2]; p = 0.25; partial η² = 0.04) following the exercise session.

DISCUSSION

Low IC is associated with a blunted acute exercise‐induced cognitive enhancement in mid to late adulthood. Future research is justified to determine the physiological mechanisms underpinning this novel finding.

Highlights

• Adults with overweight/obesity show cognitive gains after endurance exercise.

• Poor locomotor function limits cognitive gains from exercise in overweight adults.

• IC better predicts exercise‐related cognitive gains than cognition.

1. INTRODUCTION

In the United States, the cumulative impact of both an increasing aging population and an obesity epidemic has led to more than 40% of middle‐aged and older adults meeting the criteria for overweight or severe obesity (body mass index [BMI] ≥ 25 kg∙m²). ¹ This maladaptive shift in body composition, characterized by adipose accumulation and age‐related loss of skeletal muscle mass, promotes a pro‐inflammatory milieu and mitochondrial dysfunction that substantially elevates the risk of developing physical and/or cognitive frailty – an increased susceptibility to disease and loss of resilience. ² , ³ Yet, despite frailty being a precipitating risk factor for severe cognitive and physical impairment, such as dementia and functional disability, ³ , ⁴ the routine comprehensive assessment of body composition along with physical and cognitive abilities, especially among individuals in mid to late adulthood, is not standard of care. ⁵

To address this emerging public health concern, the World Health Organization (WHO) advocates for a societal shift from a disease‐centered to capacity‐centered model for understanding healthy aging. ⁵ In the WHO World Report on Ageing and Health, the authors propose assessing and monitoring an individual's intrinsic capacity (IC), a composite of physical and cognitive abilities, to identify adults at risk for transitioning to functional disability or cognitive impairment. ⁵ The five functional aging domains that make up one's IC are locomotor function, cognition, vitality (e.g., body composition or energy), psychological health, and sensory (i.e., hearing and vision). ⁵ However, chief among these is locomotor function as it shows strong interconnectedness with the other four domains. ⁶ At its core, IC is a holistic concept used to determine an individual's resiliency capacity to efficiently mobilize reserves in response to a stressor (i.e., adaptive behavior). Importantly, the stressor can be negative – causing poor health or maladaptation – or therapeutic, enhancing reserve capacity and physiological function.

Sun and colleagues recently showed that older adults with high IC (fewer deficits) have a lower risk of dementia compared to those with low IC. ⁷ Consistent with this result, the 2024 Lancet Commission on dementia prevention identified several midlife (ages 45 to 65 years) risk factors – such as obesity and hearing loss – that are closely linked to the five IC domains. ⁸ The authors also reported the benefits of aerobic exercise to mitigate dementia risk. ⁸ However, one study found that about 30% of individuals with moderate to high aerobic capacity in midlife still developed dementia, though onset was later than in those with low aerobic capacity. ⁹ This suggests that intrinsic factors beyond aerobic capacity contribute to dementia risk in physically active aging adults. Nonetheless, appropriately dosed aerobic exercise is widely recognized as a key acute and chronic stressor that may mitigate age‐related cognitive decline, potentially by optimizing IC. ¹⁰ , ¹¹ The suitability of an acute exercise dose depends primarily on duration and intensity and should foster cognitive resilience (i.e., adaptive recovery) rather than fatigue. Further, Voss et al. demonstrated that the anticipated long‐term neurocognitive benefit following chronic exercise training can be predicted from the magnitude of cognitive enhancement in response to a single exercise session. ¹¹ Therefore, maximizing the effectiveness of a single exercise session is necessary to reap optimal chronic cognitive adaptations. Yet, there remains much heterogeneity in the magnitude of cognition‐enhancing benefit that healthy aging adults can expect to achieve after a single exercise session. ¹² , ¹³

Although acute exercise affects global cognition, executive function (working memory, cognitive flexibility, and inhibitory control) is more responsive to an acute exercise bout ¹³ and strongly predicts functional disability ¹⁴ and prodromal dementia. ¹⁵ Consistent with a meta‐analysis of individual participant data, ¹³ we previously showed that variability in exercise effects on executive function partly reflected pre‐exercise performance. ¹⁶ After an aerobic endurance exercise session (161‐km cycling event), participants with the slowest pre‐exercise executive function task completion time experienced the largest post‐exercise improvement (i.e., faster completion time). ¹⁶ The magnitude of executive function task improvement we observed was comparable to that seen at shorter durations or smaller doses of acute exercise. ¹⁰ , ¹² , ¹³ In the context of IC, executive function shares unique bi‐directional relationships with locomotor function and vitality domains. For instance, habitual gait speed (locomotor function) is directly linked to executive function, with declines in one predicting declines in the other. ¹⁷ , ¹⁸ Similarly, increasing body mass index (BMI), a vitality parameter, is linked to executive function decline, while reducing BMI improves it. ¹⁹ Further, in a cross‐sectional study of mostly older adults with overweight/obesity, combined poor exercise performance (vitality) and slow gait speed (<1.0 m/s; locomotor) were linked to higher mild cognitive impairment and dementia risk than slow gait alone. ²⁰ Despite this evident biological plausibility, it remains unknown if IC influences the magnitude of executive function improvement following a single exercise bout.

This study aimed to examine how IC affects executive function gains after aerobic endurance exercise in physically active middle‐aged and older adults. We tested the hypothesis that heterogeneity in the magnitude of improvement in executive function task performance was partly attributable to differences in IC. Specifically, despite similar baseline cognitive abilities, we anticipated that adults aged 45 to 70 years with poor vitality and locomotor function would show less improvement in executive function than those with poor vitality but robust locomotor function.

2. METHODS

2.1. Study population

We performed a secondary analysis of our prospective field‐based cohort study that demonstrated significant improvement in executive function after an aerobic endurance exercise session in physically active adults (21 to 70 years). ¹⁶ Since executive and physical function declines are recognized beginning as early as midlife (45 years), ²¹ , ²² we enrolled participants who were ≥45 years of age. Considering that IC is a composite measure, we further restricted this analysis to those with BMI ≥ 24.9 kg/m² to capture individuals at risk of cognitive decline and to limit the variability across IC domains. In addition to meeting age and BMI criteria, participants were included if they met the following criteria from the parent study: cognitively normal as determined by the Mini Cog assessment (score was ≥ 3/5 au units; 1 point each for three‐word recall and 2 points for correct clock draw), free of musculoskeletal injury, free of a fluid balance altering illness or medication (e.g., diuretic), no dietary restrictions (e.g., vegetarian, vegan), not a current smoker or tobacco user, and had previously completed a similar aerobic endurance exercise event.

2.2. Pre‐exercise measures

Prior to the day of exercise (within 48 h) we measured participants’ anthropometrics (e.g., height) and collected medical history as previously detailed. ¹⁶ During the same study visit, habitual gait speed (m/s) was measured over a 4‐m distance. The fastest of two trials was used for statistical analysis. To attenuate the influence of a learning effect, participants were then familiarized with the executive function task – Trail Making Test Parts A and B (TMT A+B). TMT A required participants to connect scattered encircled numbers (1 to 25), and TMT B required participants to alternate between scattered encircled numbers and letters (e.g., 1‐A‐2‐B) placed on an 8×10 white sheet of paper. At the same study visit, participants were familiarized with the Rating of Perceived Exertion (RPE) scale (scores ranged from 6 representing no exertion at all to 20 representing maximal exertion) – a measure of subjective exercise intensity.

2.3. IC assessments

Data were available on three out of five IC domains – vitality, cognition, and locomotor function. As an intentional part of the inclusionary criteria, all participants had unimpaired cognition but poor vitality (overweight/obesity). Since locomotor function is closely related to the other four domains, ⁶ participants were stratified by locomotor function into low IC (gait speed ≤1.0 m/s; LOW‐IC) and normal IC (gait speed > 1.0 m/s; NORM‐IC). A cut‐off of 1.0 m/s was selected for this study because a gait speed > 1.0 m/s is associated with better health‐related outcomes in well‐functioning aging adults. ²³ In total, NORM‐IC experienced one IC deficit (vitality) and LOW‐IC experienced two deficits (vitality and locomotor function). The three IC domains were operationally defined as follows:

RESEARCH IN CONTEXT

1. Systematic Review: We reviewed the literature on the impact of IC on the magnitude of cognition‐enhancing benefits of a single exercise session in mid to late adulthood using traditional sources (e.g., PubMed). Our search revealed that little is known about the impact of IC on acute exercise‐induced cognitive benefits.

2. Interpretation: We reported that the low IC (poor vitality [high BMI] and locomotor function [slow gait speed] but robust cognitive function) was associated with a blunted post‐exercise cognitive enhancement compared to those with normal IC (poor vitality but robust locomotor [normal gait speed] and cognitive function). Thus, increasing IC may be necessary to maximize the benefits of aerobic exercise on brain health.

3. Future directions: The findings reported here set the stage for studies to investigate the biological mechanisms underpinning the relationship between IC and cognition in response to acute and long‐term exercise.

Vitality: In agreement with the WHO working definition of vitality, ²⁴ BMI was calculated as a measure of body composition. At the end of the exercise bout, participants provided a study staff member with the total time to complete the exercise session and the accompanying post‐exercise RPE. Total exercise time was compared with or captured from official time using the cyclist bib number when possible. Both measures were used as a measure of aerobic fitness/endurance.

Cognition: In our prior work, we established that pre‐exercise TMT A+B was a key predictor of post‐exercise executive function improvement (r ²  = 0.23, p < 0.0001). ¹⁶ Therefore, in addition to the Mini Cog screening assessment (global cognition), participant pre‐exercise TMT A+B task performance (executive function) was used as a measure of cognitive abilities.

Locomotor function: Habitual gait speed was used as a measure of mobility/physical function.

2.4. Exposure

Aerobic endurance exercise session: All participants completed a 161‐km mass participation cycling event (>3300 cyclists, Hotter N’ Hell Hundred in Wichita Falls, Texas) using their own bicycle. The temperature on the day of the event ranged from 21°C to 31°C, and precipitation was zero. On average, most cyclists, including those in this study, completed the cycling event in 6 to 9 h.

2.5. Primary outcome

Prior to and at completion (within 15 min) of the exercise session, participants completed the TMT A+B in sequential order (A before B). The total time to complete the task was recorded using a stopwatch. The change in time to complete the TMT A+B (before vs after) was used as the primary outcome.

2.6. Statistical analysis

Levene's statistic was used to assess data normality. An independent sample Student's t‐test or Mann–Whitney U test was used to compare group differences between baseline characteristics and post‐exercise performance measures. ANOVA was used to compare before versus after difference in time to complete the TMT A+B within the entire group. A two‐way repeated measure analysis of covariance (ANCOVA) (group × time), controlling for baseline TMT A+B, was conducted to explore interaction effects. Post hoc pairwise comparisons (Bonferroni corrected) were used to identify simple main effect differences. Effect sizes are reported as partial eta‐squared (partial η² ), where values of 0.01, 0.06, and 0.14 correspond to small, medium, and large effects, respectively.  Statistical significance was set at p < 0.05. Data are presented as either adjusted mean difference (95% confidence interval [CI]) or mean ± standard deviation unless designated otherwise. All analyses were performed using SPSS Statistics, version 29.0 (IBM Corp., Armonk, NY, USA).

2.7. Power analysis

To detect statistically significant group differences in the magnitude of change time to complete the TMT A+B (before vs after), at an α level of p < 0.05, power of 0.80, at a partial η² of 0.20, and using an ANCOVA, a sample size of 17 per group was required (G*Power, version 3.1.9, Aichach, Germany).

3. RESULTS

3.1. Participants

A total of 40 participants were enrolled (age = 55 ± 6 years; mean ± SD), and most identified as male (93%). Significant differences between groups confirmed sufficient IC stratification by locomotor function (habitual gait speed [p < 0.05], Table 1). Participants’ pre‐exercise vitality and cognitive abilities were statistically similar (p > 0.05, Table 1). Further, groups did not differ in total exercise time or subjective rating of exercise intensity (i.e., RPE). Complete participant characteristics are presented in Table 1.

TABLE 1.

Participant characteristics for entire group and when stratified by intrinsic capacity.

Characteristics	Entire sample (N = 40)	NORM‐IC (N = 23)	LOW‐IC (N = 17)	P
Anthropometrics
Age (years)	55 (45–70)	53 ± 5	57 ± 7	0.07
Female (%)	8	4	12	0.39
Vitality domain
Body weight (kg)	88.1 (73.7 to 124)	90.2 ± 12.9	85.3 ± 8.7	0.19
Height (cm)	176 (167 to 193)	177 ± 6	174 ± 6	0.15
BMI (kg/m2)	28.5 (24.9 to 36.3)	28.8 ± 3.2	28.1 ± 3.1	0.56
Exercise duration (min)	365 (274 to 510) a	358 ± 56 b	373 ± 64 c	0.49
Rating of perceived exertion (au)	16 (11 to 19) d	17 (3) e	16 (2)	0.68
Locomotor function domain
Habitual Gait speed (m/s)	1.07 (0.76 to 1.55)	1 .17 ± 0.14	0.93 ± 0.08	<0.001
Cognitive function domain
TMT A+B (s)	83 (40 to 128)	81 ± 23	87 ± 24	0.39

Note: Values are displayed as mean (min–max), mean ± standard deviation, or median (interquartile range).

Bold value statistically significant p < 0.0005.

Abbreviations: au, arbitrary unit; BMI, body mass index; SLOW‐IC, low intrinsic capacity; NORM‐IC, normal intrinsic capacity; TMT A+B, Trail Making Test Parts A + B.

^a Denotes sample size = 32.

^b Sample size = 18.

^c Sample size = 14.

^d Sample size = 39.

^e Sample size = 22.

3.2. Influence of IC on post‐exercise executive function

After the aerobic endurance exercise bout, a significant performance improvement in the time to complete TMT A+B (F_1,.39 = 16.423; −9 s (−13 to −4); p < 0.001; partial η² = 0.30) was observed in the entire sample. This result recapitulated our prior finding from a larger cohort. ¹⁶ After stratifying by IC, a significant group × time interaction (F_1,37 = 7.874; p = 0.008; partial η² = 0.18) was observed (Figure 1). In post hoc analyses, NORM‐IC completed the TMT A+B faster after exercise (−13 s [−18 to −8]; p < 0.001) compared to LOW‐IC (−3 s [−9 to 2]; p = 0.25) (Figure 1). The effect size was large in NORM‐IC (partial η² = 0.47) but small in the LOW‐IC (partial η² = 0.04) group (Figure 2).

FIGURE 1.

Exercise‐induced differences in time to complete TMT A+B as a factor of intrinsic capacity. Individual raw times to complete TMT A+B are represented by shapes. P values are from an analysis of covariance adjusting for differences in baseline TMT A+B performance. Following the completion of the endurance exercise session, a significant group interaction was detected (p = 0.008). Participants with a NORM‐IC (>1.0 m/s) significantly reduced their time to complete the TMT A+B, whereas participants with a LOW‐IC (≤1.0 m/s) saw no improvement in time to complete the TMT A+B. LOW‐IC, low intrinsic capacity; NORM‐IC, normal intrinsic capacity; TMT A+B, Trail Making Test Parts A + B.

FIGURE 2.

Conceptual model of exercise responses and magnitude of cognitive enhancement after aerobic endurance exercise for entire sample and as a factor of IC. (A) Conceptual model demonstrating potential dynamic responses to stress of physical exercise. (B) Display of magnitude of cognitive enhancement demonstrated by entire sample (n = 40; partial η² = 0.30) in response to a single exercise session. (C) Display of difference in magnitude of cognitive enhancement in response to single exercise session when stratified by IC (partial η² = 0.47 vs 0.04 [NORM‐IC vs LOW‐IC]). LOW‐IC participants maintained whereas NORM‐IC improved their executive function in response to the single exercise session. LOW‐IC, low intrinsic capacity; NORM‐IC, normal intrinsic capacity.

4. DISCUSSION

In this study of physically active middle‐aged and older adults, exercise‐induced cognitive responses varied by pre‐exercise IC. This novel finding adds further nuance to our prior study showing pre‐exercise executive function predicted post‐exercise executive function improvement. ¹⁶ In the current study, both groups exhibited similar pre‐exercise executive function; however, heterogeneities in the magnitude of post‐exercise improvement were revealed. Indeed, the acute aerobic endurance exercise bout produced large improvements in executive function (faster completion) in participants with robust IC compared to those with low IC (Figure 2). Most notably, the exercise stressor revealed differences in cognitive resilience not detected by pre‐exercise cognitive testing (Figure 2). Together, these data suggest that factors beyond pre‐exercise cognitive abilities influence the therapeutic benefit of exercise on the aging brain. To our knowledge, we are among the first to identify IC as a potential moderator of the exercise‐cognition relationship in mid to late adulthood. These findings further support emerging evidence linking IC to cognitive impairment ⁷ and may explain variability in exercise‐induced cognitive gains reported previously. ¹⁰ , ¹² , ²⁵ , ²⁶

With advancing age, habitual gait speed is increasingly correlated to peak aerobic capacity, ²⁷ a well‐established moderator of the cognition‐enhancing benefit following a single exercise session. ¹² When considered alongside Boidin and colleagues’ work demonstrating a direct relationship between peak aerobic capacity and executive function in older adults with obesity, ²⁸ our findings may be partly explained by studies highlighting the influence of aerobic capacity on the exercise–cognition relationship. For instance, Chang et al. exposed older adults, stratified by peak aerobic capacity, to 20 min of moderate exercise and found an inverse relationship between aerobic capacity and post‐exercise executive function task completion time. ²⁹ Chu et al. also observed better executive function performance in participants with higher aerobic capacity. ³⁰ Notably, we had comparable sample sizes (n = 40 vs 46) and observed an interaction effect size identical to that observed by Chu et al. (partial η² = 0.18), ³⁰ despite our exercise condition being, on average, 18‐fold longer in duration. Conversely, Netz and colleagues observed no impact of aerobic capacity on post‐exercise cognitive function. ³¹ This discrepancy may be consequent to participants in the Netz et al. study exhibiting a lower aerobic capacity (25.9 ± 4.2 mL·kg⁻¹·min⁻¹) than the higher aerobic capacity groups in both the Chang et al. (36.0 ± 2.9 mL·kg⁻¹·min⁻¹) and Chu et al. (36.0 ± 1.2 mL·kg⁻¹·min⁻¹) reports ²⁹ , ³⁰ ; thus, a small or negligible improvement would be expected in the study by Netz et al. compared to both Chang et al. and Chu et al. ²⁹ , ³⁰ , ³¹ In addition, slow walkers in a study by Fiser et al. used 23% greater aerobic capacity reserve during habitual walking compared to faster walkers. ²⁷ High usage of physiological reserves during normal activities of daily living increases the risk of frailty and reduced resilience. ³² Using the Fried Frailty Index criteria, slow walking participants in the present study, on average, displayed a gait speed consistent with at least a pre‐frailty status, whereas normal walkers exhibited more robustness. ³² Considering this, slow walking participants’ proclivity to resist (cognitive maintenance) stress from a single exercise session rather than adapt (cognitive improvement) can be viewed as a lack of resilience (i.e., increased frailty) in comparison to faster walkers. This is consistent with frail adults’ increased propensity to be “non‐responders” to aerobic exercise, which indicates a different dose of exercise is required to achieve a comparable benefit compared to non‐frail adults. ³²

The disparity in cognitive resilience observed in this study may represent mechanistic differences in hippocampal plasticity. Hippocampus atrophy is associated with reduced cognitive abilities, being overweight, slow gait speed, low aerobic capacity, and high utilization of aerobic capacity reserves during walking that is reversible, or the rate of decline slowed, with regular exercise training. ¹⁰ , ¹² , ³³ A single exercise session acutely induces hippocampal microstructural changes linked to neuroplasticity and cognitive improvement, ¹⁰ while hippocampal hypertrophy often accompanies cognitive gains after chronic training. ¹⁰ Additional studies are therefore justified to elucidate if hippocampal structure affects the relationship between IC and executive function performance following acute and chronic exercise.

Although able to complete a 161‐km cycling event, our participants with high BMI and slow gait may be at risk of severe geriatric syndromes linked to cognitive frailty and dementia, such as sarcopenic obesity, osteosarcopenia, and motoric cognitive risk syndrome. ³⁴ , ³⁵ , ³⁶ First, the screening criteria for sarcopenic obesity consist of the co‐existence of high BMI and diminished muscle mass or function, which are attributes of our LOW‐IC group. ³⁴ However, it is recommended that follow‐up with more precise measures of adiposity and skeletal muscle occur before a clinical diagnosis of sarcopenic obesity can be determined. ³⁴ Secondly, the combination of osteoporosis and sarcopenia is termed osteosarcopenia. ³⁵ Skeletal muscle and bone exchange mechanical, biological, and endocrine signals that result in the health of one organ being indicative of the health of the other. ³⁷ Bearing in mind that frequent long‐duration cycling exercise is associated with low bone mineral density or osteoporosis, ³⁸ it is possible that our LOW‐IC participants – particularly given their slow gait speed – may also be at risk of lower bone quality, and subsequently osteosarcopenia, compared to those with NORM‐IC. Lastly, the motoric cognitive risk syndrome is a prodromal dementia syndrome, which is defined as the co‐existence of slow gait and subjective cognitive complaints without cognitive or functional disability. ³⁶ Slowing of gait speed can occur a decade before a diagnosis of cognitive impairment or complaints. ³⁹ Thus, our LOW‐IC participants are plausibly at a higher risk for developing motoric cognitive risk syndrome compared to those with NORM‐IC. Longitudinal studies to determine if physically active adults with LOW‐IC are at risk for transitioning to more severe geriatric syndromes, including dementia, are therefore warranted.

The major strengths of our study are twofold: (1) it involved middle‐aged and older adults exercising in their preferred environment and mode, rather than in a lab under forced conditions; and (2) our participants were middle‐aged and older adults with overweight/obesity – an at‐risk group for cognitive and physical decline who may benefit most from exercise. Our study also has several limitations to be noted. Due to the type of individuals who participate in endurance exercise of this magnitude, we have an inherent selection bias. In addition, the combination of a convenience sample and a secondary analysis collectively warrants caution in the interpretation of our findings. BMI is a crude, but practical, measure of body mass that fails to delineate the components of body composition. Thus, we were unable to ascertain if differences in adipose or lean mass impacted our findings. In addition, we measured only three IC domains and therefore could not determine if our findings were due to group differences in sensory and psychological status. However, in a network analysis of the five IC domains, l ocomotor function was the largest node demonstrating interconnectedness with the other four. ⁶ Hence, a difference in sensory or psychological status is likely to be reflected in locomotor function. Lastly, our sample consisted mostly of males, and participants performed outdoor cycling, which may enhance the cognitive benefits of exercise. ⁴⁰ As such, results may not generalize to females, indoor exercisers, or other exercise modes.

5. CONCLUSION

In summary, of the IC domains measured herein, participants presented with similar pre‐exercise cognitive abilities and vitality and only differed in locomotor function. It was not until participants were exposed to the stress of a single endurance exercise session that disparities in their cognitive resilience were made manifest. Exercise is already routinely used in clinical settings to assess cardiovascular resilience, ⁴¹ and, given the heat–brain axis, ⁴² there may also be clinical utility in assessing post‐exercise brain resilience. Beyond providing support for assessing and monitoring IC, our findings highlight the need for precision rehabilitation to address IC deficits and potentially augment cognitive resiliency in seemingly healthy middle‐aged and older adults. Moreover, the ecological nature of our study greatly enhances the generalizability of our data to real‐world settings but limits our interpretation of the mechanistic underpinnings and veracity of our results. Therefore, there remains a need for well‐controlled studies to determine if cognitive resilience is indeed blunted in response to a single exercise session in persons with low IC and what underlying physiological mechanisms account for this disparity.

CONFLICT OF INTEREST STATEMENT

The authors declare no competing interests. Author disclosures are available in the Supporting Information.

CONSENT STATEMENT

This study was reviewed and approved by the Institutional Review Board for Human Studies at in the University of North Texas (USA), and all participants provided written informed consent prior to data collection.

Supporting information

Supporting information

Yates BA, Orkaby AR, Vingren JL, Armstrong LE. Low intrinsic capacity is associated with a blunted exercise‐induced cognitive enhancement in physically active middle‐aged and older adults. Alzheimer's Dement. 2025;11:e70141. 10.1002/trc2.70141