Skip to main content
Download PDF

Enhancing cognitive performance and mitigating dyslipidemia: the impact of moderate aerobic training on sedentary older adults

BMC Geriatrics volume 24, Article number: 678 (2024) Cite this article

Abstract

Background

The present study aimed to evaluate the effects of 24 weeks of moderate aerobic exercise on lipids and lipoprotein levels; Lipo (a) markers, and their association with cognitive performance in healthy older adults.

Methods

A total of 150 healthy subjects (100 males and 50 females; age range: 65–95 years) were recruited for this study. Based on the LOTCA test score, subjects were classified into two groups: the control group (n = 50) and the cognitive impairment group (n = 100). Cognitive functioning, leisure-time physical activity (LTPA), lipid profile, total cholesterol, TG, HDL-c, LDL-C, and lipo(a) were assessed at baseline and post-24-week aerobic exercise interventions using LOTCA battery, pre-validated Global Physical Activity Questionnaire (GPAQ) version II, colorimetric, and immunoassay techniques, respectively.

Results

Significant improvements in cognitive function and modulation in lipid profile and lipoprotein (a) markers were reported in all older subjects following 24 weeks of moderate exercise. LOTCA-7-sets scores significantly correlated with physical activity status and the regulation of lipids and Lipo (a) markers. Physically active persons showed higher cognitive performance along with a reduction in the levels of T-Cholest., TG, LDL-C, Lipo (a), and an increase in the levels of HDL-C and aerobic fitness VO2max compared with sedentary participants. Cognitive performance correlated positively with increased aerobic fitness, HDL-C, and negatively with T-Cholest., TG, LDL-C, and Lipo (a). However, a significant increase in the improvement of motor praxis, vasomotor organization, thinking operations, attention, and concentration were reported among older adults.

Conclusions

The study findings revealed that supervised moderate aerobic training for 24 weeks significantly enhances cognitive functions via mitigating older adults’ lipid profiles and lipoprotein (a). Cognitive performance is positively correlated with aerobic fitness and HDL-C level and negatively with T-Cholest., TH, LDL-C, and Lipo (a).

Peer Review reports

Introduction

Cognitive abilities refer to all essential mental skills that the various processes and capacities of the mind that enable us to acquire, process, store, and apply knowledge. These abilities play a crucial role in how we perceive and interact with the world, solve problems, make decisions, and engage in complex thinking task that control the behavioral lifestyle of humans, including day routine work [1]. It’s important to note that these changes in cognitive abilities can vary widely among individuals, and not everyone will experience the same degree or pattern of decline with aging [2, 3].

Declines in cognitive abilities were shown to produce more drastic problems for older adults in performing their daily life activities [2]. However, more studies tried to maintain or enhance cognitive abilities in older adults by enhancing or delaying functional disabilities [3]. The results of these trials are not precise; this may be because most of these trials concentrated on treatment schedules rather than prevention in older subjects with cognitive deficits or functional disabilities. Previously it was reported that prevention or improvement of cognitive deficits among normal older adults is accessible, but the treatment parameters did not include the outcome measures, which may relate to the limited and lack of sample randomization [4, 5]. Thus, there are more pathological and physiological parameters or factors were involved in the progression of cognitive decline among both young and older ages [4,5,6,7]. The impairment in brain function in older age is performed via many pathological mechanisms [6, 7]. The most important is tissue damage and neural cell death, which occur via the interaction of complex path physiological processes [8]. In addition to that, decline in cognitive abilities among older adults were significantly associated with many severe age-related diseases, such as inflammation which is related to chronic pathological processes. Moreover, the incidence of inflammation and poor in immunosenescence resulted in a decline of multiple physiological systems and functional dependence in brain among the elderly [9,10,11]. Besides, abnormal in the cellular levels of lipid profiles is another physiological factor reported to be associated with cognitive decline among older adults [11, 12]. Many research studies reported that cognitive impairment and increased risk for CVD among older subjects are associated with abnormal lipid profiles [12,13,14], higher levels of low-density lipoprotein (LDL) cholesterol, total cholesterol levels, and lower high-density lipoprotein (HDL) cholesterol were significantly linked with lower scores of cognitive impairment older subjects with dementia [15, 16]. However, lower LDL, HDL, and higher HDL were associated with reduced or improved cognitive impairment [17, 18]. Similarly, lipoprotein (a) was reported as a possible risk factor for vascular dementia and cognitive impairments in older subjects [19, 20]. Lipoprotein (a) in many studies was reported as one of the cholesterol derivatives that exist in human plasma and structurally similar to low-density lipoprotein (LDL), but with a glycoprotein called [21, 22]. Thus, collectively both cellular physiological changes in lipid profiles are in connection in such away with the status of cognitive abilities and essential mental skills which are interconnected and contribute to overall cognitive functioning and performance in various domains of life, including academics, work, and daily activities [19,20,21,22]. These essential physiological and behavioral factors can be developed and improved through practice, learning, and engaging in activities that challenge and stimulate the mind.

Previous studies have shown that appropriate physical exercise and physical activity are effective means for cardiopulmonary function and brain cognition, which can enhance the cognitive ability of stroke patients, reduce pain, relieve cardiovascular pressure, and improve walking ability [23,24,25,26].

Physical activity of all kinds with a variety of intensities, ranging between light, moderate, and vigorous (or high) intensity are beneficial for human health. Light-intensity activities require the least amount of effort (< 3METS) compared to moderate (3–6 METS) and vigorous activities (> 6 METS). Many researchers showed that the therapeutic effect of aerobic exercise with different intensities, like light, moderate, and sternness is the most significant for improving cardiopulmonary function and brain cognition [27,28,29].

In this regard, many studies focused on the importance of body physical activity and its positive effects on cognitive abilities, especially in older ages. Physical exercise was shown to play a protective role against hippocampal cell injury, which produces brain memory loss [30]. Whereas physical facilitate recovery from injury and improves cognitive function via an increase in the expression of many neurotrophic and physiological factors involved in neural survival, differentiation, and improvement of memory function [31].

Recent studies reported the potential action of exercise as an anti-apoptotic parameter against many brain diseases such as brain inflammatory conditions [32], mice Parkinson’s disease [33], in the improvement of depressive symptoms [34], traumatic brain injury [35, 36], and alleviation of memory impairment [37].

It was reported that physical exercise performs sound effects on cognitive abilities in different ways, which argues its importance as non-drug and non-invasive essential targets for long-term health programs for all ages [38, 39]. The marked improvement was manifested in both function and biomarker integrity, as shown in recent studies [40, 41]. This indicates the non-drug efficiency of exercise, especially of moderate type, to change lifestyle and improve lipoprotein and lipid levels in adults [42]. A significant positive change in the levels of lipids and lipoproteins was reported among both men and women following aerobic exercise [43, 44].

Most research topics studied the combined effects of exercise and diet on lipids and lipoproteins furthermore, few studies concentrated on the effects of physical exercise alone [45, 46]. Thus, the benefits of regular physical exercise as a health-ensuring necessity over age, gender, occupation, and affective status cannot be overestimated [47, 48]. In this study, it was hypothesized that moderate aerobic exercise as non-drug remedy for 24 weeks might have a potential role in the improvement of cognitive abilities among older adults via reducing the levels of lipid profiles.

Therefore, the present study was designed to evaluate the effects of 24 weeks of moderate aerobic exercise on the levels of lipids and lipoprotein (a) markers and their association with cognitive performance in healthy older adults.

Materials and methods

Subjects

A total of 200 subjects were invited to participate in this study. Only, one-hundred-fifty healthy subjects (100 males, 50 females; mean age between 65 and 95 years) who matched inclusion criteria were recruited for this study. Subjects with physical disability and endocrine, immune, psychiatric illness, eating disorders, and taking glucocorticoid medication that could interfere with lipid profile and cognitive ability measurements were excluded from this study. In addition, subjects who are the overweight and obese (body mass index [BMI] ≥ 25 and ≥ 30 kg/m2 were also excluded. Also, subjects who participated in other exercise programs were excluded from this study. Based on the LOTCA test scores, subjects were classified into two groups, the control group (n = 50) and the cognitive impairment group (n = 100). To record any drop out, the diet or lifestyle of all participants were observed and subjected under follow up for any change during the period of the exercise program (24 weeks). Demographic and anthropometric data of participants were included in Table (1).

Training procedure

Participants were involved in an exercise program designed according to Karvonen’s formula [49] thrice weekly for 24 weeks. Whereas the training intensity of each intervention was prepared according to each participant’s maximum and resting heart rate. During warming, the subject performed stretching exercises and walking for 5 to 10 min. During the active phase, the subject could reach his pre-calculated training heart rate (THR max; 60 to 70% for 45–60 min) in bouts form using a treadmill, bicycle, and stair master [50, 51]. Each participant’s exact calculated heart rate was monitored via a wearable automatic portable heart rate meter (Polar Electro, Kempele, Finland). The exercise test gave the participants physical activities corresponding to 30–45% of VO2 max uptake [52].

Assessment of leisure-time physical activity (LTPA)

A pre-validated global physical activity questionnaire version II (GPAQ v. II) calculates a leisure-time physical activity (LTPA). The energy expenditure rates were calculated weekly in metabolic equivalents per hour/week (T-LPTA-MET/H/W), as previously reported [53].

Assessment of cognitive abilities

Instrument

Trained research assistants assessed the cognitive abilities of older adults at pre and post-supervised aerobic exercise using the Loewenstein Occupational Therapy Cognitive Assessment (LOTCA) battery. Assessments are required between 45 and 90 min. The LOTCA consists of seven main domains divided into 26 subtests, with each subtest scored on a four- or five-point Likert scale. The assessment of the LOTCA test was performed according to instruction manuals as reported in the literature [54]. In this study, the applied LOTCA test was valid for older adults with different ages as has been evaluated in recent studies [55,56,57,58,59]. Results are presented as a profile along with all subtests. A composite score for each domain was calculated by summing the scores of the relevant subtests. The LOTCA score was calculated by summing the score of all subtests. The maximum score on the test is 123, and the minimum score is 27. A higher score indicates better cognitive performance.

LOTCA test Validity

The test has excellent intra-rater reliability (100%) and good inter-rater reliability (86%), as well as criterion validity (78%) [60]. This LOTCA test was chosen because of its psychometric properties and primarily non-verbal nature, making it more suitable for evaluating the cognitive abilities of individuals from non-Western and non-English-speaking cultures. Several studies have used this instrument on Western and Arab populations [1, 60].

Assessment of dyslipidemia

All serum samples were taken from all participants in the morning following an overnight fast at pre and post-exercise training program for estimation of the following parameters;

Analysis of lipoprotein A and lipid profile

The Immunoassay ELISA technique was performed to measure lipoprotein A levels in the serum of participants pre- and post-exercise interventions using the DRG ELISA kit of Total Human Lipoprotein (A) (DRG International Inc., USA). The serum was analyzed for total cholesterol by the enzymatic (CHOD-PAP) colorimetric method and triglycerides by the enzymatic (GPO-PAP) method [49, 50]. HDL-Cholesterol estimated by precipitant method and LDL-Cholesterol by Friede wald formula (1972) [LDL-C = TC - HDL-C – (TG/5)] [61, 62].

Sample size calculation

In this study, the power of the sample size was estimated by using the G ∗ Power program for Windows (version 3.1.9.7). A sample comprising 150 of subjects was included in this study. Using the T-test and Wilcoxan signed-rank test with a significance level of 0.05, the total sample of 150 achieves a power of 95% with effective size d of 0.276, Df = 142.23, critical t = 1.655, and noncentrality -α = 3.305.

Statistical analysis

Statistical analysis was performed using SPSS version 17. The data were expressed as mean ± SD. The comparison and correlation of the studied parameters were investigated using both student’s t-test and Pearson’s correlation coefficient, respectively. Paired t-test was used for within-group comparison. The data was deemed to be significant at P-values < 0.05.

Results

A total of 150 healthy subjects were involved in this study. 67% of the sample was male (n = 100), and 70% of subjects were highly educated (n = 105). They are classified according to LOTCA test scores into a control group (n = 50) and a cognitive impairment group (n = 100). There was a significant difference in WHR (P = 0.05), LPTA (P = 0.001), and average LOTCA scores (P = 0.01) of exercise participants compared to the control group (Table 1).

Table 1 General characteristics of subjects
Full size table

This study showed a significant (P = 0.01) improvement in all LOTCA 7 -subsets variables among subjects following 24 weeks of moderate aerobic training compared to the pre-test, and the control group showed a slight improvement in LOTCA scores, as shown in Table (2). However, significant (P = 0.001) improvements in motor praxis, vasomotor organization, thinking operations, attention, and concentration were reported among older adults following 24 weeks of aerobic exercise. The data revealed positive significant correlations between the LOTCA scores of older subjects and their performance of cognitive abilities. Moreover, significant correlations were obtained between the older subjects in the motor praxis, vasomotor organization, thinking operations, attention and concentration domains of the LOTCA –scores, and their performance of a functional physical activity, as shown in Table (3).

Table 2 LOTCA scores in studied subjects following 24 weeks supervised aerobic training program (means ± SD)
Full size table
Table 3 Post training correlation analysis of lipid and lipoprotein (a) markers, and cognitive abilities (LOTCA scores) variables according to the level of leisure-time physical activity (LPTA-MET-H /week) after 24-week of exercise
Full size table

Lipid profile and lipoprotein (a) makers, cholesterol, TG, HDL-C, LDL-C, and Lipo (a) were estimated in this study. Paired t-test and independent t-test analysis showed that participants with cognitive impairments had abnormal basal levels of lipids and lipoprotein (a) makers compared with (p = 0.001) control groups (Table 4). Paired t-test analysis within groups showed a significant reduction in the levels of TG, LDL-C, and Lipo (a), along with an increase in the level of HDL-C in participants with cognitive impairment (p = 0.001) and control (p = 0.01) compared with baseline values following 24 weeks of moderate aerobic training as shown in Table (4). The data were significantly correlated with the physical fitness of the participants. Physical fitness scores were correlated negatively with the reduction in the levels of TG, LDL-C, and Lipo (a), and positively with the increase in the level of HDL-C (Table 3).

Table 4 Changes in the levels of lipid and lipoprotein (a) markers, and leisure-time physical activity (LTPA) score of participants pre- and Post- 24 weeks supervised aerobic training program (paired t-test analysis)
Full size table

Regarding LOTCA scores, the improvements in cognitive abilities among physically active participants were significantly correlated with the change in the levels of lipids and lipo(a) markers. Cognitive parameters were correlated negatively with TG, LDL-C, and lipo (a) and positively with increased HDL-C and aerobic fitness as measured by VO2 max (Table 5).

Table 5 Post training correlation coefficients among factors involved in Dyslipidemia and cognitive parameters (n = 100)
Full size table

Discussions

Physical activity as non-drug modulates consider one of the most promising strategies to prevent or improve cognitive disabilities among elderly populations [63]. It was reported that physically active people throughout their lives minimize the incidence rates of dementia and cognitive difficulties [64,65,66]. Whereas many studies reported a lower rate of cognitive disorders among subjects who participated in higher levels of physical activity interventions than persons with lower scores of physical activity [67, 68].

Recently, many research works revealed that moderate-intensity physical exercise produces remarkably higher levels of improvement in skills, mobility, and mood in both younger [69] and older adults [70]. However, little is known about whether the positive effect of moderate exercise on cognitive abilities occurs via modulating lipid profiles and lipoprotein (a).

Therefore, the current research aimed to investigate the probable correlation between anti-dyslipidemic mechanisms of exercise on cognitive abilities among one-hundred-fifty older adults who participated in a supervised aerobic training program for 24 weeks.

In the present study, the cognitive abilities of 150 older adults of the control and exercise groups were measured using LOTCA scores, a cognitive evaluation test of 7-subsets variables. In older subjects who participated in moderate aerobic exercise for 24 weeks, there was a significant improvement in cognitive performance via an increase in all LOTCA 7-subsets variables compared to the control group. The data revealed positive significant correlations between the total LOTCA scores of older subjects and their performance of cognitive abilities. Thus, the accuracy and evaluation of the LOTCA test support its use as a diagnostic tool for cognitive function, as previously reported [1].

Moreover, a significant positive correlation was obtained between the older subjects in the motor praxis, vasomotor organization, thinking operations, attention and concentration domains of the LOTCA –scores, and their performance of the functional physical activity. The data matched with others who suggested the strongest indication of physical exercise benefits cognition function via enhancing academic performance and psychological well-being [71, 72].

Similarly, our study was in accordance with recent studies that reported improvement in cognitive performance on a working memory task among younger and older adults following moderate-intensity cycling [73]. In addition, our study supported that the positive effects of physical exercise intervention rely on enhancing psychological well-being, cognitive functioning, and quality-of-life, especially in older subjects with mild cognitive impairment, as reported recently in literature [74,75,76].

The present study showed a slightly insignificant change in cognitive ability scores and lipid profile-related markers among the control group. This change may be due to low-intensity physical activity, such as routine daytime life, which accounts for most activity energy expenditure (AEE) in people who do not regularly exercise [77]. These activities may be useful in health outcomes such as cognitive impairment. This is indicated by other research work, which reported that older women identified a positive association between cognitive performance and total daytime movement, which suggests that total activity may be necessary for cognitive outcomes [78]. Cognitive impairment and other metabolic disorders like CVD and stroke are significantly interrelated in older subjects with dyslipidemia [16, 79, 80]. However, lipid-lowering therapies have demonstrated benefits in stroke prevention and prognosis [18, 57, 81, 82].

Lipid profile and lipoprotein (a) makers, cholesterol, TG, HDL-C, LDL-C, and Lipo (a) were estimated in this study. Paired t-test and student t-test analysis showed that participants with cognitive impairments had abnormal basal levels of lipids and lipoprotein (a) makers. The data matched many studies that reported a significant relationship between abnormal lipid profiles and a negative impact on cognition in old age [83,84,85,86,87].

Also, this study had a significant association between physical activity and cognitive impairment as measured by LOTCA scores. In physically active participants, there was a significant reduction in the levels of TG, LDL-C, and Lipo (a), along with an increase in the level of HDL-C and LOTCA scores with overall cognitive improvement status following 24 weeks of moderate aerobic training. The data aligned with many studies that performed the positive effects of physical exercise as anti-dyslipidemia modulates via a significant reduction in the levels of circulating lipids and apolipoproteins (apos) induced by regular physical exercise [88,89,90]. Thus, incorporating exercise as a non-drug modulator in subjects with abnormal lipid profiles has priority among many clinical trials [91, 92]. The association between biological and cognitive aging among older ages is greatly supported by the dynamic link between physical activity and cognitive functioning via changes in biological fluids related to cognitive domains [86, 93, 94].

In the present study, cognitive parameters correlated negatively with the reduction in TG, LDL-C, and lipo (a) and positively with the increase in HDL-C and aerobic fitness levels as measured by VO2 max. The data were consistence with other studies that reported the potential positive link of many physiological mediators, including lipid profiles and aerobic fitness as potential mediators in physical activity-cognition relationships [95], and that the improved cognition significantly correlated with the increase in aerobic fitness and reduction in the levels of lipid profile [94,95,96].

Finally, the data obtained showed that physical activity status, aerobic fitness, and lipid profile played a pivotal role in the cognitive performance of healthy older adults.

Conclusions

In conclusion, the study’s results indicate that engaging in moderate exercise for a duration of 24 weeks can lead to significant improvements in cognitive function among older individuals. These improvements were accompanied by positive changes in lipid profile and lipoprotein (a) markers. The findings revealed a strong correlation between cognitive performance and physical activity status and the regulation of lipids and lipo(a) markers. Specifically, physically active individuals demonstrated higher cognitive performance, reduced levels of total cholesterol, triglycerides, LDL cholesterol, and lipoprotein (a), as well as increased levels of HDL cholesterol and aerobic fitness (VO2 max) compared to sedentary participants. Cognitive performance was positively associated with increased aerobic fitness and HDL cholesterol while displaying negative associations with total cholesterol, triglycerides, LDL cholesterol, and lipoprotein (a). Notably, among older adults, significant improvements were observed in various aspects of cognitive function, including motor praxis, vasomotor organization, thinking operations, attention, and concentration. These findings highlight the importance of regular exercise for promoting cognitive health and lipid regulation in the aging population. Further research in this field can provide additional insights into the mechanisms underlying the relationship between exercise, cognitive function, and lipid metabolism, leading to the development of targeted interventions for optimizing brain health in aging populations.

Data availability

All the data generated or analyzed during this study are included in this published article.

References

  1. Josman N, Abdallah TM, Engel-Yeger B. Using the LOTCA to measure cultural and sociodemographic effects on cognitive skills in two groups of children. Am J Occup Ther. 2011;65:29–37.

    Article  Google Scholar 

  2. Royall DR, Palmer R, Chiodo LK, PolkM J. Normal rates of cognitive change in successful aging: the freedom house study. J Int Neuropsychol Soc. 2005;11:899–909.

    Article  PubMed  Google Scholar 

  3. Cherry KE, Simmons-D’Gerolamo SS. Long-term effectiveness of spaced-retrieval memory training for older adults with probable Alzheimer’s disease. Exp Aging Res. 2005;31:261–89.

    Article  PubMed  Google Scholar 

  4. Derwinger A, Stigsdotter NA, MacDonald S, Backman L. Forgetting numbers in old age: strategy and learning speed matter. Gerontol 2005,51: 277–84.

  5. O’Hara R, Brooks JOIII, Friedman L, Schroder CM, Morgan KS, Kraemer HC. Long-term effects of mnemonic training in community-dwelling older adults. J Psychiatr Res. 2007;41(7):585–90.

    Article  PubMed  Google Scholar 

  6. Garde E, Mortensen EL, Krabbe K, et al. Relation between age-related decline in intelligence and cerebral white-matter hyperintensities in healthy octogenarians: a longitudinal study. Lancet. 2000;356:628–34.

    Article  PubMed  CAS  Google Scholar 

  7. De Groot JC, De Leeuw FE, Oudkerk M, et al. Periventricular cerebral white matter lesions predict rate of cognitive decline. Ann Neurol. 2002;52:335–41.

    Article  PubMed  Google Scholar 

  8. Dirnagl U, Iadecola C, Moskowitz MA. Pathobiology of ischaemic stroke: an integrated view. Trends Neurosci. 1999;22:391–7.

    Article  PubMed  CAS  Google Scholar 

  9. Miwa S, Beckman KB, Muller FL. Oxidative stress in aging. Totowa, NJ, USA: Humana; 2008.

    Book  Google Scholar 

  10. Paniz C, Bairros A, Valentini J, et al. The influence of the serumvitamin C levels on oxidative stress biomarkers in elderly women. Clin Biochem. 2007;40(18):1367–72.

    Article  PubMed  CAS  Google Scholar 

  11. Simen AA, Bordner KA, Martin MP, Moy LA, Barry LC. .Cognitive dysfunction with aging and the role of inflammation. Therapeutic Adv Chronic Disease. 2011;2(3):175–95.

    Article  Google Scholar 

  12. Notkola IL, Sulkava R, Pekkanen J, Erkinjuntti T, Ehnholm C, Kivinen P, Tuomilehto J, Nissinen A. Serum total cholesterol, apolipoprotein E epsilon 4 allele, and Alzheimer’s disease. Neuroepidemiology. 1998;17:14–20.

    Article  PubMed  CAS  Google Scholar 

  13. Roher AE, Kuo YM, Kokjohn KM, Emmerling MR, Gracon S. Amyloid and lipids in the pathology of Alzheimer disease. Amyloid. 1999;6:136–45.

    Article  PubMed  CAS  Google Scholar 

  14. Kivipelto M, Helkala EL, Laakso MP, et al. Midlife vascular risk factors and Alzheimer’s disease in later life: longitudinal, population based study. BMJ. 2001;322:1447–51.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  15. van Exel E, de Craen AJ, Gussekloo J, et al. Association between high-density lipoprotein and cognitive impairment in the oldest old. Ann Neurol. 2002;51:716–21.

    Article  PubMed  Google Scholar 

  16. Lesser G, Kandiah K, Libow LS, et al. Elevated serum total and LDL cholesterol in very old patients with Alzheimer’s disease. Dement Geriatr Cogn Disord. 2001;12:138–45.

    Article  PubMed  CAS  Google Scholar 

  17. Yaffe K, Barrett-Connor E, Lin F, Grady D. Serum lipoprotein levels, statin use, and cognitive function in older women. Arch Neurol. 2002;59:378–84.

    Article  PubMed  Google Scholar 

  18. Sparks DL, Sabbagh MN, Connor DJ, et al. Atorvastatin for the treatment of mild to moderate Alzheimer disease: preliminary results. Arch Neurol. 2005;62:753–7.

    Article  PubMed  Google Scholar 

  19. Urakami K, Wada-Isoe K, Wakutani Y, et al. Lipoprotein (a) phenotypes in patients with vascular dementia. Dement Geriatr Cogn Disord. 2000;11:135–8.

    Article  PubMed  CAS  Google Scholar 

  20. Matsumoto T, Fujioka T, Saito E, Yasugi T, Kanmatsuse K. Lipoprotein(a) as a risk factor for cerebrovascular disease and dementia. Nutr Metab Cardiovasc Dis. 1995;5:17–22.

    Google Scholar 

  21. Firozeh Z, Bijeh N, Atri EA, Ramazani S. Effect of 8week walking program on serum lipoprotein (a) concentration in nonathlete menopausal women. J Gorgan Univ Med Sci. 2011;13:30–8.

    Google Scholar 

  22. Almeida DR, Prado ES, Melo LA, Oliveira AC. Lipoprotein (A) and body mass in mice which were submitted to hypercholesterolemia strength and aerobic physical trainings. Fit Perform J. 2008;7:137–44.

    Article  Google Scholar 

  23. Yang B, Wang S. Meta-Analysis on Cognitive Benefit of Exercise after Stroke. Complexity. 2021 Apr 7; 2021:5569346.

  24. Ma Y, Luo J, Wang XQ. The effect and mechanism of exercise for post-stroke pain. Front Molec Neurosci. 2022 Dec;2:15:1074205.

  25. Anjos JM, Neto MG, Dos Santos FS, Almeida KDO, Bocchi EA, Lima Bitar YDS, et al. The impact of high-intensity interval training on functioning and health-related quality of life in post-stroke patients: a systematic review with meta-analysis. Clin Rehabil. 2022 Jun;36(6):726–39.

  26. Pang MYC, Charlesworth SA, Lau RWK, Chung RCK. Using Aerobic Exercise to Improve Health outcomes and Quality of Life in Stroke: evidence-based Exercise prescription recommendations. Cerebrovasc Dis. 2013;35(1):7–22.

    Article  PubMed  Google Scholar 

  27. Kendall BJ, Gothe NP. Effect of Aerobic Exercise interventions on mobility among stroke patients a systematic review. Am J Phys Med Rehabil. 2016 Mar;95(3):214–24.

  28. Tiozzo E, Youbi M, Dave K, Perez-Pinzon M, Rundek T, Sacco RL et al. Aerobic, resistance, and Cognitive Exercise Training Poststroke. Stroke 2015 Jul; 46(7):2012–6.

  29. Ploughman M, Kelly LP. Four birds with one stone? Reparative, neuroplastic, cardiorespiratory, and metabolic benefits of aerobic exercise poststroke. Curr Opin Neurol. 2016 Dec;29(6):684–92.

  30. Johansson BB, Ohlsson AL. Environment, social interaction, and physical activity adeterminants of functional outcome after cerebral infarction in the rat. Exp Neurol. 1996;139:322–7.

    Article  PubMed  CAS  Google Scholar 

  31. Trejo JL, Carro E, Torres-Aleman I. Circulating insulin-like growth factor I mediates exercise-induced increases in the number of new neurons in the adult hippocampus. J Neurosci. 2001;21:1628–34.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  32. Kim SE, Ko IG, Park CY, Shin MS, Kim CJ, Jee YS. Treadmill and wheel exercise alleviate lipo poly saccharide induced shortterm memory impairment by enhancing neuronal maturation in rats. Mol Med Rep. 2013;7:31–6.

    Article  PubMed  CAS  Google Scholar 

  33. Sung YH, Kim SC, Hong HP, et al. Treadmill exercise ameliorates dopaminergic neuronal loss through suppressing microglial activation in Parkinson’s disease mice. Life Sci. 2012;91:1309–16.

    Article  PubMed  CAS  Google Scholar 

  34. Baek SS, Jun TW, Kim KJ, Shin MS, Kang SY, Kim CJ. Effects of postnatal treadmill exercise on apoptotic neuronal cell death and cell proliferation of maternal separated rat pups. Brain Dev. 2012;34:45–56.

    Article  PubMed  Google Scholar 

  35. Kim DH, Ko IG, Kim BK, et al. Treadmill exercise inhibits traumatic brain injury induced hippocampal apoptosis. Physiol Behav. 2010a;101:660–5.

    Article  PubMed  CAS  Google Scholar 

  36. Seo TB, Kim BK, Ko IG, et al. Effect of treadmill exercise on Purkinje cell loss and a strocytic reaction in the cerebellum after traumatic brain injury. Neurosci Lett. 2010;481:178–82.

    Article  PubMed  CAS  Google Scholar 

  37. Kim SE, Ko IG, Kim BK, et al. Treadmill exercise prevents aging induced failure of memory through an increase in neurogenesis and suppression of apoptosis in rat hippocampus. Exp Gerontol. 2010b;45:357–65.

    Article  PubMed  Google Scholar 

  38. Caprara M, Molina MA, Schettini R, et al. Active aging promotion: results from the vital aging program. Curr Gerontol Geriatric Res. Article 2013;817813. https://doi.org/10.1155/2013/817813.

  39. Archer T, Garcia D. Physical exercise influences academic performance and well-being in children and adolecents. Int J School Cogn Psychol. 2014;1(e102). DOI10.4172/1234-3425.1000e102.

  40. Archer T. Influence of physical exercise on traumatic brain injury deficits: scaffolding effect. Neurotox Res. 2013;21:418–34. https://doi.org/10.1007/s12640-011-9297-0.

    Article  Google Scholar 

  41. Fredriksson A, Stigsdotter IM, Hurtig A, Ewalds-Kvist B, Archer T. Running wheel activity restores MPTP-induced deficits. J Neural Transm. 2011;118:407–20. https://doi.org/10.1007/s00702-010-0474-8.

    Article  PubMed  CAS  Google Scholar 

  42. Rosamond W, Flegal K, Furie K. Heart disease and stroke statistics—2008 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation. 2008;117:25–146.

    Google Scholar 

  43. Kelley GA, Kelley KS. Aerobic exercise and lipids and lipoproteins in men: a meta-analysis of randomized controlled trials. J Mens Health Gend. 2006;3:61–70.

    Article  PubMed  PubMed Central  Google Scholar 

  44. Kelley GA, Kelley KS, Tran Z. Aerobic exercise and lipids and lipoproteins in women: a meta-analysis of randomized controlled trials. J Womens Health. 2004;13:1148–64.

    Article  Google Scholar 

  45. Tall A. Exercise to reduce cardiovascular risk: how much is enough? N Eng J Med. 2002;347:1522–25.

    Article  Google Scholar 

  46. Crouse SF, O’Brien BC, Grandjean PW, Lowe RC, Rohack JJ, Green JS. Effects of training and a single session of exercise on lipids and apolipoproteins in hypercholesterolaemic men. J App Physiol. 1997;83:2019–28.

    Article  CAS  Google Scholar 

  47. Palomo T, Beninger RJ, Kostrzewa RM, Archer T. Affective status in relation to impulsiveness, motor and motivational symptoms: personality, development and physical exercise. Neurotox Res. 2008;14:151–68. https://doi.org/10.1007/BF03033807.

    Article  PubMed  Google Scholar 

  48. Garcia D, Archer T, Moradi S, Andersson-Arnten A-C. Exercise frequency, high activation positive affectivity, and psychological well-being: beyond age, gender, and occupation. Psychology. 2012;3:328–36. https://doi.org/10.4236/psych.2012.34047.

    Article  Google Scholar 

  49. Karvonen M, Kentala K, Mustala O. The effects of training heart rate: a longitudinal study. Ann Med Exp Biol Fenn. 1957;35:307–15.

    PubMed  CAS  Google Scholar 

  50. So WY, Choi DH. Effects of walking and resistance training on the bodycomposition, cardiorespiratory function, physical fitness and blood profiles of middle-aged obese women. Exer Sci. 2007;16:85–94.

    Google Scholar 

  51. ACSM. ACSM’s guidelines for Exercise Testing and prescription by American College of Sports Medicine. 8th ed. Lippincott Williams & Wilkins; 2009.

  52. Guezenne CY, Satabin P, Legrand H, BigardI AX. Physical performance and metabolic changes induced by combined prolonged exercise and different energy intakes in humans. Eur J Appl Physiol. 1994;68:525–30.

    Article  Google Scholar 

  53. Ainsworth BE, Haskell WL, Whitt MC, et al. Compendium of physical activities: an update of activity codes and MET intensities. Med Sci Sports Exerc. 2000;32:S498–504.

    Article  PubMed  CAS  Google Scholar 

  54. Almomani F, Josman N, Almomani MO, et al. Factors related to cognitive function among elementary school children. Scand J Occup Ther. 2014;21:191–8.

    Article  PubMed  Google Scholar 

  55. Alghadir AH, Gabr SA, Al-Momani M, Al-Momani F. Moderate aerobic training modulates cytokines and cortisol profiles in older adults with cognitive abilities. Cytokine. 2021;138:155373. https://doi.org/10.1016/j.cyto.2020.155373. Epub 2020 Nov 25. PMID: 33248912.

    Article  PubMed  CAS  Google Scholar 

  56. Alghadir AH, Gabr SA, Al-Eisa ES. Effects of Moderate Aerobic Exercise on cognitive abilities and Redox state biomarkers in older adults. Oxid Med Cell Longev. 2016;2016:2545168. https://doi.org/10.1155/2016/2545168. Epub 2016 Apr 18. PMID: 27195073; PMCID: PMC4852338.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  57. Alghadir AH, Gabr SA, Almomani M, Almomani F, Tse C. Adiponectin and nitric Oxide Deficiency-Induced Cognitive Impairment in Fatigued Home-Resident in mature and older adults: a case-control study. Pain Res Manag. 2022;2022:7480579. https://doi.org/10.1155/2022/7480579.

    Article  PubMed  PubMed Central  Google Scholar 

  58. Alghadir AH, Gabr SA, Al-Eisa ES. Assessment of the effects of glutamic acid decarboxylase antibodies and trace elements on cognitive performance in older adults. Clin Interv Aging. 2015;10:1901–7. https://doi.org/10.2147/CIA.S95974.

    Article  PubMed  PubMed Central  CAS  Google Scholar 

  59. Khalafi M, Akbari A, Symonds ME, Pourvaghar MJ, Rosenkranz SK, Tabari E. Influence of different modes of exercise training on inflammatory markers in older adults with and without chronic diseases: a systematic review and meta-analysis. Cytokine. 2023;169:156303. https://doi.org/10.1016/j.cyto.2023.156303.

    Article  PubMed  CAS  Google Scholar 

  60. Itzkovich M, Elazar B, Averbuch S. Loewenstein Occupational Therapy Cognitive Assessment (LOTCA) manual. 2nd ed. Printed in USA, Occupational Therapy Department, Loewenstein Rehabilitation Hospital. Israel: Maddac; 2000.

  61. Allain CC, Poon IS, Chan CHG, Richmond W. Enzymatic determination of serum total cholesterol. Clin Chem. 1974;20:470–1.

    Article  PubMed  CAS  Google Scholar 

  62. Jacobs NJ, Van Denmark PJ. Enzymatic determination of serum triglyceride. Biochem Biophys. 1960;88:250–5.

    Article  CAS  Google Scholar 

  63. Gordon T, Gordon M. Enzymatic method to determine the serum HDL-cholesterol. Am J Med. 1977;62:707–8.

    Article  PubMed  CAS  Google Scholar 

  64. Friedewald WT, Levy RI, Fredrickson DS. Estimation of the concentration of LDL-cholesterol. Clin Chem. 1972;18(6):499–515.

    Article  PubMed  CAS  Google Scholar 

  65. Middleton LE, Yaffe K. Promising strategies for the prevention of dementia. Arch Neurol. 2009;66(10):1210–5.

    Article  PubMed  PubMed Central  Google Scholar 

  66. Rovio S, Ka°reholt I, Helkala EL, et al. Leisure-time physical activity at midlife and the risk of dementia and Alzheimer’s disease. Lancet Neurol. 2005;4(11):705–11.

    Article  PubMed  Google Scholar 

  67. Larson EB, Wang L, Bowen JD, et al. Exercise is associated with reduced risk for incident dementia among persons 65 years of age and older. Ann Intern Med. 2006;144(2):73–81.

    Article  PubMed  Google Scholar 

  68. Rockwood K, Middleton L. Physical activity and the maintenance of cognitive function. Alzheimers Dement. 2007;3(2):S38–44.

    PubMed  Google Scholar 

  69. Yaffe K, Barnes D, Nevitt M, Lui LY, Covinsky K. A prospective study of physical activity and cognitive decline in elderly women: women who walk. Arch Intern Med. 2002;161(14):1703–8.

    Article  Google Scholar 

  70. Lytle ME, Vander Bilt J, Pandav RS, Dodge HH, Ganguli M. Exercise level and cognitive decline: the MoVIES project. Alzheimer Dis Assoc Disord. 2004;18(2):57–64.

    Article  PubMed  Google Scholar 

  71. Barnett F. The effect of exercise on affective and self-efficacy responses in older and younger women. J Phys Act Health. 2013;10:97–105.

    Article  PubMed  Google Scholar 

  72. Martins R, Coelho E, Silva M, Pindus D, Cumming S, Teixeira A, Verissimo M. Effects of strength and aerobic-based training on functional fitness, mood and the relationship between fatness and mood in older adults. J Sports Med Phys Fitness. 2011;51:489–96.

    PubMed  CAS  Google Scholar 

  73. Archer T, Garcia D. Physical exercise influences academic performance and well-being in children and adolecents. Int J School Cogn Psychol. 2014;1(e102). https://doi.org/10.4172/1234-3425.1000e102.

  74. Dunton GF, Huh J, Leventhal AM, et al. Momentary assessment of affect, physical feeling states, and physical activity in children. Health Psychol. 2014;33(3):255–63. https://doi.org/10.1037/a0032640.

    Article  PubMed  Google Scholar 

  75. Hogan CL, Mata J, Carstensen LL. Exercise holds immediate benefits for affect and cognition in younger and older adults. Psychol Aging. 2013;28:587–94. https://doi.org/10.1037/a0032634.

    Article  PubMed  PubMed Central  Google Scholar 

  76. Caprara M, Molina MA, Schettini R et al. Active aging promotion: results from the vital aging program. Curr Gerontol Geriatric Res 2013 Article 817813 https://doi.org/10.1155/2013/817813

  77. Gates N, Valenzuela M, Sachdev PS, Fiatarone, Singh MA. Psychological well-being in individuals with mild cognitive impairment. Clin Interv Aging. 2014;9:779–92. https://doi.org/10.2147/CIA.S58866.

    Article  PubMed  PubMed Central  Google Scholar 

  78. Donahoo WT, Levine JA, Melanson EL. Variability in energy expenditure and its components. Curr Opin Clin Nutr Metab Care. 2004;7(6):599–605.

    Article  PubMed  Google Scholar 

  79. Barnes DE, Blackwell T, Stone KL, Goldman SE, Hillier T, Yaffe K. Study of osteoporotic fractures. Cognition in older women: the importance of daytime movement. J Am Geriatr Soc. 2008;56(9):1658–64.

    Article  PubMed  PubMed Central  Google Scholar 

  80. Tirschwell DL, Smith NL, Heckbert SR, et al. Association of cholesterol with stroke risk varies in stroke subtypes and patient subgroups. Neurology. 2004;63:1868–75.

    Article  PubMed  CAS  Google Scholar 

  81. Alvarez-Sabin J, Huertas R, Quintana M, et al. Prior statin use may be associated with improved stroke outcome after tissue plasminogen activator. Stroke. 2007;38:1076–8.

    Article  PubMed  CAS  Google Scholar 

  82. Amarenco P, Labreuche J. Lipid management in the prevention of stroke: review and updated meta-analysis of statins for stroke prevention. Lancet Neuro. 2009;l8:453–63.

    Article  Google Scholar 

  83. Laukka EJ, Fratiglioni L, Backman L. The influence of vascular disease on cognitive performance in the preclinical and early phases of Alzheimer’s disease. Dement Geriatr Cogn Disord. 2010;29:498–503.

    Article  PubMed  CAS  Google Scholar 

  84. Alonso A, Jacobs DR Jr., Menotti A, et al. Cardiovascular risk factors and dementia mortality: 40 years of follow-up in the Seven Countries Study. J Neurol Sci. 2009;280:79–83.

    Article  PubMed  Google Scholar 

  85. Martins IJ, Hone E, Foster JK, et al. Apolipoprotein E, cholesterol metabolism, diabetes, and the convergence of risk factors for Alzheimer’s disease and cardiovascular disease. Mol Psychiatry. 2006;11:721–36.

    Article  PubMed  CAS  Google Scholar 

  86. Amarenco P, Labreuche J, Touboul PJ. High-density lipoproteincholesterol and risk of stroke and carotid atherosclerosis: a systematic review. Atherosclerosis. 2008;196:489–96.

    Article  PubMed  CAS  Google Scholar 

  87. Stein RA, Michielli DW, Glantz MD, Sardy H, Cohen GAN, Brown CD. Effects of different exercise training intensities on lipoprotein cholesterol fractions in healthy middle-aged men. Am Heart J. 1990;119:277–83.

    Article  PubMed  CAS  Google Scholar 

  88. Wood PD, Stefanick ML, Dreon DM, et al. Changes in plasma lipids and lipoproteins in overweight men during weight loss through dieting as compared with exercise. N Engl J Med. 1988;319:1173–9.

    Article  PubMed  CAS  Google Scholar 

  89. Durstine JL, Haskell WL. Effects of exercise training on plasma lipids and lipoproteins. In: Exercise and Sport Sciences Reviews, edited by Holloszy JO. Baltimore, MD: Williams &Wilkins, 1994, 477–521.

  90. Fletcher G, Blair S, Blumenthal J, et al. Benefits and recommendations for physical activity programs for all americans. A statement for health professionals by the Committee on Exercise and Cardiac Rehabilitation of the Council on Clinical Cardiology, American Heart Association. Circulation. 1992;86:340–4.

    Article  PubMed  CAS  Google Scholar 

  91. National Cholesterol Education Program. Second report of the Expert Panel on detection, evaluation, and treatment of high blood cholesterol in adults. Washington, DC: US Department of Health and Human Services, National Institutes of Health; 1993. (Report no. 93–3095: O-1-R-32).

    Google Scholar 

  92. MacDonald SW, DeCarlo CA, Dixon RA. Linking biological and cognitive aging: toward improving characterizations of developmental time. Journals Gerontol. 2011;66(1):i59–70.

    Article  Google Scholar 

  93. Spirduso W, Poon LW, Chodzko-Zaiko W. Using resources and reserves in an exercise-cognition model. In Exercise and Its Mediating Effect on Cognition. Spirduso, W.;Poon, L.W.; Chodzko-Zaiko,W.; Eds., Human Kinetics, Champaign, Ill, USA, 2008.

  94. Etnier JL. Interrelationships of exercise, mediator variables, and cognition, in Aging, Exercise and Cognition Series: Vol 2 Exercise and Its Mediating Effects on Cognition. Spirduso, W.W.; Chodzko-Zajko, W.; Poon, L.W.; Eds., pp. 13–32, Human Kinetics, Urbana-Champaign, Ill, USA, 2008.

  95. Colcombe S, Kramer AF. Fitness effects on the cognitive function of older adults: a meta-analytic study. Psychol Sci. 2003;14(2):125–30.

    Article  PubMed  Google Scholar 

  96. Etnier JL, Nowel PM, Landers DM, Sibley BA. Ameta-regression to examine the relationship between aerobic fitness and cognitive performance. Brain Res Rev. 2006;52(1):119–30.

    Article  PubMed  Google Scholar 

Download references

Acknowledgements

The authors are grateful to the Researchers Supporting Project number (RSP2024R382), King Saud University, Riyadh, Saudi Arabia for funding this research.

Funding

Researchers Supporting Project number (RSP2024R382), King Saud University, Riyadh, Saudi Arabia.

Author information

Authors and Affiliations

  1. Department of Rehabilitation Sciences, College of Applied Medical Sciences, King Saud University, P.O. Box 10219, Riyadh, 11433, Saudi Arabia

    Ahmad H. Alghadir, Sami A. Gabr & Amir Iqbal

Authors
  1. Ahmad H. Alghadir
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Sami A. Gabr
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. Amir Iqbal
    View author publications

    You can also search for this author in PubMed Google Scholar

Contributions

Conceptualization, A.H.A. S.A.G and A.I; Data curation, S.A.G and A.H.A; Formal analysis and interpretation, S.A.G and A.I; Methodology, S.A.G; Project administration, A.H.A.; Supervision, A.H.A.; Writing – original draft, A.H.A. S.A.G and A.I; Writing – review & editing, S.A.G and A.I. All authors read, understood, and approved the final manuscript version to be published.

Corresponding author

Correspondence to Amir Iqbal.

Ethics declarations

Ethics approval and consent to participate

The study was performed according to the ethical guidelines of the 2013 Declaration of Helsinki, the study protocol was reviewed and approved by the Ethics Sub-Committee, King Saud University, Kingdom of Saudi Arabia, under file number ID: RRC-2014-011. Before data collection, written informed consent was obtained from all participating patients.

Consent for publication

Not applicable.

Competing interests

The authors declare no competing interests.

Additional information

Publisher’s Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Rights and permissions

Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by-nc-nd/4.0/.

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Alghadir, A.H., Gabr, S.A. & Iqbal, A. Enhancing cognitive performance and mitigating dyslipidemia: the impact of moderate aerobic training on sedentary older adults. BMC Geriatr 24, 678 (2024). https://doi.org/10.1186/s12877-024-05276-8

Download citation

  • Received:

  • Accepted:

  • Published:

  • DOI: https://doi.org/10.1186/s12877-024-05276-8

Keywords

BMC Geriatrics

ISSN: 1471-2318

Contact us