Ejercicio y flujo cerebral
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Ejercicio y flujo cerebral
- 1. EJERCICIO Y FLUJO CEREBRAL José López Chicharro Universidad Complutense de Madrid España
- 2. Ejercicio y flujo cerebral 750 ml/min 15% GC
- 3. Ejercicio y flujo cerebral Autorregulación cerebral Flujo de sangre cerebral Presión arterial pCO2 Gasto cardiaco Actividad simpático-adrenal pO2
- 4. Ejercicio y flujo cerebral Valoración del flujo de sangre cerebral Inhalación de óxido nítrico (N2O) Radioisótopos (133Xe)
- 5. Ejercicio y flujo cerebral Valoración del flujo de sangre cerebral Inhalación de óxido nítrico (N2O) Radioisótopos (133Xe) Doppler transcraneal
- 6. Ejercicio y flujo cerebral Valoración del flujo de sangre cerebral Inhalación de óxido nítrico (N2O) Radioisótopos (133Xe) Doppler transcraneal Tomografía por emisión de positrones
- 7. Ejercicio y flujo cerebral Flujo sanguíneo cerebral y ejercicio Flujo sanguíneo Intensidad - dependiente hasta 60% VO2max > 65% VO2max Flujo regional cortical Descenso rápido post-ejercicio
- 8. Ejercicio y flujo cerebral Regulación del flujo sanguíneo cerebral en ejercicio Querido y Sheel, 2007
- 9. Ejercicio y flujo cerebral Regulación del flujo sanguíneo cerebral en ejercicio Factores químicos Dióxido de carbono (*) (CO2 + H2O CO3H2 HCO3 - + H+) Oxígeno •(pCO2 + O2 efectos sumatorios) Población general: pO2 en ejercicio Atletas: pO2 en ejercicio función cognitiva
- 10. Ejercicio y flujo cerebral Regulación del flujo sanguíneo cerebral en ejercicio Factores cardiovasculares Presión arterial ( PAM Flujo cerebral) Gasto cardiaco • (GC perfusión cerebral)
- 11. Ejercicio y flujo cerebral Ogoh y col, 2005
- 12. Ejercicio y flujo cerebral Regulación del flujo sanguíneo cerebral en ejercicio Factores cardiovasculares Presión arterial ( PAM Flujo cerebral) Gasto cardiaco • (GC perfusión cerebral) Mecanorreceptores musculares
- 13. Ejercicio y flujo cerebral Regulación del flujo sanguíneo cerebral en ejercicio Factores metabólicos Glucosa (utilización glucosa – flujo cerebral ) Lactato • (lactato/piruvato – NADH/NAD+) Catecolaminas Temperatura
- 14. Ejercicio y flujo cerebral Regulación del flujo sanguíneo cerebral en ejercicio
- 15. Impact of a physical program on cerebral vasoreactivity in sedentary elderly people Davinia Vicente-Campos, Jesús Mora, José Castro-Piñero, Jose L González- Montesinos, Julio Conde-Caveda, José López Chicharro J Sports Med Phys Fitness 212 October : 52(5): 537-544
- 16. Impact of a physical program on cerebral vasoreactivity in sedentary elderly people Vicente-Campos y col, 2012 Ultrasonidos doppler transcraneal ( acetazolamida IV, CO2 inhalado) Hipercapnia por apnea (Ratnatunga y Adiseshiah, 1990) PaCO2 VD
- 17. Impact of a physical program on cerebral vasoreactivity in sedentary elderly people Vicente-Campos y col, 2012 Edad avanzada Flujo sanguíneo cerebral Velocidad flujo sanguíneo cerebral Volumen sanguíneo cerebral
- 18. Impact of a physical program on cerebral vasoreactivity in sedentary elderly people Ainslie y col, 2008
- 19. Impact of a physical program on cerebral vasoreactivity in sedentary elderly people Vicente-Campos y col, 2012 n= 33 (62-67 años) EXP, n=22, 12 mujeres CON,n=21, 13 mujeres 7 meses programa aeróbico 3-4 sesiones/semana; 50 min/sesión 70% FCmax Ultasonidos doppler transcraneal Flujo a. cerebral media Estímulo: hipercapnia e hipocapnia PA, Colesterol total HDL-C, Triglicéridos Test caminar (2,4 km)
- 20. Impact of a physical program on cerebral vasoreactivity in sedentary elderly people Vicente-Campos y col, 2012 50 55 60 65 70 75 80 EXP CON PRE POST VmcaBH(cm·s-1) Hemisferio izq. p=0,019
- 21. Impact of a physical program on cerebral vasoreactivity in sedentary elderly people Vicente-Campos y col, 2012 50 55 60 65 70 75 80 EXP CON PRE POST VmcaBH(cm·s-1) Hemisferio dcho.p=0,02
- 22. Impact of a physical program on cerebral vasoreactivity in sedentary elderly people DeSouza y col, 2000
- 23. Impact of a physical program on cerebral vasoreactivity in sedentary elderly people Vicente-Campos y col, 2012 60 65 70 75 80 85 90 95 100 EXP CON PRE POST Testmarcha(m·s-1) P<0,001
- 24. Impact of a physical program on cerebral vasoreactivity in sedentary elderly people Vicente-Campos y col, 2012 60 70 80 90 100 110 120 130 140 150 EXP CON PRE POST PAS(mmHg) P<0,001
- 25. Impact of a physical program on cerebral vasoreactivity in sedentary elderly people Vicente-Campos y col, 2012 60 65 70 75 80 85 90 95 100 105 110 EXP CON PRE POST PAD(mmHg) P<0,05
- 26. Impact of a physical program on cerebral vasoreactivity in sedentary elderly people Vicente-Campos y col, 2012 190 195 200 205 210 215 220 225 230 EXP CON PRE POST Colesterol(mg·dl-1) P<0,001
- 27. Impact of a physical program on cerebral vasoreactivity in sedentary elderly people Vicente-Campos y col, 2012 20 25 30 35 40 45 50 EXP CON PRE POST HDL-C(mg·dl-1) P<0,001
- 28. Impact of a physical program on cerebral vasoreactivity in sedentary elderly people Vicente-Campos y col, 2012 150 155 160 165 170 175 180 185 190 EXP CON PRE POST Triglicéridos(mg·dl-1) P<0,05
- 30. Eskes y col, 2010 Ejercicio y flujo cerebral Modelo de predicción del marcador global de función cognitiva 22% 12% 21%
- 31. Ejercicio y flujo cerebral
- 32. Brown y col, 2010 Ejercicio y flujo cerebral
- 33. Ejercicio y flujo cerebral
- 34. Ejercicio y flujo cerebral Cochrane Database of Systematic Reviews 2008, Issue 2. Art. No.: CD005381. DOI: 10.1002/14651858.CD005381.pub2.
- 35. Ejercicio y flujo cerebral FITNESS CARDIORRESPIRATORIO (VO2max) ACTIVIDAD FÍSICA GENÉTICA ENFERMEDADES Incidencia Enfermedades (cardiovasculares, ictus, diabetes, hipertensión) Mejora función cerebral (producción y eficiencia neurotransmisores, Angiogénesis, sinaptogénesis, neurogénesis ) FUNCIÓN COGNITIVA
- 36. Ejercicio y flujo cerebral http: //www.fisiologiadelejercicio.com José López Chicharro Universidad Complutense de Madrid España jlchicharro@enf.ucm.es
Notas del editor
- La irrigación cerebral es fundamentalmente soportada por 4 arterias: 2 carótidas y 2 vertebrales. Los dos sistemas proveen de cantidades similares de sangre a la circulación cerebral Las principales arterias convergen en el Polígono de Willis, permitiendo que el flujo se mantenga, incluso ocluyendo una arteria principal. Tres pares de arterias, anterior, posterior y media salen del Polígono de Willis, con ramas arteriales que perfunden diferentes partes de la corteza.
- La autorregulación cerebral es el mecanismo que permite mantener constante el flujo de sangre, independientemente de los cambios en la presión arterial
- Oxido nítrico. Se basa en el principio de que la cantidad de oxido nitrico que está en la circulación venosa es dependiente del volumen de sangre que fluye a través del cerebro. Radioisótopos. Mediante inhalación o inyección de un radioisótopo inerte, que posteriormente se monitoriza extracranealmente mediante sensores.
- Doppler transcraneal. Mide la velocidad del flujo de la sangre en una arteria principal de forma no invasiva. La medida es latido a latido, pudiendose tomar con indicador de la autorregulación cerebral.
- PET. la PET se basa en detectar y analizar la distribución tridimensional que adopta en el interior del cuerpo un radiofármaco de vida media ultracorta administrado a través de una inyección intravenosa
- Distintos estudios han observado, aumentos, disminuciones y no cambios en relación al flujo sanguineo cerebral y el ejercicio; no obstante, la mayor parte observa un aumento. El aumento inicial parece relacionado con un aumento del metabolismo cerebral. El descenso o retorno a niveles pre-ejercicio en alta intensidad, parece relacionado con la hiperventilación que induce un descenso de la pCO2. Linkis y col, midieron los aumentos de flujo de la a carótida anterior durante contracciones de la mano y pie derechos, observando un aumento de la velocidad de flujo sanguíneo, en la arteria cerebral media izquierda, así como en la carótida izquierda. Esto sugiere que el aumento del flujo es regional a las arterias que irrigan la representacion cortical de la extremidad ejercitante. El tiempo de medida del flujo es muy importante, ya que se ha observado un drástico descenso del flujo cerebral a los 5 s después de cesar el ejercicio dinámico.
- Los factores químicos (PCO2) parecen ser los más importantes. El CO2 difunde facil por la barrera hematoencefálica, disociandose en H+ y HCO3-. Se ha sugerido que es el H+ el responsable de los cambios en el diametro del vaso y resistencia vascular. Por tanto no es el CO2 el responsable directo de la dilatacion. Sin embargo, un aumento sanguíneo de H+ no causa necesariamente dilatacion de los vasos cerebrales ya que los H+ cruzan la barrera hematoencefalica muy lentamente. El mecanismo responsanble del cambio de diametro del vaso parece debido al efecto del H+ sobre el potencial transmembrana de las células del ms liso. Como ocurre en los vasos del músculo esquelético, el H+ provoca relajación de las células musculares lisas. OXÍGENO. La relación entre pO2 y el flujo cerebral es curvilineal o semi-logarítmica. Bajos pO2 causa VD (quizás por la via del estímulo en la secrección de adenosina, y posiblemente K, H y prostaglandinas),mientras que la hiperoxia puede causa VC cerebral. Gonzalez Alonso demostró que aunque el flujo cerebral disminuya en ejercicio máximo, la extracción de oxígeno tisular cerebral aumentó, esto implica que el cerbro se protege bien durante el ejercicio de alta intensidad.
- El flujo cerebral es dependiente de la presión arterial, presión venosa cerebral y presión intracraneal. PRESION ARTERIAL. Aunque el flujo cerebral permanece estable en el rango de autorregulación, se ha observado cambios del 6% por cada 10 mmHg en la PAM. La PAM juega un papel relevante en la regulación de l flujo cerebral en ejercicio. Una mayor PAM se corresponde con un aumento de la velocidad de flujo cerebral durante el ejercicio. Por otra parte, en ejercicio en ambiente caluroso, suele darse un descanso de la PAM, que se acompaña con un descenso en el flujo cerebral global. GASTO CARDIACO Es considerado como un factor importante en la regulación del flujo sanguíneo cerebral durante el ejercicio. Descensos y aumentos del GC, se corresponden con descensos y aumentos del flujo cerebral, respectivamente. En reposo, esta relación es más marcada que durante el ejercicio MECANORRECEPTORES MUSCULARES El simple acto del movimiento tambien produce aumento en el flujo cerebral, lo que permite suponer un papel importante de los mecanorreceptores en la regulación del flujo cerebral en ejercicio
- Figure 1. A summary of the linear relationships between ˙Q and FBF (A) or MCA Vmean (B) at rest (•) and during exercise ( ) Symbols denote actual group data for all subjects (means ± S.E.M.). The lines represent the linear regressions calculated from the group average data.
- El flujo cerebral es dependiente de la presión arterial, presión venosa cerebral y presión intracraneal. PRESION ARTERIAL. Aunque el flujo cerebral permanece estable en el rango de autorregulación, se ha observado cambios del 6% por cada 10 mmHg en la PAM. La PAM juega un papel relevante en la regulación de l flujo cerebral en ejercicio. Una mayor PAM se corresponde con un aumento de la velocidad de flujo cerebral durante el ejercicio. Por otra parte, en ejercicio en ambiente caluroso, suele darse un descanso de la PAM, que se acompaña con un descenso en el flujo cerebral global. GASTO CARDIACO Es considerado como un factor importante en la regulación del flujo sanguíneo cerebral durante el ejercicio. Descensos y aumentos del GC, se corresponden con descensos y aumentos del flujo cerebral, respectivamente. En reposo, esta relación es más marcada que durante el ejercicio MECANORRECEPTORES MUSCULARES El simple acto del movimiento tambien produce aumento en el flujo cerebral, lo que permite suponer un papel importante de los mecanorreceptores en la regulación del flujo cerebral en ejercicio
- GLUCOSA En condiciones de reposo el cerebro es casi totalmente dependiente de la glucosa para el metabolismo oxidativo. La utilización de la glucosa por el cerebro (difA-V (glucosa) disminuye al 30% VO2max, pero aumenta con la intensidad moderada de ejercicio (>60%VO2max), sugiriendo que la utilización de glucosa por el cerebro aumenta con la intensidad de ejercicio. La velocidad de flujo aumentó en ambas intensidades, lo que sugiere que el flujo sanguíneo cerebral y la utilización de glucosa no están relacionados. LACTATO El cerebro utiliza lactato como sustrato energetico. Parece existir una relacion entre el flujo cerebral y la relación lactato/piruvato. Parece que es la relación NADH/NAD la que provoca aumentos del flujo cerebral, PERO solo cuando los niveles de lactato sean elevados, no antes. CATECOLAMINAS Es pequeña ya que atraviesan muy dificilmente la barrera hematoencefálica. Sin embargo, a altas intensidades puede tener su influencia. TEMPERATURA La hipertermia disminuye el flujo cerebral, cuando se compara con un ejercicio en ambiente neutro. Parece explicarse por la hiperventilación, al disminuir la pCO2. No obstante, corrigiendo los valores de CO2, aun se observa una disminución del flujo, poniendo por tanto en riesgo al tejido cerebral. La temperatura tambien afecta al consumo de glucosa por el cerebro.
- GLUCOSA En condiciones de reposo el cerebro es casi totalmente dependiente de la glucosa para el metabolismo oxidativo. La utilización de la glucosa por el cerebro (difA-V (glucosa) disminuye al 30% VO2max, pero aumenta con la intensidad moderada de ejercicio (>60%VO2max), sugiriendo que la utilización de glucosa por el cerebro aumenta con la intensidad de ejercicio. La velocidad de flujo aumentó en ambas intensidades, lo que sugiere que el flujo sanguíneo cerebral y la utilización de glucosa no están relacionados. LACTATO El cerebro utiliza lactato como sustrato energetico. Parece existir una relacion entre el flujo cerebral y la relación lactato/piruvato. Parece que es la relación NADH/NAD la que provoca aumentos del flujo cerebral, PERO solo cuando los niveles de lactato sean elevados, no antes. CATECOLAMINAS Es pequeña ya que atraviesan muy dificilmente la barrera hematoencefálica. Sin embargo, a altas intensidades puede tener su influencia. TEMPERATURA La hipertermia disminuye el flujo cerebral, cuando se compara con un ejercicio en ambiente neutro. Parece explicarse por la hiperventilación, al disminuir la pCO2. No obstante, corrigiendo los valores de CO2, aun se observa una disminución del flujo, poniendo por tanto en riesgo al tejido cerebral. La temperatura tambien afecta al consumo de glucosa por el cerebro.
- The capacity of the cerebral arteries to modify their diameter and thus the blood supply to the brain is known as cerebral vasomotor reactivity or vasoreactivity. The aim of the present study was to determine the effect of a physical activity program on the hemodynamic response of the brain (vasoreactivity) in elderly people.
- Transcranial Doppler ultrasound (TCD) assesses changes in blood flow produced in the cerebral arteries, mainly the middle cerebral artery, in response to vasodilatory stimuli such as the intravenous administration of acetazolamide or inhaled carbon dioxide. The vasodilation induced in arterioles by these stimuli increases regional blood flow (Q) and diminishes the pressure gradient between arteries and arterioles. Assuming no changes in the caliber of the middle cerebral artery, the vasodilatory stimulus on the arteriole will determine its increased flow according to the equation Q = V x R2, where V is the velocity of flow and R is the vessel radius. This increase manifests as an increased mean blood flow velocity and a drop in the pulsatility index. The main shortcoming of both methods is that these substances have to be exogenously administered. In 1990, Ratnatunga and Adiseshiah (9) introduced a non-invasive method in which the vasodilatory stimulus was hypercapnia induced by breath-holding. When the subject holds his or her breath, this produces an increase in the partial pressure of arterial CO2 that is able to induce vasodilation
- During resting conditions, age-related decreases in cerebral blood flow (CBF), cerebral blood volume (7), and cerebral blood flow velocity in the basal intracerebral arteries (8) have been reported. Regular physical exercise has been associated with improved systemic function of the arterial endothelium reducing the rigidity of the arteries thereby diminishing the risk of arterial atherosclerotic disease in middle aged and older individuals (11-13). The results of several studies (14-16) have shown that regular endurance training and vigorous physical activity might also reduce the age-related increase in arterial stiffness observed among men. Mayhan et al. (17) examined the effects of exercise on the nitric oxide synthase dependent reactivity of cerebral blood vessels and concluded that exercise-induced activation of the nitric oxide biosynthetic pathway could be an important factor for preventing diabetes induced cerebrovascular abnormalities, possibly including stroke. Findings from a metaanalysis also establish the clear benefits of physical activity in terms of both reducing the incidence of stroke, and the mortality rate when stroke occurred (18).
- We examined how regular aerobic exercise affects the age-related decline in blood flow velocity in the middle cerebral artery (MCAv) in healthy humans. MCAv was consistently elevated by 9.1±3.3 cm s−1 (CI=2.7–15.6, P =0.006) in endurance-trained men throughout the age range. This ∼17% difference between trained and sedentary men amounted to an approximate 10 year reduction in MCAv ‘age’ and was robust to between-group differences in BMI and blood pressure. Regular aerobic-endurance exercise is associated with higher MCAv in men aged 18–79 years. The persistence of this finding in older endurance-trained men may therefore help explain why there is a lower risk of cerebrovascular disease in this population. Figure 1. Relationship between age, cerebral blood flow velocity and physical fitness The red line represents linear regression for the endurance-trained group. The blue line represents linear regression for the sedentary group. MCAv was consistently elevated by 9.1 ± 3.3 cm s−1 [CI = 2.7–15.6, P = 0.006 (∼17%)] in endurance-trained men throughout ageing.
- Methods: 18 men and 25 women (aged 62-67 years) were randomly assigned to an experimental (EXP, n=22, 12 women) and a control (CON, n=21, 13 women) group. Subjects in EXP group were required to complete a 7-month program based on aerobic training (3-4 sessions/weekd, 50 min/session, 3-4 sessions/week, at 70% maximum heart rate). Transcranial Doppler (TCD) ultrasound was used to examine the cerebral blood flow response to hypercapnic and hypocapnic stimuli. We also determined blood pressure, total serum cholesterol, HDL and LDL cholesterol, and triglycerides, and conducted an aerobic capacity test (the 2.4-Km walking test). Physical activity program The 7-month physical activity program was conducted in three stages (I, II, III). Over the first 5 weeks (stage I or adaptation stage), the intensity and duration of exercise sessions was stepped up from two weekly 15-min sessions to three weekly 60-min sessions. Heart rate was used to control the intensity of aerobic exercise during this period, starting at 50% the maximum heart rate and ending at 60%. Stage II comprised 24 sessions, three per week. Sessions commenced with a 12-15 min warm up (pacing, moving joints and muscle stretching). During a further 50 min, circuits including aerobic work, muscle strengthening exercises and coordination exercises were completed. The intensity increased gradually from 60 to 70%. During the 15 weeks of stage III, weekly exercise sessions increased from three to four, and one of these sessions was entirely devoted to aerobic work. This involved 50 min of sustained walking at a constant intensity of 70% maximum heart rate. The remaining sessions were as in stage II, though intensity was revised.
- First, we determined baseline mean blood flow velocity in the MCA (Vmca) after several minutes of normal respiration. At least 10 cardiac cycles were selected to obtain an average value. Next, the subject was instructed to take a deep breath and then hold his/her breath for as long as possible. The variables recorded were the time it took for the maximum increase in peak MCA velocity to occur (TVmax), peak velocity during breath holding (Vmca BH) and the pulsatility of flow during breath holding (Pulsat BH).
- this is the first study to show that long-term physical exercise improves the responsiveness of cerebral hemodynamics in elderly subjects. The most significant finding supporting such improved cerebral vasomotor reactivity was an increased blood flow velocity in the middle cerebral artery in both cerebral hemispheres produced in response to a hypercapnic stimulus (breath-holding). The mechanisms underlying the reduced endothelial-dependent vasodilatory capacity of older subjects have not been well established and it remains unclear whether the vasodilatory dysfunction associated with age is related to an agonist-specific defect or to a more general endothelial vasomotor deficiency
- Background—In sedentary humans endothelium-dependent vasodilation is impaired with advancing age contributing to their increased cardiovascular risk, whereas endurance-trained adults demonstrate lower age-related risk. We determined the influence of regular aerobic exercise on the age-related decline in endothelium-dependent vasodilation. Methods and Results—In a cross-sectional study, 68 healthy men 22 to 35 or 50 to 76 years of age who were either sedentary or endurance exercise–trained were studied. Forearm blood flow (FBF) responses to intra-arterial infusions of acetylcholine and sodium nitroprusside were measured by strain-gauge plethysmography. Among the sedentary men, the maximum FBF response to acetylcholine was 25% lower in the middle aged and older compared with the young group (P,0.01). In contrast, there was no age-related difference in the vasodilatory response to acetylcholine among the endurance-trained men. FBF at the highest acetylcholine dose was almost identical in the middle aged and older (17.361.3 mL/100 mL tissue per minute) and young (17.761.4 mL/100 mL tissue per minute) endurance-trained groups. There were no differences in the FBF responses to sodium nitroprusside among the sedentary and endurancetrained groups. In an exercise intervention study, 13 previously sedentary middle aged and older healthy men completed a 3-month, home-based aerobic exercise intervention (primarily walking). After the exercise intervention, acetylcholinemediated vasodilation increased '30% (P,0.01) to levels similar to those in young adults and middle aged and older endurance-trained men. Conclusions—Our results indicate that regular aerobic exercise can prevent the age-associated loss in endotheliumdependent vasodilation and restore levels in previously sedentary middle aged and older healthy men. This may represent an important mechanism by which regular aerobic exercise lowers the risk of cardiovascular disease in this population. (Circulation. 2000;102:1351-1357.) DeSouza et al. (12) showed that regular aerobic exercise can prevent the age-associated loss in endothelium-dependent vasodilation and restore levels in previously sedentary middle aged and older healthy men They suggest that impaired endothelium-dependent vasodilation may not be an inevitable consequence of biological aging. Rather, this dysfunction may be due, at least in part, to agerelated reductions in physical activity/aerobic fitness and associated increases in body fat. Moreover, they suggest that regular aerobic exercise may be an effective lifestyle intervention strategy for improving endothelial vasodilatory function. Specifically, 3 months of regular aerobic exercise (primarily walking) resulted in a 30% increase in endothelium-dependent vasodilation in sedentary middle aged and older men
- 2.4-Km walking test Table IV (Pre- and post-intervention values for variables determined in the experimental (n=22) and control (n=21) groups) provides the results of the cardiorespiratory resistance test, revealing significant increases in mean velocity in the EXP group (89.67±7.45 vs 95.32±8.90; p<0.001) but not the CON group.
- Our findings indicate that a 7-month physical activity program was able to improve indicators of cerebral vasoreactivity in both brain hemispheres in elderly people. This improvement translates to an improved capacity of the arterioles in the brain to dilate when confronted with an adverse stimulus in an effort to maintain a constant flow of cerebral perfusion. The novel idea that physical activity could be viewed as a treatment strategy to improve cerebral blood flow and thus reduce the risk of ischemic damage to the brain warrants further investigation. Perspectives Based of these findings, and from a practical point of view, a regular physical activity in sedentary ederly people might exert a protective effect on cerebrovascular health, improving cerebral blood flow and thus reduce the risk of ischemic damage.
- Studies of the effects of physical fitness on cognition suggest that exercise can improve cognitive abilities in healthy older adults, as well as delay the onset of age-related cognitive decline. The mechanisms for the positive benefit of exercise and how these effects interact with other variables known to influence cognitive function (e.g., involvement in cognitive activities) are less well understood. The current study examined the associations between the physical fitness, cerebrovascular blood flow regulation and involvement in cognitive activities with neuropsychological function in healthy post-menopausal women. Methods: Forty-two healthy women between the ages of 55 and 90 were recruited. Physical fitness (V˙O2 max), cerebrovascular reserve (cerebral blood flow during rest and response to an increase in end-tidal (i.e., arterial) PCO2), and cognitive activity (self-reported number and hours of involvement in cognitive activities) were assessed. The association of these variables with neuropsychological performance was examined through linear regression.
- Table 4 demonstrates that, with age and education entered as a first step, the model accounted for 22% of the variance. When fitness (V˙O2 max) was entered in the second step, an additional 12% of the variance was explained, with higher fitness associated with better cognitive performance (as reported by Brown et al. 2008). The number and duration of cognitive activities was entered in the third step and accounted for an additional 21% of the variance, with the final model having an R2 = 55% (F(5,34) = 8.15, p < 0.001). In the final model age and the number of cognitive activities were the only significant predictors, with age inversely and cognitive activities directly associated with better cognitive performance. previous research has shown that physical exercise increases levels of serum antioxidant proteins and a reduction in oxidative stress (Pialoux et al., 2009). These changes may lead to improvements in cognitive function, or at least they may help delay the cognitive declines associated with advancing age. Conclusions: Cognitive function in older adults is associated with multiple factors, including physical fitness, cerebrovascular health and cognitive stimulation. Interestingly, cognitive stimulation effects appear related more to the diversity of activities, rather than the duration of activity. Further examination of these relationships is ongoing in a prospective cohort study.
- The mechanisms by which aerobic fitness confers beneficial effects on cognition with aging are unclear but may involve cerebrovascular adaptations. In a cross-sectional study of women from the community (n = 42; age range = 50–90 years), we sought to determine whether physical fitness is associated with higher cerebrovascular function, and its relationship to cognition. Main outcome measures included resting cerebral blood flow, cerebrovascular reserve, physical fitness (i.e., V˙ O2max) and cognition.
- Relation between overall cognition, age and physical fitness. Overall cognitive score was derived by converting each domain score into a Z-score, and summing these, equally weighting each domain. Scores are performance relative to the entire cohort. Cognition has a negative relationship with age and is higher in young women. Cognition has a positive relationship with physical fitness and is higher in physically active and fit women. Error bars represent S.D. Abbreviation: VO2max, maximal oxygen consumption. Physically fit women had lower resting mean arterial pressure (MAP) and higher cerebrovascular conductance (CVC) than sedentary women. Overall cognition was negatively correlated with age and positively correlated with V˙ O2max. V˙ O2max was a predictor of resting CVC and MAP, and CVC and MAP when end-tidal gases were held constant at near-resting values. MAP and CVC were predictors of cognition. This study identified strong associations between physical fitness, vascular function and cognition, and provides new understanding regarding the mechanisms by which fitness positively impacts cognition with aging. The implications of this research are considerable and warrant future investigation.
- We provide a brief review of the extant research on the influence of cardiovascular fitness training on brain and cognition. The review includes an examination of the non-human animal literature that has reported molecular, cellular, and behavioral consequences of fitness interventions. We relate this literature to human studies of the relationship between fitness and cognition, as well as the nascent literature on fitness influences on human brain structure and function with state-of-the art neuroimaging techniques. We also consider the important topic of participant adherence in clinical exercise trials. Finally, we suggest future directions for studies of cardiovascular fitness, aging, and neurocognitive function.
- There is evidence that aerobic physical activities which improve cardiorespiratory fitness are beneficial for cognitive function in healthy older adults, with effects observed for motor function, cognitive speed, delayed memory functions and auditory and visual attention. However, the majority of comparisons yielded no significant results