Exercise and Cognition in Young Adults

Exercise had been proven to have a positive effect on physical, mental and cognitive functioning in varying populations. This study looks in to the effect of exercise on episodic memory, perceptual speed and executive function in young adults. Three cognitive tasks and academic performance were correlated with exercise in high school and in college. Results showed a positive correlation between exercise and perceptual speed and a negative correlation between exercise and episodic memory. These results were inconsistent with previous findings, however it is suggested that there is a neurobiological cause underlying the results. Additionally, the assumption that young adults are at the peak of their cognitive ability means that exercise will not cause cognitive abilities to be higher or lower compared to other young adults with more or less exercise. EXERCISE AND COGNITION 3 Literature Review Exercise has been proven to have beneficial effects on both physical health and mental health. Exercise is associated with improving balance, bone density, strength and endurance, as well as with helping to prevent cardiovascular disease, obesity, and blood pressure. These physical effects of exercise have been studied and seen to have an effect on muscles and organs that in turn modify and regulate the structure and functions of the brain (Dishman et al. 2006). In addition to physical aspects of health, exercise has also been associated with cognitive function. Specifically, it is seen as a viable prevention technique to various neurodegenerative diseases, such as Alzheimer’s disease (AD) and seen as a potential way to improve academic achievement, cognitive abilities, and intellectual function in children (Tomporowski et al. 2008). Cognition is a term that describes higher brain functions such as decision-making, calculating, problem solving, producing and using language, and memory. The purpose of the present study is to examine the effects of exercise on three facets of cognition. Studies looking at exercise and cognition have focused on individuals across the lifespan. However, research in this area has been very controversial with findings that range from exercise positively affecting cognition to findings that say exercise can actually do harm to cognitive function depending on the population and the type of exercise employed. Some have sought to uncover the specific brain processes and structures that are affected by exercise. The methodology of such studies are still in the early stage of research as technology and the ability to look at people’s brains as they function during cognitive tasks are relatively new. The current hypothesis was founded on the basis of neurogenesis, or the making of new neurons and the regulation of their growth by brain derived neurotrophic factor (BDNF) or some other neuronal growth hormone. Some animal studies have focused on studying the EXERCISE AND COGNITION 4 cellular and molecular mechanisms that underlie this phenomenon. In a study done on mice, 14 days of wheel running promoted memory acquisition, memory retention, and reversal learning increased the number of maturing neurons. Mice that had been exposed to the same regime, but sacrificed before the final memory tasks, had an increase in molecules associated with neurogenesis, suggesting that neurogenesis and memory seem to be associated (Van der Borght et al. 2007). Recently researchers have begun extending studies examining the effect of exercise on brain structures to human participants. The hippocampus is located in the medial temporal lobe of the brain and is involved in the consolidation of information from short-term memory to longterm memory. In rat studies, exercise enhances learning and improves retention, which is accompanied by increased cell proliferation and survival in the hippocampus (van Praag 2005). In a human study, done with 150 older adults, aerobic exercise increased the size of the anterior hippocampus leading to improvements in spatial memory. Increased hippocampal volume is also associated with greater serum levels of BDNF, a mediator of neurogenesis. The results also suggested that physical activity may act as a buffer and protect against hippocampal volume loss. Indeed, aerobic exercise training is effective at reversing hippocampal volume loss in late adulthood, which is accompanied by improved memory function (Erickson et al. 2011). The effect of not only exercise on memory but also other cognitive functions is an important field to continue to research, as cognitive function is important at every age, from preschool to the elderly. Bunce and Murden (2006), suggest that though there is a correlation between aerobic fitness and cognition, that association weakens with age. They speculate that fitness of the neuroanatomical structures are eventually overshadowed by neurological degeneration that occurs in 70+ years of age. An interesting application of this research is to EXERCISE AND COGNITION 5 Alzheimer’s Disease (AD). In a yearlong study, aerobic exercise was observed to stabilize the cognitive functioning in patients with AD. Individuals who walked at least 2h/week saw significant improvement in the Mini-Mental State Examination (MMSE), a questionnaire used to screen for cognitive impairment, whereas those who remained sedentary saw a decline in cognitive ability (Winchester 2013). Scarmeas et al. (2009) also observed that higher physical activity reduced the risk of AD. Researchers have sought to understand the mechanisms through which exercise may improve the symptoms of AD. The two primary diagnostic characteristics of AD include two different protein deposits in the brain, “tangles” and Amyloid β (Aβ) plaques. Both of these occur naturally with age; however AD patients develop far more of both types of proteins and also follow a particular pattern of development, beginning in important regions of the brain and spreading from there to other areas. Both protein structures are associated with the severity of AD the patient has; if there are more of these protein deposits, the progression of AD is more severe. “Tangles”, also known as neurofibrillary tangles, are an abnormal form of the microtubule-associated protein tau (Perl 2010). Tau on its own is a stabilizer for the microtubules in the neuron. The forms of tau that make up the tangles are hyperphosphorylated at specific sites. The pattern of their distribution starts in the deeper layers of the brain in the neocortex, entorhinal cortex, regions of the hippocampus and the amygdala and spread outward from there (Perl 2010). Amyloid β (Aβ) protein is derived from the larger amyloid precursor protein (APP). Normal cell functioning requires APP, which is normally used in Notch processing, a highly conserved cell signaling pathway found in most multicellular organisms that is involved in neurogenesis and neuron differentiation. However, when APP is processed Aβ peptides of EXERCISE AND COGNITION 6 varying lengths are produced between 37-49 amino acids. In a normal individual, the majority of Aβ produced are 40 amino acids in length (Aβ-40), only about 5-15% of the Aβ peptides are Aβ42. Both Aβ-40 and Aβ-42 are produced by a single Υ-secretase enzyme, a type of protease that cleaves APP (Feindeis 2007). Normally the clearance rate for these Aβ peptides is high and prevents a buildup. In an AD patient, the two main Aβ peptides found in the plaques in the brain are those of primarily Aβ-42 and smaller amounts of Aβ-40 (2007). The predominant and initial Aβ peptide deposited in the brain parenchyma is Aβ-42. These initial deposits are then able to seed the formation of both long (Aβ-42) and short (Aβ-40) forms of Aβ. In transgenic animal studies, deposits are associated with high levels of Aβ-42 and then later on Aβ-40 as seen in humans (2007). The aggregation of the insoluble Aβ peptides leads to neuronal toxicity and eventual cell death. Before the death of the neuron however, the Aβ peptides interrupt the neuronal cell function, which is what is seen in mild forms of AD. In particular long-term potentiation (LTP) is the first brain function to be interrupted. LTP is important in the formation of new memories and learning, explaining why plaque formation may be important in causing the early symptoms of AD (2007). From previous studies conducted, it is clear that exercise is beneficial to AD patients; however none of these studies examined the mechanism in the brain that drives the observed improvements or lack thereof. Recent evidence has been collected that determined Aβ plaques to be part of that mechanism. Adlard et al. (2005) used a mouse model of AD to test the hypothesis that long term voluntary exercise would impact the normal progression of AD-like neuropathology. They found that after 5 months of voluntary exercise levels Aβ-40 and Aβ-42 was significantly decreased in the cortex of the mice that were given running wheels (exercise) when compared to mice that did not get a running wheel (sedentary). It was suggested that Aβ EXERCISE AND COGNITION 7 degradation pathways were activated through exercise that may involve neuronal pathways known to regulate APP processing and be reflected in a decreased production of Aβ. In another study, they found that exercise training reduces Aβ-42 deposition in mice while their sedentary counterparts had a higher Aβ-42 deposition. From these findings, they concluded that exercise training could be used to prevent accumulation of the APP because it induces increased degradation and clearance of Aβ. On the other end of the age spectrum from those experiencing AD are children. The motivation for studying the effect of exercise on cognition in children is primarily to develop interventions that can be used in the classroom. A child who cannot effectively plan, inhibit impulsive behavior, update working memory, or shift tasks is going to be hard pressed to perform in a classroom se