The objective of this study was to examine the effects of physical exercise on parahippocampal function.
Studies were identified using electronic databases, including PubMed, PsychInfo, Sports Discus, and Google Scholar. In total, 28 articles met the inclusionary criteria. Among these, 20 were among humans and 8 in animal models. Among the 20 human studies that examined some aspects of the parahippocampal gyrus, 5 evaluated the entorhinal cortex and 1 evaluated the perirhinal cortex. Among the 20 human studies, 3 evaluated neural activity (or BOLD-signal changes), 14 evaluated brain volume (gray or white matter), 2 examined fractional anisotropy, 1 examined glucose metabolism, and 1 examined functional connectivity between the parahippocampal gyrus and a proximal brain tissue. Among the 8 animal studies, 4 evaluated the entorhinal cortex, with the other 4 examining the perirhinal cortex.
The results demonstrated that, among both animal and human models, exercise had widespread effects on parahippocampal function. These effects, included, for example, increased neural excitability in the parahippocampal gyrus, increased gray/white matter, reduced volume of lesions, enhanced regional glucose metabolism, increased cerebral blood flow, augmented markers of synaptic plasticity, and increased functional connectivity with other proximal brain structures.
Exercise appears to have extensive effects on parahippocampal function.
This review discusses the potential role that glial cells may play in influencing the relationship between exercise and episodic memory function. A narrative review methodology is employed. Herein, the different types of glial cells, their implications in subserving episodic memory function, and how exercise can modulate glial cell activity, particularly astrocyte functionality, are discussed. Although additional experimental work is needed, astrocytes appear to play an important role in the exercise–memory interaction. Exercise may increase astrocytic size, attenuate astrogliodegeneration, improve astrocytic aquaporin-4 expression, and increase astrocytic transporter levels. These effects, in turn, may help to increase the number of synapses that neurons form, increase the number of synaptic structures, and increase presynaptic function and postsynaptic receptor localization. Ultimately, these effects may help influence long-term potentiation and episodic memory function.
Emerging research demonstrates that exercise is favorably associated with several cognitive outcomes, including episodic memory function. The majority of the mechanistic work describing the underlying mechanisms of this effect has focused on chronic exercise engagement. Such mechanisms include, e.g., chronic exercise-induced neurogenesis, gliogenesis, angiogenesis, cerebral circulation, and growth factor production. Less research has examined the mechanisms through which acute (vs. chronic) exercise subserves episodic memory function. The purpose of this review is to discuss these potential underlying mechanisms, which include, e.g., acute exercise-induced (via several pathways, such as vagus nerve and muscle spindle stimulation) alterations in neurotransmitters, synaptic tagging/capturing, associativity, and psychological attention.
Prior research has evaluated the effects of acute exercise on episodic memory function. These studies have, on occasion, demonstrated that acute exercise may enhance both short- and long-term memory. It is uncertain as to whether the acute exercise improvements in long-term memory are a result of acute exercise attenuating declines in long-term memory, or rather, are driven by the enhancement effects of acute exercise on short-term memory. The present empirical study evaluates whether the decline from short- to long-term is influenced by acute exercise. This relationship is plausible as exercise has been shown to activate neurophysiological pathways (e.g., RAC1) that are involved in the mechanisms of forgetting.
To evaluate the effects of acute exercise on forgetting, we used data from 12 of our laboratory's prior experiments (N = 538). Across these 12 experiments, acute exercise ranged from 10 to 15 mins in duration (moderate-to-vigorous intensity). Episodic memory was assessed from word-list or paragraph-based assessments. Short-term memory was assessed immediately after encoding, with long-term memory assessed approximately 20-min later. Forgetting was calculated as the difference in short- and long-term memory performance.
Acute exercise (vs. seated control) was not associated with an attenuated forgetting effect (d = 0.10; 95% CI: −0.04, 0.25, P = 0.17). We observed no evidence of a significant moderation effect (Q = 6.16, df = 17, P = 0.17, I2 = 0.00) for any of the evaluated parameters, including study design, exercise intensity and delay period.
Across our 12 experimental studies, acute exercise was not associated with an attenuated forgetting effect. We discuss these implications for future research that evaluates the effects of acute exercise on long-term memory function.
No previous studies have evaluated the potential combined effects of acute exercise and acute hypoxia exposure on memory function, which was the purpose of this study. Twenty-five participants (Mage = 21.2 years) completed two laboratory visits in a counterbalanced order, involving 1) acute exercise (a 20-min bout of moderate-intensity exercise) and then 30 min of exposure to hypoxia (FIO2 = 0.12), and 2) exposure to hypoxia alone (FIO2 = 0.12) for 30 min. Following this, participants completed a cued-recall and memory interference task (AB/AC paradigm), assessing cued-recall memory (recall 1 and recall 2) and memory interference (proactive and retroactive interference). For cued-recall memory, we observed a significant main effect for condition, with Exercise + Hypoxia condition having significantly greater cued-recall performance than Hypoxia alone. Memory interference did not differ as a function of the experimental condition. This experiment demonstrates that engaging in an acute bout of exercise prior to acute hypoxia exposure had an additive effect in enhancing cued-recall memory performance.