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. 2016 Dec 29;595(1):7–8. doi: 10.1113/JP272761

Exercise becomes brain: sustained aerobic exercise enhances hippocampal neurogenesis

Tharmegan Tharmaratnam 1,, Robert A Civitarese 2, Tyler Tabobondung 3, Taylor A Tabobondung 4
PMCID: PMC5199726  PMID: 28035680

Chronic exercise has been shown to induce favourable adaptations in brain structure through the phenomenon of synaptic plasticity. These changes may attenuate age‐related declines in cognitive function and curtail the risk of neurodegenerative disease. Investigations of exercise‐induced neurogenesis have largely focused on endurance exercise. Particularly, these studies show endurance training is a potent stimulus in augmenting neurogenesis through neurotrophic factor‐mediated signalling. Less is known on whether other forms of exercise may elicit similar adaptations in brain structure and function. The optimal duration, intensity and type of exercise necessary to stimulate neurogenesis are also not well defined in the literature. Using an adult male rodent model, Nokia et al. (2016) recently implemented a 6–8 week training programme to examine whether high intensity interval training (HIT) and resistance training (RT) were comparable to aerobic exercise in stimulating adult hippocampal neurogenesis (AHN).

In experiment 1, Nokia et al. (2016) compared the effects on AHN of 7 weeks of HIT, consisting of 20 min of increased intensity exercise, with 7 weeks of voluntary aerobic exercise. HIT had a modest but non‐significant effect on AHN, whereas voluntary and sustained aerobic exercise enhanced AHN. In experiment 2, the authors then compared the effects on AHN of 6 weeks of RT, consisting of resistance ladder climbing, with 8 weeks of aerobic training on a motorized treadmill. Similar to the first experiment, AHN was significantly enhanced in the aerobic training group compared with the RT group. Finally, in their last experiment, the authors assessed whether 8 weeks of similar RT elicited benefits to AHN in comparison with sedentary controls (ST). Contrary to previous findings, RT did not elicit any changes in AHN compared with ST. Taken together, these findings support previous work suggesting that exercise modality, particularly aerobic exercise, is an important factor in exercise‐induced changes in hippocampal neurogenesis.

The novelty of this study lies in using a heterogeneous rodent model that demonstrated high and low responsiveness to aerobic exercise (HRT and LRT, respectively). This additional parameter accounts for the genetic disparities in the observed training response. HRT rats demonstrated a greater response to training in most modalities in comparison with LRT rats. Overall, this study revealed greater levels of AHN in HRT compared with LRT rats during aerobic exercise. This interesting finding suggests that there may be genetic factors influencing exercise‐induced benefits on AHN. Furthermore, despite low responsiveness to training, there were equivalent increases in maximal aerobic endurance in both HRT and LRT rat models. These findings suggest that aerobic training can improve overall endurance and induce physiological adaptations despite a genetically unfavourable profile for training responsiveness.

Nokia et al. (2016) were the first to investigate the relationship between HIT and AHN. The findings from postmortem neural tissue analysis demonstrate a trend towards an increase in neuronal cell density within the hippocampus. However, there was no statistically significant increase in AHN. This may be attributed to the short duration (20 min) and high intensity nature of the protocol. Significant changes in AHN may be expected with a longer training protocol. Furthermore, considering stress beyond optimal limits has deleterious effects on neurogenesis (Costa et al. 2015), reduced intensity training (i.e. alternating 50% of maximal aerobic capacity) may also promote more favourable changes in synaptic plasticity. While difficult to assess in rodents, an increasingly popular form of HIT is the use of circuit training, which incorporates both aerobic and resistance training. As such, exploring alternative forms of HIT is necessary to understand the potential benefits on AHN.

Nokia et al. (2016) demonstrate that aerobic exercise promotes hippocampal neurogenesis. This interesting finding could have benefited from assessing both younger (childhood/adolescent) and older animals. It is widely described that specific stressors influence neurogenesis in different ways depending on the period of time the stressor is introduced (Ortega‐Martínez, 2015). Multiple studies have shown that brain function is affected by different kinds of neural precursors and is regulated by gene expression at particular points in development (Ortega‐Martínez, 2015). Specifically, childhood and adolescence are characterized by significant hippocampal‐dependent functions, including learning and memory, spatial information processing, response to stress and cognitive performance (Rola et al. 2004). Furthermore, maintaining AHN is critical in old age to counteract the intellectual decline and disease‐related cognitive impairment in older adults (Costa et al. 2015). As such, exploring the effect of different exercise modalities (aerobic vs. resistance training) on early and late hippocampal neurogenesis would have provided increased insight into the benefits of exercise on the brain.

A pivotal conclusion from Nokia and colleagues (2016) was that increased AHN was dependent on the amount of aerobic exercise. To complement this finding, the authors could have explored whether extended cessation of aerobic exercise post‐training reversed the increase in AHN or whether this effect was sustained. Van der Borght et al. (2009) demonstrated that hippocampal neurogenesis was significantly elevated in mice after 10 days of aerobic exercise, but that this increase returned to baseline just 24 h after cessation of physical activity. Interestingly, Nishijima and colleagues (2013) demonstrated that cessation of physical activity after long‐term aerobic exercise training (8 weeks) in mice decreased hippocampal neurogenesis in comparison with sedentary mice, suggesting physical inactivity may impair a component of hippocampal neurogenesis. Collectively, these results suggest that exercise‐related improvements in AHN are dependent on continued exercise compliance. Given that compliance to physical activity remains a challenge for a significant portion of society, knowledge translation could have been improved by examining the short‐term vs. long‐term benefits of exercise on AHN.

The findings demonstrated by Nokia et al. (2016) may support the clinical utility of aerobic exercise for improving AHN in humans. Several studies have shown a link between hippocampal neurogenesis and adverse clinical manifestations, including depression, anxiety and cognitive impairment (Costa et al. 2015). Specifically, Alzheimer's disease (AD), the most common cause of dementia in the elderly, is characterized by altered hippocampal neurogenesis, which may account for some aspects of the cognitive decline in patients with AD (Costa et al. 2015). As such, preserving or enhancing hippocampal neurogenesis has been suggested to be a potential therapeutic strategy to delay or halt the cognitive decline in AD. Indeed, exercise has been shown to improve cognitive performance in rodent models of AD (Costa et al. 2015). Future studies are warranted to determine whether improvements in AHN via aerobic exercise can improve clinical outcomes in diseases related to the hippocampus.

In conclusion, this study provided novel insight on the effects of different exercise modalities on AHN, while taking into account genetic variations in exercise response. Future studies are warranted to determine the benefits of exercise on hippocampal neurogenesis in different forms of HIT and across age groups, as well as the duration of improvements and the clinical relevance of these findings.

Additional information

Competing interests

None declared.

Author contributions

All authors have approved the final version of the manuscript and agree to be accountable for all aspects of the work. All persons designated as authors qualify for authorship, and all those who qualify for authorship are listed. The authors would like to thank Dr. Stephen S. Cheung for careful review and editing of the manuscript.

Linked articles This Journal Club article highlights an article by Nokia et al. To read this article, visit http://dx.doi.org/10.1113/JP271552.

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