Abstract
Alzheimer's disease (AD) is characterized by the accumulation of β-amyloid (Aβ) plaques and tau neurofibrillary tangles in the brain. Although the exact details of the neuronal protective effect of high-intensity interval training (HIIT) on AD remain unclear, the preclinical phase of AD appears to be the important time point for such intervention. The described experiment investigates the neuroprotective effect of HIIT on AD in APP/PS1 mice. In total, 14 C57BL6 healthy control (C) mice and 14 APP/PS1 AD mice were each randomly assigned into two groups, one that did not participate in HIIT (C and AD groups, respectively) and the other subject to HIIT intervention (control HIIT (CE) and AD HIIT (ADE) groups, respectively). Visualization of hippocampal neuronal cells via HE and Congo red staining showed significant improvement in cell status and a significant reduction in amyloidosis in ADE compared with AD. The results of behavioral analysis show that the HIIT intervention significantly improved cognitive decline and reduced spatial exploration in both the C and AD groups. Immunofluorescence showed that the overall brain and the hippocampus of aged rats in the C and AD groups had different degrees of neuroglial responses and astrocyte GFAP proliferation and hypertrophy, with obvious improvement in the CE and ADE groups after 10 weeks of HIIT intervention. These results show that HIIT significantly improves the status of mitochondrial kinetic proteins and related proteins, with the mechanism differing between the normal aging C and the AD groups. 10 weeks of HIIT improved the imbalance in mitochondrial dynamics present in normal control mice and in AD mice. We conclude that preclinical training intervention has a significant positive effect on the exploratory behavior and cognitive functioning of mice.
Highlights
Alzheimer’s disease (AD) is the main cause of dementia, which seriously impacts human health, and the incidence is rising along with the increase in life expectancy
Studies have shown [12] that impaired mitochondrial dynamics is an important early event in AD pathogenesis, and a Oxidative Medicine and Cellular Longevity growing number of studies have demonstrated [13, 14] that high-intensity interval training (HIIT) induces altered mitochondrial dynamics and mitochondrial autophagy and plays an important role in maintaining mitochondrial homeostasis
In comparison with the AD group, there was a clear improvement in the AD with high-intensity interval training (ADE) group when considering the number of hippocampus nerve cells, nuclear condensation, glial and neuronal cell necrosis, and status of cell structure disruption
Summary
Alzheimer’s disease (AD) is the main cause of dementia, which seriously impacts human health, and the incidence is rising along with the increase in life expectancy. Studies have demonstrated that regular physical activity can delay or assist in the avoidance of neurological and psychiatric disorders and is effective in treating neurological disorders [5–7]. HIIT can be an effective alternative to traditional endurance training and induce similar or even better physiological adaptations in both healthy individuals and diseased populations. Studies have shown that high-intensity interval exercise is more effective than traditional aerobic exercise in promoting brain health and enhancing cognitive functioning in the brain [10, 11]. Studies have shown [12] that impaired mitochondrial dynamics is an important early event in AD pathogenesis, and a Oxidative Medicine and Cellular Longevity growing number of studies have demonstrated [13, 14] that HIIT induces altered mitochondrial dynamics and mitochondrial autophagy and plays an important role in maintaining mitochondrial homeostasis
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