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Regular exercise has many beneficial effects on health because it triggers stress response mechanisms that work to maintain cell quality and function. It is worth noting that it isn’t as good at this as the practice of calorie restriction, however. This might be expected from the differing effects of exercise and calorie restriction on life span in short lived species such as laboratory mice. Calorie restriction can improve maximum life span by as much as 40%, while exercise can only improve healthy life span. This isn’t a case of do one or the other, of course. Do both.
Age is associated with rising levels of chronic inflammation, and in the brain this correlates with the dysfunction of microglia, supporting immune cells with a range of important roles. They don’t just clear up debris, but also participate in many of the functions of neurons and neural connections. Needless to say, when they start to be inflammatory and overactive, this is not good for brain health. It is connected to the progression of all of the most common neurodegenerative conditions. Exercise is well known to reduce inflammation, and the research here adds to the existing mountain of data on this front.
Exercise impacts our body at multiple levels, including the central nervous system (CNS). In responding to exercise-related stress (e.g., hypoxia, heat, free radicals, etc.) and injuries, the body launches multiple endogenous protective and repair systems by altering gene expression and releasing a range of factors that prepare the body for the next challenge. These factors, amongst others, involve trophic effects, anti-oxidation, energy metabolism, and anti-inflammation.
Some of these factors enhance brain function and ameliorate brain disorders by inducing neuroplasticity, increasing metabolic efficiency, and improving anti-oxidative capacity. Others maintain brain homeostasis and protect brain from pathological insults by regulating glial activation and neuroinflammation. Activated microglia and several pro-inflammatory cytokines play active roles in the pathogenesis of neurodegenerative diseases, such as Alzheimer’s disease (AD) and Parkinson’s disease (PD). It has been well-documented that although acute, high-intensity exercise may cause muscle injury and induce inflammation, long-term exercise at low-to-moderate intensity negatively regulates the inflammatory response.
Considerable evidence also suggests that exercise may inhibit microglial activation by downregulation of the levels of pro-inflammatory factors. However, the mechanism for the exercise-related downregulation of pro-inflammatory factors is less clear, as pro-inflammatory cytokines can be secreted from various sources (e.g., injured neurons, astrocytes, and microglia). Thus, the anti-microglial activation effect of exercise can be interpreted indirectly by upregulating the levels of trophic factors, which then lead to reduced neuronal injury and degrees of microglial activation.
Furthermore, there are a few reports suggesting that physical exercise can shift the composition of the gut microbiome, which then affects both peripheral and central inflammation, including microglial activation in the CNS. Although some mechanisms are still waiting to be determined, it should be emphasized that physical activity represents a natural strong anti-inflammatory strategy to improve brain function.