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Fig. 2 | Immunity & Ageing

Fig. 2

From: SARS-CoV-2 and mitochondrial health: implications of lifestyle and ageing

Fig. 2

Resistance to SARS-CoV-2: mitochondrial and redox reserve, hormesis and the metabolic/inflammatory see-saw. Data strongly support that people who are aerobically fit, and follow a healthy lifestyle, tend to have a greater metabolic and anti-oxidant reserve related to training-induced mitochondrial adaptation; this is associated with less disease and a longer “healthspan”. The underlying principle that leads to this is described by hormesis and is the product of humans having evolved, along with most other animals, in an environment where this adaptation was constantly induced due to the need to move, and food was less available. As a phenotype, they tend to have greater muscle to fat ratio, and exhibit few, if any symptoms of the metabolic syndrome, such as increased liver fat and visceral adipose tissue (VAT) volume, insulin resistance, or markers of chronic inflammation. In this context, data suggest that muscle, as an organ, tends to be anti-inflammatory when used regularly, whereas adipose, in particular, in VAT is inflammatory if it becomes overloaded. As the virus seems to induce oxidative stress [164] and aerobic glycolysis to enhance its own replication, it could be argued that in a person with poor mitochondrial and anti-oxidant reserve, infection will tend to tip towards chronic inflammation and incomplete resolution. In this scenario, it is important to suppress either inflammation itself, or provide extra anti-oxidant power to damp down the potential for a feed-forward inflammatory spiral

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