Effects of Intermittent Hypoxia Training on Mitochondrial Function and Longevity

Summary

Intermittent hypoxia training (IHT) refers to episodic exposure to reduced oxygen in the inspired air

separated by periods of normoxia (IHNT) or hyperoxia (IHHT). Exposure to IHT causes an increase in

the total number of mitochondria, a reduction in the number of structurally modified organelles, and the

appearance of energetically active mitochondria. IHT leads to the reprogramming of mitochondrial

metabolism ensuring adequate ATP production. The use of IHHT greatly inhibits the development of

mitochondrial dysfunction under severe hypoxia, lowers oxidative damage of mitochondria, and

increases the capacity of the endogenous antioxidant system. IHT significantly improves the control of

mitochondrial quality by eliminating damaged and dysfunctional mitochondria through autophagy

(mitophagy) and generating new and healthy mitochondria through the processes of biogenesis and

fusion. Previous studies have shown that IHT influences several underlying aging mechanisms and

increases longevity. IHT diminishes the basal level of mitochondria-dependent oxidative stress that is

supposed to be the key factor modulating life span and health span in aerobes. Furthermore, IHT

influences longevity and speed of development of age-related diseases via several mitochondriaindependent

pathways. Studies have shown that both IHNT and IHHT protocols are safe interventions

to use in humans. In conclusion, intermittent hypoxia training has considerable safe therapeutic potential

to treat multiple clinical conditions and increase mitochondrial function, healthy life, and longevity in

humans