Mitochondria produce ATP that provides readily releasable energy to cells [1]. In order to maintain proper function, the mitochondrial network undergoes fission to separate damaged mitochondrial fragments from the healthy, and fusion to reduce mitochondrial dysfunction [2,3]. Dynamin-related proteins that are known to regulate mitochondrial fusion include Mitofusin 1 (Mfn1), Mitofusin 2 (Mfn2) and Optic atrophy gene 1 (Opa1), whereas the major effector of fission is Dynamin-related protein 1 (Drp1) which has been most frequently associated with pathological conditions [4].
During aging, mitochondrial performance declines as the balance between fusion and fission is often compromised [5,6]. This imbalance has been implicated in neurodegenerative diseases [6], sarcopenic muscles [2] and various other pathological conditions [2,4]. Exercise has been reported to increase mitochondrial biogenesis, remove damaged mitochondria, stimulate mitochondrial function [5,7] and delay aging associated decline in physical fitness [8-10] and cognitive function [11]. Exercise in the elderly has also been reported to improve mitochondrial efficiency as observed with the increase in Ser637 phosphorylation in Drp1 [12].
Therefore, promoting exercise is a promising strategy to improve lifestyle of the current aging society, requiring further research to better understand the mechanisms of mitochondrial dynamics.
PDF Links
PubReader
ePub Link
XML Download
Full text via DOI
Download Citation
Print
