PMID- 19756719
OWN - NLM
STAT- MEDLINE
DCOM- 20100323
LR  - 20220316
IS  - 1432-2013 (Electronic)
IS  - 0031-6768 (Print)
IS  - 0031-6768 (Linking)
VI  - 459
IP  - 2
DP  - 2010 Jan
TI  - Mitochondrial function as a determinant of life span.
PG  - 277-89
LID - 10.1007/s00424-009-0724-5 [doi]
AB  - Average human life expectancy has progressively increased over many decades 
      largely due to improvements in nutrition, vaccination, antimicrobial agents, and 
      effective treatment/prevention of cardiovascular disease, cancer, etc. Maximal 
      life span, in contrast, has changed very little. Caloric restriction (CR) 
      increases maximal life span in many species, in concert with improvements in 
      mitochondrial function. These effects have yet to be demonstrated in humans, and 
      the duration and level of CR required to extend life span in animals is not 
      realistic in humans. Physical activity (voluntary exercise) continues to hold 
      much promise for increasing healthy life expectancy in humans, but remains to 
      show any impact to increase maximal life span. However, longevity in 
      Caenorhabditis elegans is related to activity levels, possibly through 
      maintenance of mitochondrial function throughout the life span. In humans, we 
      reported a progressive decline in muscle mitochondrial DNA abundance and protein 
      synthesis with age. Other investigators also noted age-related declines in muscle 
      mitochondrial function, which are related to peak oxygen uptake. Long-term 
      aerobic exercise largely prevented age-related declines in mitochondrial DNA 
      abundance and function in humans and may increase spontaneous activity levels in 
      mice. Notwithstanding, the impact of aerobic exercise and activity levels on 
      maximal life span is uncertain. It is proposed that age-related declines in 
      mitochondrial content and function not only affect physical function, but also 
      play a major role in regulation of life span. Regular aerobic exercise and 
      prevention of adiposity by healthy diet may increase healthy life expectancy and 
      prolong life span through beneficial effects at the level of the mitochondrion.
FAU - Lanza, Ian R
AU  - Lanza IR
AD  - Division of Endocrinology, Endocrinology Research Unit, Mayo Clinic College of 
      Medicine, Rochester, MN, USA.
FAU - Nair, K Sreekumaran
AU  - Nair KS
LA  - eng
GR  - R01 DK041973/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Review
DEP - 20090911
PL  - Germany
TA  - Pflugers Arch
JT  - Pflugers Archiv : European journal of physiology
JID - 0154720
RN  - 0 (DNA, Mitochondrial)
RN  - 0 (Reactive Oxygen Species)
RN  - EC 3.5.1.- (Sirtuins)
SB  - IM
MH  - Adiposity/physiology
MH  - Aging/*physiology
MH  - Animals
MH  - Apoptosis/physiology
MH  - Caloric Restriction
MH  - DNA, Mitochondrial/metabolism
MH  - Exercise/physiology
MH  - Humans
MH  - Life Expectancy
MH  - Longevity/*physiology
MH  - Mitochondria/*physiology
MH  - Mitochondria, Muscle/physiology
MH  - Reactive Oxygen Species/metabolism
MH  - Sirtuins/physiology
PMC - PMC2801852
EDAT- 2009/09/17 06:00
MHDA- 2010/03/24 06:00
PMCR- 2009/09/11
CRDT- 2009/09/17 06:00
PHST- 2009/07/23 00:00 [received]
PHST- 2009/08/26 00:00 [accepted]
PHST- 2009/09/17 06:00 [entrez]
PHST- 2009/09/17 06:00 [pubmed]
PHST- 2010/03/24 06:00 [medline]
PHST- 2009/09/11 00:00 [pmc-release]
AID - 724 [pii]
AID - 10.1007/s00424-009-0724-5 [doi]
PST - ppublish
SO  - Pflugers Arch. 2010 Jan;459(2):277-89. doi: 10.1007/s00424-009-0724-5. Epub 2009 
      Sep 11.