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Difference between revisions of "Rasmussen 2003 Eur J Physiol"

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|abstract=The mitochondrial theory of ageing was tested. Isolated mitochondria from the quadriceps muscle from normal, healthy, young (age 20+ years, n=12) and elderly (70+ years, n=11) humans were studied in respiratory experiments and the data expressed as activities of the muscle. In each group, the subjects exhibited a variation of physical activity but, on average, the groups were representative for their age with maximum O(2) consumption rate of 50+/-9 and 34+/-13 ml min(-1) kg(-1) (mean+/-SD), respectively. Thirteen different activities were assayed. alpha-Glycerophosphate oxidation was lower in the 70+ group (38%, P~0.001), as was the respiratory capacity for fatty acids (19%, P~0.03). The remaining eleven activities, including those of the central bioenergetic reactions, were not lower in the 70+ group. Pyruvate and alpha-ketoglutarate dehydrogenase activities (i.e. the tricarboxylic acid cycle turnover) and the respiratory chain activity could all account for ~14 mmol O(2) min(-1) kg(-1) muscle (37 degrees C). The capacity for aerobic ATP synthesis was ~35 mmol ATP min(-1) kg(-1). The mitochondrial capacities were far in excess of whole-body performance. They were related to physical activity, but not to age. The mitochondrial theory of ageing, which attributes the age-related decline of muscle performance to decreased mitochondrial function, is incompatible with these results.
|abstract=The mitochondrial theory of ageing was tested. Isolated mitochondria from the quadriceps muscle from normal, healthy, young (age 20+ years, n=12) and elderly (70+ years, n=11) humans were studied in respiratory experiments and the data expressed as activities of the muscle. In each group, the subjects exhibited a variation of physical activity but, on average, the groups were representative for their age with maximum O(2) consumption rate of 50+/-9 and 34+/-13 ml min(-1) kg(-1) (mean+/-SD), respectively. Thirteen different activities were assayed. alpha-Glycerophosphate oxidation was lower in the 70+ group (38%, P~0.001), as was the respiratory capacity for fatty acids (19%, P~0.03). The remaining eleven activities, including those of the central bioenergetic reactions, were not lower in the 70+ group. Pyruvate and alpha-ketoglutarate dehydrogenase activities (i.e. the tricarboxylic acid cycle turnover) and the respiratory chain activity could all account for ~14 mmol O(2) min(-1) kg(-1) muscle (37 degrees C). The capacity for aerobic ATP synthesis was ~35 mmol ATP min(-1) kg(-1). The mitochondrial capacities were far in excess of whole-body performance. They were related to physical activity, but not to age. The mitochondrial theory of ageing, which attributes the age-related decline of muscle performance to decreased mitochondrial function, is incompatible with these results.
|keywords=Age effects, Ageing, Human skeletal muscle, Isolated mitochondria, Oxidative phosphorylation, Oxygen uptake, Quadriceps muscle, Respiration
|keywords=Age effects, Ageing, Human skeletal muscle, Isolated mitochondria, Oxidative phosphorylation, Oxygen uptake, Quadriceps muscle, Respiration
|editor=[[Gnaiger E]],
}}
}}
{{Labeling
{{Labeling
|area=Exercise physiology;nutrition;life style
|diseases=Aging;senescence
|organism=Human
|organism=Human
|tissues=Skeletal muscle
|tissues=Skeletal muscle
|preparations=Isolated mitochondria
|preparations=Isolated mitochondria
|enzymes=Complex I, Complex II;succinate dehydrogenase, Complex V;ATP synthase
|enzymes=Complex I, Complex II;succinate dehydrogenase, Complex V;ATP synthase
|diseases=Aging;senescence
|topics=Substrate
|topics=Substrate
|pathways=N, NS
|additional=MitoEAGLE BME,
}}
}}
__TOC__
__TOC__
==References==
== MitoEAGLE ''V''<sub>O2max</sub>/BME data base ==
 
:::* Human vastus lateralis
:::* 12 males
:::* 24 years
:::* Range of differenct endurance activities
:::* ''h'' = 1.79 m
:::* ''m'' = 75 kg
:::* [[BME]] = 1.12
:::* BMI = 23.4 kg·m<sup>-2</sup>
:::* ''V''<sub>O2max/BM</sub> = 50.0 mL·min<sup>-1</sup>·kg<sup>-1</sup>
:::* Isolated mitochondria; 25 °C; GS<sub>''P''</sub>; conversions: [[Gnaiger 2009 Int J Biochem Cell Biol]]
:::* ''J''<sub>O2,''P''</sub>(NS) = 120.6 µmol·s<sup>-1</sup>·kg<sup>-1</sup> wet muscle mass (37 °C)
::::* 10.3 µM mt-protein/mg ''m''<sub>w</sub>
----
:::* Human vastus lateralis
:::* 1 female & 10 males
:::* 72 years
:::* Range of differenct endurance activities
:::* ''h'' = 1.75 m
:::* ''m'' = 80 kg
:::* [[BME]] = 1.28
:::* BMI = 26.1 kg·m<sup>-2</sup>
:::* ''V''<sub>O2max/BM</sub> = 34.0 mL·min<sup>-1</sup>·kg<sup>-1</sup>
:::* Isolated mitochondria; 25 °C; GS<sub>''P''</sub>; conversions: [[Gnaiger 2009 Int J Biochem Cell Biol]]
:::* ''J''<sub>O2,''P''</sub>(NS) = 115.1 µmol·s<sup>-1</sup>·kg<sup>-1</sup> wet muscle mass (37 °C)
::::* 10.3 µM mt-protein/mg ''m''<sub>w</sub>
----
 
 
== References ==


====Both muscle strength and peak contraction velocity decline, in some muscles even from the age of 20====
==== Both muscle strength and peak contraction velocity decline, in some muscles even from the age of 20 ====
::[8, 15, 16 17, 22, 23, 26, 27, 28, 29, 30, 32, 36, 37]
::[8, 15, 16 17, 22, 23, 26, 27, 28, 29, 30, 32, 36, 37]
====The response to training is independent of age====
==== The response to training is independent of age ====
::[8, 9, 15, 17, 22, 23, 30, 32, 36, 37].
::[8, 9, 15, 17, 22, 23, 30, 32, 36, 37].
====Loss of type-II fibres is greater than that of type-I====
==== Loss of type-II fibres is greater than that of type-I ====
::[15, 16, 22, 23, 26, 27, 28, 37].  
::[15, 16, 22, 23, 26, 27, 28, 37].  
====Cytochrome oxidase deficient fibres appear later in increasing, but very small numbers====
==== Cytochrome oxidase deficient fibres appear later in increasing, but very small numbers ====
::[8, 9, 10, 33, 35, 44, 52].
::[8, 9, 10, 33, 35, 44, 52].



Revision as of 23:48, 8 December 2019

Publications in the MiPMap
Rasmussen UF, Krustrup P, Kjaer M, Rasmussen HN (2003) Human skeletal muscle mitochondrial metabolism in youth and senescence: no signs of functional changes in ATP formation and mitochondrial oxidative capacity. Pflugers Arch – Eur J Physiol 446:270-78.

» PMID: 12739165

Rasmussen UF, Krustrup P, Kjaer M, Rasmussen HN (2003) Eur J Physiol

Abstract: The mitochondrial theory of ageing was tested. Isolated mitochondria from the quadriceps muscle from normal, healthy, young (age 20+ years, n=12) and elderly (70+ years, n=11) humans were studied in respiratory experiments and the data expressed as activities of the muscle. In each group, the subjects exhibited a variation of physical activity but, on average, the groups were representative for their age with maximum O(2) consumption rate of 50+/-9 and 34+/-13 ml min(-1) kg(-1) (mean+/-SD), respectively. Thirteen different activities were assayed. alpha-Glycerophosphate oxidation was lower in the 70+ group (38%, P~0.001), as was the respiratory capacity for fatty acids (19%, P~0.03). The remaining eleven activities, including those of the central bioenergetic reactions, were not lower in the 70+ group. Pyruvate and alpha-ketoglutarate dehydrogenase activities (i.e. the tricarboxylic acid cycle turnover) and the respiratory chain activity could all account for ~14 mmol O(2) min(-1) kg(-1) muscle (37 degrees C). The capacity for aerobic ATP synthesis was ~35 mmol ATP min(-1) kg(-1). The mitochondrial capacities were far in excess of whole-body performance. They were related to physical activity, but not to age. The mitochondrial theory of ageing, which attributes the age-related decline of muscle performance to decreased mitochondrial function, is incompatible with these results. Keywords: Age effects, Ageing, Human skeletal muscle, Isolated mitochondria, Oxidative phosphorylation, Oxygen uptake, Quadriceps muscle, Respiration Bioblast editor: Gnaiger E


Labels: MiParea: Exercise physiology;nutrition;life style  Pathology: Aging;senescence 

Organism: Human  Tissue;cell: Skeletal muscle  Preparation: Isolated mitochondria  Enzyme: Complex I, Complex II;succinate dehydrogenase, Complex V;ATP synthase  Regulation: Substrate 

Pathway: N, NS 


MitoEAGLE BME 

MitoEAGLE VO2max/BME data base

  • Human vastus lateralis
  • 12 males
  • 24 years
  • Range of differenct endurance activities
  • h = 1.79 m
  • m = 75 kg
  • BME = 1.12
  • BMI = 23.4 kg·m-2
  • VO2max/BM = 50.0 mL·min-1·kg-1
  • Isolated mitochondria; 25 °C; GSP; conversions: Gnaiger 2009 Int J Biochem Cell Biol
  • JO2,P(NS) = 120.6 µmol·s-1·kg-1 wet muscle mass (37 °C)
  • 10.3 µM mt-protein/mg mw

  • Human vastus lateralis
  • 1 female & 10 males
  • 72 years
  • Range of differenct endurance activities
  • h = 1.75 m
  • m = 80 kg
  • BME = 1.28
  • BMI = 26.1 kg·m-2
  • VO2max/BM = 34.0 mL·min-1·kg-1
  • Isolated mitochondria; 25 °C; GSP; conversions: Gnaiger 2009 Int J Biochem Cell Biol
  • JO2,P(NS) = 115.1 µmol·s-1·kg-1 wet muscle mass (37 °C)
  • 10.3 µM mt-protein/mg mw


References

Both muscle strength and peak contraction velocity decline, in some muscles even from the age of 20

[8, 15, 16 17, 22, 23, 26, 27, 28, 29, 30, 32, 36, 37]

The response to training is independent of age

[8, 9, 15, 17, 22, 23, 30, 32, 36, 37].

Loss of type-II fibres is greater than that of type-I

[15, 16, 22, 23, 26, 27, 28, 37].

Cytochrome oxidase deficient fibres appear later in increasing, but very small numbers

[8, 9, 10, 33, 35, 44, 52].

8. Brierley EJ, Johnson MA, James OFW, Turnbull DM (1996) Effects of physical activity and age on mitochondrial function. Q J Med 89: 251–258.

9. Brierley EJ, Johnson MA, Bowman A, Ford GA, Subhan F, Reed JW, James OFW, Turnbull DM (1997) Mitochondrial function in muscle from elderly athletes. Ann Neurol 41: 114–116.

10. Brierley EJ, Johnson MA, Lightowlers RN, James OFW, Turnbull DM (1998) Role of mitochondrial DNA mutations in human aging: implications for the central nervous system and muscle. Ann Neurol 43: 217–223.

15. Coggan AR, Spina RJ, Rogers MA, King DS, Brown M, Nemeth PM, Holloszy JO (1990) Histochemical and enzymatic characteristics of skeletal muscle in master athletes. J Appl Physiol 68: 1896–1901.

16. Coggan AR, Spina RJ, King DS, Rogers MA, Brown M, Nemeth PM, Holloszy JO (1992) Histochemical and enzymatic comparison of the gastrocnemius muscle of young and elderly men and women. J Gerontol 47: B71–B76.

17. Coggan AR, Abduljalil AM, Swanson SC, Earle MS, Farris JW, Mendenhall LA, Robitaille P-M (1993) Muscle metabolism during exercise in young and older untrained and endurance-trained men. J Appl Physiol 75: 2125–2133.

22. Kent-Braun JA, NG AV (2000) Skeletal muscle oxidative capacity in young and older women and men. J Appl Physiol 89: 1072–1078.

23. Klitgaard H, Mantoni M, Schiaffino S, Ausoni S, Gorza L, Laurent-Winter C, Schnohr P, Saltin B (1990) Function, morphology and protein expression of ageing skeletal muscle: a cross-sectional study of elderly men with different training backgrounds. Acta Physiol Scand 140: 41–54.

26. Larsson L, Grimby G, Karlsson J (1979) Muscle strength and speed of movement in relation to age and muscle morphology. J Appl Physiol 46: 451–456.

27. Lexell J (1995) Human aging, muscle mass, and fiber type composition. J Gerontol 50: A11–A16.

28. Lexell J, Taylor CC, Sjöström M (1988) What is the cause of the ageing atrophy? Total number, size and proportion of different fiber types studied in whole vastus lateralis muscle from 15- to 83-year-old men. J Neurol Sci 84: 275–294.

29. McCully KK, Fielding RA, Evans WJ, Leigh JS, Posner JD (1993) Relationships between in vivo and in vitro measurements of metabolism in young and old human calf muscles. J Appl Physiol 75: 813–819.

30. Meredith CN, Frontera WR, Fisher EC, Hughes VA, Herland JC, Edwards J, Ewans WJ (1989) Peripheral effects of endurance training in young and old subjects. J Appl Physiol 66: 2844–2849.

32. Örlander J, Aniansson A (1980) Effects of physical training on skeletal muscle metabolism and ultrastructure in 70 to 75-year-old men. Acta Physiol Scand 109: 149–154.

33. Ozawa T (1997) Genetic and functional changes in mitochondria associated with aging. Physiol Rev 77: 425–464.

35. Pesce V, Cormio A, Fracasso F, Vecchiet J, Felzani G, Lezza AMS, Cantatore P, Gadaleta MN (2001) Age-related mitochondrial genotypic and phenotypic alterations in human skeletal muscle. Free Radic Biol Med 30: 1223–1233.

36. Proctor DN, Joyner MJ (1997) Skeletal muscle mass and the reduction of VO2,max in trained older subjects. J Appl Physiol 82: 1411–1415.

37. Proctor DN, Sinning WE, Walro JM, Sieck GC, Lemon PWR (1995) Oxidative capacity of human muscle fiber types: effects of age and training status. J Appl Physiol 78: 2033–2038.

44. Rifai Z, Welle S, Kamp C, Thornton CA (1995) Ragged red fibers in normal aging and inflammatory myopathy. Ann Neurol 37: 24–29.

52. Wilson PD, Franks LM (1975) The effect of age on mitochondrial ultrastructure and enzymes. Adv Exp Med Biol 53: 171–183.