Rasmussen 2003 Eur J Physiol
|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.|
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
MitoEAGLE VO2max/BME database
- Human vastus lateralis
- 12 males
- 24 years
- Range of differenct endurance activities
- H = 1.79 m
- M = 75 kg
- BME = 0.12
- BMI = 23.4 kg·m-2
- VO2max/M = 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 = 0.28
- BMI = 26.1 kg·m-2
- VO2max/M = 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
Both muscle strength and peak contraction velocity decline, in some muscles even from the age of 20
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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].
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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.
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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.
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References: BME and VO2max
- » VO2max
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MitoPedia: BME and mitObesity
» Body mass excess and mitObesity | BME and mitObesity news | Summary |
|BME cutoff points||BME cutoff||Obesity is defined as a disease associated with an excess of body fat with respect to a healthy reference condition. Cutoff points for body mass excess, BME cutoff points, define the critical values for underweight (-0.1 and -0.2), overweight (0.2), and various degrees of obesity (0.4, 0.6, 0.8, and above). BME cutoffs are calibrated by crossover-points of BME with established BMI cutoffs.|
|Body fat excess||BFE||In the healthy reference population (HRP), there is zero body fat excess, BFE, and the fraction of excess body fat in the HRP is expressed - by definition - relative to the reference body mass, M°, at any given height. Importantly, body fat excess, BFE, and body mass excess, BME, are linearly related, which is not the case for the body mass index, BMI.|
|Body mass||m [kg]; M [kg·x-1]||The body mass M is the mass (kilogram [kg]) of an individual (object) [x] and is expressed in units [kg/x]. Whereas the body weight changes as a function of gravitational force (you are weightless at zero gravity; your floating weight in water is different from your weight in air), your mass is independent of gravitational force, and it is the same in air and water.|
|Body mass excess||BME||The body mass excess, BME, is an index of obesity and as such BME is a lifestyle metric. The BME is a measure of the extent to which your actual body mass, M [kg/x], deviates from M° [kg/x], which is the reference body mass [kg] per individual [x] without excess body fat in the healthy reference population, HRP. A balanced BME is BME° = 0.0 with a band width of -0.1 towards underweight and +0.2 towards overweight. The BME is linearly related to the body fat excess.|
|Body mass index||BMI||The body mass index, BMI, is the ratio of body mass to height squared (BMI=M·H-2), recommended by the WHO as a general indicator of underweight (BMI<18.5 kg·m-2), overweight (BMI>25 kg·m-2) and obesity (BMI>30 kg·m-2). Keys et al (1972; see 2014) emphasized that 'the prime criterion must be the relative independence of the index from height'. It is exactly the dependence of the BMI on height - from children to adults, women to men, Caucasians to Asians -, which requires adjustments of BMI-cutoff points. This deficiency is resolved by the body mass excess relative to the healthy reference population.|
|Comorbidity||Comorbidities are common in obesogenic lifestyle-induced early aging. These are preventable, non-communicable diseases with strong associations to obesity. In many studies, cause and effect in the sequence of onset of comorbidities remain elusive. Chronic degenerative diseases are commonly obesity-induced. The search for the link between obesity and the etiology of diverse preventable diseases lead to the hypothesis, that mitochondrial dysfunction is the common mechanism, summarized in the term 'mitObesity'.|
|Healthy reference population||HRP||A healthy reference population, HRP, establishes the baseline for the relation between body mass and height in healthy people of zero underweight or overweight, providing a reference for evaluation of deviations towards underweight or overweight and obesity. The WHO Child Growth Standards (WHO-CGS) on height and body mass refer to healthy girls and boys from Brazil, Ghana, India, Norway, Oman and the USA. The Committee on Biological Handbooks compiled data on height and body mass of healthy males from infancy to old age (USA), published before emergence of the fast-food and soft-drink epidemic. Four allometric phases are distinguished with distinct allometric exponents. At heights above 1.26 m/x the allometric exponent is 2.9, equal in women and men, and significantly different from the exponent of 2.0 implicated in the body mass index, BMI [kg/m2].|
|Height of humans||h [m]; H [m·x-1]||The height of humans, h, is given in SI units in meters [m]. Humans are countable objects, and the symbol and unit of the number of objects is N [x]. The average height of N objects is, H = h/N [m/x], where h is the heights of all N objects measured on top of each other. Therefore, the height per human has the unit [m·x-1] (compare body mass [kg·x-1]). Without further identifyer, H is considered as the standing height of a human, measured without shoes, hair ornaments and heavy outer garments.|
|Length||l [m]||Length l is an SI base quantity with SI base unit meter m. Quantities derived from length are area A [m2] and volume V [m3]. Length is an extensive quantity, increasing additively with the number of objects. The term 'height' h is used for length in cases of vertical position (see height of humans). Length of height per object, LUX [m·x-1] is length per unit-entity UX, in contrast to lentgth of a system, which may contain one or many entities, such as the length of a pipeline assembled from a number NX of individual pipes. Length is a quantity linked to direct sensory, practical experience, as reflected in terms related to length: long/short (height: tall/small). Terms such as 'long/short distance' are then used by analogy in the context of the more abstract quantity time (long/short duration).|
|MitObesity drugs||Bioactive mitObesity compounds are drugs and nutraceuticals with more or less reproducible beneficial effects in the treatment of diverse preventable degenerative diseases implicated in comorbidities linked to obesity, characterized by common mechanisms of action targeting mitochondria.|
|Obesity||Obesity is a disease resulting from excessive accumulation of body fat. In common obesity (non-syndromic obesity) excessive body fat is due to an obesogenic lifestyle with lack of physical exercise ('couch') and caloric surplus of food consumption ('potato'), causing several comorbidities which are characterized as preventable non-communicable diseases. Persistent body fat excess associated with deficits of physical activity induces a weight-lifting effect on increasing muscle mass with decreasing mitochondrial capacity. Body fat excess, therefore, correlates with body mass excess up to a critical stage of obesogenic lifestyle-induced sarcopenia, when loss of muscle mass results in further deterioration of physical performance particularly at older age.|
|VO2max||VO2max; VO2max/M||Maximum oxygen consumption, VO2max, is and index of cardiorespiratory fitness, measured by spiroergometry on human and animal organisms capable of controlled physical exercise performance on a treadmill or cycle ergometer. VO2max is the maximum respiration of an organism, expressed as the volume of O2 at STPD consumed per unit of time per individual object [mL.min-1.x-1]. If normalized per body mass of the individual object, M [kg.x-1], mass specific maximum oxygen consumption, VO2max/M, is expressed in units [mL.min-1.kg-1].|
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, BMI, VO2max, BME