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Biochemical adaptation of mitochondria, muscle, and whole-animal respiration to endurance training
Ist Teil von
Archives of biochemistry and biophysics, 1981-07, Vol.209 (2), p.539-554
Ort / Verlag
United States: Elsevier Inc
Erscheinungsjahr
1981
Quelle
Elsevier Journal Backfiles on ScienceDirect (DFG Nationallizenzen)
Beschreibungen/Notizen
The experimental intervention of exercise training has been used to study mitochondrial biosynthesis, and the physiologic integration of subcellular, cellular, and whole-animal energetics. Gross mitochondrial composition was unchanged in rat muscle by a 10-week program of endurance treadmill running. The mitochondrial concentration of iron-sulfur clusters, cytochromes, flavoprotein, dehydrogenases, oxidases, and membrane protein and lipid, as well as the ratios of each component to the others, maintained constant proportions. The mitochondrial content of muscle, however, increased by approximately 100% as did absolute tissue oxidative capacity. The soluble portions of mitochondria maintained a constant total protein content and mass, relative to the membrane fraction, despite adaptive changes in the specific activities of some citric acid-cycle enzymes. Mitochondria from endurance-trained muscles generated normal transmembrane potentials, ADP/O ratios, and respiratory control ratios. Muscle oxidase activity was highly correlated (
r = 0.92) with endurance capacity, which increased 403%. Whole-animal maximal O
2 consumption (
V
̇
O
2
max
), however, increased only 14% and was a relatively poor predictor of endurance. Thus, mitochondrial factors, rather than
V
̇
O
2
max
, must play an important role in dictating the limits of endurance activity. Conversely,
V
̇
O
2
max
was strongly related to the maximal intensity of work which could be attained aerobically (
r = 0.82). Comparison of O
2 consumption at the mitochondrial, muscle, and whole-animal levels revealed that maximal muscle oxidase activity was not an absolute limitation to
V
̇
O
2
max
: It is concluded that other factors intervene to control the percentage of muscle O
2 consumption capacity which may be utilized during exercise.