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Oxygen uptake kinetics: Why are they so slow? And what do they tell us?

100%

Grassi B.

Journal of Physiology and Pharmacology. Supplement

2006

tom 57

nr 10

53-65

O2 kinetics and O2 deficit are important determinants of exercise tolerance. In "normal" conditions convective and diffusive O2 delivery to skeletal muscle fibers do not represent important determinants of O2 kinetics, whose limiting factors seem mainly located within muscle fibers. Whereas a limiting role by PDH has not been confirmed, the role of inhibition of mitochondrial respiration by NO needs further investigations. Important determinants of skeletal muscle O2 kinetics likely reside in the interplay between bioenergetic mechanisms at exercise onset. By acting as high-capacitance energy buffers, PCr hydrolysis and anaerobic glycolysis would delay or attenuate the increase in [ADP] within muscle fibers following rapid increases in ATP demand, preventing a more rapid activation of oxidative phosphorylation. The different "localization" of the main limiting factors for O2 kinetics and O2max offers the opportunity to perform a functional evaluation of oxidative metabolism at two different levels of the pathway for O2, from ambient air to mitochondria. WhereasO2max is mainly limited by the capacity of the cardiovascular system to deliver O2 to exercising muscles, by analysis of O2 kinetics the functional evaluation is mainly related to skeletal muscle. In pathological conditions the situation may be less clear, and warrants further investigations.

Training-induced acceleration of oxygen uptake kinetics in skeletal muscle: the underlying mechanisms

51%

Zoladz J. A., Korzeniewski B., Grassi B.

Journal of Physiology and Pharmacology. Supplement

2006

tom 57

nr 10

67-84

It is well known that the oxygen uptake kinetics during rest-to-work transition (O2 on-kinetics) in trained subjects is significantly faster than in untrained individuals. It was recently postulated that the main system variable that determines the transition time (t1/2) of the O2 on-kinetics in skeletal muscle, at a given moderate ATP usage/work intensity, and under the assumption that creatine kinase reaction works near thermodynamic equilibrium, is the absolute (in mM) decrease in [PCr] during rest-to-work transition. Therefore we postulate that the training-induced acceleration of the O2 on-kinetics is a marker of an improvement of absolute metabolic stability in skeletal muscles. The most frequently postulated factor responsible for enhancement of muscle metabolic stability is the training-induced increase in mitochondrial proteins. However, the mechanism proposed by Gollnick and Saltin (1982) can improve absolute metabolic stability only if training leads to a decrease in resting [ADPfree]. This effect is not observed in many examples of training causing an acceleration of the O2 on-kinetics, especially in early stages of training. Additionally, this mechanism cannot account for the significant training-induced increase in the relative (expressed in % or as multiples of the resting values) metabolic stability at low work intensities, condition in which oxidative phosphorylation is not saturated with [ADPfree]. Finally, it was reported that in the early stage of training, acceleration in the O2 on-kinetics and enhancement of muscle metabolic stability may precede adaptive responses in mitochondrial enzymes activities or mitochondria content. We postulate that the training-induced acceleration in the O2 on-kinetics and the improvement of the metabolite stability during moderate intensity exercise in the early stage of training is mostly caused by an intensification of the “parallel activation” of ATP consumption and ATP supply pathways. A further acceleration in O2 on-kinetics, resulting from prolonged periods of training, may be caused by a further and more pronounced improvement in the muscles’ absolute metabolic stability, caused by an intensification of the “parallel activation” as well as by an increase in mitochondrial proteins.

Ograniczanie wyników

2 Journal of Physiology and Pharmacology. Supplement

2 Grassi B.

1 Korzeniewski B.

1 Zoladz J. A.

2 2006

Wyniki wyszukiwania

Oxygen uptake kinetics: Why are they so slow? And what do they tell us?

Training-induced acceleration of oxygen uptake kinetics in skeletal muscle: the underlying mechanisms