These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: Physiological background of the change point in VO2 and the slow component of oxygen uptake kinetics. Author: Zoładź JA, Korzeniewski B. Journal: J Physiol Pharmacol; 2001 Jun; 52(2):167-84. PubMed ID: 11453098. Abstract: It is generally believed that oxygen uptake during incremental exercise--until VO2max, increases linearly with power output (see eg. Astrand & Rodahl, 1986). On the other hand, it is well established that the oxygen uptake reaches a steady state only during a low power output exercise, but during a high power output exercise, performed above the lactate threshold (LT), the oxygen uptake shows a continuous increase until the end of the exercise. This effect has been called the slow component of VO2 kinetics (Whipp & Wasserman, 1972). The presence of a slow component in VO2 kinetics implies that during an incremental exercise test, after the LT has been exceeded, the VO2 to power output relationship has to become curvilinear. Indeed, it has recently been shown that during the incremental exercise, the exceeding of the power output, at which blood lactate begins to accumulate (LT), causes a non-proportional increase in VO2 (Zoladz et al. 1995) which indicates a drop in muscle mechanical efficiency. The power output at which VO2 starts to rise non-proportionally to the power output has been called "the change point in VO2" (Zoladz et al. 1998). In this paper, the significance of the factors most likely involved in the physiological mechanism responsible for the change point in oxygen uptake (CP-VO2) and for the slow component of VO2 kinetics, including: increase of activation of additional muscle groups, intensification of the respiratory muscle activity, recruitment of type II muscle fibres, increase of muscle temperature, increase of the basal metabolic rate, lactate and hydrogen ion accumulation, proton leak through the inner mitochondrial membrane, slipping of the ATP synthase and a decrease in the cytosolic phosphorylation potential, are discussed. Finally, an original own model describing the sequence of events leading to the non-proportional increase of oxygen cost of work at a high exercise intensity is presented.[Abstract] [Full Text] [Related] [New Search]