%0 Journal Article
%T VO2 Kinetics during Moderate Effort in Muscles of Different Masses and Training Level
%A Omri Inbar
%A Marcello Faina
%A Sabrina Demarie
%A Brian J. Whipp
%J ISRN Physiology
%D 2013
%R 10.1155/2013/101565
%X Purpose. To examine the relative importance of central or peripheral factors in the on-transient VO2 response dynamics to exercise with ¡°trained¡± and relatively ¡°untrained¡± muscles. Methods. Seven professional road cyclists and seven elite kayak paddlers volunteered to participate in this study. Each completed two bouts of constant-load ¡°square-wave¡± rest-to-exercise transition cycling and arm-cranking exercise at a power output 50¨C60% of the mode-specific VO2peak presented in a randomized order. Results. In the cyclists, the mean response time (MRT) as well as the phase II VO2 time constant ( ) was significantly slower in the untrained compared with the trained muscles. The opposite was the case in the kayakers. With respect to the relatively untrained muscle groups, while both demonstrated faster VO2 kinetics than normal (moderately fit) subjects, the kayakers evidenced faster VO2 kinetics than the cyclists. This suggests that there is a greater stabilizing-counterforce involvement of the legs in the task of kayaking than of the arms for cycling. Conclusions. The results of the present study provide no support for the ¡°transfer¡± of a training effect onto the VO2 on-transient response for moderate exercise, but rather support earlier reports demonstrating that peripheral effects may be important in dictating this kinetics. 1. Introduction The time course of the pulmonary oxygen uptake (VO2) response to constant-load exercise of moderate intensity can be characterized by two transient phases. In Phase I, the initial, usually rapid, increase in VO2 is mediated by an increase in cardiac output, or more properly pulmonary blood flow, whilst the gas contents of the mixed-venous blood perfusing the lungs remain similar to those at rest. Phase II transition is triggered by the gas contents of the blood perfusing the lungs being altered by the influence of active muscle metabolism; it therefore represents the blood transport delay between the active muscles and the lungs. During Phase II VO2 reflects the decreasing mixed venous O2 content supplementing the continuing increase in pulmonary blood flow. This is characterized by a monoexponential rise in VO2 up to the asymptotic or steady-state level (Phase III), the time course of which closely reflects that of the increased muscle oxygen consumption [1, 2]. However, if the work rate is appreciably above the individual¡¯s lactate threshold (LT), VO2 may not reach a steady state, associated with a continued slower rise in VO2 (slow component; VO2slow) of a delayed onset. Opinions are divided over whether VO2
%U http://www.hindawi.com/journals/isrn.physiology/2013/101565/