ABSTRACT
Oxygen uptake (V̇O2) measured via respired gas analysis ultimately reflects O2 utilization by the mitochondria within the cells of the body. This is true despite the interposition of gas stores for example within the lungs, muscles and venous blood in addition to circulatory transit delays from the exercising muscles to the lungs. At the onset of contractions, the working skeletal muscles are the predominant users of the increased V̇O2 and as shown in Chapter 6, muscle V̇O2 begins to increase without discernible delay (Behnke et al., 2002a). Despite V̇O2 max being lowered, the absolute V̇O2 necessary to perform a given amount of constant-load submaximal work may not be affected by the disease processes and thus the steady-state V̇O2 per se provides no information about the underlying pathology (Wasserman et al., 1994). However, the superb coordination among the respiratory, cardiovascular and muscle systems required for the rapid V̇O2 kinetics observed in healthy individuals is very sensitive to dysfunction at multiple steps in the O2 transport pathway (Figure 14.1). Thus, evaluation of V̇O2 kinetics can provide a powerful method for detecting problems within the oxygen transport/utilization systems. This chapter will present the broad alterations in V̇O2 kinetics manifested in disease conditions that perturb those key systems responsible for delivering O2 to and within the exercising muscles and will address briefly changes in skeletal muscle oxidative enzymes that may contribute to those alterations (Dernevik et al., 1988; Drexler et al., 1992; Mattson and Poole, 1998; Casaburi, 2000; Diederich et al., 2002). Recent mechanistic insights that link the slowed pulmonary V̇O2 kinetics to impaired microvascular exchange profiles within the contracting muscles will be presented.
