Any transition in muscular Selisistat work from rest to short duration bouts of movement requires a rapid adjustment in ATP synthesis in order to match ATP usage.33 This is met initially by the ATP-CP system and anaerobic glycolysis. If the activity remains low intensity, reliance on anaerobic glycolysis is fleeting and oxidative metabolism attends to ATP synthesis. If PA is performed at higher intensities, the contribution of anaerobic glycolysis becomes more significant.

Pulmonary oxygen uptake (VO2) has traditionally been used as a marker of oxidative metabolism and it is generally assumed that VO2 is linearly related to work rate, and at a given intensity, VO2 remains constant.34 These assumptions are however, not strictly true. The pulmonary oxygen uptake kinetic response to exercise has fast (primary) Nutlin-3 cell line and slow components, reflecting the efficiency of skeletal muscle oxidative metabolism, the relative degree of fatigue and affording an understanding of the interplay between cardiopulmonary and metabolic processes during PA and how these may be affected by conditions such as obesity.35 The pulmonary

oxygen uptake kinetic response to low-to-moderate intensity exercise (i.e., intensity below the gas exchange threshold) has been described by three phases. Phase I begins as soon as the child transits from a period of rest to a bout of PA. First there is a delay, followed by a rapid rise in oxygen uptake. This first phase is also known as the cardiodynamic phase and reflects cardiovascular and pulmonary adaptations. Phase I is not dependent on VO2, rather it is largely a marker of the increase in pulmonary blood flow. Phase I is followed by an exponential increase in VO2 (phase II) that drives VO2 to steady state (phase III). Phase II kinetics are also known as the primary (fast) component and are described by a time constant revealing the time taken to achieve 63% of the change in oxygen uptake. Thiamine-diphosphate kinase The primary component provides a very close reflection (within about 10%) of the kinetics of oxygen uptake at the muscle. In phases I and

II, when ATP re-synthesis cannot be fully supported by oxidative phosphorylation, the additional energy requirements are met from oxygen stores, PCr, and glycolysis. The oxygen equivalent of these energy sources is known as the oxygen deficit and the faster the time constant the smaller the oxygen deficit.35 During higher intensity PA, activity that is above the gas exchange threshold, a slow component manifests at phase III. During low to moderate intensity activity, there is no phase III slow component, with VO2 attaining steady-state at the end of phase II. In comparison, during more vigorous intensity activity above the gas exchange threshold VO2 continues to rise above what would have been steady-state and this reflects a loss of muscle efficiency and ensuing fatigue.