Regulation of Oxygen Consumption at Exercise Onset: Is It Really Controversial?

Abstract

GRASSI, B. Regulation of oxygen consumption at exercise onset: is it really controversial? Exerc. Sport Sci. Rev., Vol. 29, No. 3, pp 134 -138, 2001.

Kinetics of O2uptake, leg blood flow, and muscle deoxygenation are slowed in the upper compared with lower region of the moderate-intensity exercise domain

“…The factors responsible for limiting the rate of V O 2 adaptation during the transition toward a new exercise steady-state broadly are categorized as being related to limitations imposed by 1) the adaptation of muscle blood flow and muscle O 2 delivery, and 2) the activation of muscle enzymes and provision of substrates (other than O 2 ) to the mitochondrial TCA cycle and electron transport chain (16,24,37). Hughson and Morrissey (22,23) suggested that the slower adaptation of V O 2 in the S2 compared with S1 could be a consequence of an O 2 transport limitation, as suggested by slower HR kinetics (i.e., greater HR MRT) (23).…”

Prior heavy exercise elevates pyruvate dehydrogenase activity and muscle oxygenation and speeds O2uptake kinetics during moderate exercise in older adults

“…V O2 kinetics; ageing; pyruvate dehydrogenase; phosphocreatine DURING THE TRANSITION TO moderate-intensity exercise there is a delay in the full activation of mitochondrial oxidative phosphorylation, as estimated by pulmonary O 2 uptake (V O 2p ) kinetics (2, 21, 38), such that it can take several minutes before a new steady-state in aerobic ATP production meets ATP demand (55). It has been suggested that this delay is a result of either a slowed activation of oxidative enzymes and provision of substrates other than O 2 to the mitochondrial tricarboxylic acid (TCA) cycle and electron transport chain (ETC) (e.g., acetyl-CoA; NADH) (20,42), an inadequate supply of O 2 during the transition to exercise (33), or the interaction between these two (22,54). In older compared with young adults, V O 2p kinetics, reflecting the adaptation of muscle O 2 utilization, are slowed during the transition to moderate-and heavyintensity exercise (1, 5, 9, 11).…”

“…It has been suggested that this delay is a result of either a slowed activation of oxidative enzymes and provision of substrates other than O 2 to the mitochondrial tricarboxylic acid (TCA) cycle and electron transport chain (ETC) (e.g., acetyl-CoA; NADH) (20,42), an inadequate supply of O 2 during the transition to exercise (33), or the interaction between these two (22,54). In older compared with young adults, V O 2p kinetics, reflecting the adaptation of muscle O 2 utilization, are slowed during the transition to moderate-and heavyintensity exercise (1,5,9,11).…”

Skeletal muscle metabolic changes in peripheral arterial disease contribute to exercise intolerance: a point-counterpoint discussion

“…'Metabolic inertia', which describes a sluggishness of mitochondrial metabolism (independent of O 2 supply) to respond immediately to an increase in ATP hydrolysis, is likely to retard the increase in O 2 consumption at the onset of exercise in all people. 78,79 However, there is no evidence that such metabolic inertia is more pronounced in PAD or that differences in it explain differences in exercise performance amongst claudicants. It was stated in the affirmative argument that a role of blood flow in the impaired VO 2 kinetics seen in PAD was inexplicable because the rise in blood flow during the early stage of exercise was normal.…”