No acetyl group deficit is evident at the onset of exercise at 90% of maximal oxygen uptake in humans

Marwood, Simon; Constantin‐Teodosiu, Dumitru; Casey, Edel; Whyte, Martin; Boobis, L.; Bowtell, Joanna L.

doi:10.1080/02640410903440884

Cited by 4 publications

(3 citation statements)

References 39 publications

(63 reference statements)

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“…Hence, rapid muscle oxygen consumption kinetics require strong parallel activation of ATP-consuming and ATP-producing pathways (14,15), high oxidative enzyme activity, and sufficient mitochondrial ADP delivery regulated by the CK kinase reaction (11). Pharmacological activation of pyruvate dehydrogenase did not speed muscle oxygen uptake kinetics in most experimental preparations (for discussion, see (16)), suggesting that reducing equivalent delivery to the electron transport chain is not a limiting factor. There may, however, be a role for mitochondrial enzyme activity to speed V˙O 2 kinetics in aged muscles (17).…”

Section: V˙o2 Kinetics and The O2 Deficitmentioning

confidence: 99%

Bioenergetic Mechanisms Linking V˙O2 Kinetics and Exercise Tolerance

Goulding¹,

Rossiter

Marwood

et al. 2021

Exercise and Sport Sciences Reviews

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We hypothesize that the V˙O2 time constant (τV˙O2) determines exercise tolerance by defining the power output associated with a “critical threshold” of intramuscular metabolite accumulation (e.g., inorganic phosphate), above which muscle fatigue and work inefficiency are apparent. Thereafter, the V˙O2 “slow component” and its consequences (increased pulmonary, circulatory, and neuromuscular demands) determine performance limits.

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Section: V˙o2 Kinetics and The O2 Deficitmentioning

confidence: 99%

Bioenergetic Mechanisms Linking V˙O2 Kinetics and Exercise Tolerance

Goulding¹,

Rossiter

Marwood

et al. 2021

Exercise and Sport Sciences Reviews

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“…Activation of the PDC prior to exercise via DCA infusion has on a number of occasions been shown to reduce the muscle lactate accumulation and phosphocreatine degradation during subsequent constant load exercise, suggesting a role of the PDC in determining intracellular metabolic inertia (Howlett et al, 1999;Timmons et al, 1998a;Timmons et al, 1998b). Despite these findings, a number of studies have found no effect of DCA infusion on the fundamental time constant of pulmonary oxygen uptake kinetics at the onset of exercise (Koppo et al, 2004;Jones et al, 2004b;Marwood et al, 2010;Rossiter et al, 2003). During incremental exercise, it was recently demonstrated that…”

Section: Discussionmentioning

confidence: 79%

No effect of glutamine ingestion on indices of oxidative metabolism in stable COPD

Marwood

Jack

Patel

et al. 2011

Respiratory Physiology & Neurobiology

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“…However, DCA administration has failed to demonstrate any effect on O 2 kinetics in humans. For instance, no effect of DCA on the fundamental phase O 2 kinetics during moderate- [ 150 ], heavy- [ 151 ] and severe-intensity exercise [ 152 ] has been demonstrated in humans, despite a four- to eight-fold increase in PDH activation occurring in some studies [ 153 ]. DCA administration did not reduce either or the time constant for muscle PCr kinetics during heavy knee-extension exercise in humans, but rather reduced the amplitude of the fundamental O 2 and PCr responses.…”

Section: Mechanisms Underpinning the Priming Effectmentioning

confidence: 99%

How Priming Exercise Affects Oxygen Uptake Kinetics: From Underpinning Mechanisms to Endurance Performance

Goulding

Wüst

2023

Sports Med

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The observation that prior heavy or severe-intensity exercise speeds overall oxygen uptake ($$\dot{V}$$ V ˙ O2) kinetics, termed the “priming effect”, has garnered significant research attention and its underpinning mechanisms have been hotly debated. In the first part of this review, the evidence for and against (1) lactic acidosis, (2) increased muscle temperature, (3) O2 delivery, (4) altered motor unit recruitment patterns and (5) enhanced intracellular O2 utilisation in underpinning the priming effect is discussed. Lactic acidosis and increased muscle temperature are most likely not key determinants of the priming effect. Whilst priming increases muscle O2 delivery, many studies have demonstrated that an increased muscle O2 delivery is not a prerequisite for the priming effect. Motor unit recruitment patterns are altered by prior exercise, and these alterations are consistent with some of the observed changes in $$\dot{V}$$ V ˙ O2 kinetics in humans. Enhancements in intracellular O2 utilisation likely play a central role in mediating the priming effect, probably related to elevated mitochondrial calcium levels and parallel activation of mitochondrial enzymes at the onset of the second bout. In the latter portion of the review, the implications of priming on the parameters of the power–duration relationship are discussed. The effect of priming on subsequent endurance performance depends critically upon which phases of the $$\dot{V}$$ V ˙ O2 response are altered. A reduced $$\dot{V}$$ V ˙ O2 slow component or increased fundamental phase amplitude tend to increase the work performable above critical power (i.e. W´), whereas a reduction in the fundamental phase time constant following priming results in an increased critical power.

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No acetyl group deficit is evident at the onset of exercise at 90% of maximal oxygen uptake in humans

Cited by 4 publications

References 39 publications

Bioenergetic Mechanisms Linking V˙O2 Kinetics and Exercise Tolerance

Bioenergetic Mechanisms Linking V˙O2 Kinetics and Exercise Tolerance

No effect of glutamine ingestion on indices of oxidative metabolism in stable COPD

How Priming Exercise Affects Oxygen Uptake Kinetics: From Underpinning Mechanisms to Endurance Performance

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