Negative accumulated oxygen deficit during heavy and very heavy intensity cycle ergometry in humans

Özyener, Fadıl; Rossiter, Harry B.; Ward, Susan A.; Whipp, Brian J.

doi:10.1007/s00421-003-0870-y

Cited by 27 publications

(21 citation statements)

References 25 publications

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“…Our findings that the magnitude of the AOD in the FS condition was inversely related to the time to exhaustion and that the AOD actually became negative in two subjects (Fig. 6) confirms the earlier observations of Özyener et al (2003), and supports their conclusion that the existence of the V̇O 2 slow component during exercise >CP confounds the calculation of AOD and challenges the validity of the AOD concept.…”

Section: Discussionsupporting

confidence: 89%

Influence of pacing strategy on O₂ uptake and exercise tolerance

Jones

Wilkerson

Vanhatalo

et al. 2008

Scandinavian Med Sci Sports

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Seven male subjects completed cycle exercise bouts to the limit of tolerance on three occasions: (1) at a constant work rate (340+/-57 W; even-pace strategy; ES); (2) at a work rate that was initially 10% lower than that in the ES trial but which then increased with time such that it was 10% above that in the ES trial after 120 s of exercise (slow-start strategy; SS); and, (3) at a work rate that was initially 10% higher than that in the ES trial but which then decreased with time such that it was 10% below that in the ES trial after 120 s of exercise (fast-start strategy; FS). The expected time to exhaustion predicted from the pre-established power-time relationship was 120 s in all three conditions. However, the time to exhaustion was significantly greater (P<0.05) for the FS (174+/-56 s) compared with the ES (128+/-21 s) and SS (128+/-30 s) conditions. In the FS condition, (.)VO2 increased more rapidly toward its peak such that the total O2 consumed in the first 120 s of exercise was greater (ES: 5.15+/-0.78; SS: 5.07+/-0.83; FS: 5.36+/-0.84 L; P<0.05 for FS vs ES and SS). These results suggest that a fast-start pacing strategy might enhance exercise tolerance by increasing the oxidative contribution to energy turnover and hence "sparing" some of the finite anaerobic capacity across the transition to high-intensity exercise.

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Section: Discussionsupporting

confidence: 89%

Influence of pacing strategy on O₂ uptake and exercise tolerance

Jones

Wilkerson

Vanhatalo

et al. 2008

Scandinavian Med Sci Sports

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“…If PDC activation increases carbohydrate oxidation, then up to ∼12% less oxygen utilization is required for the same ATP regeneration when using lipid as the fuel. A recent study highlighted several problems associated with the OD calculation, derived from respiratory gas values (Özyener et al 2003), further indicating that it is not a useful approach to studying the acetyl group deficit. One further recent study (Koppo et al 2004) failed to design the study to ensure that PDC activation differed between control and DCA‐treated conditions (they could not measure PDC status but plasma lactate concentrations during exercise supported the contention that no substantial ‘metabolic’ intervention took place) highlighting the importance of a rational experimental design when investigating the OD.…”

Section: Discussionmentioning

confidence: 99%

Acetyl group availability influences phosphocreatine degradation even during intense muscle contraction

Timmons

Constantin‐Teodosiu

Poucher

et al. 2004

The Journal of Physiology

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We previously established that activation of the pyruvate dehydrogenase complex (PDC) using dichloroacetate (DCA) reduced the reliance on substrate-level phosphorylation (SLP) at the onset of exercise, with normal and reduced blood flow. PDC activation also reduced fatigue development during contraction with reduced blood flow. Since these observations, several studies have re-evaluated our observations. One study demonstrated a performance benefit without a reduction in SLP, raising a question mark over PDC's role in the regulation of ATP regeneration and our interpretation of fatigue mechanisms. Using a model of muscle contraction similar to the conflicting study (i.e. tetanic rather than twitch stimulation), we re-examined this question. Using canine skeletal muscle, one group was infused with saline while the other was pretreated with 300 mg (kg body mass) −1 DCA. Muscle biopsies were taken at rest, peak tension (1 min) and after 6 min of tetanic electrical stimulation (75 ms on−925 ms off per second) and blood flow was limited to 25% of normal values observed during contraction. DCA reduced phosphocreatine (PCr) degradation by 40% during the first minute of contraction, but did not prevent the almost complete depletion of PCr stores at 6 min, while muscle fatigue did not differ between the two groups. During intermittent tetanic stimulation PCr degradation was 75% greater than with our previous 3 Hz twitch contraction protocol, despite a similar rate of oxygen consumption at 6 min. Thus, in the present study enhanced acetyl group availability altered the time course of PCr utilization but did not prevent the decline towards depletion. Consistent with our earlier conclusions, DCA pretreatment reduces muscle fatigue only when SLP is attenuated. The present study and our met-analysis indicates that enhanced acetyl group availability results in a readily measurable reduction in SLP when the initial rate of PCr utilization is ∼1 mmol (kg dry mass) −1 s −1 or less (depending on intrinsic mitochondrial capacity). When measured early during an uninterrupted period of muscle contraction, acetyl group availability is likely to influence SLP under any condition where mitochondria are responsible for a significant proportion of ATP regeneration.

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“…The most commonly used method to determine the time constant is based on calculations of a mono-exponential function describing the rise and adaptation of _ VO 2 in a single steady-state exercise test (Wasserman et al, 1994a;Cooper & Storer, 2001). This model is used primarily to determine the time constant for exercise in the moderate intensity domain, while at higher intensities there is an addition of a slow component of _ VO 2 (Roston et al, 1987;Whipp et al, 2002;Ozyener et al, 2003). The amount of O 2 required at each load, is commonly determined either from a constant load test (Å strand & Rodahl, 1986) or from a linear function of _ VO 2 versus load obtained during an incremental exercise test.…”

Section: Introductionmentioning

confidence: 99%

“…This model is used primarily to determine the time constant for exercise in the moderate intensity domain, while at higher intensities there is an addition of a slow component of _ VO 2 (Roston et al, 1987;Whipp et al, 2002;Ozyener et al, 2003). The amount of O 2 required at each load, is commonly determined either from a constant load test (Å strand & Rodahl, 1986) or from a linear function of _ VO 2 versus load obtained during an incremental exercise test.…”

Section: Introductionmentioning

confidence: 99%

Determination of both the time constant of v̇O₂ and Δv̇O₂/ΔW from a single incremental exercise test: validation and repeatability

Wisén

Wohlfart

2004

Clin Physio Funct Imaging

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SummaryA single incremental cycle exercise test including a steady-state load, combined with respiratory gas exchange, was performed with the objective of determining the time constant (s _ V O 2 ) and the amount of oxygen required at each load (D _ V O 2 /DW) by using a novel equation. The protocol was validated using four exercise tests at different constant loads and conventionally fitted mono-exponential functions to determine s _ V O 2 , and interpolation of _ V O 2 versus load to determine D _ V O 2 /DW. No significant differences were seen between the means of either s _ V O 2 or D _ V O 2 /DW determined with the two protocols. The correlation coefficient was 0AE62 for s _ V O 2 and 0AE48 for D _ V O 2 /DW. The absolute differences (2 SD) were 11AE6 s for s _ V O 2 and 1AE1 ml minThe equations were compared in the same steady-state test and good agreement of s _ V O 2 was obtained (R ¼ 0AE99). The 5-6-week repeatability (incremental test) was evaluated. No statistical differences were seen between the mean of the repeated tests. The difference between the tests (2 SD) were 20 s for s _ V O 2 and 1AE2 ml minV O 2 /DW can be determined from a single incremental test. The validation showed an acceptable agreement, although the variations in absolute values were not negligible. This could partly be explained by the natural day-to-day variation and fluctuations in incoming raw data. The test-retest variation in absolute values was considerable, which must be taken into account when using s _ V O 2 and D _ V O 2 /DW for evaluation of aerobic function.

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Negative accumulated oxygen deficit during heavy and very heavy intensity cycle ergometry in humans

Cited by 27 publications

References 25 publications

Influence of pacing strategy on O₂ uptake and exercise tolerance

Influence of pacing strategy on O₂ uptake and exercise tolerance

Acetyl group availability influences phosphocreatine degradation even during intense muscle contraction

Determination of both the time constant of v̇O₂ and Δv̇O₂/ΔW from a single incremental exercise test: validation and repeatability

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Negative accumulated oxygen deficit during heavy and very heavy intensity cycle ergometry in humans

Cited by 27 publications

References 25 publications

Influence of pacing strategy on O2 uptake and exercise tolerance

Influence of pacing strategy on O2 uptake and exercise tolerance

Acetyl group availability influences phosphocreatine degradation even during intense muscle contraction

Determination of both the time constant of v̇O2 and Δv̇O2/ΔW from a single incremental exercise test: validation and repeatability

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Product

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About

Influence of pacing strategy on O₂ uptake and exercise tolerance

Influence of pacing strategy on O₂ uptake and exercise tolerance

Determination of both the time constant of v̇O₂ and Δv̇O₂/ΔW from a single incremental exercise test: validation and repeatability