The Accumulated Oxygen Deficit Measure and Its Application in Pediatric Exercise Science

1998 ◽  
Vol 10 (1) ◽  
pp. 13-20 ◽  
Author(s):  
Geraldine A. Naughton ◽  
John S. Carlson
Keyword(s):  
High Intensity ◽  
Anaerobic Metabolism ◽  
High Intensity Exercise ◽  
Exhaustive Exercise ◽  
Oxygen Deficit ◽  
Exercise Science ◽  
Energy Contribution ◽  
Accumulated Oxygen Deficit ◽  
Anaerobic Energy ◽  
The Subject

A definitive measure for assessing the energy contribution of anaerobic pathways during exhaustive exercise remains inconclusive. The accumulated oxygen deficit (AOD) has been used in several studies to estimate energy contribution. The underlying assumptions of the AOD measure have been criticized for underestimating the true contribution of anaerobic metabolism in high intensity exercise. Indeed, the AOD measure has been the subject of much controversy. Several of the physiological exercise responses of children may lead to an even greater underestimation of the anaerobic energy contribution to high intensity exercise in children than adults when AOD measures are calculated.

Accumulated oxygen deficit measurements during and after high-intensity exercise in trained male and female adolescents

1997 ◽  
Vol 76 (6) ◽  
pp. 525-531 ◽  
Author(s):  
G. A. Naughton ◽  
J. S. Carlson ◽  
D. C. Buttifant ◽  
S. E. Selig ◽  
K. Meldrum ◽  
...  
Keyword(s):  
High Intensity ◽  
High Intensity Exercise ◽  
Oxygen Deficit ◽  
Female Adolescents ◽  
Male And Female ◽  
Accumulated Oxygen Deficit

Method-Induced Differences of Energy Contributions in Women’s Kayaking

2018 ◽  
Vol 13 (1) ◽  
pp. 9-13
Author(s):  
Yongming Li ◽  
Margot Niessen ◽  
Xiaoping Chen ◽  
Ulrich Hartmann
Keyword(s):  
Relative Energy ◽  
Oxygen Deficit ◽  
Energy Calculation ◽  
Longitudinal Assessment ◽  
Energy Contribution ◽  
Training Experience ◽  
Incremental Exercise Test ◽  
Accumulated Oxygen Deficit ◽  
Anaerobic Energy ◽  
Gas Metabolism

Context: Different relative aerobic energy contribution (WAER%) has been reported for the 2 women’s Olympic kayaking disciplines (ie, 200 and 500 m). Purpose: To investigate whether the adopted method of energy calculation influences the value of WAER% during kayaking time trials. Methods: Eleven adolescent female kayakers (age 14 ± 1 y, height 172 ± 4 cm, body mass 65.4 ± 4.2 kg, VO2peak 42.6 ± 4.9 mL·min−1·kg−1, training experience 1.5 ± 0.3 y) volunteered to participate in 1 incremental exercise test and 2 time trials (40 and 120 s) on the kayak ergometer. A portable spirometric system was used to measure gas metabolism. Capillary blood was taken from the ear lobe during and after the tests and analyzed for lactate afterward. The method of modified maximal accumulated oxygen deficit (m-MAOD) and the method based on the fast component of oxygen-uptake off-kinetics (PCr-La-O2) were used to calculate the energy contributions. Results: The anaerobic energy portions from m-MAOD were lower than those from PCr-La-O2 in the 40-s (41.9 ± 8.8 vs 52.8 ± 4.0 kJ, P > .05) and 120-s (64.1 ± 27.9 vs 68.2 ± 10.0 kJ, P > .05) time trials, which induced differences of WAER% between m-MAOD and PCr-La-O2 (36.0% vs 30.0% in 40 s, P > .05; 60.9% vs 57.5% in 120 s, P > .05). Conclusions: The reported different WAER% in women’s Olympic kayaking could be partly attributed to the adopted method of energy calculation (ie, m-MAOD vs PCr-La-O2). A fixed method of energy calculation is recommended during the longitudinal assessment on the relative energy contribution in women’s Olympic kayaking.

High intensity exercise conditioning increases accumulated oxygen deficit of horses

2010 ◽  
Vol 34 (1) ◽  
pp. 9-16 ◽  
Author(s):  
K. W. HINCHCLIFF ◽  
M. A. LAUDERDALE ◽  
J. DUTSON ◽  
R. J. GEOR ◽  
V. A. LACOMBE ◽  
...  
Keyword(s):  
High Intensity ◽  
High Intensity Exercise ◽  
Oxygen Deficit ◽  
Accumulated Oxygen Deficit

Furosemide reduces accumulated oxygen deficit in horses during brief intense exertion

1996 ◽  
Vol 81 (4) ◽  
pp. 1550-1554 ◽  
Author(s):  
K. W. Hinchcliff ◽  
K. H. McKeever ◽  
W. W. Muir ◽  
R. A. Sams
Keyword(s):  
Blood Lactate ◽  
High Intensity ◽  
Lactate Concentration ◽  
Blood Lactate Concentration ◽  
High Intensity Exercise ◽  
Oxygen Deficit ◽  
Specific Rate ◽  
Rate Of Increase ◽  
Accumulated Oxygen Deficit ◽  
Plasma Lactate Concentration

Hinchcliff, K. W., K. H. McKeever, W. W. Muir, and R. A. Sams. Furosemide reduces accumulated oxygen deficit in horses during brief intense exertion. J. Appl. Physiol. 81(4): 1550–1554, 1996.—We theorized that furosemide-induced weight reduction would reduce the contribution of anaerobic metabolism to energy expenditure of horses during intense exertion. The effects of furosemide on accumulated O2 deficit and plasma lactate concentration of horses during high-intensity exercise were examined in a three-way balance randomized crossover study. Nine horses completed each of three trials: 1) a control (C) trial, 2) a furosemide-unloaded (FU) trial in which the horse received furosemide 4 h before running, and 3) a furosemide weight-loaded (FL) trial during which the horse received furosemide and carried weight equal to the weight lost after furosemide administration. Horses ran for 2 min at ∼120% maximal O2 consumption. Furosemide (FU) increased O2 consumption (ml ⋅ 2 min−1 ⋅ kg−1) compared with C (268 ± 9 and 257 ± 9, P < 0.05), whereas FL was not different from C (252 ± 8). Accumulated O2 deficit (ml O2 equivalents/kg) was significantly ( P < 0.05) lower during FU (81.2 ± 12.5), but not during FL (96.9 ± 12.4), than during C (91.4 ± 11.5). Rate of increase in blood lactate concentration (mmol ⋅ 2 min−1 ⋅ kg−1) after FU (0.058 ± 0.001), but not after FL (0.061 ± 0.001), was significantly ( P < 0.05) lower than after C (0.061 ± 0.001). Furosemide decreased the accumulated O2 deficit and rate of increase in blood lactate concentration of horses during brief high-intensity exertion. The reduction in accumulated O2 deficit in FU-treated horses was attributable to an increase in the mass-specific rate of O2 consumption during the high-intensity exercise test.

scholarly journals Acute administration of high doses of taurine does not substantially improve high-intensity running performance and the effect on maximal accumulated oxygen deficit is unclear

2016 ◽  
Vol 41 (5) ◽  
pp. 498-503 ◽  
Author(s):  
Fabio Milioni ◽  
Elvis de Souza Malta ◽  
Leandro George Spinola do Amaral Rocha ◽  
Camila Angélica Asahi Mesquita ◽  
Ellen Cristini de Freitas ◽  
...  
Keyword(s):  
Oxygen Uptake ◽  
Exercise Intensity ◽  
Maximal Oxygen Uptake ◽  
High Intensity ◽  
Treadmill Running ◽  
Oxygen Deficit ◽  
Time To Exhaustion ◽  
Acute Administration ◽  
Running Performance ◽  
Accumulated Oxygen Deficit

The aim of the present study was to investigate the effects of acute administration of taurine overload on time to exhaustion (TTE) of high-intensity running performance and alternative maximal accumulated oxygen deficit (MAODALT). The study design was a randomized, placebo-controlled, crossover design. Seventeen healthy male volunteers (age: 25 ± 6 years; maximal oxygen uptake: 50.5 ± 7.6 mL·kg−1·min−1) performed an incremental treadmill-running test until voluntary exhaustion to determine maximal oxygen uptake and exercise intensity at maximal oxygen uptake. Subsequently, participants completed randomly 2 bouts of supramaximal treadmill-running at 110% exercise intensity at maximal oxygen uptake until exhaustion (placebo (6 g dextrose) or taurine (6 g) supplementation), separated by 1 week. MAODALT was determined using a single supramaximal effort by summating the contribution of the phosphagen and glycolytic pathways. When comparing the results of the supramaximal trials (i.e., placebo and taurine conditions) no differences were observed for high-intensity running TTE (237.70 ± 66.00 and 277.30 ± 40.64 s; p = 0.44) and MAODALT (55.77 ± 8.22 and 55.06 ± 7.89 mL·kg−1; p = 0.61), which seem to indicate trivial and unclear differences using the magnitude-based inferences approach, respectively. In conclusion, acute 6 g taurine supplementation before exercise did not substantially improve high-intensity running performance and showed an unclear effect on MAODALT.

scholarly journals Antioxidants Facilitate High–intensity Exercise IL–15 Expression in Skeletal Muscle

2018 ◽  
Vol 40 (01) ◽  
pp. 16-22 ◽  
Author(s):  
Alberto Pérez-López ◽  
Marcos Martin-Rincon ◽  
Alfredo Santana ◽  
Ismael Perez-Suarez ◽  
Cecilia Dorado ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Protein Expression ◽  
High Intensity ◽  
Human Skeletal Muscle ◽  
Vastus Lateralis ◽  
Acute Hypoxia ◽  
High Intensity Exercise ◽  
Oxygen Deficit ◽  
Post Exercise ◽  
Sprint Exercise

AbstractInterleukin (IL)-15 stimulates mitochondrial biogenesis, fat oxidation, glucose uptake and myogenesis in skeletal muscle. However, the mechanisms by which exercise triggers IL-15 expression remain to be elucidated in humans. This study aimed at determining whether high-intensity exercise and exercise-induced RONS stimulate IL-15/IL-15Rα expression and its signaling pathway (STAT3) in human skeletal muscle. Nine volunteers performed a 30-s Wingate test in normoxia and hypoxia (PIO2=75 mmHg), 2 h after placebo or antioxidant administration (α-lipoic acid, vitamin C and E) in a randomized double-blind design. Blood samples and muscle biopsies (vastus lateralis) were obtained before, immediately after, and 30 and 120 min post-exercise. Sprint exercise upregulated skeletal muscle IL-15 protein expression (ANOVA, P=0.05), an effect accentuated by antioxidant administration in hypoxia (ANOVA, P=0.022). In antioxidant conditions, the increased IL-15 expression at 120 min post-exercise (33%; P=0.017) was associated with the oxygen deficit caused by the sprint (r=–0.54; P=0.020); while, IL-15 and Tyr705-STAT3 AUCs were also related (r=0.50; P=0.036). Antioxidant administration promotes IL-15 protein expression in human skeletal muscle after sprint exercise, particularly in severe acute hypoxia. Therefore, during intense muscle contraction, a reduced PO2 and glycolytic rate, and possibly, an attenuated RONS generation may facilitate IL-15 production, accompanied by STAT3 activation, in a process that does not require AMPK phosphorylation.

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