O2 Deficit

2012 ◽  
pp. 653-653
Author(s):  
Marleen A. Baak ◽  
Bernard Gutin ◽  
Kim A. Krawczewski Carhuatanta ◽  
Stephen C. Woods ◽  
Heinz W. Harbach ◽  
...  
Keyword(s):  
O2 Deficit

Sex-related differences in accumulated O2 deficit incurred by high-intensity rowing exercise during childhood and adolescence

2021 ◽  
Author(s):  
Joffrey Bardin ◽  
Hugo Maciejewski ◽  
Allison Diry ◽  
Neil Armstrong ◽  
Claire Thomas ◽  
...  
Keyword(s):  
High Intensity ◽  
Childhood And Adolescence ◽  
O2 Deficit

Effects of Walking with Blood Flow Restriction on Excess Post-exercise Oxygen Consumption

2015 ◽  
Vol 36 (03) ◽  
pp. e11-e18 ◽  
Author(s):  
G. Mendonca ◽  
J. Vaz ◽  
P. Pezarat-Correia ◽  
B. Fernhall
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Relative Intensity ◽  
Walking Speed ◽  
Treadmill Exercise ◽  
Young Men ◽  
Blood Flow Restriction ◽  
Post Exercise ◽  
Flow Restriction ◽  
O2 Deficit

AbstractThis study determined the influence of walking with blood flow restriction (BFR) on the excess post-exercise oxygen consumption (EPOC) of healthy young men. 17 healthy young men (22.1±2.9 years) performed graded treadmill exercise to assess VO2peak. In a randomized fashion, each participant performed 5 sets of 3-min treadmill exercise at their optimal walking speed with 1-min interval either with or without BFR. Participants were then seated in a chair and remained there for 30 min of recovery. Expired gases were continuously monitored during exercise and recovery. BFR increased the O2 cost of walking as well as its relative intensity and cumulative O2 deficit (p<0.05). The EPOC magnitude after walking with BFR was greater than in the non-BFR condition (p<0.05). No differences between conditions were seen for the duration of EPOC. The EPOC magnitude was no longer different between conditions after controlling for the differences in relative intensity and in the cumulative O2 deficit (p>0.05). These data indicate that walking with BFR increases the magnitude of EPOC. Moreover, they also demonstrate that such increment in EPOC is likely explained by the effects of BFR on walking relative intensity and cumulative O2 deficit.

Maximum O2 uptake, O2 debt and deficit, and muscle metabolites in Thoroughbred horses

1988 ◽  
Vol 64 (2) ◽  
pp. 781-788 ◽  
Author(s):  
R. J. Rose ◽  
D. R. Hodgson ◽  
T. B. Kelso ◽  
L. J. McCutcheon ◽  
T. A. Reid ◽  
...  
Keyword(s):  
Peak Plasma ◽  
Co2 Production ◽  
Human Beings ◽  
O2 Uptake ◽  
Thoroughbred Horses ◽  
Muscle Ph ◽  
Exercise Muscle ◽  
Muscle Biopsies ◽  
O2 Deficit ◽  
O2 Debt

This study determined maximal O2 uptake (VO2max), maximal O2 deficit, and O2 debt in the Thoroughbred racehorse exercising on an inclined treadmill. In eight horses the O2 uptake (VO2) vs. speed relationship was linear until 10 m/s and VO2max values ranged from 131 to 153 ml.kg-1.min-1. Six of these horses then exercised at 120% of their VO2max until exhaustion. VO2, CO2 production (VCO2), and plasma lactate (La) were measured before and during exercise and through 60 min of recovery. Muscle biopsies were collected before and at 0.25, 0.5, 1, 1.5, 2, 5, 10, 15, 20, 40, and 60 min after exercise. Muscle concentrations of adenosine 5'-triphosphate (ATP), phosphocreatine (PC), La, glucose 6-phosphate (G-6-P), and creatine were determined, and pH was measured. The O2 deficit was 128 +/- 32 (SD) ml/kg (64 +/- 13 liters). The O2 debt was 324 +/- 62 ml/kg (159 +/- 37 liters), approximately two to three times comparative values for human beings. Muscle [ATP] was unchanged, but [PC] was lower (P less than 0.01) than preexercise values at less than or equal to 10 min of recovery. [PC] and VO2 were negatively correlated during both the fast and slow phases of VO2 during recovery. Muscle [La] and [G-6-P] were elevated for 10 min postexercise. Mean muscle pH decreased from 7.05 (preexercise) to 6.75 at 1.5 min recovery, and the mean peak plasma La value was 34.5 mmol/l.(ABSTRACT TRUNCATED AT 250 WORDS)

VO2 kinetics of constant-load exercise following bed-rest-induced deconditioning

1984 ◽  
Vol 57 (5) ◽  
pp. 1545-1550 ◽  
Author(s):  
V. A. Convertino ◽  
D. J. Goldwater ◽  
H. Sandler
Keyword(s):  
Steady State ◽  
Supine Position ◽  
Bed Rest ◽  
Constant Load ◽  
Submaximal Exercise ◽  
Delayed Response ◽  
Total Recovery ◽  
Vo2 Kinetics ◽  
O2 Deficit ◽  
Constant Load Exercise

The purpose of this study was to determine the effects of bed-rest-induced deconditioning on changes in O2 uptake (VO2) kinetics, O2 deficit, steady-state VO2, and recovery VO2 during the performance of constant-load exercise. Five male subjects (36–40 yr) underwent 7 days of continuous bed rest (BR) in the head-down (-6 degrees) position. Two days before (pre) and the day after (post) BR each subject performed one submaximal exercise test in the supine and one in the upright position consisting of 5 min of rest, 5 min of cycle ergometer exercise at 700 kg.m/min, and 10 min of recovery from exercise. VO2 was measured continuously in all tests from 2-liter aliquot gas samples collected every 30 s. Following BR steady-state VO2 was unchanged in supine and upright exercise. In the supine position BR did not change total exercise VO2, O2 deficit, or total recovery VO2. However, compared with pre-BR, total exercise VO2 decreased (P less than 0.05) from 7.41 +/- 0.11 to 7.23 +/- 0.17 liters, O2 deficit increased (P less than 0.05) from 1.15 +/- 0.05 to 1.41 +/- 0.07 liters, and total recovery VO2 increased (P less than 0.05) from 5.17 +/- 0.11 to 5.47 +/- 0.17 liters during the post-BR upright test. Despite the ability to attain similar steady-state VO2 within 5 min, bed-rest-induced deconditioning resulted in a reduction of total VO2 capacity and an increase in the O2 deficit during submaximal constant-load exercise. This change in VO2 kinetics is found only with exercise in the upright rather than supine position implicating orthostatic mechanisms in the delayed response to submaximal exercise.

Limb skeletal muscle adaptation in athletes after training at altitude

1990 ◽  
Vol 68 (2) ◽  
pp. 496-502 ◽  
Author(s):  
M. Mizuno ◽  
C. Juel ◽  
T. Bro-Rasmussen ◽  
E. Mygind ◽  
B. Schibye ◽  
...  
Keyword(s):  
Sea Level ◽  
Enzyme Activities ◽  
Buffer Capacity ◽  
Altitude Training ◽  
Mitochondrial Enzyme ◽  
Muscle Adaptation ◽  
Short Term ◽  
Vo2 Max ◽  
Capillary Supply ◽  
O2 Deficit

Morphological and biochemical characteristics of biopsies obtained from gastrocnemius (GAS) and triceps brachii muscle (TRI), as well as maximal O2 uptake (VO2 max) and O2 deficit, were determined in 10 well-trained cross-country skiers before and after a 2-wk stay (2,100 m above sea level) and training (2,700 m above sea level) at altitude. On return to sea level, VO2 max was the same as the prealtitude value, whereas an increase in O2 deficit (29%) and in short-term running performance (17%) was observed (P less than 0.05). GAS showed maintained capillary supply but a 10% decrease in mitochondrial enzyme activities (P less than 0.05), whereas an increase in capillary supply (P less than 0.05) but unchanged mitochondrial enzyme activities were observed in TRI. Buffer capacity was increased by 6% in both GAS and TRI (P less than 0.05). A positive correlation was found between the relative increase in buffer capacity of GAS and short-term running time (P less than 0.05). Thus the present study indicates no effect of 2 wk of altitude training on VO2 max but provides evidence to suggest an improvement in short-term exercise performance, which may be the result of an increase in muscle buffer capacity.

The Effect of Pacing Strategy on O2 Deficit During the First 5K of a 20K Cycling Time Trial

2006 ◽  
Vol 38 (Supplement) ◽  
pp. S224
Author(s):  
Tim Streeper ◽  
Jeremiah Peiffer ◽  
Irvin E. Faria ◽  
Roberto Quintana ◽  
Daryl L. Parker
Keyword(s):  
Time Trial ◽  
Cycling Time Trial ◽  
Pacing Strategy ◽  
Cycling Time ◽  
O2 Deficit

O2 uptake kinetics and the O2 deficit as related to exercise intensity and blood lactate

1993 ◽  
Vol 75 (2) ◽  
pp. 755-762 ◽  
Author(s):  
T. J. Barstow ◽  
R. Casaburi ◽  
K. Wasserman
Keyword(s):  
Blood Lactate ◽  
Time Constant ◽  
Exercise Intensity ◽  
Power Output ◽  
Cycle Ergometer ◽  
O2 Uptake ◽  
Ergometer Exercise ◽  
Lactate Levels ◽  
Power Outputs ◽  
O2 Deficit

The dynamic responses of O2 uptake (VO2) to a range of constant power output levels were related to exercise intensity [as percent maximal VO2 and as below vs. above lactic acid threshold (LAT)] and to the associated end-exercise lactate in three groups of subjects: group I, untrained subjects performing leg cycle ergometer exercise; group II, the same subjects performing arm cycle exercise; and group III, trained cyclists performing leg cycle ergometer exercise. Responses were described by a double-exponential equation, with each component having an independent time delay, which reduced to a monoexponential description for moderate (below-LAT) exercise. When a second exponential component to the VO2 response was present, it did not become evident until approximately 80–100 s into exercise. An overall time constant (tau T, determined as O2 deficit for the total response divided by net end-exercise VO2) and a primary time constant (tau P, determined from the O2 deficit and the amplitude for the early primary VO2 response) were compared. The tau T rose with power output and end-exercise lactate levels, but tau P was virtually invariant, even at high end-exercise lactate levels. Moreover the gain of the primary exponential component (as delta VO2/delta W) was constant across power outputs and blood lactate levels, suggesting that the primary VO2 response reflects a linear system, even at higher power outputs. These results suggest that elevated end-exercise lactate is not associated with any discernible slowing of the primary rise in VO2.(ABSTRACT TRUNCATED AT 250 WORDS)

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