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Добірка наукової літератури з теми "VO2 slow component"

Автор: Grafiati

Опубліковано: 11 березня 2023

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Статті в журналах з теми "VO2 slow component"

Fontana, Federico Y., Giorgia Spigolon, and Silvia Pogliaghi. "VO2 Slow Component." Medicine & Science in Sports & Exercise 48 (May 2016): 200. http://dx.doi.org/10.1249/01.mss.0000485602.73906.88.

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Wasserman, K. "Coupling of external to cellular respiration during exercise: the wisdom of the body revisited." American Journal of Physiology-Endocrinology and Metabolism 266, no. 4 (1994): E519—E539. http://dx.doi.org/10.1152/ajpendo.1994.266.4.e519.

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The changes in cellular respiration needed to increase energy output during exercise are intimately and predictably linked to external respiration through the circulation. This review addresses the mechanisms by which lactate accumulation might influence O2 uptake (VO2) and CO2 output (VCO2) kinetics. Respiratory homeostasis (a steady state with respect to VO2 and VCO2) is achieved by 3-4 min for work rates not associated with an increase in arterial lactate. When blood lactate increases significantly above rest for constant work rate exercise, VO2 characteristically increases past 3 min (slow component) at a rate proportional to the lactate concentration increase. The development of a similar slow component in VCO2 is not evident. The divergence of VCO2 from VO2 increase can be accounted for by extra CO2 release from the cell as HCO3- buffers lactic acid. Thus the slow component of aerobic CO2 production (parallel to VO2) is masked by the increase in buffer VCO2. This CO2, and the consumption of extracellular HCO3- by the lactate-producing cells, shifts the oxyhemoglobin dissociation curve rightward (Bohr effect). The exercise lactic acidosis has been observed to occur after the minimal capillary PO2 is reached. Thus the lactic acidosis serves to facilitate oxyhemoglobin dissociation and O2 transport to the muscle cells without a further decrease in end-capillary PO2. From these observations, it is hypothesized that simultaneously measured dynamic changes in VO2 and VCO2 might be useful to infer the aerobic and anaerobic contributions to exercise bioenergetics for a specific work task.

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Colosio, Alessandro L., Kevin Caen, Jan G. Bourgois, Jan Boone, and Silvia Pogliaghi. "Bioenergetics of the VO2 slow component between exercise intensity domains." Pflügers Archiv - European Journal of Physiology 472, no. 10 (2020): 1447–56. http://dx.doi.org/10.1007/s00424-020-02437-7.

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Abstract During heavy and severe constant-load exercise, VO2 displays a slow component (VO2sc) typically interpreted as a loss of efficiency of locomotion. In the ongoing debate on the underpinnings of the VO2sc, recent studies suggested that VO2sc could be attributed to a prolonged shift in energetic sources rather than loss of efficiency. We tested the hypothesis that the total cost of cycling, accounting for aerobic and anaerobic energy sources, is affected by time during metabolic transitions in different intensity domains. Eight active men performed 3 constant load trials of 3, 6, and 9 min in the moderate, heavy, and severe domains (i.e., respectively below, between, and above the two ventilatory thresholds). VO2, VO2 of ventilation and lactate accumulation ([La−]) were quantified to calculate the adjusted oxygen cost of exercise (AdjO2Eq, i.e., measured VO2 − VO2 of ventilation + VO2 equivalent of [La−]) for the 0–3, 3–6, and 6–9 time segments at each intensity, and compared by a two-way RM-ANOVA (time × intensity). After the transient phase, AdjO2Eq was unaffected by time in moderate (ml*3 min−1 at 0–3, 0–6, 0–9 min: 2126 ± 939 < 2687 ± 1036, 2731 ± 1035) and heavy (4278 ± 1074 < 5121 ± 1268, 5225 ± 1123) while a significant effect of time was detected in the severe only (5863 ± 1413 < 7061 ± 1516 < 7372 ± 1443). The emergence of the VO2sc was explained by a prolonged shift between aerobic and anaerobic energy sources in heavy (VO2 − VO2 of ventilation: ml*3 min−1 at 0–3, 0–6, 0–9 min: 3769 ± 1128 < 4938 ± 1256, 5091 ± 1123, [La−]: 452 ± 254 < 128 ± 169, 79 ± 135), while a prolonged metabolic shift and a true loss of efficiency explained the emergence of the VO2sc in severe.

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Womack, C. J., S. E. Davis, J. L. Blumer, E. Barrett, A. L. Weltman, and G. A. Gaesser. "Slow component of O2 uptake during heavy exercise: adaptation to endurance training." Journal of Applied Physiology 79, no. 3 (1995): 838–45. http://dx.doi.org/10.1152/jappl.1995.79.3.838.

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Seven untrained male subjects [age 25.6 +/- 1.5 (SE) yr, peak O2 uptake (VO2) 3.20 +/- 0.19 l/min] trained on a cycle ergometer 4 days/wk for 6 wk, with the absolute training workload held constant for the duration of training. Before and at the end of each week of training, the subjects performed 20 min of constant-power exercise at a power designed to elicit a pronounced slow component of VO2 (end-exercise VO2-VO2 at minute 3 of exercise) in the pretraining session. An additional 20-min exercise bout was performed after training at this same absolute power output during which epinephrine (Epi) was infused at a rate of 100 ng.kg-1.min-1 between minutes 10 and 20. After 2 wk of training, significant decreases in VO2 slow component, end-exercise VO2, blood lactate ([La-] and glucose concentrations, plasma Epi ([Epi]) and norepinephrine concentrations, ventilation (VE), and heart rate (HR) were observed (P < 0.05). Although the rapid attenuation of the VO2 slow component coincided temporally with reductions in plasma [Epi], blood [La-], and VE, the infusion of Epi after training significantly increased plasma [Epi] (delta 2.22 ng/ml), blood [La-] (delta 2.4 mmol/l) and VE (delta 10.0 l/min) without any change in exercise VO2. We therefore conclude that diminution of the VO2 slow component with training is attributable to factors other than the reduction in plasma [Epi], blood [La-] and VE.

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Heck, Kristen L., Jeffrey A. Potteiger, Karen L. Nau, and Jan M. Schroeder. "Sodium Bicarbonate Ingestion Does Not Attenuate the VO2 Slow Component during Constant-Load Exercise." International Journal of Sport Nutrition 8, no. 1 (1998): 60–69. http://dx.doi.org/10.1123/ijsn.8.1.60.

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We examined the effects of sodium bicarbonate ingestion on the VO2 slow component during constant-load exercise. Twelve physically active males performed two 30-min cycling trials at an intensity above the lactate threshold. Subjects ingested either sodium bicarbonate (BIC) or placebo (PLC) in a randomized. counterbalanced order. Arterialized capillary blood samples were analyzed for pH, bicarbonate concentration ([HCO3−), and lactate concentration ([La]). Expired gas samples were analyzed for oxygen consumption (VO2). The VO2 slow component was defined as the change in VO2 from Minutes 3 and 4 to Minutes 28 and 29. Values for pH and [HCO3−] were significantly higher for BIC compared to PLC. There was no significant difference in [La] between conditions. For both conditions there was a significant time effect for VO2 during exercise: however, no significant difference was observed between BIC and PLC. While extracellular acid-base measures were altered during the BIC trial, sodium bicarbonate ingestion did not attenuate the VO2 slow component during constant-load exercise.

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Billat, V. L. "VO2 slow component and performance in endurance sports." British Journal of Sports Medicine 34, no. 2 (2000): 83–85. http://dx.doi.org/10.1136/bjsm.34.2.83.

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Lucia, A. "The slow component of VO2 in professional cyclists." British Journal of Sports Medicine 34, no. 5 (2000): 367–74. http://dx.doi.org/10.1136/bjsm.34.5.367.

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Jones, A. "VO2 slow component and performance in endurance sports." British Journal of Sports Medicine 34, no. 6 (2000): 473. http://dx.doi.org/10.1136/bjsm.34.6.473.

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Poole, D. C., W. Schaffartzik, D. R. Knight, et al. "Contribution of excising legs to the slow component of oxygen uptake kinetics in humans." Journal of Applied Physiology 71, no. 4 (1991): 1245–60. http://dx.doi.org/10.1152/jappl.1991.71.4.1245.

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Rates of performing work that engender a sustained lactic acidosis evidence a slow component of pulmonary O2 uptake (VO2) kinetics. This slow component delays or obviates the attainment of a stable VO2 and elevates VO2 above that predicted from considerations of work rate. The mechanistic basis for this slow component is obscure. Competing hypotheses depend on its origin within either the exercising limbs or the rest of the body. To resolve this question, six healthy males performed light nonfatiguing [approximately 50% maximal O2 uptake (VO2max)] and severe fatiguing cycle ergometry, and simultaneous measurements were made of pulmonary VO2 and leg blood flow by thermodilution. Blood was sampled 1) from the femoral vein for O2 and CO2 pressures and O2 content, lactate, pH, epinephrine, norepinephrine, and potassium concentrations, and temperature and 2) from the radial artery for O2 and CO2 pressures, O2 content, lactate concentration, and pH. Two-leg VO2 was thus calculated as the product of 2 X blood flow and arteriovenous O2 difference. Blood pressure was measured in the radial artery and femoral vein. During light exercise, both pulmonary and leg VO2 remained stable from minute 3 to the end of exercise (26 min). In contrast, during severe exercise [295 +/- 10 (SE) W], pulmonary VO2 increased 19.8 +/- 2.4% (P less than 0.05) from minute 3 to fatigue (occurring on average at 20.8 min). Over the same period, leg VO2 increased by 24.2 +/- 5.2% (P less than 0.05). Increases of leg and pulmonary VO2 were highly correlated (r = 0.911), and augmented leg VO2 could account for 86% of the rise in pulmonary VO2.(ABSTRACT TRUNCATED AT 250 WORDS)

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Jones, Andrew M., and Mark Burnley. "Oxygen Uptake Kinetics: An Underappreciated Determinant of Exercise Performance." International Journal of Sports Physiology and Performance 4, no. 4 (2009): 524–32. http://dx.doi.org/10.1123/ijspp.4.4.524.

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The rate at which VO2 adjusts to the new energy demand following the onset of exercise strongly influences the magnitude of the “O2 defcit” incurred and thus the extent to which muscle and systemic homeostasis is perturbed. Moreover, during continuous high-intensity exercise, there is a progressive loss of muscle contractile efficiency, which is reflected in a “slow component” increase in VO2. The factors that dictate the characteristics of these fast and slow phases of the dynamic response of VO2 following a step change in energy turnover remain obscure. However, it is clear that these features of the VO2 kinetics have the potential to influence the rate of muscle fatigue development and, therefore, to affect sports performance. This commentary outlines the present state of knowledge on the characteristics of, and mechanistic bases to, the VO2 response to exercise of different intensities. Several interventions have been reported to speed the early VO2 kinetics and/or reduce the magnitude of the subsequent VO2 slow component, and the possibility that these might enhance exercise performance is discussed.

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