Literatura académica sobre el tema "VO2 slow component"

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.

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.

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.

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.

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)

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.

Established models of endurance performance (Costill et al. (1973) Med Sci Sports 5(4): 248-252 and Coyle (1995) Ex. Sport Sci. Rev. 23:25-63) are based on the athlete's ability to maintain a fixed %V02peak, normally within the severe intensity domain, e.g. 88 %V02peak (exercise intensity domains being defined as; rest-moderate-heavy-severe-V02peak; Whipp (1994) Med. Sci. Sports Exerc. 26(11): 1319-13-26). The V02 slow component (V02SC) concept (Gaesser and Poole, 1996, Ex. Sport Sci. Rev. 24:35-70), which is based on observations from a healthy/sedentary populations', states that V02 continually increases within the severe intensity domain, and therefore undermines the validity of the performance models. This thesis examined the V02SC in an endurance trained cyclist population. Within the models, V02peak sets the ceiling for endurance performance. Current V02SC theory suggests that V02p"k assessment is protocol independent, as V02 continually increases within the severe intensity domain. This thesis demonstrated that V02peak was protocol dependent for 3 ramp protocols (35, 20 and 5 W.min-'), the V02SC being unable to generate a V02peak response from the 5 W.min-' protocol even though the subjects worked within the severe intensity domain. The V02SC definition states that V02 is elevated above values predicted from moderate intensity exercise at heavy, and increases continually, at severe exercise intensities. The endurance trained subjects demonstrated elevated steady state V02 responses at exercise intensities up to their endurance performance V02. This was within the severe intensity domain, thus validating the performance models for this subject population. The V02SC response in endurance trained cyclists differed from that previously observed for a sedentary/healthy population, therefore the currently accepted cause, increased fast twitch (FT) muscle fibre recruitment, may be questioned. Evidence from EMG studies suggest that muscle recruitment patterns differ between muscles, with increasing intensity (Green and Patla (1992) Med. Sci. Sports Ex. 24(1): 38-46). The recruitment patterns of three muscles were examined during incremental exercise to establish changes in both the magnitude of activation, and potential changes in fibre type recruitment (via the median frequency response). The pattern of muscle recruitment varied between both subjects and muscles. Changes in the recruitment patterns of a number of individual muscles were coincidental with the initiation of the V02SC. No coincidence between muscle fibre type recruitment (assessed via the EMG median frequency response) and the V02SC in endurance trained cyclists was observed. Therefore the V02SC may be due to changes in muscle recruitment patterns as well as FT fibre recruitment. The results of this thesis suggest that current models of endurance performance are valid for the endurance trained cyclist population studied, and that the V02SC concept should be redefined for this population. The V02SC response observed may be due to changes in muscle recruitment patterns and an increase in the number of motor units recruited, as median frequency EMG measures did not support the hypothesis that the V02SC is principally caused by an increased recruitment of FT muscle fibres.

L'objectif de cette thèse était triple 1)- Etudier la fonction ventilatoire durant un exercice incrémental maximal et un exercice sous-maximal prolongé chez des sportifs porteurs de trait drépanocytaire (PTD) 2)- Etudier la performance de la fonction ventilatoire durant un exercice à charge constante chez des sujets ayant une β-thalassémie mineure, 3)- Evaluer l'adaptation physiologique durant un effort sous-maximal prolongé chez des sportifs atteints de drépanocytose hétérozygote. La première étude a montré que l'exercice incrémental maximal et l'exercice à charge constante induisent une fatigue spirométrique, de la force et de l'endurance des muscles respiratoires chez les sujets porteurs de trait drépanocytaire. L'exercice rectangulaire affecte de façon importante la force et l'endurance musculaire respiratoire que l'exercice triangulaire. La deuxième étude a montré par ailleurs, une altération de la performance de la fonction ventilatoire après la réalisation d'un exercice sous-maximal prolongé chez les sujets ayant une β-thalassémie mineure. Ainsi, une diminution importante de l'endurance des muscles respiratoires a été constatée chez ces individus pathologiques en réponse à l'exercice à charge constante par rapport aux sujets sains. Ces résultats confirment que les sujets ayant des hémoglobinopathies n'ont pas la capacité de maintenir des niveaux élevés de ventilation pendant un exercice physique intense. Ensuite, lors de la troisième étude, la détermination de la PMA a permis d'affirmer que la forme hétérozygote de la drépanocytose n'est pas un facteur limitant de l'aptitude physique aérobie maximale. L'adaptation à un effort sous-maximal, évaluée par la phase rapide est parfaitement normale chez les sujets ayant un trait drépanocytaire. Par contre, l'amplitude de la composante lente de VO2, plus élevée chez les PTD suggère que ces individus pathologiques se caractérisent par une mauvaise tolérance à l'effort. Cette élévation était corrélée avec l'HbO2 et HHb qui étaient stables durant l'effort. Cette stabilité confirme la génération du mécanisme de remodelage vasculaire chez les PTD en réponse à des problèmes hémorhéologiques produits par l'effort. Une augmentation précoce du RMS et une diminution linéaire de 25,63% de MPF corrélée avec HHb, ont été constatées durant l'effort chez les individus pathologiques par rapport aux sujets sans hémoglobinopathie, affirmant que la baisse de déformabilité des globules rouges dont sont signalés généralement les sujets porteurs de trait drépanocytaire bouleverse de façon accrue la microcirculation musculaire qui pourrait être responsable de la composante lente de VO2. Ces résultats montrent que les sujets ayant une hémoglobinopathie pourraient avoir une fonction ventilatoire moins performante durant un effort physique intense que les sujets sains. Également, ces individus pourraient avoir une fatigue musculaire périphérique plus importante que les sujets à hémoglobine normale et une oxygénation musculaire stable durant un exercice rectangulaire. Ils présentent une capacité aérobie et une tolérance à l'effort d'endurance, inférieures aux sujets sains durant un effort sous-maximal
The aim of this thesis was threefold 1)- To study the ventilatory function during a maximal incremental exercise and a prolonged submaximal exercise in athletes with sickle cell trait (SCT), 2)- To study the performance of the ventilatory function during a constant load exercise in subjects with minor β-thalassemia, 3)- Evaluate the physiological adaptation during prolonged submaximal exercise in athletes with heterozygous sickle cell disease. The first study showed that maximal incremental exercise and constant load exercise induce spirometric fatigue, and decreased strength and endurance of the respiratory muscles in subjects with sickle cell trait. Rectangular exercise significantly affects respiratory muscle strength and endurance than triangular exercise. The second study was showed an impairment of the performance of ventilatory function after performing prolonged submaximal exercise in subjects with minor β-thalassemia. Thus, a significant decrease in the endurance of the respiratory muscles was observed in these pathological individuals in response to constant load exercise compared to healthy subjects. These results confirm that hemoglobinopathic subjects do not have the ability to maintain high levels of ventilation during intense physical exercise. Then, in the third study, the determination of the MAP confirmed that the heterozygous form of sickle cell disease is not a limiting factor in maximal aerobic physical fitness. Adaptation to submaximal effort, assessed by the rapid phase, is perfectly normal in subjects with sickle cell trait. In contrast, the amplitude of the slow component of VO2, which is higher in SCT, suggests that these pathological individuals are characterized by weak tolerance to exercise. This rise was correlated with HbO2 and HHb which were satble during exercise. This stability confirms the generation of the vascular remodeling mechanism in SCT in response to hemorheological problems produced by exercise. An precocious increase in RMS and a 25.63% linear decrease in MPF correlated with HHb, were observed during exercise in pathologic individuals compared to subjects without hemoglobinopathy, affirming that the decrease in erythrocyte deformabilities which are generally reported in subjects with sickle cell trait disrupts the muscular microcirculation in an increased manner which could be responsible for the slow component of VO2. These results show that subjects with hemoglobinopathy could have a less efficient ventilatory function during intense physical exertion than healthy subjects. Also, these individuals might have more significant peripheral muscle fatigue than subjects with normal hemoglobin and stable muscle oxygenation during rectangular exercise. They exhibit aerobic capacity and tolerance to endurance effort inferior than healthy subjects during submaximal effort