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Journal articles on the topic 'Slow component of VO2'

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Published: 18 October 2022

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1

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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2

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 (April 1, 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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3

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 (July 14, 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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4

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 (September 1, 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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5

Billat, V. L. "VO2 slow component and performance in endurance sports." British Journal of Sports Medicine 34, no. 2 (April 1, 2000): 83–85. http://dx.doi.org/10.1136/bjsm.34.2.83.

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6

Lucia, A. "The slow component of VO2 in professional cyclists." British Journal of Sports Medicine 34, no. 5 (October 1, 2000): 367–74. http://dx.doi.org/10.1136/bjsm.34.5.367.

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7

Jones, A. "VO2 slow component and performance in endurance sports." British Journal of Sports Medicine 34, no. 6 (December 1, 2000): 473. http://dx.doi.org/10.1136/bjsm.34.6.473.

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8

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 (March 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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9

Poole, D. C., W. Schaffartzik, D. R. Knight, T. Derion, B. Kennedy, H. J. Guy, R. Prediletto, and P. D. Wagner. "Contribution of excising legs to the slow component of oxygen uptake kinetics in humans." Journal of Applied Physiology 71, no. 4 (October 1, 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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10

Fawkner, S. G., and N. Armstrong. "VO2 SLOW COMPONENT RELATIVE TO CRITICAL POWER IN CHILDREN." Medicine & Science in Sports & Exercise 34, no. 5 (May 2002): S86. http://dx.doi.org/10.1097/00005768-200205001-00481.

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11

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 (December 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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12

Poole, D. C., L. B. Gladden, S. Kurdak, and M. C. Hogan. "L-(+)-lactate infusion into working dog gastrocnemius: no evidence lactate per se mediates VO2 slow component." Journal of Applied Physiology 76, no. 2 (February 1, 1994): 787–92. http://dx.doi.org/10.1152/jappl.1994.76.2.787.

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Constant-load exercise that engenders a sustained lactic acidosis (i.e., above the lactate threshold) is accompanied by a slow component of O2 uptake (VO2) kinetics that increases VO2 above rather than toward the predicted value. This response arises predominantly from within the exercising limbs and is temporally correlated with that of blood lactate. Lactate exerts a disproportionate metabolic stimulatory effect on gluconeogenic tissues, and there is a strong indication that lactate infusions may increase VO2 of resting tissues. To investigate the potential role of lactate in the VO2 slow component, we infused lactate in 20-min square-wave pulses (change of 10 mM) into the arterial blood supply of an electrically stimulated and surgically isolated dog gastrocnemius preparation (2 x 60-min bouts, approximately 30–40% peak VO2; n = 5) under iso-pH conditions at constant muscle temperature. With lactate infusions, intramuscular lactate concentration ([La]) rose proportionally with inflowing [La] (muscle [La] = 6.34 + 0.38 blood [La]; r = 0.642, P < 0.05) to approximately 80% of arterial blood [La], and neither blood (control, 7.39 +/- 0.01; high lactate, 7.40 +/- 0.01; P > 0.05) nor muscle (control, 7.02 +/- 0.03; high lactate, 7.00 +/- 0.04; P > 0.05) pH was changed. Compared with control values, lactate infusion decreased muscle VO2 from 5.1 +/- 0.3 to 4.1 +/- 0.2 ml.min-1.100 g-1 (P < 0.05). However, VO2 relative to tension remained constant. Notwithstanding the obvious differences between this preparation and the exercising human, this finding does not support a role for lactate per se in driving the VO2 slow component during intense exercise.

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13

Hagberg, J. M., D. S. King, M. A. Rogers, S. J. Montain, S. M. Jilka, W. M. Kohrt, and S. L. Heller. "Exercise and recovery ventilatory and VO2 responses of patients with McArdle's disease." Journal of Applied Physiology 68, no. 4 (April 1, 1990): 1393–98. http://dx.doi.org/10.1152/jappl.1990.68.4.1393.

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This study was designed to determine whether patients with McArdle's disease, who do not increase their blood lactate levels during and after maximal exercise, have a slow “lactacid” component to their recovery O2 consumption (VO2) response after high-intensity exercise. VO2 was measured breath by breath during 6 min of rest before exercise, a progressive maximal cycle ergometer test, and 15 min of recovery in five McArdle's patients, six age-matched control subjects, and six maximal O2 consumption- (VO2 max) matched control subjects. The McArdle's patients' ventilatory threshold occurred at the same relative exercise intensity [71 +/- 7% (SD) VO2max] as in the control groups (60 +/- 13 and 70 +/- 10% VO2max) despite no increase and a 20% decrease in the McArdle's patients' arterialized blood lactate and H+ levels, respectively. The recovery VO2 responses of all three groups were better fit by a two-, than a one-, component exponential model, and the parameters of the slow component of the recovery VO2 response were the same in the three groups. The presence of the same slow component of the recovery VO2 response in the McArdle's patients and the control subjects, despite the lack of an increase in blood lactate or H+ levels during maximal exercise and recovery in the patients, provides evidence that this portion of the recovery VO2 response is not the result of a lactacid mechanism. In addition, it appears that the hyperventilation that accompanies high-intensity exercise may be the result of some mechanism other than acidosis or lung CO2 flux.

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14

Oliveira, Diogo R., Lio F. Gonçalves, António M. Reis, Ricardo J. Fernandes, Nuno D. Garrido, and Victor M. Reis. "The oxygen uptake slow component at submaximal intensities in breaststroke swimming." Journal of Human Kinetics 51, no. 1 (June 1, 2016): 165–73. http://dx.doi.org/10.1515/hukin-2015-0179.

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Abstract The present work proposed to study the oxygen uptake slow component (VO2 SC) of breaststroke swimmers at four different intensities of submaximal exercise, via mathematical modeling of a multi-exponential function. The slow component (SC) was also assessed with two different fixed interval methods and the three methods were compared. Twelve male swimmers performed a test comprising four submaximal 300 m bouts at different intensities where all expired gases were collected breath by breath. Multi-exponential modeling showed values above 450 ml·min−1 of the SC in the two last bouts of exercise (those with intensities above the lactate threshold). A significant effect of the method that was used to calculate the VO2 SC was revealed. Higher mean values were observed when using mathematical modeling compared with the fixed interval 3rd min method (F=7.111; p=0.012; η2=0.587); furthermore, differences were detected among the two fixed interval methods. No significant relationship was found between the SC determined by any method and the blood lactate measured at each of the four exercise intensities. In addition, no significant association between the SC and peak oxygen uptake was found. It was concluded that in trained breaststroke swimmers, the presence of the VO2 SC may be observed at intensities above that corresponding to the 3.5 mM-1 threshold. Moreover, mathematical modeling of the oxygen uptake on-kinetics tended to show a higher slow component as compared to fixed interval methods.

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15

Casaburi, R., T. J. Barstow, T. Robinson, and K. Wasserman. "Influence of work rate on ventilatory and gas exchange kinetics." Journal of Applied Physiology 67, no. 2 (August 1, 1989): 547–55. http://dx.doi.org/10.1152/jappl.1989.67.2.547.

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A linear system has the property that the kinetics of response do not depend on the stimulus amplitude. We sought to determine whether the responses of O2 uptake (VO2), CO2 output (VCO2), and ventilation (VE) in the transition between loadless pedaling and higher work rates are linear in this respect. Four healthy subjects performed a total of 158 cycle ergometer tests in which 10 min of exercise followed unloaded pedaling. Each subject performed three to nine tests at each of seven work rates, spaced evenly below the maximum the subject could sustain. VO2, VCO2, and VE were measured breath by breath, and studies at the same work rate were time aligned and averaged. Computerized nonlinear regression techniques were used to fit a single exponential and two more complex expressions to each response time course. End-exercise blood lactate was determined at each work rate. Both VE and VO2 kinetics were markedly slower at work rates associated with sustained blood lactate elevations. A tendency was also detected for VO2 (but not VE) kinetics to be slower as work rate increased for exercise intensities not associated with lactic acidosis (P less than 0.01). VO2 kinetics at high work rates were well characterized by the addition of a slower exponential component to the faster component, which was seen at lower work rates. In contrast, VCO2 kinetics did not slow at the higher exercise intensities; this may be the result of the coincident influence of several sources of CO2 related to lactic acidosis. These findings provide guidance for interpretation of ventilatory and gas exchange kinetics.

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16

Hallen, J., G. K. Resaland, and S. B. Aasen. "INTERMITTENT ISOMETRIC EXERCISE, A NEW MODEL TO STUDY VO2 SLOW COMPONENT." Medicine & Science in Sports & Exercise 33, no. 5 (May 2001): S326. http://dx.doi.org/10.1097/00005768-200105001-01830.

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17

Pedersen, P. K., J. Franch, K. Madsen, and M. S. Djurhuus. "SHORT-INTERVAL RUN TRAINING REDUCES THE SLOW VO2 COMPONENT DURING RUNNING." Medicine & Science in Sports & Exercise 30, Supplement (May 1998): 190. http://dx.doi.org/10.1097/00005768-199805001-01080.

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18

Lucía, Alejandro, Jesús Hoyos, Margarita Pérez, and José L. Chicharro. "Thyroid Hormones May Influence the Slow Component of VO2 in Professional Cyclists." Japanese Journal of Physiology 51, no. 2 (2001): 239–42. http://dx.doi.org/10.2170/jjphysiol.51.239.

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19

Faina, M., G. B. Mirri, F. Felici, and A. Rosponi. "COMPARISON BETWEEN VO2 SLOW COMPONENT AT SEA LEVEL AND AT HIGH ALTITUDE." Medicine & Science in Sports & Exercise 31, Supplement (May 1999): S182. http://dx.doi.org/10.1097/00005768-199905001-00811.

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20

Bernasconi, Sylvain, Nicolas Tordi, Stéphane Perrey, Bernard Parratte, and Guy Monnier. "Is the VO2 slow component in heavy arm-cranking exercise associated with recruitment of type II muscle fibers as assessed by an increase in surface EMG?" Applied Physiology, Nutrition, and Metabolism 31, no. 4 (August 2006): 414–22. http://dx.doi.org/10.1139/h06-021.

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The recruitment of additional type II muscle fibers is one mechanism often suggested to be responsible for the slow component of oxygen uptake (VO2 SC). We hypothesized that surface electromyogram (EMG) of the biceps brachii, triceps brachii, anterior deltoid, and infraspinatus muscles could be related to the VO2 SC amplitude during arm-cranking exercises above ventilatory threshold (VT). Eight healthy subjects performed transitions from rest to 6-min heavy exercise at a constant power output of approximately 40% between VT and peak VO2. A 2-component exponential model was used to fit the VO2 response. EMG were recorded the last 15 s of each minute to obtain root mean square (RMS) and mean power frequency (MPF). Mean EMG responses for RMS and MPF were calculated by averaging EMG responses of the 4 muscles. The VO2 SC amplitude was of 530 ± 166 mL/min and occurred after 134 ± 31 s of exercise onset. Significant correlations were found for most of the subjects between EMG parameters and the VO2 SC amplitude as determined between the 2nd and the 6th minute. For all muscles, RMS values significantly increased over time during the VO2 SC, whereas MPF decreased significantly. These results suggest a relation between the recruitment of additional type II muscle fibers and the VO2 SC in arm-cranking exercises.

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21

Ferri, Alessandra, Mauro Marzorati, Saverio Adamo, Francesca Lanfranconi, Angelo Colombini, Paolo Capodaglio, Antonietta Marchi, and Bruno Grassi. "Absence Of A Slow Component Of Pulmonary VO2 Kinetics In Very Old Subjects." Medicine & Science in Sports & Exercise 36, Supplement (May 2004): S10. http://dx.doi.org/10.1097/00005768-200405001-00046.

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22

Ferri, Alessandra, Mauro Marzorati, Saverio Adamo, Francesca Lanfranconi, Angelo Colombini, Paolo Capodaglio, Antonietta Marchi, and Bruno Grassi. "Absence Of A Slow Component Of Pulmonary VO2 Kinetics In Very Old Subjects." Medicine & Science in Sports & Exercise 36, Supplement (May 2004): S10. http://dx.doi.org/10.1249/00005768-200405001-00046.

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23

Shelden, Melissa A., Vassilios G. Vardaxis, Julian Rivera, Brooke A. Boley, and Joseph P. Weir. "Lack of Association Betyween Changes In Running Mechanics and the VO2 Slow Component." Medicine & Science in Sports & Exercise 43, Suppl 1 (May 2011): 386. http://dx.doi.org/10.1249/01.mss.0000401064.09437.1b.

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24

Cleland, Sarah Margaret, Juan Manuel Murias, John Michael Kowalchuk, and Donald Hugh Paterson. "Effects of prior heavy-intensity exercise on oxygen uptake and muscle deoxygenation kinetics of a subsequent heavy-intensity cycling and knee-extension exercise." Applied Physiology, Nutrition, and Metabolism 37, no. 1 (February 2012): 138–48. http://dx.doi.org/10.1139/h11-143.

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This study examined the effects of prior heavy-intensity exercise on the adjustment of pulmonary oxygen uptake (VO2p) and muscle deoxygenation Δ[HHb] during the transition to subsequent heavy-intensity cycling (CE) or knee-extension (KE) exercise. Nine young adults (aged 24 ± 5 years) performed 4 repetitions of repeated bouts of heavy-intensity exercise separated by light-intensity CE and KE, which included 6 min of baseline exercise, a 6-min step of heavy-intensity exercise (H1), 6-min recovery, and a 6-min step of heavy-intensity exercise (H2). Exercise was performed at 50 r·min–1 or contractions per minute per leg. Oxygen uptake (VO2) mean response time was ∼20% faster (p < 0.05) during H2 compared with H1 in both modalities. Phase 2 time constants (τ) were not different between heavy bouts of CE (H1, 29.6 ± 6.5 s; H2, 28.0 ± 4.6 s) or KE exercise (H1, 31.6 ± 6.7 s; H2, 29.8 ± 5.6 s). The VO2 slow component amplitude was lower (p < 0.05) in H2 in both modalities (CE, 0.19 ± 0.06 L·min–1; KE, 0.12 ± 0.07 L·min–1) compared with H1 (CE, 0.29 ± 0.09 L·min–1; KE, 0.18 ± 0.07 L·min–1), with the contribution of the slow component to the total VO2 response reduced (p < 0.05) in H2 during both exercise modes. The effective τHHb was similar between bouts for CE (H1, 18.2 ± 3.0 s; H2, 18.0 ± 3.6 s) and KE exercise (H1, 26.0 ± 7.0 s; H2, 24.0 ± 5.8 s). The ΔHHb slow component was reduced during H2 in both CE and KE (p < 0.05). In conclusion, phase 2 VO2p was unchanged with priming exercise; however, a faster mean response time of VO2p during the heavy-intensity exercise preceded by a priming heavy-intensity exercise was attributed to a smaller slow component and reduced muscle deoxygenation indicative of improved muscle O2 delivery during the second bout of exercise.

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Casaburi, R., T. W. Storer, I. Ben-Dov, and K. Wasserman. "Effect of endurance training on possible determinants of VO2 during heavy exercise." Journal of Applied Physiology 62, no. 1 (January 1, 1987): 199–207. http://dx.doi.org/10.1152/jappl.1987.62.1.199.

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When moderate exercise begins, O2 uptake (VO2) reaches a steady state within 3 min. However, with heavy exercise, VO2 continues to rise beyond 3 min (VO2 drift). We sought to identify factors contributing to VO2 drift. Ten young subjects performed cycle ergometer tests of 15 min duration for each of four constant work rates, corresponding to 90% of the anaerobic threshold (AT) and 25, 50, and 75% of the difference between maximum VO2 (VO2 max) and AT for that subject. Time courses of VO2, minute ventilation (VE), and rectal temperature were recorded. Blood lactate, norepinephrine, and epinephrine were measured at the end of exercise. Eight weeks of cycle ergometer endurance training improved average VO2 max by 15%. Subjects then performed four tests identical to pretraining studies. For the above AT tests, training reduced VO2 drift substantially; reduction in each of the possible mediators we measured was also demonstrated. The training-induced decrease in VO2 drift was well correlated with decreases in end exercise lactate and less well correlated with the drift in VE seen at above AT work rates. The training-induced reduction in VO2 drift was not significantly correlated with attenuation of rectal temperature rise or decrease in end-exercise level of the catecholamines. Thus the slow rise in VO2 during heavy exercise seems linked to lactate, though a component dictated by the work of breathing cannot be ruled out.

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WOMACK, CHRISTOPHER J., JUDITH A. FLOHR, ARTHUR WELTMAN, and GLENN A. GAESSER. "The Effects of a Short-Term Training Program on the Slow Component of Vo2." Journal of Strength and Conditioning Research 14, no. 1 (February 2000): 50–53. http://dx.doi.org/10.1519/00124278-200002000-00009.

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27

Lauver, Jakob D., Timothy R. Rotarius, and Barry W. Scheuermann. "The Effect of Continuous versus Intermittent Exercise on VO2 Slow Component and Muscle Activation." Medicine & Science in Sports & Exercise 49, no. 5S (May 2017): 640. http://dx.doi.org/10.1249/01.mss.0000518684.52735.77.

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28

Machado, Fabiana A., >Luiz G. A. Guglielmo, Camila C. Greco, and Benedito S. Denadai. "Effects of Exercise Mode on the Oxygen Uptake Kinetic Response to Severe-Intensity Exercise in Prepubertal Children." Pediatric Exercise Science 21, no. 2 (May 2009): 159–70. http://dx.doi.org/10.1123/pes.21.2.159.

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The objective of this study was to verify the effect of the exercise mode on slow component of VO2 (VO2SC) in children aged 11–12 years during severe-intensity exercise. After determination of the lactate threshold (LT) and peak VO2 (VO2peak) in both cycling (CE) and running exercise (TR), fourteen active boys completed a series of “square-wave” transitions of 6-min duration at 75%∆ [75%∆ = LT + 0.75 × (VO2peak—LT)] to determine the VO2 kinetics. The VO2SC was significantly higher in CE (180.5 ± 155.8 ml • min−1) than in TR (113.0 ± 84.2 ml · min−1). We can conclude that, although a VO2SC does indeed develop during TR in children, its magnitude is considerably lower than in CE during severe-intensity exercise.

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Reis, Joana F., Gregoire P. Millet, Davide Malatesta, Belle Roels, Fabio Borrani, Veronica E. Vleck, and Francisco B. Alves. "Are Oxygen Uptake Kinetics Modified When Using a Respiratory Snorkel?" International Journal of Sports Physiology and Performance 5, no. 3 (September 2010): 292–300. http://dx.doi.org/10.1123/ijspp.5.3.292.

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Purpose:The aim of this study was to compare VO2 kinetics during constant power cycle exercise measured using a conventional facemask (CM) or a respiratory snorkel (RS) designed for breath-by-breath analysis in swimming.Methods:VO2 kinetics parameters—obtained using CM or RS, in randomized counterbalanced order—were compared in 10 trained triathletes performing two submaximal heavy-intensity cycling square-wave transitions. These VO2 kinetics parameters (ie, time delay: td1, td2; time constant: τ1, τ2; amplitude: A1, A2, for the primary phase and slow component, respectively) were modeled using a double exponential function. In the case of the RS data, this model incorporated an individually determined snorkel delay (ISD).Results:Only td1 (8.9 ± 3.0 vs 13.8 ± 1.8 s, P < .01) differed between CM and RS, whereas all other parameters were not different (τ1 = 24.7 ± 7.6 vs 21.1 ± 6.3 s; A1 = 39.4 ± 5.3 vs 36.8 ± 5.1 mL·min−1·kg−1; td = 107.5 ± 87.4 vs 183.5 ± 75.9 s; A2' (relevant slow component amplitude) = 2.6 ± 2.4 vs 3.1 ± 2.6 mL·min−1·kg−1 for CM and RS, respectively).Conclusions:Although there can be a small mixture of breaths allowed by the volume of the snorkel in the transition to exercise, this does not appear to significantly influence the results. Therefore, given the use of an ISD, the RS is a valid instrument for the determination of VO2 kinetics within submaximal exercise.

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Santalla, Alfredo, Alejandro Lucía, and Margarita Pérez. "Caffeine Ingestion Attenuates the VO2 Slow Componnt during Intense Exercise." Japanese Journal of Physiology 51, no. 6 (2001): 761–64. http://dx.doi.org/10.2170/jjphysiol.51.761.

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31

Reis, Victor M., Eduardo B. Neves, Nuno Garrido, Ana Sousa, André L. Carneiro, Carlo Baldari, and Tiago Barbosa. "Oxygen Uptake On-Kinetics during Low-Intensity Resistance Exercise: Effect of Exercise Mode and Load." International Journal of Environmental Research and Public Health 16, no. 14 (July 15, 2019): 2524. http://dx.doi.org/10.3390/ijerph16142524.

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Oxygen uptake (VO2) kinetics has been analyzed through mathematical modeling of constant work-rate exercise, however, the exponential nature of the VO2 response in resistance exercise is currently unknown. The present work assessed the VO2 on-kinetics during two different sub maximal intensities in the inclined bench press and in the seated leg extension exercise. Twelve males (age: 27.2 ± 4.3 years, height: 177 ± 5 cm, body mass: 79.0 ± 10.6 kg and estimated body fat: 11.4 ± 4.1%) involved in recreational resistance exercise randomly performed 4-min transitions from rest to 12% and 24% of 1 repetition maximum each, of inclined bench press (45°) and leg extension exercises. During all testing, expired gases were collected breath-by-breath with a portable gas analyzer (K4b2, Cosmed, Italy) and VO2 on-kinetics were identified using a multi-exponential mathematical model. Leg extension exercise exhibited a higher R-square, compared with inclined bench press, but no differences were found in-between exercises for the VO2 kinetics parameters. VO2 on-kinetics seems to be more sensitive to muscle related parameters (upper vs. lower body exercise) and less to small load variations in the resistance exercise. The absence of a true slow component indicates that is possible to calculate low-intensity resistance exercise energy cost based solely on VO2 measurements.

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Womack, C. J., D. J. Sieminski, L. I. Katzel, A. Yataco, and A. W. Gardner. "EXERCISE REHABILITATION DECREASES THE SLOW COMPONENT OF VO2 IN PATIENTS WITH PERIPHERAL ARTERIAL DISEASE 955." Medicine &amp Science in Sports &amp Exercise 29, Supplement (May 1997): 167. http://dx.doi.org/10.1097/00005768-199705001-00954.

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33

Powell, Slater K., Emilie M. Hauser, Nathan D. Dicks, Robert W. Pettitt, and Cherie D. Pettitt. "Recreationally-Trained Subjects are Unable to Attenuate VO2 Slow Component During Severe Exercise Using RPE." Medicine & Science in Sports & Exercise 49, no. 5S (May 2017): 116. http://dx.doi.org/10.1249/01.mss.0000517143.45951.dd.

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34

Poole, D. C., G. A. Gaesser, M. C. Hogan, D. R. Knight, and P. D. Wagner. "Pulmonary and leg VO2 during submaximal exercise: implications for muscular efficiency." Journal of Applied Physiology 72, no. 2 (February 1, 1992): 805–10. http://dx.doi.org/10.1152/jappl.1992.72.2.805.

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Insights into muscle energetics during exercise (e.g., muscular efficiency) are often inferred from measurements of pulmonary gas exchange. This procedure presupposes that changes of pulmonary O2 (VO2) associated with increases of external work reflect accurately the increased muscle VO2. The present investigation addressed this issue directly by making simultaneous determinations of pulmonary and leg VO2 over a range of work rates calculated to elicit 20–90% of maximum VO2 on the basis of prior incremental (25 or 30 W/min) cycle ergometry. VO2 for both legs was calculated as the product of twice one-leg blood flow (constant-infusion thermodilution) and arteriovenous O2 content difference across the leg. Measurements were made 3–5 min after each work rate imposition to avoid incorporation of the VO2 slow component above the lactate threshold. For all 17 subjects, the slope of pulmonary VO2 (9.9 +/- 0.2 ml O2.W-1.min-1) was not different (P greater than 0.05) from that for leg VO2 (9.2 +/- 0.6 ml O2.W-1.min-1). Estimation of “delta” efficiency (i.e., delta work accomplished divided by delta energy expended, calculated from slope of VO2 vs. work rate and a caloric equivalent for O2 of 4.985 cal/ml) using pulmonary VO2 measurements (29.1 +/- 0.6%) was likewise not significantly different (P greater than 0.05) from that made using leg VO2 measurements (33.7 +/- 2.4%). These data suggest that the net VO2 cost of metabolic “support” processes outside the exercising legs changes little over a relatively broad range of exercise intensities. Thus, under the conditions of this investigation, changes of VO2 measured from expired gas reflected closely those occurring within the exercising legs.

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35

Roth, D. A., W. C. Stanley, and G. A. Brooks. "Induced lactacidemia does not affect postexercise O2 consumption." Journal of Applied Physiology 65, no. 3 (September 1, 1988): 1045–49. http://dx.doi.org/10.1152/jappl.1988.65.3.1045.

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To study the effects of circulatory occlusion on the time course and magnitude of postexercise O2 consumption (VO2) and blood lactate responses, nine male subjects were studied twice for 50 min on a cycle ergometer. On one occasion, leg blood flow was occluded with surgical thigh cuffs placed below the buttocks and inflated to 200 mmHg. The protocol consisted of a 10-min rest, 12 min of exercise at 40% peak O2 consumption (VO2 peak), and a 28-min resting recovery while respiratory gas exchange was determined breath by breath. Occlusion (OCC) spanned min 6-8 during the 12-min work bout and elicited mean blood lactate of 5.2 +/- 0.8 mM, which was 380% greater than control (CON). During 18 min of recovery, blood lactate after OCC remained significantly above CON values. VO2 was significantly lower during exercise with OCC compared with CON but was significantly higher during the 4 min of exercise after cuff release. VO2 was higher after OCC during the first 4 min of recovery but was not significantly different thereafter. Neither total recovery VO2 (gross recovery VO2 with no base-line subtraction) nor excess postexercise VO2 (net recovery VO2 above an asymptotic base line) was significantly different for OCC and CON conditions (13.71 +/- 0.45 vs. 13.44 +/- 0.61 liters and 4.93 +/- 0.26 vs. 4.17 +/- 0.35 liters, respectively). Manipulation of exercise blood lactate levels had no significant effect on the slow ("lactacid") component of the recovery VO2.

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Lai, Nicola, Melita M. Nasca, Marco A. Silva, Fatima T. Silva, Brian J. Whipp, and Marco E. Cabrera. "Influence of exercise intensity on pulmonary oxygen uptake kinetics at the onset of exercise and recovery in male adolescents." Applied Physiology, Nutrition, and Metabolism 33, no. 1 (February 2008): 107–17. http://dx.doi.org/10.1139/h07-154.

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The dynamics of the pulmonary oxygen uptake (VO2) responses to square-wave changes in work rate can provide insight into bioenergetic processes sustaining and limiting exercise performance. The dynamic responses at the onset of exercise and during recovery have been investigated systematically and are well characterized at all intensities in adults; however, they have not been investigated completely in adolescents. We investigated whether adolescents display a slow component in their VO2 on- and off-kinetic responses to heavy- and very heavy-intensity exercise, as demonstrated in adults. Healthy African American male adolescents (n = 9, 14–17 years old) performed square-wave transitions on a cycle ergometer (from and to a baseline work rate of 20 W) to work rates of moderate (M), heavy (H), and very heavy (VH) intensity. In all subjects, the VO2 on-kinetics were best described with a single exponential at moderate intensity (τ1, on = 36 ± 11 s) and a double exponential at heavy (τ1, on = 29 ± 9 s; τ2, on = 197 ± 92 s) and very heavy (τ1, on = 36 ± 9 s; τ2, on = 302 ± 14 s) intensities. In contrast, the VO2 off-kinetics were best described with a single exponential at moderate (τ1, off = 48 ± 9 s) and heavy (τ1, off = 53 ± 7 s) intensities and a double exponential at very heavy (τ1, off = 51 ± 3 s; τ2, off = 471 ± 54 s) intensity. In summary, adolescents consistently displayed a slow component during heavy exercise (on- but not off- transition) and very heavy exercise (on- and off-transitions). Although the overall response dynamics in adolescents were similar to those previously observed in adults, their specific characterizations were different, particularly the lack of symmetry between the on- and off-responses.

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Carmines, A. A., L. Wideman, J. Y. Weltman, M. L. Hartman, A. Weltman, and G. A. Gaesser. "HIGH-CARBOHYDRATE AND HIGH-FAT DIETS DO NOT ALTER SLOW COMPONENT OF VO2 DURING HEAVY EXERCISE." Medicine & Science in Sports & Exercise 27, Supplement (May 1995): S9. http://dx.doi.org/10.1249/00005768-199505001-00053.

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38

Pedersen, Preben K., Martin Mogensen, Malene Bagger, Maria Fernström, and Kent Sahlin. "Vo2 Slow Component Correlates With Skeletal Muscle Mitochondrial UCP3 In Untrained But Not In Trained Individuals." Medicine & Science in Sports & Exercise 39, Supplement (May 2007): S359. http://dx.doi.org/10.1249/01.mss.0000274409.22439.e1.

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39

Faisal, Azmy, Keith R. Beavers, Andrew D. Robertson, and Richard L. Hughson. "Priming Exercise Induced Attenuation Of VO2 Slow Component Is Associated With Changes In Muscle EMG Activity." Medicine & Science in Sports & Exercise 43, Suppl 1 (May 2011): 385. http://dx.doi.org/10.1249/01.mss.0000401062.07651.d2.

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40

Draper, Stephen B., Dan M. Wood, Jo Corbett, David V. B. James, and Christopher R. Potter. "The Effect of Prior Moderate- and Heavy-Intensity Running on the VO2 Response to Exhaustive Severe-Intensity Running." International Journal of Sports Physiology and Performance 1, no. 4 (December 2006): 361–74. http://dx.doi.org/10.1123/ijspp.1.4.361.

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We tested the hypothesis that prior heavy-intensity exercise reduces the difference between asymptotic oxygen uptake (VO2) and maximum oxygen uptake (VO2max) during exhaustive severe-intensity running lasting ≍2 minutes. Ten trained runners each performed 2 ramp tests to determine peak VO2 (VO2peak) and speed at venti-latory threshold. They performed exhaustive square-wave runs lasting ≍2 minutes, preceded by either 6 minutes of moderate-intensity running and 6 minutes rest (SEVMOD) or 6 minutes of heavy-intensity running and 6 minutes rest (SEVHEAVY). Two transitions were completed in each condition. VO2 was determined breath by breath and averaged across the 2 repeats of each test; for the square-wave test, the averaged VO2 response was then modeled using a monoexponential function. The amplitude of the VO2 response to severe-intensity running was not different in the 2 conditions (SEVMOD vs SEVHEAVY; 3925 ± 442 vs 3997 ± 430 mL/min, P = .237), nor was the speed of the response (τ; 9.2 ± 2.1 vs 10.0 ± 2.1 seconds, P = .177). VO2peak from the square-wave tests was below that achieved in the ramp tests (91.0% ± 3.2% and 92.0% ± 3.9% VO2peak, P < .001). There was no difference in time to exhaustion between conditions (110.2 ± 9.7 vs 111.0 ± 15.2 seconds, P = .813). The results show that the primary VO2 response is unaffected by prior heavy exercise in running performed at intensities at which exhaustion will occur before a slow component emerges.

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di Prampero, P. E., P. B. Mahler, D. Giezendanner, and P. Cerretelli. "Effects of priming exercise on VO2 kinetics and O2 deficit at the onset of stepping and cycling." Journal of Applied Physiology 66, no. 5 (May 1, 1989): 2023–31. http://dx.doi.org/10.1152/jappl.1989.66.5.2023.

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Breath-by-breath O2 uptake (VO2) kinetics and increase of blood lactate concentration (delta Lab) were determined at the onset of square-wave stepping (S) or cycling (C) exercise on six male subjects during 1) transition from rest (R) to constant work load, 2) transition from lower to heavier work loads, wherein the baseline VO2 (VO2 s) was randomly chosen between 20 and 65% of the subjects' maximal O2 uptake (VO2 max), and 3) inverse transition from higher to lower work loads and/or to rest. VO2 differences between starting and arriving levels were 20–60% VO2 max. In C, the VO2 on-response became monotonically slower with increasing VO2 s, the half time (t1/2) increasing from approximately 22 s for VO2 s = R to approximately 63 s when VO2 s approximately equal to 50% VO2 max. In S, the fastest VO2 kinetics (t1/2 = 16 s) was attained from VO2 s = 15–30% VO2 max, the t1/2 being approximately 25 s when starting from R or from 50% VO2 max. The slower VO2 kinetics in C were associated with a much larger delta Lab. The VO2 kinetics in recovery were essentially the same in all cases and could be approximated by a double exponential with t1/2 of 21.3 +/- 6 and 93 +/- 45 s for the fast and slow components, respectively. It is concluded that the O2 deficit incurred is the sum of three terms: 1) O2 stores depletion, 2) O2 equivalent of early lactate production, and 3) O2 equivalent of phosphocreatine breakdown.(ABSTRACT TRUNCATED AT 250 WORDS)

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42

Cochrane, J. E., and R. L. Hughson. "319 EVIDENCE FOR A SLOW DRIFT COMPONENT IN OXYGEN UPTAKE (VO2) KINETICS BELOW THE VENTILATORY THRESHOLD (VT)." Medicine & Science in Sports & Exercise 22, no. 2 (April 1990): S54. http://dx.doi.org/10.1249/00005768-199004000-00319.

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43

DeLorey, Darren S., Aaron P. Heenan, Greg R. duManoir, John M. Kowalchuk, and Donald H. Paterson. "The Effect of Prior Exercise on the Slow Component of VO2, Leg Blood Flow and Muscle Deoxygenation." Medicine & Science in Sports & Exercise 38, Supplement (May 2006): S221. http://dx.doi.org/10.1249/00005768-200605001-01856.

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44

Pogliaghi, Silvia, Alessandro L. Colosio, Kevin Caen, Jan G. Bourgois, Jan Boone, Øyvind Nøstdahl Gløersen, and Carlo Capelli. "Response to the commentary on our paper “bioenergetics of the VO2 slow component between exercise intensity domains”." Pflügers Archiv - European Journal of Physiology 472, no. 12 (November 9, 2020): 1665–66. http://dx.doi.org/10.1007/s00424-020-02489-9.

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45

Barstow, T. J., and P. A. Mole. "Linear and nonlinear characteristics of oxygen uptake kinetics during heavy exercise." Journal of Applied Physiology 71, no. 6 (December 1, 1991): 2099–106. http://dx.doi.org/10.1152/jappl.1991.71.6.2099.

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We assessed the linearity of oxygen uptake (VO2) kinetics for several work intensities in four trained cyclists. VO2 was measured breath by breath during transitions from 33 W (baseline) to work rates requiring 38, 54, 85, and 100% of maximal aerobic capacity (VO2max). Each subject repeated each work rate four times over 8 test days. In every case, three phases (phases 1, 2, and 3) of the VO2 response could be identified. VO2 during phase 2 was fit by one of two models: model 1, a double exponential where both terms begin together close to the start of phase 2, and model 2, a double exponential where each of the exponential terms begins independently with separate time delays. VO2 rose linearly for the two lower work rates (slope 11 ml.min-1 W-1) but increased to a greater asymptote for the two heavier work rates. In all four subjects, for the two lighter work rates the double-exponential regression reduced to a single value for the time constant (average across subjects 16.1 +/- 7.7 s), indicating a truly monoexponential response. In addition, one of the responses to the heaviest work rate was monoexponential. For the remaining seven biexponential responses to the two heaviest work rates, model 2 produced a significantly better fit to the responses (P less than 0.05), with a mean time delay for the slow component of 105 +/- 46 s.(ABSTRACT TRUNCATED AT 250 WORDS)

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Cannon, Daniel T., Fred W. Kolkhorst, and Daniel J. Cipriani. "Electromyographic Data Do Not Support a Progressive Recruitment of Muscle Fibers during Exercise Exhibiting a VO2 Slow Component." Journal of PHYSIOLOGICAL ANTHROPOLOGY 26, no. 5 (2007): 541–46. http://dx.doi.org/10.2114/jpa2.26.541.

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47

Ocel, J., S. Davis, F. Gwasdauskas, J. Myers, L. Craft, L. Bullock, E. Walker, and W. Herbert. "ADAPTATION OF THE SLOW COMPONENT OF ??VO2 (SC) FOLLOWING 6 WEEKS OF HIGH OR LOW INTENSITY EXERCISE TRAINING." Medicine & Science in Sports & Exercise 30, Supplement (May 1998): 166. http://dx.doi.org/10.1097/00005768-199805001-00944.

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48

Zuniga, Jorge, Kris Berg, John Noble, Jeanette Harder, Morgan Chaffin, and Vidya Sagar Hanumanthu. "Physiological Responses and Role of VO2 slow Component to Interval Training with Different Intensities and Durations of Work." Medicine & Science in Sports & Exercise 40, Supplement (May 2008): S173. http://dx.doi.org/10.1249/01.mss.0000322213.21626.2d.

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49

Moral-González, Susana, Javier González-Sánchez, Pedro L. Valenzuela, Sonia García-Merino, Carlos Barbado, Alejandro Lucia, Carl Foster, and David Barranco-Gil. "Time to Exhaustion at the Respiratory Compensation Point in Recreational Cyclists." International Journal of Environmental Research and Public Health 17, no. 17 (August 31, 2020): 6352. http://dx.doi.org/10.3390/ijerph17176352.

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The time to exhaustion (tlim) at the respiratory compensation point (RCP) and whether a physiological steady state is observed at this workload remains unknown. Thus, this study analyzed tlim at the power output eliciting the RCP (tlim at RCP), the oxygen uptake (VO2) response to this effort, and the influence of endurance fitness. Sixty male recreational cyclists (peak oxygen uptake [VO2peak] 40–60 mL∙kg∙min−1) performed an incremental test to determine the RCP, VO2peak, and maximal aerobic power (MAP). They also performed constant-load tests to determine the tlim at RCP and tlim at MAP. Participants were divided based on their VO2peak into a low-performance group (LP, n = 30) and a high-performance group (HP, n = 30). The tlim at RCP averaged 20 min 32 s ± 5 min 42 s, with a high between-subject variability (coefficient of variation 28%) but with no differences between groups (p = 0.788, effect size = 0.06). No consistent relationships were found between the tlim at RCP and the different fitness markers analyzed (RCP, power output (PO) at RCP, VO2peak, MAP, or tlim at MAP; all p > 0.05). VO2 remained steady overall during the tlim test, although a VO2 slow component (i.e., an increase in VO2 >200 mL·min−1 from the third min to the end of the tests) was present in 33% and 40% of the participants in HP and LP, respectively. In summary, the PO at RCP could be maintained for about 20 min. However, there was a high between-subject variability in both the tlim and in the VO2 response to this effort that seemed to be independent of fitness level, which raises concerns on the suitability of this test for fitness assessment.

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Miyamoto, Y., and Y. Niizeki. "Dynamics of ventilation, circulation, and gas exchange to incremental and decremental ramp exercise." Journal of Applied Physiology 72, no. 6 (June 1, 1992): 2244–54. http://dx.doi.org/10.1152/jappl.1992.72.6.2244.

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Transient responses of minute volume (VE), O2 uptake (VO2), CO2 output (VCO2), heart rate (HR), and cardiac output (Q) to a step change and ramp changes with slopes ranging from 33.3 to 14.3 W/min were studied in five healthy human subjects over the load range from 25 to 125 W. The ramp responses were fitted to a first-order model with a pure time delay (td) and a time constant (TC), while most of the step responses fitted better to a second-order model, consisting of a fast and a slow component. No significant asymmetry was observed between the on- and off-responses to step forcing. The mean response time (MRT = td+TC) of the incremental ramp response was prolonged, whereas the MRT of the decremental ramp response was shortened or unchanged, with decreasing ramp slope. The asymmetry was commonly observed in respiratory and gas exchange variables and, to a lesser extent, also in circulatory variables. Neural and humoral factors that might be responsible for this phenomenon are discussed.

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