Abstract
In response to an increase in the metabolic demand the oxygen uptake (VO2) increases in an exponential fashion in exercising muscles and stabilizes after 1-2 min eventually reaching a plateau or steady state where the energy demand is matched by the l vel of VO2. VO2 kinetics describes the distinct phases of the VO2 response at the onset of exercise. Fast VO2 kinetics are considered to be beneficial in intense endurance sports with competitions lasting ~2-8 min, whereas low VO2 at steady state (high efficiency) is considered beneficial especially in events of longer duration. To improve the understanding of which mechanisms are regulating VO2 kinetics, in particular at the onset of exercise, five studies were performed manipulating oxygen delivery, dietary nitrate, training intensity and prior exercise intensity. Also the influence on performance capacity was evaluated with some of the interventions.
In study I a modest reduction in oxygen delivery of ~6% and a large reduction in arterial oxygen pressure of ~40% in the early phase of high intensity knee-extensor exercise, caused by breathing air simulating altitude of ~3500 m (hypoxia), did not slow the VO2 response measured at the muscular level. This is in contrast to the frequent observation of slower VO2 kinetics with hypoxia measured in the whole body across the lungs which may imply that hypoxia slows VO2 in tissues other than the muscle or that the measuring sensitivity in
study I was not high enough to detect a small “real” difference. In study II during high intensity kneeextensor exercise a blockade of two systems implicated in blood flow regulation caused a reduction in blood flow of 25-50% in the early part of exercise. This resulted in oxygen delivery being less than VO2 in the control setting, thereby causing lower VO2 values. Modeling of data from that study revealed that the VO2 response in both the normal situation and even with reduced oxygen delivery could be limited by factors within the muscle and not oxygen delivery. Support for a limitation from oxygen delivery could also be found when modeling the response. In an additional study it was found that a prior high intensity exercise bout caused a faster VO2 response in subsequent high intensity exercise bout. This was due to increased oxygen extraction in the second exercise bout and not increased oxygen delivery showing that the capacity for muscle to extract oxygen was limiting VO2 in the first exercise bout. In study III increased dietary nitrate intake in the form of beetroot juice – expected to increase nitric oxide levels - did not improve exercise economy or performance in highly trained cyclists unlike previous observations in untrained or moderately trained subjects. This was speculated to relate to a high capacity to produce nitric oxide in the trained state with no further advantage of supplementing with nitrate. In study IV rather trained cyclists intensified their training and reduced training volume by performing repeated 30-s sprints and 4-min intervals designed to increase content of oxidative enzymes in fast twitch muscle fibres and thus the capacity to extract oxygen from the blood. This did not increase oxidative enzyme levels in fast twitch muscle fibres and VO2 kinetics was not faster and exercise economy was unaltered. In an additional training study it was observed that intensified training – in the form of repeated sprints with a duration of 30 to 60 s – added to the normal training of world-class rowers did not speed VO2 kinetics. In this group of rowers fast VO2 kinetics was associated with superior 2000-m rowing performance lasting ~6.5 min. In study V three different preparation protocols was performed by highly trained cyclists prior to a 4-min maximal performance test. Progressive high intensity exercise coupled with 6 min of recovery was associated with lower blood pH before the test. This was speculated to be implicated in reduced performance during the test relative to when extending recovery to 20 min after the prior high intensity exercise or when performing prior moderate exercise. Moreover, in the first condition the low pH was speculated to be implicated in the faster VO2 response observed due to faster oxygen off-loading of the red blood cells, and without this faster VO2 response performance might have been even worse.
Regulation of VO2 kinetics is influenced by numerous factors and holds great complexity. Whether oxygen delivery under “normal” upright exercise such as cycling and running limits the primary VO2 response from the exercising muscle is not clear. A key factor is distribution of blood flow which at present cannot be determined in absolute terms. However reductions of oxygen delivery in the range of 25-50% can attenuate the rise in muscle VO2 during high intensity exercise. There appears to be limited benefits from supplementing with nitrate to improve exercise efficiency and performance in endurance trained subjects. Furthermore it appears difficult to improve VO2 kinetics with intensified training in trained athletes; however intense exercise can amplify the VO2 response during subsequent high intensity exercise and also influence exercise performance.
In study I a modest reduction in oxygen delivery of ~6% and a large reduction in arterial oxygen pressure of ~40% in the early phase of high intensity knee-extensor exercise, caused by breathing air simulating altitude of ~3500 m (hypoxia), did not slow the VO2 response measured at the muscular level. This is in contrast to the frequent observation of slower VO2 kinetics with hypoxia measured in the whole body across the lungs which may imply that hypoxia slows VO2 in tissues other than the muscle or that the measuring sensitivity in
study I was not high enough to detect a small “real” difference. In study II during high intensity kneeextensor exercise a blockade of two systems implicated in blood flow regulation caused a reduction in blood flow of 25-50% in the early part of exercise. This resulted in oxygen delivery being less than VO2 in the control setting, thereby causing lower VO2 values. Modeling of data from that study revealed that the VO2 response in both the normal situation and even with reduced oxygen delivery could be limited by factors within the muscle and not oxygen delivery. Support for a limitation from oxygen delivery could also be found when modeling the response. In an additional study it was found that a prior high intensity exercise bout caused a faster VO2 response in subsequent high intensity exercise bout. This was due to increased oxygen extraction in the second exercise bout and not increased oxygen delivery showing that the capacity for muscle to extract oxygen was limiting VO2 in the first exercise bout. In study III increased dietary nitrate intake in the form of beetroot juice – expected to increase nitric oxide levels - did not improve exercise economy or performance in highly trained cyclists unlike previous observations in untrained or moderately trained subjects. This was speculated to relate to a high capacity to produce nitric oxide in the trained state with no further advantage of supplementing with nitrate. In study IV rather trained cyclists intensified their training and reduced training volume by performing repeated 30-s sprints and 4-min intervals designed to increase content of oxidative enzymes in fast twitch muscle fibres and thus the capacity to extract oxygen from the blood. This did not increase oxidative enzyme levels in fast twitch muscle fibres and VO2 kinetics was not faster and exercise economy was unaltered. In an additional training study it was observed that intensified training – in the form of repeated sprints with a duration of 30 to 60 s – added to the normal training of world-class rowers did not speed VO2 kinetics. In this group of rowers fast VO2 kinetics was associated with superior 2000-m rowing performance lasting ~6.5 min. In study V three different preparation protocols was performed by highly trained cyclists prior to a 4-min maximal performance test. Progressive high intensity exercise coupled with 6 min of recovery was associated with lower blood pH before the test. This was speculated to be implicated in reduced performance during the test relative to when extending recovery to 20 min after the prior high intensity exercise or when performing prior moderate exercise. Moreover, in the first condition the low pH was speculated to be implicated in the faster VO2 response observed due to faster oxygen off-loading of the red blood cells, and without this faster VO2 response performance might have been even worse.
Regulation of VO2 kinetics is influenced by numerous factors and holds great complexity. Whether oxygen delivery under “normal” upright exercise such as cycling and running limits the primary VO2 response from the exercising muscle is not clear. A key factor is distribution of blood flow which at present cannot be determined in absolute terms. However reductions of oxygen delivery in the range of 25-50% can attenuate the rise in muscle VO2 during high intensity exercise. There appears to be limited benefits from supplementing with nitrate to improve exercise efficiency and performance in endurance trained subjects. Furthermore it appears difficult to improve VO2 kinetics with intensified training in trained athletes; however intense exercise can amplify the VO2 response during subsequent high intensity exercise and also influence exercise performance.
| Original language | English |
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| Publisher | Department of Nutrition, Exercise and Sports, Faculty of Sciences, University of Copenhagen |
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| Number of pages | 162 |
| Publication status | Published - 2013 |