I like to use Daniele's data of his three assessments of a 4/ 1 to re-engage some open minds in a more critical look at VO2 max, VO2 max intensities or training and ideas of using VO2 as a " zoning" idea.
One of the most intriguing ideas or studies done in Cape town from a group is a VO2 tests , like we did in the late 1980 the lactate balance point test.
In short : The outcome was that any kind of step test does not end up with a VO2 max or VO2 peak , but rather the highest readings of VO2 showed up in post step test loads depending how we create them and what we load. The unfortunate result for all of us this is, that we would have to accept that many or all of the Vo2 max studies , where we use % of VO2 max to define a training intensity , would have to be reviewed and who would actually do this despite the fact that many of the drawn conclusion may be at least not completely correct, to avoid the word, wrong.
Than there is the review of great studies and the end result on how many time a VO2 max plateau was found is very limited to say the least.
But it is getting somewhat more intriguing, when we know that the same VO2 max % from you and from me are not at all the same physiological effort. So groups and studies, where we have 6 or 10 or hopefully more people involved who where all stressed by a the same 80 % of their individual VO2 peak result in fact may have stressed very different physiological systems and as such we can not at all look at the general results of the full group , but have to look very individual.
So when we ever look at a VO2 max involved studies, even when the studies pledge to use " accepted " ideas and protocols for VO2 max , we have to ask ourself , who accepted this protocol and how good is it justified.
I will show you later how we started to look at our own ideas more critical when comparing VO2 max or VO2 datas with NIRS as NIRS is a direct feedback and VO2 datas have like lactate datas a lag time as well a physiological reaction delay time.
How long does it take to have the MCT carrier for lactate working in an optimal way ? Now here some interesting reading in regard to % of VO2 max and performance and efficiency.
Try to keep in mind our ideas of LIMITER and compensator and the whole idea about priorities on who is getting the available O2 .
VO2 MAX AND CYCLISTS: IMPORTANT OR IRRELEVANT
June 16, 2012 by peakcentre
VO2 max is one of the most commonly measured physiological variables. Endurance athletes spend countless hours discussing, comparing and worrying about their VO2 max scores. Cyclists are always quoting VO2 max scores for one top rider or another. Is all the attention that this physiological variable gets really worth all the effort?
VO2 max is the maximum amount of oxygen that your body can take in and use. It is a function of both the body’s ability to deliver oxygen via the heart, lung and blood and the body’s ability to use oxygen in the working muscles and other tissues.
What could happen if there is a delivery limitation with O2 how would VO2 max react?
What happens when there is a leg VO2 utilization limitation can we still increase VO2 max ?
While there are some exceptions, Elite cyclists typically have VO2 max scores in the 70-75 ml/kg/min range, similar to that seen in well trained amateur cyclists and some very fit age group riders. In an aerobic sport oxygen consumption is tightly tied to energy expenditure and generally producing more energy means more power and work. The relationship between power and oxygen consumption is not perfect; efficiency or economy play an important role in determining how strong the relationship is in each person.
Gross efficiency, the ratio of power output to power input, is a key determinant of cycling performance (1). A higher efficiency allows a cyclist to work at lower percentages of the VO2 max to accomplish the same or more work as a less efficient cyclist. In fact, a high efficiency rating can make up for lower VO2 max scores. Alejandro Lucia and coworkers (2) from the Universidad Europea de Madrid examined the relationship between VO2 max and cycling efficiency and gross efficiency in a group of elite cyclists. The subjects in this study were all world class riders having won at least one major professional race, defined as stage in the Tour de France, Giro d’Italia or the Vuelta a Espana, or finished in the top three at the World Championships. Hemoglobin and hematocrit levels were measured prior to the start of the study to ensure they were within normal physiological ranges. All subjects performed a VO2 max test following standard protocols. Later the same day they performed a 20 minute constant load test where they road at 80% of their VO2 max. VO2max values in the subjects varied from a high of 82.5 ml/kg/min to a low of 65.5 ml/kg/min. Cycling efficiency varied from 97.9 watts/L O2/min to 72.1 watts/L O2/min. There was a significant inverse correlation between VO2 max and cycling efficiency.
Question comes up who used the O2 but did not delivered the use as a better performance ?
This means that those with the higher VO2 max scores had the lowest efficiencies and those with lower VO2 max scores had higher efficiency. A similar pattern was seen in gross efficiency. Power to weight ratio at VO2 max was not significantly different between riders, they were all in the 4.9-5.4 W/kg range. Interestingly two of the most accomplished riders, a road race and time trial world champion and climbing specialist who had won five stages in the Tour de France both had VO2 max score under 70 ml/kg/min.
This study clearly shows that VO2 max is less important than efficiency in cycling performance and that a high level of efficiency can make up for a lower VO2 max. This pattern is not unique to cycling it has also been seen in running (3) and rowing. In an upcoming article we will look at the various factors that contribute to efficiency and how to improve your cycling efficiency.
So the next time someone start bragging about their VO2 max score ask them about their efficiency rating. Their high VO2 max may just mean that they are very inefficient riders.
- Coyle, E. (1995). Integration of the physiological factors determining endurance performance ability. Exerc Sport Sci rev. 23: 25-64.
- Lucia, A. et al. (2002). Inverse relationship between VO2 max and economy/efficiency in world class cyclists. Med Sci Sports Exerc. 34: 2079-2084.
- Saltin et al. (1995). Morphology, enzyme activities, and buffer capacity of Kenyan and Scandinavian runners. Scand J. Med Sci Sports. 5: 222-230.
Do Increases in VO2max Cause Improved Performance?
If you are an experienced runner then you have likely heard it many times – VO2max limits performance and increasing VO2max causes improvements in performance.
This belief is both widely held and commonly promoted within the running community and has led to runners and coaches devising workouts specifically designed to increase VO2max. For example, Pfitzinger & Douglas, in their bookRoad Racing for Serious Runners, devote an entire chapter to training methods for improving VO2max and speed.(1) In the introduction to the chapter titled Training to Improve VO2max and Speed they write “Many serious runners know that improving VO2max, or aerobic capacity, is key to racing better.” and “In this chapter, we’ll show you why and how to improve the two main components of racing fitness that runners try to develop with hard workouts – VO2max and basic speed.” In their view VO2max isn’t just important, it is key to racing well. They spend much of the chapter explaining what VO2max is and prescribing workouts specifically designed to increase it.
Another example comes from Dr Jack Daniels in his book, Daniels Running Formula. He writes “To optimize VO2max, the runner must stress the oxygen delivery and processing system to its limit while performing the act of running. I assign a phase of interval training…to accomplish this goal.”(2) Dr. Daniels thinks VO2max is important enough that he assigns an entire phase of training to optimizing VO2max.
Runners and coaches aren’t alone in this belief; exercise scientists believe it too. The link between VO2max and performance is strong enough that physiologists have conducted research studies designed to identify training techniques that will maximize VO2max.(3)
Which, of course, brings us to an obvious question; what does the research have to say on the subject? After all, any physiological belief this strongly-held and generally taught must be supported by the research, right?
Actually, no, it isn’t supported by the research.
A review of the research (4) on this topic actually reveals that:
· “…in well trained athletes VO2max remains stable even when performance is shown to increase.”
· “…in these athletes the correlation between VO2max and aerobic performance can be poor.”
· “…although rarely acknowledged, in the small longitudinal studies that have linked changes in VO2max with changes in aerobic performance, the data have been unconvincing.”
· “…studies using chronic obstructive pulmonary disease patients, recreationally active subjects, and endurance-trained athletes did not observe a correlation between the magnitude of training-induced improvements in VO2max and aerobic performance.”
All of these quotes indicate that the link between VO2max and performance is not what many have long believed and promoted. The fact is that changes in VO2max and performance are not cause/effect as runners have been taught for so many years. The data does not prove that improving VO2max is what causes improvement in performance; in actuality, the data in support of that belief is slim at best.
In 2009 a group of scientists who knew and acknowledged that the data was equivocal decided to revisit this topic. They designed a study to settle the issue by having a relatively large cohort of previously untrained subjects undergo a supervised six week cycling program. By monitoring changes in performance and various physiological parameters, such as VO2max, they were able to provide definitive insights about the link between changes in performance and aerobic capacity.
The basic finding was this – “This study demonstrates that improvements in high-intensity aerobic performance in humans are not related to altered maximal oxygen transport capacity.”
In other words, changes in VO2max did not cause improvements in performance.
Yes, VO2max improved in the subjects. And, yes, performance improved too. But the changes are not related to each other. “The change in VO2max was not related to the change in time trial performance.”
Training does improve both VO2max and performance but these researchers “…demonstrated that these adaptations do not occur in proportion to each other and do not appear to be determined by the same physiological or biochemical parameters.” In others words, the physiological factors within the body that cause performance to improve are not the same factors that cause VO2max to improve. The things within the body responsible for VO2max improvements are not the same things within the body that cause performance to improve.
The practical implication of this research is this – training specifically designed to optimize VO2max may or may not be the best training to maximize performance. Since different factors are responsible for changes in VO2max and performance, then training to optimize VO2max may not fully train those factors responsible for maximizing performance.
Does this mean you should abandon training designed to maximize VO2max? No, it doesn’t. It means that coaches and runners should not have a goal to maximize VO2max. Instead the goal should be to maximize performance. They should ignore VO2max and focus on performance. There is no need to ever measure VO2max in an effort to evaluate the effectiveness of a workout or a program. The only standard by which to judge training effectiveness is performance.
1. Pfitzinger P, Douglass S, Road Racing for Serious Runners, 1999, Chapter 2
2. Daniels, Jack, Daniels Running Formula, 1st edition, 1998, page 39
3. Midgley A, McNaughton L, Wilkinson M., Is there an optimal training intensity for enhancing the maximum oxygen uptake of distance runners? Empirical research findings, current opinions, physiological rationale and practical recommendations. Sports Med, 35: 117-132, 2006
4. Vollard N, Constantin-Teodosiu D, Fredriksson K, Rooyackers O, Jansson E, greenhaff P, Timmons J, Sundberg C., Systematic analysis of adaptations in aerobic capacity and submaximal energy metabolism provides a unique insight into determinants of human aerobic performance, J. Appl. Physiol., 106: 1279-1286, 2009
Non-linear relationships between central cardiovascular variables and VO2 during incremental cycling exercise in endurance-trained individuals.
Vella CA1, Robergs RA.
- 1Exercise Physiology Laboratories, The University of New Mexico, Albuquerque, NM, USA. firstname.lastname@example.org
The purpose of this study was to examine the relationships between the central cardiovascular variables (cardiac output, stroke volume and heart rate) and oxygen uptake (VO2) during continuous, incremental cycle exercise to maximal aerobic capacity (VO2max).
Twenty-one moderately to highly trained males (n=19) and females (n=2) participated in the study. A baseline maximal exercise test was performed to measure VO2max. Following the initial VO2max test, cardiac output was measured (CO2 rebreathing technique) at rest and 3 times during each of 4 exercise trials (2 submaximal tests to 90% VO2max and 2 maximal tests). Stroke volume and arteriovenous O2 difference were calculated using standard equations.
Significant non-linear relationships were found between all central cardiovascular variables and VO2 (P<0.01). A plateau in cardiac output at VO2max was identified in 3 subjects. Stroke volume plateaued at an average of 37+/-12.5% of VO2max in 18 subjects and increased continuously to VO2max in 3 subjects. The arteriovenous O2 difference progressively increased to VO2max in 17 subjects and revealed a plateau response in 4 subjects.
Our data suggest that there is a significant non-linear relationship between the central cardiovascular variables and VO2 during incremental exercise to VO2max. Furthermore, depending on the person, VO2max may be limited by cardiac output (evidence of cardiac output[Q] plateau) or peripheral factors (continued increase in Q).
The limitation to VO2 max is central!
Proposition for Debate - by Alison Low and Carolee Hatch
Statement of the Topic
Affirmative Argument by Alison Low
Negative Argument by Carolee Hatch
Statement of the Topic
The limitation to VO2 max is central!
Affirmative Argument by Alison Low
V02 max is traditionally defined as the maximal rate at which the body consumes oxygen during each minute of exercise (Basset and Howley 1997, Seiler 1996). As oxygen consumption is linearly related to energy expenditure it is therefore an indirect calculation of an individuals' maximal ability to work aerobically (Seiler 1996). High level aerobic capacity or endurance is a product of three physiological factors; a high VO2 max, a high lactate threshold and the efficient use of the three energy systems. Consequently as athletes strive to push endurance to its limits there has been a great body of research performed into what limits VO2 max and how it can be improved.
VO2 max is determined by incremental exercise testing, and is the point at which oxygen uptake reaches a peak and additional power production fails to elicit further gains in VO2 (Lindstedt et al 1988). The concept of VO2 max can be attributed to Archibald Vivian Hill who won a Nobel Prize in 1922 for his work in the area. After conducting, in his own words, "many careful and elegant experiments on exercising man" he concluded that VO2 max was limited by the capacity of the cardiovascular and respiratory systems to transport oxygen (Basset and Howley 1997). This is exactly the viewpoint of the debate today, that the limitation to VO2 max is central and the negative speaker is challenged to dispute the findings of a Nobel Prize winner!
There are several elements in the oxygen transport pathway from mouth to mitochondria that have the individual potential to limit oxygen supply and therefore VO2 max (Wagner 1995). These structures (in order) are pulmonary diffusion capacity, cardiac output and therefore muscle blood flow, haemoglobin concentration and diffusional transport of oxygen between muscle microcirculatory red cells and mitochondria (Wagner 1995). For the purposes of this debate all structure and functions that occur outside the perimysium will be considered as driven by central mechanisms, as maximal VO2 and blood flow are inextricably linked (Cain 1995). Each of these structures will now be examined separately and it will be proved that the limitation to VO2 max is centrally driven.
The lung can increase pulmonary surface area (and hence diffusing capacity for oxygen) in response to an increase in oxygen demand. This has been determined in the laboratory with the increase in demand for oxygen created artificially in animals through genetics, drugs and manipulation of temperature. Similarly it has been demonstrated that humans who are native to the Andes have relatively large lungs (Lindstedt et al 1988). These observations demonstrate a consistent response of an increase in diffusing capacity for oxygen to a chronic reduction in oxygen supply. If the lung does not limit VO2 max (i.e. there is already more lung structure than is necessary to meet demand), it is valid to ask why does the diffusing capacity for oxygen increase in response to oxygen demand?Therefore available lung structure has been postulated to limit VO2 max, however in reality this is most likely to only occur at altitude.
There have been a number of studies that have measured the response of VO2 max to hyperoxic and hypoxic situations. It would appear that the reduction in VO2 max in response to hypoxia is much more significant than the increase demonstrated in hyperoxia (Basset and Howley 1997,Wagner 1995). These effects closely mimic the oxygen-haemoglobin dissociation curve (fig 1). During high PO2 there are only moderate increases in haemoglobin saturation as haemoglobin are close to maximal capacity (flat part of the curve), whereas during low PO2 there are sharp decreases in heamoglobin saturation in response to lower levels of inspired oxygen (steep part of the curve).
Fig 1 (from McArdle, Katch and Katch 1986)
The exception to this situation has been demonstrated by Powers et al (cited in Wagner 1995) who increased inspired PO2 in elite endurance athletes. In this group of subjects VO2 max was increased by breathing higher levels of oxygen, as this corrected an arterial hypoxaemia induced by intense exercise. The phenomenon of arterial hypoxaemia was seen in the 70-80 ml/min/kg VO2 max range, which according to Frontera and Adams (1986) places an individual in a 'world class runner' category. Consequently the results of this study were very impressive as already high VO2 max values were pushed even higher. It is postulated that this phenomenon occurs because of the decreased transit time of the RBC's in the pulmonary capillaries of elite athletes resulting in a pulmonary diffusion limitation (Basset and Howley 1997, Frontera and Adams 1988). This provides greater evidence that pulmonary diffusing capacity can limit VO2 max, particularly in the elite athlete.
Lastly it has been proposed by Wagner (cited in Ranson 1997) that the pulmonary system may limit the VO2 max of elite athletes by way of CO2 poisoning. In the average person PCO2 fall toward VO2 max suggesting that there are expiratory flow limitations. However in elite athletes CO2 levels actually rise as VO2 reaches its maximum secondary to their greater capacity to utilise oxygen, and potentially CO2 may limit VO2 max.
Although there is some support in the literature for pulmonary diffusion capacity being the principal limitation to VO2 max, the prevailing opinion is that VO2 max is primarily limited by cardiac function. Evidence in support of this comes from experimental manipulation of haemoglobin (Hb) concentration, cardiac output and partial pressure of oxygen in arterial blood (PaO2) (Lindstedt 1988). It has been shown that in anaemia, VO2 max drops as a linear function of Hb, with similar responses demonstrated by subjecting humans to conditions whereby the Hb is preferentially bound to CO (Lindstedt 1988). More compelling evidence is generated by studies, which directly manipulate RBC's within the blood stream. It has been found that reinfusion of stored blood leads to a significant increase in VO2 max, with a proportional decrease in VO2 max demonstrated if RBC's are withdrawn (Poole and Richardson 1997). This raises another question to the negative speaker; if VO2 max was driven by the rate of mitochondrial utililisation of oxygen there should always be a circulating supply of surplus oxygen. Consequently if oxygen supply levels were reduced by way of limiting the carrier cells (as in the aforementioned experiment) it would be reasonable to expect very little reduction in VO2 max.
Cardiac output has been manipulated in a number of studies. Perhaps the most well known method of augmenting cardiac output is 'blood doping'. Oxygen delivery has also been enhanced in pericardectomised dogs (Wagner et al cited in Poole and Richardson 1997). This procedure split the pericardium of dogs to allow 20% increases in ventricular volume. The research demonstrated that in the absence of any peripheral training effect that this procedure facilitated an increased stroke volume, cardiac output and thus VO2 max during maximal exercise.
Just as diffusion of oxygen through the lungs may limit oxygen uptake so might the diffusion between the capillaries and the mitochondria (Lindstedt 1988). Wagner and colleagues (cited in Lindstedt 1988) have presented evidence implicating a limitation to oxygen flow at the level of tissue diffusing capacity. They postulated that at low capillary PaO2 there might not be adequate driving force for oxygen to diffuse to the mitochondria. If the mitochondria were hypoxic they would consequently suffer a reduction in oxygen consumption. The negative speaker may argue that this mechanism is a good example of peripheral limitation to VO2 max, however capillary PaO2 is governed by the cardiovascular system and they are therefore inextricably linked.
From the evidence presented thus far it would seem that the limitation to VO2 max might not be a single factor, but a combination of a number of elements of the cardiopulmonary systems. Further evidence supporting this concept is generated by studies investigating the concept that it is O2 delivery not utilisation that remains the limiting factor. A number of studies have examined the effects of active muscle mass (and hence oxygen utilisation) on VO2 max. In general these researchers have found that VO2 max for combined leg and arm work was similar to that elicited by legwork alone (Basset and Howley 1997). This poses the question that if limitation to VO2 max was generated peripherally as the negative speaker would have you believe, why are values of VO2 max for exercise that involves both arm and leg work not greater than those generated by leg work alone?
In 1979 Secher and colleagues (cited in Basset and Howley 1997) had subjects cycle for 10 minutes at 68% of VO2 max, they then added arm cranking whilst continuing to maintain power output with the legs. The added arm work led to a reduction in leg blood flow and oxygen uptake with no change in mean arterial pressure. They concluded that the blood flow to the exercising legs became limited by vasoconstriction once another large muscle mass was activated. They postulate that this mechanism occurred in order for the cardiac output to maintain blood pressure and it provides further support for central limitation of VO2 max.
Recently, investigators have designed the human-knee extensor model to aid in the study of metabolic capacity of human muscle (Anderson et al cited in Poole and Richardson 1997). This model allows for the measurement of blood flow, VO2 and work rate in a functionally isolated muscle group. Data obtained from this exercise model have led to the conclusion that the small muscle mass of the quadriceps (≈2.5kg) can achieve a very high perfusion to muscle mass ratio that can exceed 3.9L/kg/min. These values were compared with peak mass specific blood flows of 1.5L/kg/min found during conventional cycling. Inspired hyperoxia did not alter these flows, which provides strong evidence that when a small muscle mass is used cardiac out put can easily meet muscular needs and therefore limitation to VO2 max can not be on a peripheral level.
Three different research approaches have been taken to investigate the limitation to VO2 max. These three aspects were; the manipulation of inspired PO2, the manipulation of circulating PaO2 and the manipulation of muscle perfusion. It is highly unlikely that all of the studies quoted are incorrect in their assumption that the limitation to VO2 max is central, therefore the logical conclusion is to agree with this assumption.
Response to Statements by the Negative Speaker
The negative speaker has introduced some interesting points, and it may be conceded that the transport of blood to exercising muscle is indeed part of the peripheral mechanism of limitation to VO2 max, however the circulating blood is inextricably linked to the central mechanisms that drive it (Cain 1995). Furthermore the author agrees that the limitation to VO2 max is multifactorial, however the factors that drive this limitation are central. The negative speaker has demonstrated that mitochondrial density is proportional to VO2 max and hence it is mitochondrial activity that limits oxygen consumption. This conclusion is not the only one that may be made from this observation, for it could equally be that gains in central oxygen delivery facilitate increases in mitochondria. Another point raised was that subjects with metabolic deficiencies (such as McArdle's disease) have a low a-VO2 difference and this is what leads to their correspondingly low VO2 max, this example is surely too simplistic as many factors may lead to a poor VO2 max in these patients.
To conclude, the majority of data presented in today's debate points to oxygen supply (and not oxygen utilisation at a peripheral level) as the broad process that sets VO2 max for an individual, under a given set of conditions. Therefore it can clearly be stated that the limitation to VO2 max (and thus aerobic capacity) is central. This has been demonstrated in numerous ways:
The lung will increase in size in response to chronic low PO2.
Manipulation of inspired oxygen will alter an individuals VO2 max, hyperoxia increases VO2 max and hypoxia will decrease VO2 max.
Elite athletes will demonstrate a rise in CO2 towards VO2 max, which may lead to limitation by way of CO2 poisoning.
Increasing Hb levels and/or CO will lead to a corresponding increase in VO2 max.
Low capillary PO2 may limit the diffusing capacity of O2 to the mitochondria at a tissue level.
There is no difference between VO2 max during cycling and cycling with arm cranking.
If muscles are exercised individually they have a great capacity for perfusion which is not demonstrated during exercise large muscle mass.
Short Answer Review Questions
- How can the pulmonary system limit VO2 max?
- What would create the greatest alteration in VO2 max: increasing or decreasing PO2? How does the oxyhaemoglobin curve affect this?
- How does the cardiac system limit VO2 max?
- Explain another way of investigating the limitation to VO2 max, other than altering inspired gases of altering cardiac function (i.e. cardiac output and haemoglobin levels).
Basset DR and Howley ET (1997)
maximal oxygen uptake: "classical" versus "contemporary" viewpoints. Medicine and Science in Sport and Exercise 29:591-603.
Cain SM (1995)
Mechanisms which control VO2 nearVO2 max: an overview. Medicine and Science in Sport and Exercise 27:60-64.
Frontera WR and Adams RP (1986)
Endurance exercise: normal physiology and limitations imposed by pathological processes (part 1). Physician and Sports Medicine 14:95-105.
Lindstedt SL, Wells DJ, Jones JH, Hoppeler H and Thronsen Jr HA (1988)
Limitations to aerobic performance in mammals: interaction of structure and demand. International Journal of Sports Medicine 9:210-217.
McArdle WD, Katch FI and Katch VL(1986)
Exercise Physiology. (2nd Ed.) Philadelphia: Lea and Febiger.
Poole DC and Richardson RS (1997)
Determinants of oxygen uptake: implications for exercise testing. Sports Medicine 24:308-320.
Ranson C (1997)
Limitation to VO2. URL http://physiotherapy.curtin.edu.au/resources/educational-resources/exphys/97/limit.cfm: accessed 3 October 1998. Perth: Curtin University of Technology.
Seiler S (1996)
Exercise physiology: The methods and mechanisms underlying performance. URL http://home.hia.no/~stephens/exphys.htm accessed 3 October 1998.
Wagner PD (1995)
Muscle O2 transport and O2 dependent control of metabolism. Medicine and Science in Sport and Exercise 27:47-53.
Negative Argument by Carolee Hatch
The limit to VO2 max is central?.........or is it?
For some years there has been debate over whether the factors limiting VO2 max are central or peripheral or a combination of both. Central factors limiting VO2 max are thought to be the oxygen provided to the tissues as a result of pulmonary ventilation (to achieve oxygen into the blood) and cardiac output (the mechansim providing oxygen availability to the working muscles). Peripheral mechanisms are thought to be oxygen perfusion of muscle, oxygen diffusion and uptake by the mitochondria (Cain 1995).
Contemporary viewpoints on factors limiting VO2 max appear to point to multifactorial mechanisms including both central and peripheral mechanisms (Cain 1995).
The theory of symmorphosis preposes that central mechanisms are alterred in order to meet the needs of the peripheral system, that is oxygen requirements of a specific muscle mass comprising a certain number of mitochondria, impose a demand on the respiratory system and cardiac output which correspond by increasing proportional output. What is know however is that cardiac ouput reaches a point where it can no longer meet the demands of the exercising muscle and for this reason cardiac output has been regarded as one of the main mechanisms limiting VO2 max (Saltin and Strange, 1992). What has not been considered by supporters of this theory however is what is happening at a muscular level at the point of VO2 max. As central mechanisms are reaching their limit it may be that the mitochondrial ability to extract and process oxygen may have been exceeded which may limit further oxygen uptake. The rate at which mitochondria can use oxygen is set at 5ml O2 per cm of mitochondria per minute. Muscle with many mitochondria (high aerobic power) will therefore be able to uptake large amounts of oxygen resulting in a large arteriovenous oxygen difference (Lindstedt et al 1988).
Some might argue that increasing oxygen consumption to the mitochondria results in greater VO2 max and therefore the mitochondria are not the limiting factor. Indeed under artificially induced hyperoxia, the mitochondrial enzymes are able to respond by uptaking and processing more oxygen. Under normal circumstances however it is the mitochondria density and activity is matched with haemaglobin and oxygen availability and therefore the uptake of oxygen matches the demand of the mitochondria (Lindstedt et al 1988).
Aerobic training is known to increase the number of mitochondria in active muscle and increase ability to uptake oxygen proportionately that is mitochondrial density in the muscle is proportional to VO2 max. In addition altitude and hypoxic training has been found to increase oxidative muscle enzymes (Boning 1997). Further supporting the limiting role of the mitochondria are the finding of low VO2 in persons with muscle metabolic diseases including McArdle's disease - myophosphorylase deficiency and PFK (phosphofructokinase) deficiency. In such diseases the ability of the mitochondria to extract oxygen from the muscle capillary is altered and arteriovenous difference is low (Bassett and Howley 1997).
Perfusion of muscle or conductance of oxygen to the active muscle is another peripheral mechanisms which may limit VO2 max. Evidence of perfusion limiting VO2 max is the finding that exercise of a single muscle group (the knee extensors) versus mutiple groups (as in cycle ergometry) results in a disproportionately high ability to extract oxygen for the single muscle group. This limitation may be seen as central limitation of cardiac output however it is possibly the competition for peripheral perfusion (or distribution of the cardiac ouput) that limits the VO2 max in the mutiple muscle task (Lindsted et al 1988).
Robergs et al (1997), exercised individuals under hypobaric hypoxic conditions to determine the effect on VO2 max. The authors found that males with large lean body masses and low lactate threshold experienced the greater decriments in VO2 max than individuals with small lean body mass and high lactate threshold when compared with normoxic VO2 max. Such a finding may represent that greater competiton for perfusion across a greater muscle mass may occur when oxygen availability is low. Peripheral perfusion may thus be a limiting factor in this situation. The finding that low lactate threshold resulted in larger decrements in VO2 max under hypoxic versus normoxic situations may represent the limitation imposed on VO2 max by low oxidative capacity of the muscle or low density of mitochondria.
Aerobic training is known to increase capillary density to exercising muscle which may explain why training increases VO2 max. Training also reduces shunting of blood to non active muscle which may reduce competition for peripheral perfusion thereby increasing available oxygen (Poole and Richardson 1997).
Arterial pressures of oxygen in elite athletes are often lower than in untrained subjects. This may result from red blood cells spending less time in the pulmonary capillary resulting in less time to bind with oxygen diffusing across the pulmonary membrane.
Haemaglobin concentration in athletes may also be lower as a result of expanded plasma volume which may lower conduction of oxygen to the muscles. Interestingly studies of anaemic individuals and individuals with artificially enhanced erythrocyte populations have been used to explain central mechanisms controlling VO2 max (Lindstedt et al 1988).
Wagner 1995 investigated the effect of presenting the same muscle with oxygen at high and low pressure to determine the effect of diffusion from capillary to mitochondria on maximal oxygen uptake. Wagner found that reducing pressure of oxygen reduced maximum VO2 and muscle venous and mean capillary PO2. Such a finding highlight the effect of oxygen diffusion on VO2 max.
The theory of a respiratory limitation to VO2 max is negated by the finding that pulmonary diffusion and airway conductivity cannot adapt significantly to training. Increases in the resistance of the airways and changes in lung volumes may not alter VO2 max. Evidence supporting this theory is the finding that VO2 max between smokers and nonsmokers are not significantly different whilst lung volume and function in the smoking group are significantly lower than the nonsmoking group (Lindstedt et al 1988).
Whilst the pumonary diffusing capacity is essentially fixed changes in cardiac output, capillary density and muscle mitochondrial volume can all be alterred to increase VO2 max (Bassett and Howley, 1997).
Lindstedt et al (1988)postulate that the highly tuned athlete has no one single factor limiting maximal oxygen consumption. Rather changes in the muscle requirements for oxygen impose demands on the cardiac ouput, peripheral perfusion, mitochondria and diffusion across the capillary/mitochondrian junction which collectively produce maximal levels of VO2. Therefore changes to any of these factors may result in alterations in VO2 max.