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Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #1 
Here a very interesting paper:

It is one of the opposing groups  towards  T.D. Noakes  ideas  and  therefor very interesting to see what they  tell us.
 The idea  of VO2  max is nicely summarized in this  abstract  and you can see, why   many coaches  and  people  may  have some problems  with our ideas of NIRS information.
 I case   we really can show , how  VO2 values change  by altering the a-v O2  difference, than this paper  may need some critical reviews  .
 The interesting point is the   fixed  info,  that VO2  is  basically only dependent on the CO  ( delivery system  ) but not on the a-v O2 difference.
  If that is the case why is the Fick formula not  simply  CO = VO2  max. Why  do so many discuss the a-v O2  difference.
   See at the end    some ideas   you can try  as a new MOXY user.

Limiting factors for maximum oxygen

uptake and determinants of

endurance performance

DAVID R. BASSETT, JR. and EDWARD T. HOWLEY

Department of Exercise Science and Sport Management, University of Tennessee, Knoxville, TN

ABSTRACT

BASSETT, D. R., JR. and E. T. HOWLEY. Limiting factors for maximum oxygen uptake and determinants of endurance performance.

Med. Sci. Sports Exerc., Vol. 32, No. 1, pp. 70–84, 2000. In the exercising human, maximal oxygen uptake (V˙ O2max) is limited by the ability of the cardiorespiratory system to deliver oxygen to the exercising muscles. This is shown by three major lines of evidence:

 

1) when oxygen delivery is altered (by blood doping, hypoxia, or beta-blockade), V˙ O2max changes accordingly;

 

2) the increase in V˙O2max with training results primarily from an increase in maximal cardiac output (not an increase in the a-vO2 difference); and

 

 3) when a small muscle mass is overperfused during exercise, it has an extremely high capacity for consuming oxygen.

 

 Thus, O2 delivery,not skeletal muscle O2 extraction, is viewed as the primary limiting factor for V˙ O2max in exercising humans.

 

Metabolic adaptations in skeletal muscle are, however, critical for improving submaximal endurance performance. Endurance training causes an increase in mitochondrial enzyme activities, which improves performance by enhancing fat oxidation and decreasing lactic acid accumulation at

a givenV˙ O2. V˙ O2max is an important variable that sets the upper limit for endurance performance (an athlete cannot operate above 100%

V˙O2max. for extended periods). Running economy and fractional utilization of V˙ O2max also affect endurance performance. The speed at lactate threshold (LT) integrates all three of these variables and is the best physiological predictor of distance running performance.

 

Key Words: CARDIORESPIRATORY, FITNESS, EXERCISE, OXYGEN TRANSPORT, MARATHON, RUNNING, RUNNING

ECONOMY, LACTATE THRESHOLD   

If we can't alter a-v O2 difference  how come:
  a)  make a VO2  test  and   change in one step  your respiration  from " normal  to very fast  and hypocapnic   and than repeat the same step  but breathe  slow  and deep  hypercapnic  sent us the result of the VO2   volume in ml / min.
 What   do you see and what  can we see ???

 2. Use a physio flow  and  change  cardiac output  by changing   SV.  than play as well with   hyper an hypocapnia  and look what happens  with VO2.

 3. Train an athlete  and  see how VO2  changes,  without changes of CO   but with a much better utilization of  O2    shown over NIRS   testing.

Last but not least here some  numbers  to look at.
 This was a research project  done  by Red Bull in Death Valley  and in altitude  combining  different e equipment like Physio flow , SEMG,  NIRS,  lactate, VO2  . The  same as we show  since many years  on the fact forum.
 They had  an incredible group of people together to collect  data's  and as set of world class athletes.

 Here my question.
  See pic  1.  VO2  values  in  death valley  top  info  and altitude bottom info.
 Red VO2  values.
  Where was VO2   higher.
 Than  pic 2 NIRS info    from death valley  and  altitude  same  test  protocol. See  one of teh pics  showes a great O2  utilization an the other less optimal.
 So if  VO2   would not be influenced  by  a- v  O2  difference we would   now  have to argue, that in death valley the VO2  is higher because of  CO  higher and SV  higher.
 Now  CO = SV  x HR.
 So last pic see  irst column : death valley  HR  and SV  values  and  second row  altitude.
 Where is HR x SV higher  .
 Why is  VO2  lower,
 where is a-v O2  difference higher   ?
  Just some  critical questions  as  paper like the one   I showed  you confuse  me.  Now just for fun finish  the  loud thinking:
 If   yo move fast  to altitude , what system often gas to compensate  immediately ???
 If that is the case   would it be possible that this could be a reason of a  much lower utilization in altitude   ?


 

 

 

 

 

 

 

 

 

 

 

 

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Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #2 
Here another interesting study  with some questions:  look to key elements.
  a) a-v O2 difference  was  CALCULATED)

 AND THEY  NEEDED TO USE THE vo2  RESULT  , WHICH HAS A   NICE LAG TIME AS IT IS AN INDIRECT  ASSESSMENT IN YOUR MOUTH  COMPARED WITH THE RELATIVE DIRECT ASSESSMENT OF THE CARDIAC  READINGS.
 SO  IF WE  TAKE A- V o2 DIFFERENCE  FROM vo2  WE HAVE THE  TIME LAG PUSHED  UPON US  AND THEREFOR THE vo2   SEEMS TO BE INFLUENCED   IMMEDIATELY  FROM co  AND    NOT  FROM A-V  o2 DIFFERENCE.
 IF WE LOOK AT DIRECT INFO    WITH HR  AND PHYSIOFLOW  AND moxy WE  WOULD  DISAGREE. WE SEE AN IMMEDIATE  DROP IN sMo2  AS A SIGN OF A  CHANGE IN A- V  o2  DIFFERENCE.   AND THAN,    MORE OR LESS  AT THE SAME TIME  A CHANGE IN CO OVER HR AND SV. BUT FOR SURE NOT FASTER. HR  AND SV WILL INCREASE  WITH  INDIVIDUAL REACTIONS.DEPENDING ON THE  BACK FLOW OF BLOOD TO THE HEART.
 SO READ THIS STUDY  AND SEE THE CONCLUSIONS  WE GET  BUT   ASK THE QUESTION:
 WHAT IF  WE  WOULD TEST A- V o2 DIFFERENCE   NOT  MATHEMATICALLY BUT   AS A  DIRECT INFO DATA COLLECTION AS WELL. ( moxy  TREND )
 

Cardiac output, oxygen consumption and arteriovenous oxygen difference following a sudden rise in exercise level in humans.

 

Abstract

1. To investigate the relative contributions of increases in cardiac output and arteriovenous oxygen difference to the increase in oxygen consumption during exercise, the ventilatory and cardiovascular responses to a sudden transition from unloaded cycling to 70 or 80 W were measured in six normal healthy subjects. 2. Oxygen consumption (VO2) was measured breath-by-breath and corrected for changes in lung gas stores. Cardiac output (Q) was measured beat-by-beat using pulsed Doppler ultrasound, and blood pressure was measured beat-by-beat using a non-invasive finger cuff (Finapres). All data were calculated off-line, second-by-second. 3. Arteriovenous oxygen difference (A-VO2) was calculated from Q and VO2 using the Fick Principle. Left ventricular afterload was calculated by dividing Q by mean blood pressure. 4. The data for Q and VO2 were closely fitted by single exponential curves (mean r2 0.84 and 0.90 respectively; r is the correlation coefficient). These curves yielded mean time constants for the increases in Q and VO2 of 28 and 55 s respectively following the increase in exercise level. In each individual subject, the time course of adjustment of Q was faster than that of VO2. There was a mean lag of 15 s from the start of the new exercise level before the derived A-V O2 began to increase; the mean time constant for A-V O2 was 57 s. 5. If A-V O2 had remained constant, the observed rise in Q alone would have resulted in an average of 87% of the increase in VO2 which was observed after 5 s. If Q had remained constant, the observed increase in A-V O2 would have led to only 8% of the actual increase in VO2 after 5 s. 6. Mean and systolic blood pressure rose and afterload fell immediately after the onset of the increased workload. The time constants of the systolic blood pressure and afterload responses to exercise varied widely and ranged from 37 to 81 and 10 to 26 s respectively (n = 4). 7. We conclude that Q is responsible for most of the early increase in VO2 following a sudden increase in exercise workload. Blood pressure responses to exercise are slower than Q and VO2 responses, probably due to the rapid decrease in afterload. 8. The dominant contribution of Q to adaptation to changing workload may be physiologically important particularly in heart disease, where decreased ability to increase cardiac output may limit the capacity to cope with changing metabolic needs during everyday activitie

Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #3 
Are we  BIASED ?
 For sure  , when ever you get involved over 30 years in ideas   you  have the risk of being biased.
  Nevertheless  we try here to  have  an open directions in all  ideas.
 Here I like to show you  where some of the  ideas are miss matching  and   it is  hard  to   k=just believe   when you read  this ideas.
 The discussion is:
  VO2  max is only dependent on CO.
 versus  the idea, that in a  idea  where  VO2 max  = CO  x a- v O2 difference. it is hard to believe  than  one side  is  of no interest  in this   equation.
 Here  first  one side  of the discussion : 

Limiting factors for maximum oxygen

uptake and determinants of

endurance performance

DAVID R. BASSETT, JR. and EDWARD T. HOWLEY

Department of Exercise Science and Sport Management, University of Tennessee, Knoxville, TN

ABSTRACT

BASSETT, D. R., JR. and E. T. HOWLEY. Limiting factors for maximum oxygen uptake and determinants of endurance performance.

Med. Sci. Sports Exerc., Vol. 32, No. 1, pp. 70–84, 2000. In the exercising human, maximal oxygen uptake (V˙ O2max) is limited by the ability of the cardiorespiratory system to deliver oxygen to the exercising muscles. This is shown by three major lines of evidence:

 

1) when oxygen delivery is altered (by blood doping, hypoxia, or beta-blockade), V˙ O2max changes accordingly;

 

2) the increase in V˙O2max with training results primarily from an increase in maximal cardiac output (not an increase in the a-vO2 difference); and

 

 3) when a small muscle mass is overperfused during exercise, it has an extremely high capacity for consuming oxygen.

 

 Thus, O2 delivery,not skeletal muscle O2 extraction, is viewed as the primary limiting factor for V˙ O2max in exercising humans.

 

Metabolic adaptations in skeletal muscle are, however, critical for improving submaximal endurance performance. Endurance training causes an increase in mitochondrial enzyme activities, which improves performance by enhancing fat oxidation and decreasing lactic acid accumulation at

a givenV˙ O2. V˙ O2max is an important variable that sets the upper limit for endurance performance (an athlete cannot operate above 100%

V˙O2max. for extended periods). Running economy and fractional utilization of V˙ O2max also affect endurance performance. The speed at lactate threshold (LT) integrates all three of these variables and is the best physiological predictor of distance running performance.

 

Key Words: CARDIORESPIRATORY, FITNESS, EXERCISE, OXYGEN TRANSPORT, MARATHON, RUNNING, RUNNING

ECONOMY, LACTATE THRESHOLD  

well some other studies  would dispute the  statement  and we for  sure, when looking at MOXY infos  see the  picture somewhat different.

You are the judge  but you can see, why we  "play"  so much  with  respiration and the O2  diss curve. Just simpler  as in this study.

Increased V˙o2 maxwith right-shifted Hb-O2dissociation curve at a constant O2 delivery in dog muscle in situ

 

1.   Russell S. Richardson,

 

2.   Kuldeep Tagore,

 

3.   Luke J. Haseler,

 

4.   Maria Jordan, and

 

5.   Peter D. Wagner

 

*       Submitted 17 April 1997.

 

*       accepted in final form 31 October 1997.

 

 

 

Abstract

 

If the diffusive component of O2 transport in muscle is important in determining exercise capacity, an increased capillary-to-tissue difference should enhance gas exchange from blood to skeletal muscle during exercise. Thus a rightward shift in the O2 dissociation curve should theoretically increase O2extraction and improve maximal O2uptake (V˙o2 max). To test this hypothesis, we used the canine gastrocnemius muscle to study maximal exercise in eight dogs at a normal P50 (33.1 ± 0.4 Torr) and with the O2 dissociation curve shifted to the right by an allosteric modifier of hemoglobin (Hb) (methylpropionic acid, RSR-13; P50 = 53.2 ± 5.0 Torr). Four control dogs were also studied before and after infusion of vehicle. O2 (100%) was inspired during exercise to maintain arterial saturation in both conditions. The muscle was surgically isolated and electrically stimulated (tetanic train: 0.2-ms stimuli for 200-ms duration at 50 Hz, once per s). To maintain O2 delivery (pre-RSR-13 = 19.1 ± 2.9; RSR-13 = 19.6 ± 2.5 ml ⋅ 100 g−1 ⋅ min−1), the muscle was pump perfused. At a constant O2 delivery, RSR-13 significantly increased percent O2 extraction (pre-RSR-13 = 61 ± 4.0; RSR-13 = 75.5 ± 4.7) and muscle V˙o2 max(pre-RSR-13 = 11.8 ± 2.1; RSR-13 = 14.2 ± 1.5 ml ⋅ 100 g−1 ⋅ min−1). This improvement inV˙o2 max with increased P50 demonstrates its O2 supply dependence when P50 is normal and the importance of O2 diffusive transport to muscle at maximal exercise.

 

oxygen delivery to skeletal muscle is dependent on the interaction between the convective transport of O2 in blood and, once released from the hemoglobin (Hb) carrier molecule, its subsequent diffusion down an O2 tension () gradient to the mitochondria. Convective O2 delivery is set by muscle blood flow (Q˙) and arterial O2 content (), whereas the diffusive component is determined by the magnitude of the gradient from blood to the O2-consuming mitochondria and the physical conductance for O2 of the pathway between them. The gradient itself is the consequence of O2 delivery, the affinity of Hb for O2, the muscle metabolic rate, and the O2 conductance from blood to muscle (24, 30).

 

Thus the position of the O2dissociation curve (ODC), conveniently described by P50( at which 50% Hb is saturated), has an important role in O2transport. Of course, variations in P50 have ramifications not only in the periphery but also during O2loading in the lungs. A high P50opposes the association of O2 in the lungs but favors its release to the tissues and vice versa. Thus, if arterial is maintained to permit normal O2 saturation, a right-shifted ODC may be advantageous during exercise conditions, since it allows Hb desaturation to occur at higher levels of mean capillary(), increasing the gradient and thus promoting a greater O2 flux from capillary blood to skeletal muscle (25). There is now considerable experimental evidence, collected in animal and human skeletal muscle, that indicates that O2conductance (), from blood to mitochondria, is an important determinant of maximal muscle O2 uptake (V˙o2 max ) (3, 18, 21,29). These data have recently been supported by evidence of a large difference in between blood and the intracellular compartment in normal human muscle, as measured by myoglobin-associated , across a wide range of exercise intensities (19).

 

In the ongoing search to find methods to increase O2 delivery to ischemic tissue, recent pharmaceutical developments have lead to the discovery of allosteric effectors of Hb-O2affinity, which are active in whole blood (17). These allosteric effectors result in a similar right shift of the ODC to the naturally occurring erythrocyte allosteric effector 2,3-diphosphoglyceric acid (2,3-DPG), but they bind at a different site and so may produce an additive right shift in the ODC in the presence of 2,3-DPG. One compound of this series, 2-(4-{[(3,5-dimethylanilino)carbonyl]methyl}phenoxy)-2-methylpropionic acid (RSR-13), significantly increases the P50 in vivo but has a lower affinity for serum albumin than the other compounds from this series and therefore may be the preferred allosteric effector to study clinically (1).

 

It has previously been illustrated that in the presence of a right shift in the ODC produced by allosteric Hb-O2 modifiers [with constant convective O2 delivery and O2 uptake (V˙o2)], venous and tissue are both increased (9,32). Thus manipulations of the P50offer the opportunity to vary O2delivery to the tissues without altering blood flow and and therefore isolating the specific effects of diffusive O2 movement into the tissue. Using this approach, Hogan et al. (4) demonstrated that an increased Hb affinity (low P50) resulted in a diminished V˙o2 max in the isolated canine gastrocnemius muscle. Because the estimated was not different in the normal and left-shifted conditions and the decline inV˙o2 max was proportional to the fall in calculated, it was concluded that peripheral (blood to muscle) played a role in determiningV˙o2 max. However, these data illustrate the O2 supply dependence ofV˙o2 max only under conditions in which the gradient from blood to tissue is reduced and do not address the issue of whetherV˙o2 max is O2 supply dependent under normal conditions and thus could be increased by producing a larger gradient. This would provide a better understanding of the relationship between maximal mitochondrial respiration rate and O2 supply under normal physiological conditions. Consequently, the purpose of this study was to determine the effect of a decreased Hb affinity produced by an infusion of RSR-13 on skeletal muscleV˙o2 max, while ensuring constant O2delivery by controlling Q˙ and

 

 




Juerg Feldmann

Fortiori Design LLC
Registered:
Posts: 1,530
 #4 
Here an article  I got mailed  to me a few days back.
 The question  or   info was:
 " You are not alone  on  the VO2  max issue  as it is worthless  for the majority of the sports . A  bike VO2  test  may in the best case  be okay  for people  using a spinning bike  an that's it.
  True  and here my take on  how we  would test the wrestler.
  .  A MOXY on  the upper body ,lower body  and core  muscle  for a sport specific   activity   an than look  at the limitation of the bodies  respond.
  Delivery  problem versus   utilization problem.  than who is the limiter   an than  set up a program  controlled  and h=guided  by oxygenation demands..
 Price  tag.
  A   decent  good VO2  equipment  will be  around 10'000 $   and it is nothing  extreme  special. Than you need  masks  and more and a bike.
  A  great    wrestling assessment kit  would cost you 3  MOXY units  and a PC  software program  and 3  cheap  FR 70 watches  and you have all you need  and even can use  it later on three athletes during a workout. Cost  of this is  about  3'000 $
  Seems to  me a no brainer.
 

VO2 max: Not the gold standard?

Tony Leyland

In my article on exercise science in last month’s CFJ, I highlighted the difficulty of scientifically determining optimal training methods. Most often, it is coaches working hands-on using a trial-and-error methodology that actually push the science ahead. Eventually, scientists notice that most coaches are doing a particular thing with success and then design a study to determine why it is effective.

However, coaches’ practical, field-tested insights and clinical experience don’t necessarily translate into the realm of scientific testing and study design. I was recently contacted by a coach working with the Canadian National wrestling team. One of the wrestlers was competing in the 62 kg class, but the coaches thought that if he could drop down a weight class he would be able to medal at the Olympics. They wanted him to drop from 62 to 55 kg, but realized that he was, understandably, concerned about how he would perform after dropping over 11 percent of his body weight. So they wanted him to get a few weight-cutting practice trials in before he actually had to do it in competition. He was to act like it was a wrestling meet and cut down for weigh-in at 6 p.m., rehydrate overnight, and then go through some physiological fitness tests in the morning. They wanted to see how his body handled the cut-down and hopefully give him confidence that he could maintain fitness and perform normally while dropping that much weight. That is where I come in: they wanted me to conduct the morning fitness tests at my university.

The tests they wanted to use were a VO2 max test (aerobic capacity measured while working to exhaustion on a treadmill or stationary bike) and a Wingate test (a bike test designed to assess both anaerobic pathways). Not a good idea in my book, as those tests do not mirror the performance required by the wrester in his sport. They would not very effectively test the wrestler’s ability to perform at the tasks required for his event—which was the whole point of the experiment.

So why did they suggest tests that are clearly not the best to assess the athlete’s performance? I think it is because we all have a tendency to work with standards that are universally accepted. (Maybe this is why CrossFit is viewed with suspicion by some: it doesn’t put much stock in the standard tests for evaluating fitness. How can people compare CrossFit’s methods and results with others? How can they evaluate and quantify the fitness it produces? Nobody else uses tests called “Fran,” “Linda,” etc., to measure progress. The unfamiliar is always suspect.)

of 3

VO2 max: Not the gold standard? (continued...)

of 3

The VO2 max test on a treadmill or stationary bike measuring gas exchange is considered the “gold standard” of laboratory tests to assess VO2 max (the conventional measure of aerobic fitness), which is why the wrestling coaches wanted to use it for their athlete. But does it transfer to a wrestling match? Olympic freestyle wrestling bouts consist of three rounds of two minutes each. Wrestling is an exceptionally demanding sport using multiple lines of action (pushes, pulls, and static grips with both the arms and legs) and demanding both cardiovascular endurance and muscular stamina, so why not asses all these abilities in one test? You could do three two-minute rounds of one minute of thrusters and then one minute of pull-ups (like a Fran), or maybe three sets of two minutes of clean and jerks (like a Grace). This would tax the cardiovascular system as well as muscular strength, power, and endurance, and the athlete’s scores for each would measure changes in his fitness. You could also develop a continuous six-minute test similar to Fight Gone Bad that would cover many of these aspects and be indicative of the wrestler’s VO2 max. To break the testing into a VO2 max test (which would quantify how well he pumps blood to his leg muscles and the stamina of those muscles) and a Wingate test (which is a 30-second maximal-output bike test to assess phosphagen and glycolytic energy pathways) doesn’t adequately test the demands of the sport.

If you wanted to assess other energy systems separately, you could test the phosphagen system with a maximal sprint (say, 60 meters) or, if you wanted a very short-duration power test, you could use a vertical jump or clean and jerk. As for the glycolytic system…well, I think any self-respecting CrossFitter could think of something extremely intense using multiple muscle groups that you could sustain for only 90 seconds before collapsing in a heap on the floor.

When I discussed these issues with the wrestling coach, I got a very positive response. It made a lot of sense to him (as did the thought that he wouldn’t have to pay for expensive tests). Also he now has complete control on the timing of the test and he can repeat it more frequently than relying on my university to conduct the test.

Athletes are competitive by nature and love to challenge themselves, so I frequently get calls asking me to measure VO2 max and body fat percentages. As with the wrestling coach, I usually tell people to save their money. There is no need for expensive tests to measure these variables and there is good science to prove you shouldn’t. I’ll talk about percent body fat at another time but this month I want to focus on VO2 max.

VO2 max is a measure of your body’s ability to take up and utilize oxygen. VO2 max is measured by determining the amount of oxygen in the inspired air and the expired air. The difference is the amount of oxygen used by the body. This is usually done by analyzing inspired and expired gases while having the subject run on a treadmill with ever-increasing speed and/or incline until exhaustion.

At sea level, the most important physiological factors that determine VO2 max in a given person are:

the ability of the heart to pump blood

the oxygen-carrying capacity of the blood (hemoglobin content)

the ability of the working muscles to accept a large blood supply (amount of capillarization within a muscle)

the ability of the muscle cells to extract oxygen from the capillary blood and use it to produce energy (number of mitochondria and aerobic enzymes)

Delivery of oxygen to the blood via the lungs is important, but at sea level it is not a limiting factor. Most people can get adequate amounts of air into the lungs. The last two points in the list above are really why I thought that a running or biking VO2 max test for the wrestler wasn’t a good idea. A runner may have a large stroke volume (amount of blood pumped by the heart per beat, #1 above) but if you put him on a bike, his VO2 max measurement will come out lower than when he is tested on a treadmill. Similarly, a cyclist will not do as well on a treadmill. This is because of the difference between systemic adaptations to the training impulse and peripheral adaptations. Both runner and cyclist have large stroke volumes but the runner’s quads cannot accept as large a volume of blood and extract oxygen as efficiently as the cyclist’s quads. Likewise, the hamstrings and especially the ankle extensors (gastrocnemius and soleus) of the runner are able to receive larger amounts of blood and extract oxygen more effectively than those of the cyclist. So VO2 max is specific to what you are doing. In truth, there is no single, movement-agnostic

VO2 max. There is a “running VO2 max,” a “cycling VO2 max,” a “thruster VO2 max,” etc.

The highest VO2 maximums recorded are for cross-country skiers, as they utilize the most muscle tissue in their event. I wonder what the VO2 max of an elite CrossFit athlete would be while doing thrusters. You could have a series of barbells set up with different weights and increase the weight being thrusted every three minutes until the athlete couldn’t sustain that power output (similar to increasing the speed and/or inclination of the treadmill). Not an easy test to administer, but it is interesting to consider. The VO2 max recorded would undoubtedly be a very high value.

Another important point to keep in mind about measuring athletic performance is that there is daily variation in our physiological parameters. If you measure your heart rate upon waking each morning, it will vary from day to day. So will the maximum heart rate you can achieve on any given day. It has been reported that there can be up to an 8% variation in the VO2 max due to this natural daily variation (we are not robots responding to stimuli exactly the same way every time). So why pay for one VO2 max test when you are trying to determine change? You need at least two measures. But even two tests aren’t ideal, as the difference is likely to be affected by daily variation and other factors such as hydration, nutrition, and environmental temperature, rather than changed VO2 max per se.

So the best thing is to have simple tests such as a 5k run that you can easily repeat six or seven or more times a year. If your time improves consistently, you know your running VO2 max has improved. Over the year and multiple tests, variation due to factors other than improved running VO2 will cancel out. This is why it is so easy to test yourself while following CrossFit: the benchmark workouts become the standardized tests. You might not hit a PR every time, but you will see which direction you are heading in and how steep the trend curve is.

If you actually want a specific numeric measure of your VO2 max (in ml of oxygen utilized per kg of body weight per minute), you can run a 1.5-mile test (6 laps of a standard 400-meter track) or run for as far as you can on the track in 12 minutes. The links below will take you to calculators that will estimate your VO2 max based on your results:

Sure, there are errors in these predictions compared to a test that actually measures the O2 content in your inspired and expired breath (the gold standard of testing, remember), but they are free and repeatable whenever you can find a 400-meter track and a stopwatch.

Not a runner? Test yourself at 150 wall-ball shots for time. If over the year your time decreases, your VO2 max for wall ball has improved. And that is good to know. However, you must be able to sustain any movement you want to use to test VO2 max continuously for about 6 minutes or more. If wall ball with a 20-pound ball overloads your arms so that you have to break sets and rest, it wouldn’t be the best choice for evaluating VO2 max. Using a lighter ball (and maybe even adding to the number of shots) so that you can work continuously for 6 minutes or more would make it work as a test of your wall-ball VO2 max. So for anyone thinking of getting an expensive fitness test done, don’t bother. Spend your money on useful things, like the CrossFit Journal or another medicine ball or another set of rings so your friends can join you in actually improving your fitness rather than worrying about how to quantify it.

 

Tony Leyland is Senior Lecturer at the School of Kinesiology at Simon Fraser University in Vancouver, Canada. He has taught at the university level for 24 years and has been heavily involved in competitive sports such as soccer, tennis, squash, and rugby as both an athlete and a coach for over 40 years. He is a professional member of the National Strength and Conditioning Association, a Canadian National B-licensed soccer

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