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LisaS
06-09-2006, 11:55 PM
I was reading back in the June challenge section – and realized that I had somewhat “committed” to writing up something about VO2 max – so here it is. I'm kinda long winded ;)

Technically, I'll be talking about V-dot O2 max (written as http://jap.physiology.org/content/vol98/issue4/fulltext/1371/f1.gifO2 ) (but I'm too lazy to keep formatting it that way each time). The “dot” in V-dot indicates that we are talking about a rate and not an absolute value. V-dot O2 max refers to the maximum amount of O2 that a person can utilize in a period of time. It can either be expressed in absolute units like L O2 per minute, or in size adjusted units of ml O2/kg/min. The “dot” in V-dot indicates that we are talking about a rate and not an absolute value. But only physio texts call it V-dot or bother to write with the V and the little dot ahove – so I'll quit that and just call it VO2 max – but you remember what it means.

I'll reference some good physiology sites & articles discussion VO2 max at the end. Exercise Physiology is one of my favorite subjects.

You all remember that the endpoint of cellular respiration is the reduction of O2 to H2O while producing ATP. So, the amount of O2 that you can maximally consume (use up) is an indirect measure of how much energy you are able to produce at your max capacity. What can influence VO2? Well, let's look at the road that O2 travels to get to those cellular factories we call mitochondria. First, air (at 21% O2) has to enter your lungs and get down to your alveoli. Then the O2 has to diffuse across the alveoli and get picked up by the hemoglobin (Hb) in red blood cells (RBC). Each Hb molecule can bind up to 4 O2 molecules. Hb has iron as a main component.

Your now oxygenated blood goes from the lungs to the left side of the heart, where it is squirted out into your aorta and on to the rest of the cells in your body. Once it finds a target tissue (like skeletal muscle) and the blood is in the capillary bed, the Hb releases the O2 which again has to diffuse to its destination – your cell. The O2 makes its way to the mitochondria in the cell where it can act as the final electron receptor and be reduced to water – as you are making ATP . The now deoxygenated blood flows back through the venous system (carrying CO2) and enters the right side of the heart. The heart pumps this deoxygenated blood to the lungs, where the CO2 is offload (for you to breathe out) and the cycle starts again.

So where can things go wrong and where can we have improvements in this system? Well, these are many. We'll look at lungs, heart, blood, circulatory system and cells.

Lungs
You need lung volume; you need your lungs to properly expand and contract to exchange the “used air” for the “new air”; you need to get the new air down the pipes to the alveoli; you need proper conditions for O2 to diffuse into the blood; you need working alveoli. You need enough RBC to pick up the O2 and enough Hb in the RBC to carry it all.

If you have asthma, your pipes are inflamed, making the openings narrow. It is hard to get new air in and old air out – like using a really narrow straw. If you have COPD (like emphysema or chronic bronchitis) you have problems. Emphysema destroys the small airways and causes them to collapse – this reduces the alveoli available for gas exchange. Chronic bronchitis makes excessive mucous in the broncii – and one effect is that mucuos makes it more difficult for O2 to get across the alveoli walls into the blood. Other than avoiding diseases or improving them up to your “normal” there isn't much that training does for the lungs. Your lungs are the size they are and your vital capacity (lung volume) is whatever your body size says it is.

RBC & Hb & circulation
This is a little like a logistics problem. Lets say your packing college students into phone booths, four to a booth, and then transporting the booths on flat bed trucks. You want to transport the maximum number of students per minute to work in your factories. Assume you have an endless supply of college students. First you need lots of trucks (RBC) and you need them to be full to capacity with empty phone booths. You need to get the trucks close to the students so they can pile in quickly, and then you can race off to the factories.

If you are anemic and not making enough Hb, you don't have enough phone booths. If you are iron deficient, you hare not making enough phone booths. If you have a low RBC count, you don't have enough trucks. If you're really in trouble, you're short on trucks, and they each are carrying less than their capacity of phone booths. If you have sickle-cell anemia, most of your phone booths are deformed and can't hold students and make the trucks misshapen too. If you have sickle cell trait (a carrier), you might only have a few misshapen phone booths and you don't really have any problems unless you are in an area with fewer students than usual (like high altitudes).

If you move to an area with relatively fewer students available (high altitude), your body will adapt by building more trucks & phone booths so you can get the same amount of students to your factories from the smaller pool of students. If you have too many RBC, you can get gridlock on the highway, but this is a fairly rare problem. If you step up demand in your factories (exercise), to a certain extent your body will build more trucks & phone booths to meet the increased demand, but there are limits. This is why athletes often train or live in higher altitudes to make more RBC & Hb and then compete at lower altitudes.

The highways and offramps and streets to the factories have to be adequate to handle the traffice load. That is, you must have enough capillaries near the working muscle to supply the cells' needs. If you exercise, your body will build new capillaries to increase the flow of O2 in and CO2 out.

Heart
The heart needs to pump regularly and with force – think of a sponge filled with water – you can barely squish it and get a little water out or you can give it a might squeeze and get a lot of water out per pump. You need a big sponge (heart size), a strong squeeze and enough water (blood volume) to move things along.

Under the right (good) physiologic conditions, your heart can increase its capacity (bigger sponge) and increase its muscle to squeeze harder (increase stroke volume). Regular exercise can also increase blood volume over time, which increases the amount that fills the heart each cycle. There is a mechanism that the more the heart is stretched by the returning blood, the harder it can contract – and thereby increase stroke volume (Frank-Starling mechanism). So this increased stroke volume delivers more blood per stroke to the cells.

Cells
The organelle in the cell that is the primary user of O2 is the mitochondria. This is the factory that produces energy – the last stop for our students. If you exercise and increase the energy demands on your body, your body will respond by building more factories (mitochondria) and more roads to the area (more capillaries) to deliver more O2.

So – lets summarize – how can training increase your VO2 max? What limits VO2 max – the delivery system or the capacity to use O2?

In untrained people, the first thing that happens is that the usage capacity is increased. Capillaries increase, mitochondrial density increases, enzymes needed to support cellular respiration are increased. At first, you have adequate delivery but need to step up consumption. Later, as you become a trained athelete, the delivery system seems to be the limiting factor. This is why the elite athletes turn to high altitude training or, for the unscrupulous, things like blood doping and EPO loading.

This is why, as we exercise, we can all chant with Covert Bailey "I'm building better butter burners...I'm building better butter burners" - as we increase our capacity to use O2.

In the mean time, if I haven't totally turned you off to the concept of VO2 Max – here are some articles by real writers:

good explanation of the concept
http://home.hia.no/~stephens/vo2max.htm (http://home.hia.no/%7Estephens/vo2max.htm)

how do you improve it ?
http://www.coolrunning.com/major/97/training/hampson.html
(http://www.coolrunning.com/major/97/training/hampson.html)
Respiratory Physiology
http://www.medicine.mcgill.ca/physio/resp-web/intr-idx.htm

Heart adaptations to Exercise
http://home.hia.no/~stephens/hrttrn.htm (http://home.hia.no/%7Estephens/hrttrn.htm)

Other Exercise Adaptations
http://home.hia.no/~stephens/timecors.htm (http://home.hia.no/%7Estephens/timecors.htm)

just FYI: HIIT in kids with asthma and effects on VO2 max
http://tinyurl.com/jz5c8

postscript:

I can't find the article now, but I recently read an article by the physiologist who has tested Lance Armstrong over the years. Lance has amazing VO2 max (about 85 ml/kg/min) and he also can generate a great deal of power for a long period of time. Here's the thing – a normal adult male might have 45 ml/kg/min – and a highly trained perons might get up to 60 ml/kg/min. After Lance's cancer treatments, and without really returning to much training, he was tested. His de-trained VO2 max was at the level of a highly trained normal person. And after training again, he returned to his prior level. I'll keep looking for that reference.

LisaS
06-10-2006, 01:01 AM
So, how is VO2 max measured and how can you exercise at 110% of VO2 max? I knew you'd be wondering about that.

As some of the links explain, VO2 max is measured in a lab (although there are ways to estimate it in the field). Basically you wear a contraption that measures O2 in and O2 out - the difference is what you "used up" or consumed (very basic explanation).

So you strap this thing on and begin to exercise - usually either a treadmill or a ergonometer (cycle) is used. After you warm-up, they tell you to maintain a speed - mph running or rpm cycling. Then every minute, they make it harder - increase the incline or increase the resistance. Harder, harder, ever harder. You use more and more O2 each minute.

Let's say you get to 100 watts (just for easy math) and your VO2 is 50 ml/kg/min. They increase the resistance and you keep the rpms and your power is now 105 watts. Your VO2 is still 50. Another increase, 110 watts - still VO2 of 50. They suspect you have plateau-ed - reached your VO2 max. They increase again, your rpms drop and you are at 108 watts. You are done.

What did we learn? your VO2 max is 50 (ml/kg/min) and you made 100 watts. But what about your 110 watts? That is exercising at 110% VO2 Max. You are using the max O2 you can - and then doing the rest of the work anaerobically - just glycolysis. You've been making lactic acid, but since maybe 60 watts you're at capacity, so lactic acid starts to build in the blood. Your blood gets a little acidic -- and you can pick up a little more O2 per Hb on average - its a little easier to get the students in the booth when the environment is more acidic. At some point, your performance drops - you can't do any more.

read more about the "Lactate Threshold"
http://home.hia.no/%7Estephens/lacthres.htm

Billie
06-10-2006, 06:56 AM
Lisa, I will read your post carefully this afternoon. I have printed it so I can make some notes, and will get back I am sure with some questions. Thank you so much!

Gaelen
06-10-2006, 09:08 AM
In the mean time, if I haven't totally turned you off to the concept of VO2 Max – here are some articles by real writers:

You not only did NOT 'totally turn me off'--you made a relatively inaccessible subject easy to understand, and you used a minimum of subject-specific jargon in the process. In my experience, those are the defining skills of a 'real writer,' especially a technical and/or scientific writer. ;) Never underestimate your skills, Lisa.

BTW--I've seen the same reference about Lance Armstrong's VO2 Max capacity. He might even have referred to it in one of his own books. I'll check, too.

Missy
06-10-2006, 09:45 AM
I recommend Two Men and a Truck and some Cell Phones....:D lol...sorry...:D :rolleyes:

Interesting subject...I'll reread it...and I like the comparision to something I CAN understand. :D Good Job Lisa!

I'm someone who, in the past has "suffered" from chronic bronchitis...many many winters...and I found that when I was eating better I had less problems with this. When I was eating badly...the chronic bronchitis would return with a vengence. So, I wonder what effect "carbs" might have on this subject as well???

Gabriel Guzman
06-10-2006, 11:17 AM
Great contribution! :thumbsup: One detail to mention here is the actual role that muscles play in the whole oxygen dynamics. Besides having good lungs or lungs in good shape, it is also important to have muscles that are able to extract oxygen from the blood to be used. Muscles have an important protein called 'myoglobin', which acts in a similar way as hemoglobin; it transports oxygen. So, the importance of muscle development in the Vo2 dynamics is that the lungs are pretty much at the mercy of what the muscles do. That also means that another way to improve Vo2 is to work the muscles aerobically (something a lot of people don't think is possible but it is, depending on how you work the muscles out). The actual word 'aerobism', far from meaning how fast a person breaths during exercise, means how efficient the microscopic exchange of oxygen takes places in the muscles.

In other words, as one gets fitter, our heart, blood and muscles become more effective delivering and utilizing oxygen; less CO2 is produced and the response signals from the muscles and joints are dampened. That means that our lungs don't have to work so hard at the same exercise level compared to when we are less fit. There is no actual change to the lungs -they're simply a filter for air, at the mercy of what our heart and muscles demand.

I guess this also links nicely to your previous discussion about resistance exercise... not futile!:)

Billie
06-10-2006, 01:29 PM
Lisa what timing on this article since I just got down from the mountains in Colorado and suffered a little with the thin air. It really does take a bit of body adjustment. We were about 10,000 feet and that didn't bother me as much as the adjustment to the 6500 feet mark at the beginning of the trip. We were walking one day and it was so dang hot, about 94, I saw an elderly lady with an oxygen tank and I did have to contain myself not to go over and take a deep breath!:eek:

Your analyis so nicely painted what was going on in the body, thank you very much. Once again the resistance exercise and building the muscle capacity is a player. I still have to read all the other studies, but gosh thanks so much for putting them up! Gabe's at work this afternoon and dinner is in the crock pot, cold and rainy day so I am going to curl up and do some reading. Back later!

banshee
06-12-2006, 08:53 AM
Nice info Lisa! And very pertinent for me, since I have asthma, and one of my long term goals is to increase my VO2 max. It seems to be taking a long time because of the asthma, but maybe your info/articles will help me speed up the process a bit! :rolleyes:

laughingW
06-12-2006, 10:42 AM
How does insulin resistance fit into this, if at all?

I saw that interesting article "problems in the furnace" which talks about the details on how insulin resistance makes us less efficient at making energy.

The article might only apply to ATP and not aerobic style burning but I thought I'd ask anyway.

http://www.hhmi.org/news/shulman3.html

LisaS
06-12-2006, 11:44 AM
these articles don't really have to do with VO2 Max - but they do deal with cellular respiration in skeletal muscle. Looking at just this study http://medicine.plosjournals.org/perlserv?request=get-document&doi=10.1371/journal.pmed.0020289 it seems like the jist of the story is that in the IR persons they looked at, the muscles seem to "idle" at a lower metabolic rate. So when you read that muscle burns energy just sitting around - it seems like IR muscle burns less when just sitting around. Here is what the author says about another groups study:

ATP in resting fasted muscles is only produced for purposes of cell maintenance and survival functions (for example, maintenance of sodium and potassium gradients, amino acid gradients, protein synthesis rates, and functional organelles and membranes). Hence, Petersen et al.'s observations suggest that either the basal energy requirement is reduced in muscles of individuals with IR (potentially at the expense of the maintenance of cell functions) or the major control systems for mitochondrial respiration (simultaneous ATP synthesis and consumption) are not properly working (Figure 1 (http://medicine.plosjournals.org/perlserv?request=get-document&doi=10.1371/journal.pmed.0020289#JOURNAL-PMED-0020289-G001)).
Petersen and colleagues favour the first explanation. They suggest that their combined observations point to a general mitochondrial dysfunction that impairs the ability of the mitochondria to synthesise ATP and oxidise fatty acids (FAs) at the normal resting rate, both in the basal overnight-fasted condition and after stimulation by insulin [2 (http://medicine.plosjournals.org/perlserv?request=get-document&doi=10.1371/journal.pmed.0020289#JOURNAL-PMED-0020289-B2),3 (http://medicine.plosjournals.org/perlserv?request=get-document&doi=10.1371/journal.pmed.0020289#JOURNAL-PMED-0020289-B3)]. They also suggest that it is this mitochondrial dysfunction that causes IR.


however, the author pursues other explanations in the remainder of the article, and then summarizes:
Failure of insulin to stimulate muscle ATP production in offspring with IR may have multiple causes. A general mitochondrial dysfunction, as proposed by Petersen and colleagues, is one possibility, but the failure of insulin to (1) stimulate the insulin signalling cascade in muscle, (2) stimulate central thermogenic-control mechanisms of mitochondrial respiration, and (3) recruit muscle fibre capillaries are other potential mechanisms.


finally, the author suggests:
Regular exercise and training should be considered interventions to correct the reduction in insulin-induced muscle ATP turnover. Endurance exercise performed three to four times per week may lead to more than 5-fold increases in the mitochondrial density (concentration) of a previously sedentary muscle [15 (http://medicine.plosjournals.org/perlserv?request=get-document&doi=10.1371/journal.pmed.0020289#JOURNAL-PMED-0020289-B15)], and will increase the ATP generating capacity. Both endurance and resistance exercise increase insulin sensitivity at the molecular level in the muscle, and they have also been suggested to increase the sensitivity of adrenergic control in both skeletal muscle and adipose tissue [15 (http://medicine.plosjournals.org/perlserv?request=get-document&doi=10.1371/journal.pmed.0020289#JOURNAL-PMED-0020289-B15)]. Exercise and training open muscle capillaries and increase glucose uptake in skeletal muscle by contraction-induced mechanisms that are independent of insulin action [12 (http://medicine.plosjournals.org/perlserv?request=get-document&doi=10.1371/journal.pmed.0020289#JOURNAL-PMED-0020289-B12),14 (http://medicine.plosjournals.org/perlserv?request=get-document&doi=10.1371/journal.pmed.0020289#JOURNAL-PMED-0020289-B14)]. The measurement of muscle ATP turnover with magnetic resonance spectroscopy, as used in Petersen et al. [2 (http://medicine.plosjournals.org/perlserv?request=get-document&doi=10.1371/journal.pmed.0020289#JOURNAL-PMED-0020289-B2)], seems to be an ideal noninvasive method to investigate one critically important question: can changes towards a more active lifestyle reverse the observed reduction in insulin-induced muscle ATP turnover in the offspring with IR, and, in parallel, restore insulin sensitivity of muscle and precapillary arterioles and delay or prevent the later development of type 2 diabetes that was present in the parents?

LisaS
06-12-2006, 03:05 PM
I'm accumulating a file on exercise effects for this week - but as a sneak preview - here is a feature article that has exercise recommendations specific to increasing insulin sensitivity
http://spectrum.diabetesjournals.org/cgi/content/full/14/2/93

the authors of this review appear to believe that the current ACSM recommendations for exercise have a preventative effect but that a different prescription is needed for remediation/rehabilitation for those with impaired glucose tolerance.
see here:

Further evidence supporting the importance of exercise intensity comes from investigations in which the total caloric expenditure in high- and low-intensity exercise sessions was equal, i.e., eucaloric. Kang et al.14 (http://spectrum.diabetesjournals.org/cgi/content/full/14/2/93#R14) found that insulin action increased to a greater extent following high-intensity exercise than it did after a eucaloric low-intensity exercise session. That is, less intense exercise performed for a longer duration, resulting in an energy expenditure equivalent to that of a more intense exercise session, did not result in similar improvements in glucose metabolism in obese subjects. More intense exercise prescriptions, performed in a semi-acute fashion, can significantly improve insulin action and glucose metabolism. The current guidelines, although not specifically designed to elicit acute changes in health-related physiological variables, do not appear to significantly affect glucose homeostasis after 1 week. The strength of the current recommendations may lie in a preventive role. Chronic, life-long utilization of intermittent moderate-intensity exercise may reduce the incidence of diabetes, obesity, and other diseases thought to be lifestyle-related.

and then here:

Both acute and long-term exercise interventions indicate that the primary determinant of changes in insulin action is exercise intensity. The more intense the exercise stimulus that one prescribes, the greater the acute benefit will be. Moreover, more intense exercise will result in a greater caloric deficit increasing the likelihood of long-term weight loss. The relationship between exercise intensity and the benefits associated with exercise can be best represented by a dose-response curve (Figure 1 (http://spectrum.diabetesjournals.org/cgi/content/full/14/2/93#FIG1)).
The ACSM and CDC guidelines suggest that the largest relative benefits in health status can be achieved from moving from a sedentary state to one in which moderate-intensity physical activity is employed.
Current research would seem to suggest that those with IGT might improve insulin action to the greatest extent by the incorporation of more moderately intense exercise prescriptions.

here is the conclusion from this paper:
The CDC, ACSM, and SG have recently advocated the use of intermittent, moderate-intensity exercise. The use of this form of exercise is supported by epidemiological evidence. Those who accumulate 30 min of moderate-intensity physical activity on most, if not all, days of the week will have lower rates of mortality and morbidity than those who are inactive.

If followed at an early age and performed chronically, the guidelines may offer a preventive benefit. However, clinical investigations both chronic and semi-acute do not support the efficacy of the guidelines acting as a rehabilitative modality. Specifically, exercise performed in excess of 70% of maximum heart rate improves insulin sensitivity to a greater extent than intermittent, moderate-intensity physical activity, if performed semi-acutely or chronically. While there are many disease complications associated with type 2 diabetes that may be contraindicated for vigorous exercise, those with IGT are often free of complications. If contranindications are not present, we recommend that vigorous exercise programs be encouraged for individuals with IGT.