V02 Max: Questions & Answers

 By Ted Lambrinides, PhD.

 Presented at the 2000 NCES Health & Fitness Symposium 
Chicago, Illinois October 28, 2000

 

 What is the definition of V02 max?             

The maximal rate at which oxygen can be consumed per minute.
 

What are the controlling factors of V02 max?

The term central command refers to a motor signal developed within the brain. The central command theory of cardiovascular control argues that the initial cardiovascular changes at the beginning of exercise are due to centrally generated cardiovascular motor signals, which set the general pattern of the cardiovascular response. However, it is commonly believed that cardiovascular activity can be and is modified by muscle chemoreceptors, muscle mechanoreceptors, and pressure-sensitive receptors (baroreceptors) located within the carotid arteries and the aortic arch. Muscle
chemoreceptors are sensitive to increases in muscle metabolites (e.g. potassium, lactic
acid, etc.) and send messages to higher brain centers to “fine-tune” the cardiovascular
responses to exercise. This is called peripheral feedback.

 In a recent research study by Hagberg and associates, older endurance trained athletes had greater V02 max than their sedentary peers, and this difference was associated with significantly expanded intravascular volumes in these athletes (particularly plasma and total blood volume). The improvement in cardiovascular parameters in these endurance­ trained men during peak exercise correlated significantly with the expanded intravascular volumes. The fact that the high V02 max is associated with an increased plasma volume emphasizes the point that many of the gains expected from training can develop quite rapidly through a change in fluid balance, rather than through structural changes. This was pointed out by Holmgren in a 1967 paper, distinguishing between regulatory and dimensional aspects of training.            


How important is specificity of exercise with regard to the controlling factors?


Very! Saltin had subjects train one leg on a bicycle ergometer while the other served as an untrained control. Maximal oxygen intake and muscle enzyme levels were only improved in the trained leg. The heart rate response during exercise was lower than pretest values when the trained leg was exercised, but not when the untrained leg was tested. Saltin attributed the differences in the heart rate response to small nerve endings located in the skeletal muscle fibers. The nerves somehow sense the metabolic environment within the muscle and influence the heart rate response via connections to the cardiac control center in the brain. The slower heart rate with the trained leg provides more filling time for the heart and allows a greater end diastolic and stroke volume. Thus, it appears that some cardiovascular effects of training are subject to some degree of control from events in the muscles. This study indicates that the controlling mechanisms for such changes are to a large extent influenced by the skeletal muscles themselves.

Magel and his associates studied the V02 max improvements with swim training (1hr/day, 3 days/wk, for 10 wk). Subjects performed maximal treadmill running and tethered swimming tests both before and after training. The swimming V02 max increased by 11.2% following the 10 week swim training period. However, the running V02 max increased by only 1.5%, not a statistically significant change from the pre-training value. If the treadmill alone had been used for testing, the researchers would have concluded that swim training had no influence on cardiorespiratory endurance capacity.

 “The use of the training heart rate and emphasis on cardiovascular effects of training has diverted attention from the true target of training, skeletal muscle. Training is specific to the muscle fibers used in an activity. Training does not transfer well from one activity to another”.

Dr. Brian J. Sharkey, New Dimensions in Aerobic Fitness

 To accurately measure endurance improvement, athletes should be tested while they are engaged in an activity similar to the sport or activity in which they usually participate. For most athletes, V02 max values are substantially higher during their sport-specific activity.

 
How much of an influence does genetics have upon V02 max?
 

Maximal oxygen consumption levels depend on genetic limits. This should not be taken to mean that each individual has an exact V02 max that cannot be exceeded. Both genetic and environmental factors influence V02 max values. The genetic factors probably establish the boundaries for the athlete, but endurance training can push V02 max to the upper limit of these boundaries.

 Intraclass Correlations From Twin Studies of Aerobic Performance

Source

Test

MZ

DZ

Klissouras

VO2 max/kg

0.91

0.44

Klissouras et al.

VO2 max/kg

0.95

0.36

Komi et al.

PWC 205/kg

0.83

0.43

Engstrom and Fischbein

PWC max/kg

0.74

0.53

Bouchard et al.

PWC15o/kg

0.60

0.41

Bouchard et al.

V02 max/kg

0.71

0.51

Fagard et al.

V02 max/kg

0.77

0.04

Maes et al.

V02 max/kg

0.85

0.56

Sundet et al.

V02 max/kg

0.62

0.29

 

 

 

 

 

 

 

How much can V02 max be improved? 

For years, researchers have found wide variations in improvement in V02 max with training. In one study, men and women endurance trained for 9 to 12 months. Improvement in V02 max ranged from 0% to 43%, even though all the subjects completed exactly the same training program. 

Bouchard has now clearly established that the response to a training program is genetically determined. Ten pairs of identical twins completed a 20 week endurance training program. Improvements varied from 0% to nearly 40%. These results, and those from other studies, indicate that there will be responders (large improvement) and non-responders (little or no improvement) among groups of people who experience identical training programs. 

Costill and Wilmore suggest that in fully mature athletes, the highest attainable V02 max is reached within 8 to 18 months of heavy endurance training, indicating that each athlete has a finite attainable level of oxygen consumption. However, endurance performance continues to improve with continued training for many additional years. Factors contributing to this continued endurance performance are lactate threshold and economy of movement.

 
Can V02 max predict performance?
 

It appears that the V02 max may predict performance “when a heterogeneous group of athletes with quite different athletic abilities is studied, but “it is a relatively poor predictor when athletes of similar ability are evaluated”.
 

Can anaerobic training improve V02 max? 

Researchers at McMaster University examined the effect of sprint training on a bicycle ergometer. The subjects progressed from 4-30 second interval sprints to 10-30 second interval sprints during the seven-week study. The researchers found that intense sprint interval training increases glycolytic and oxidative muscle enzyme activity, peak power output, and oxygen consumption. The authors noted that training at an intensity that exceeds V02 max may be a more important component than the volume of training to stimulate an increase in muscle oxidative potential.
 

What are the cardiovascular benefits of high intensity resistance exercise? 

High intensity resistance training has been shown to produce minimal changes in V02 max as measured on a treadmill. The conclusions drawn from such studies are erroneous. The specific V02 changes produced from high intensity resistance exercise over several months of training have no be studied. 

High intensity resistance training has produced dramatic increases in endurance performance in both normal and cardiac populations. Hickson found small increases in V02 max but large increases in time to exhaustion on both a cycle ergometer and a treadmill. Explanations for such outcomes are 1) Increased strength. As each motor unit becomes stronger with resistance training, fewer motor units would be needed at a given submaximal workload, thus creating a greater motor unit reserve. 2) Increase lactate threshold. Researchers at the University of Maryland found that high intensity resistance training increased endurance time by rising the lactate threshold of the subjects in their study.   

Some of the additional cardiovascular benefits seen in some but not all studies are as follows: 

·         Improvements in blood lipid profiles in individuals with abnormal levels at the start of the study.

·         Decreases in blood pressure in individuals with borderline to high blood pressure at the start of the study.

·         Decreases in blood pressure in other activities after engaging in a resistance training program.
 

What is the association between V02 max and health? 

In general, physically active individuals have higher V02 values than sedentary individuals. As a result, they typically have lower mortality rates. An individual with a genetically high V02 max who smokes and leads a sedentary lifestyle is at high risk. There are numerous risk factors for cardiovascular disease: elevated cholesterol, high blood pressure, smoking, genetics, obesity, diet, homocysteine levels, elevated levels of C-reactive protein, clotting factors, and physical activity. The physiological benefits of resistance exercise are numerous and as such should enable one to stay in the low risk category provided their other risk factors are in recommended ranges.

Improvements in V02 max should not be the main focus of an exercise program. In fact the American College of Sports Medicine states “It is now clear that lower levels of physical activity may reduce the risk of certain chronic degenerative diseases and yet may not be of sufficient quantity or quality to improve V02 max”.

 Key Terms: 

Preload: The degree of stretch of the muscle when it begins to contract. For cardiac contraction, the preload is considered to be the volume of blood in the ventricle at the end of diastole, that is, the end-diastolic volume. However, sometimes this preload is expressed as the end-diastolic pressure that fills the ventricle. 

Afterload: The load against which the muscle exerts its contractile force. The afterload of the ventricle is the pressure in the arteries leading from the ventricles. 

Reactive Hyperemia: When the blood supply to a tissue is blocked for a few seconds to several hours and then is unblocked, the flow through the tissue usually increases to about five time normal; the increased flow will continue for a few seconds if the block has lasted a few seconds and sometimes for as long as many hours if the blood flow has been stopped for an hour or more. 

Active Hyperemia: When any tissue becomes highly active, such as a muscle during exercise, the rate of blood flow through the tissue increases. The increase in local metabolism causes the cells to devour the tissue fluid nutrients extremely rapidly and also to release large quantities of vasodilator substances. The result obviously would be to dilate the local blood vessels, and therefore, to increase local blood flow. In this way, the active tissue will receive the additional nutrients required to sustain its new level of function.