Entries in Oxygen Uptake (3)

Saturday
Jul302011

The Lactate Threshold

By: Sports Advisor.
Site link: Sports Advisor.
Article Link: The Lactate Threshold


If VO2 max is your aerobic endurance potential then your lactate threshold plays a significant role in how much of that potential you are tapping.

Lactate threshold has been defined as:

The point during exercise of increasing intensity at which blood lactate begins to accumulate above resting levels, where lactate clearance is no longer able to keep up with lactate production. (3)

During low intensity exercise, blood lactate remains at or near to resting levels. As exercise intensity increases there comes a break point where blood lactate levels rise sharply (4,5). Researchers in the past have suggested that this signifies a significant shift from predominantly aerobic metabolism to predominantly anaerobic energy production.

Several terms have been used to describe this shift and many coaches and athletes believe it is the same phenomenon:

  • Lactate threshold
  • Anaerobic threshold
  • Aerobic threshold
  • Onset of blood lactate accumulation (OBLA)
  • Maximal lactate steady state

Although these terms are used interchangeably, they do not describe the same thing. Lactate accumulation only determines the balance between lactate production and its clearance and suggests nothing about the availability or lack of oxygen so the terms aerobic and anaerobic become a bit misleading.

The reasons for lactate accumulation are complex and varied and not yet fully understood. For more information on this topic see the lactic acid article.

OBLA

At a slightly higher exercise intensity than lactate threshold a second increase in lactate accumulation can be seen and is often referred to as the onset of blood lactate accumulation or OBLA. OBLA generally occurs when the concentration of blood lactate reaches about 4mmol/L (6,7). The break point that corresponds to lactate threshold can often be hard to pinpoint and so some Exercise Physiologists often prefer using OBLA.

Maximal Lactate Steady State

Maximal lactate steady state is defined as the exercise intensity at which maximal lactate clearance is equal to maximal lactate production (8). Maximal lactate steady state is considered one of the best indicators of performance perhaps even more efficient than lactate threshold (8,9). 

Lactate Threshold as a Percentage of VO 2 Max

The lactate threshold is normally expressed as a percentage of an individuals VO2 max. For example, if VO2 max occurs at 24 km/h on a treadmill test and a sharp rise in blood lactate concentration above resting levels is seen at 12 km/h then the lactate threshold is said to be 50% VO2 max.

In theory, an individual could exercise at any intensity up to their VO2 max indefinitely. However, this is not the case even amongst elite athletes. As the exercise intensity draws closer to that at VO2 max, a sharp increase in blood lactate accumulation and subsequent fatigue occurs the lactate threshold is broken. In world-class athletes lactate threshold typically occurs at 70-80% VO2 max. In untrained individuals it occurs much sooner, at 50-60% VO2 max (10,11).

Generally, in two people with the same VO2 max, the one with a higher lactate threshold will perform better in continuous-type endurance events. See the graph below:

Although both Athlete 1 and Athlete 2 reach VO2 max at a similar running speed, Athlete 1 has a lactate threshold at 70% and Athlete 2 has a lactate threshold at 60%. Theoretically, Athlete 1 can maintain a pace of about 7.5 mph (12 km/h) compared to Athlete 2s pace of about 6.5 mph (10.5km/h).

VO2 max has been used to predict performance in endurance events such as distance running and cycling but the lactate threshold is much more reliable. Race pace has been closely associated with lactate threshold (11).

There are several non-invasive methods used to determine the lactate or anaerobic threshold. For more information see How to Determine Your Anaerobic Threshold.

Lactate Threshold and Training

With training, lactate threshold as a percentage of VO2 max can be increased. Even if there are no improvements in maximal oxygen uptake, increasing the relative intensity or speed at which lactate threshold occurs will improve performance. In effect, proper training can shift the lactate curve to the right:

Following training, the reductions in lactate concentration at any given intensity may be due to a decrease in lactate production and an increase in lactate clearance (12). However, Donovan and Brooks (13) suggest that endurance training affects only lactate clearance rather than production.

Blood lactate levels after an intense exercise bout are also lower following training. For example, immediately after a 200m swim at a fixed pace, blood lactate may be as high as 13-14 mmol/L. Following 7 months of training these levels can decrease to under 4mmol/L (14). Before training, a swim leading to such high levels of lactate would force the swimmer to slow down dramatically or stop after the 200m. But following training, lactate levels of under 4mmol/L would probably allow the swimmer to continue after 200m, at the same pace, indefinitely.

Studies have shown that training at or slightly above the lactate threshold can increase the relative intensity at which it occurs (4,13).

References

1) Baechle TR and Earle RW. (2000) Essentials of Strength Training and Conditioning: 2nd Edition. Champaign, IL: Human Kinetics

2) McArdle WD, Katch FI and Katch VL. (2000) Essentials of Exercise Physiology: 2nd Edition Philadelphia, PA: Lippincott Williams & Wilkins

3) Wilmore JH and Costill DL. (2005) Physiology of Sport and Exercise: 3rd Edition. Champaign, IL: Human Kinetics

4) Davis JA, Frank MH, Whipp BJ, Wasserman K. Anaerobic threshold alterations caused by endurance training in middle-aged men. J Appl Physiol. 1979 Jun;46(6):1039-46

5) Kindermann W, Simon G, Keul J. The significance of the aerobic-anaerobic transition for the determination of work load intensities during endurance training. Eur J Appl Physiol Occup Physiol. 1979 Sep;42(1):25-34

6) Sjodin B, Jacobs I. Onset of blood lactate accumulation and marathon running performance. Int J Sports Med. 1981 Feb;2(1):23-6

7) Tanaka K, Matsuura Y, Kumagai S, Matsuzaka A, Hirakoba K, Asano K. Relationships of anaerobic threshold and onset of blood lactate accumulation with endurance performance. Eur J Appl Physiol Occup Physiol. 1983;52(1):51-6

8) Beneke R. Anaerobic threshold, individual anaerobic threshold, and maximal lactate steady state in rowing. Med Sci Sports Exerc. 1995 Jun;27(6):863-

9) Foxdal P, Sjodin B, Sjodin A, Ostman B. The validity and accuracy of blood lactate measurements for prediction of maximal endurance running capacity. Dependency of analyzed blood media in combination with different designs of the exercise test. Int J Sports Med. 1994 Feb;15(2):89-95

10) Cerretelli P, Ambrosoli G, Fumagalli M. Anaerobic recovery in man. Eur J Appl Physiol Occup Physiol. 1975 Aug 15;34(3):141-8

11) Farrell PA, Wilmore JH, Coyle EF, Billing JE, Costill DL. Plasma lactate accumulation and distance running performance. Med Sci Sports. 1979 Winter;11(4):338-44

12) Bergman BC, Wolfel EE, Butterfield GE, Lopaschuk GD, Casazza GA, Horning MA, Brooks GA. Active muscle and whole body lactate kinetics after endurance training in men. J Appl Physiol. 1999 Nov;87(5):1684-96

13) Donovan CM, Brooks GA. Endurance training affects lactate clearance, not lactate production. Am J Physiol. 1983 Jan;244(1):E83-92

14) Costill DL, Thomas R, Robergs RA, Pascoe D, Lambert C, Barr S, Fink WJ. Adaptations to swimming training: influence of training volume. Med Sci Sports Exerc. 1991 Mar;23(3):371-7


Saturday
Jul302011

How To Determine Lactate / Anaerobic Threshold

By: Sports Advisor.
Site link: Sports Advisor.

There are several methods used to determine an athletes lactate or anaerobic threshold. While the most accurate and reliable is through the direct testing of blood samples during a graded exercise test, this is often inaccessible to most performers.

There are several field tests that can also be used to estimate lactate threshold. They vary in their reliability but some offer an acceptable alternative for most amateur athletes.

Several terms such as onset of blood lactate accumulation and maximal lactate steady state are used interchangeably with anaerobic threshold. Technically, they do not describe precisely the same thing. In fact, although lactate threshold and anaerobic threshold occur together under most conditions, strictly speaking even these two terms are not the same (1). For this article however, lactate threshold and anaerobic threshold will be used interchangeably. See the lactate threshold article for more details on this topic.

It is also worth bearing in mind that blood lactate and lactic acid are not the same substance. Blood lactate production is actually thought to be beneficial to endurance performance and may delay fatigue. Nevertheless, its accumulation still remains a good marker for the onset of fatigue. 

Laboratory Testing of Anaerobic Threshold

The most accurate way to determine lactate threshold is via a graded exercise test in a laboratory setting (2). During the test the velocity or resistance on a treadmill, cycle ergometer or rowing ergometer is increased at regular intervals (i.e. every 1min, 3min or 4min) and blood samples are taken at each increment. Very often VO2 max, maximum heart rate and other physiological kinetics are measured during the same test (3).

Blood lactate is then plotted against each workload interval to give a lactate performance curve. Heart rate is also usually recorded at each interval often with a more accurate electrocardiogram as opposed to a standard heart rate monitor.

Once the lactate curve has been plotted, the anaerobic threshold can be determined. A sudden or sharp rise in the curve above base level is said to indicate the anaerobic threshold. However, from a practical perspective this sudden rise or inflection is often difficult to pinpoint.

Assuming the inflection is clear (as in the graph above), the relative speed or workload at which it occurs can be determined. In this example, the athletes anaerobic threshold occurs at about 12km/h. This means, in theory they can maintain a pace at or just below 2km/h for a prolonged period, indefinitely. Of course, this is purely hypothetical as there are many other factors involved in fatigue not least the amount of carbohydrate stores an athlete has in reserve (1). A crossover to fat metabolism will significantly reduce the athletes race pace (2).

By recording heart rate data alongside workload and blood lactate levels, an athlete can use a heart rate monitor to plan and complete training sessions. Although monitoring heart rate is never completely reliable and varies greatly between and within individuals (1,2,3) combining it with lactate measurements is probably more reliable than using the Conconi test (see below) for example.

Confirmatory Test

When anaerobic threshold is read from the lactate curve, an additional test can be used to verify its accuracy. Using the example above, the athletes threshold is thought to occur at about 12km/h on the treadmill. The confirmatory test involves running for 15 minutes at a pace just below threshold, 15 minutes at threshold and 15 minutes at a pace just above threshold. See the curves below of three athletes whose thresholds have all been determined to occur at approximately 12kmh.

Notice that for Athlete 1, blood lactate remains steady at their estimated anaerobic threshold (12km/h) and lactate begins to accumulate when the pace is increased to 13km/h in the final 15 minutes. For athlete 1, this is confirmation that their anaerobic threshold pace is reasonably accurate.

For Athlete 2, lactate begins to accumulate during the middle 15minute segment (their estimated threshold) and continues to do so during the final 15 minutes. For this athlete, anaerobic threshold occurs at a slightly slower pace than was determined originally.

Finally, Athlete 3s lactate curve does not rise significantly even during the final 15 minutes segment. Anaerobic threshold for them occurs at a slightly higher pace then was originally determined.

Assuming, you dont have access to facilities that directly monitor your or your athletes lactate response, are there other acceptable alternatives?

Portable Lactate Analyzer

Portable lactate analysers are becoming more popular amongst coaches and athletes at all levels. A good portable analyzer should have the same validity and reliability as laboratory testing equipment. The Accutrend Lactate Analyzer for example, has been tested using guidelines of the European Committee for Clinical Laboratory Standards and is cleared for sports medicine use by the Federal Drug Administration in the United States.

Needless to say a portable analyser is only one half of the equation. A suitable and sport-specific exercise test is still required and selecting the most appropriate protocol takes knowledge and experience. Any physiological test is only as reliable as the testers ability to follow a set protocol. Even when a suitable assessment has been chosen, numerous variables must be kept constant for the test to remain accurate and reliable.   

Conconi Test

In 1982 Conconi et a (4) stated that the anaerobic threshold correlated to a deflection point in the heart rate. Essentially, heart rate and exercise intensity is linear i.e. as exercise intensity increases so will heart rate. However, Conconi et a found that in all their tested subjects, including those in a follow up test (5), heart rate reached a plateau at near maximal exercise intensities.

Although this is a relatively simple field test that would be useful for coaches and athletes at all levels, its accuracy has been contested by subsequent researchers (6,7,8). Studies have found that the deflection point or plateau in heart rate only occurs in a certain number of individuals and that when it does, it significantly overestimates directly measured lactate threshold. Conconi and co-workers (9) themselves acknowledge this controversy and cite studies that both support and contradict their original findings. 

10km Run, 30Km Cycle, 30 Min Time Trial

More experienced athletes often run a 10km race or cycle 30km race at or close to anaerobic threshold. By simulating a race in training and recording heart rate, the anaerobic threshold may be determined. Alternatively, exercising for 30 minutes at the fastest sustainable pace can be used. The key is to sustain a steady pace which is why this test is more suited to experienced athletes who can gauge how fast to set off. A heart rate monitor with split time facility is required to record heart rate at each 1-minute interval. Take the average heart rate over the final 20 minutes as the heart rate corresponding to anaerobic threshold.  

Heart Rate Percentage

A very simply method for estimating the anaerobic threshold is to assume anaerobic threshold occurs at 85-90% maximum heart rate (220-age). As mentioned earlier, heart rate varies greatly between individuals and even within the same individual so this is not a reliable test.

The Lactate Threshold Debate

Some researchers have questioned the validity of determining the lactate or anaerobic threshold even in laboratory settings (10,11). Yet more researchers question whether a definite point or threshold exists at all (10,12,13,14). Instead they suggest blood lactate accumulation is continuous in nature and no specific point can be determined.

Rather than get bogged down in the debate it is sensible to remember that regardless of the underlying mechanisms, the physiological changes that accompany lactate accumulation have important implications for endurance athletes. Any delay in the blood lactate accumulation that can be achieved through training is beneficial to performance.

References

1) Wilmore JH and Costill DL. (2005) Physiology of Sport and Exercise: 3rd Edition. Champaign, IL: Human Kinetics

2) McArdle WD, Katch FI and Katch VL. (2000) Essentials of Exercise Physiology: 2nd Edition Philadelphia, PA: Lippincott Williams & Wilkins

3) Maud PJ and Foster C (eds.). (1995) Physiological Assessment Of Human Fitness. Champaign, IL: Human Kinetics

4) Conconi, F., M. Ferrrari, P. G. Ziglio, P. Droghetti, and L. Codeca. Determination of the anaerobic threshold by a noninvasive field test in runners. J. Appl. Physiol. 1982, 52: 862-873

5) Ballarin, E., C. Borsetto, M. Cellini, M. Patracchini, P. Vitiello, P. G. Ziglio, and F. Conconi. Adaptation of the "Conconi test" to children and adolescents. Int. J. Sports Med. 1989, 10: 334-338

6) Parker, D., R. A. Robergs, R. Quintana, C. C. Frankel, and G. Dallam. Heart rate threshold is not a valid estimation of the lactate threshold. Med. Sci. Sports Exerc. 1997, 29: S235

7) Tokmakidis, S. P., and L. A. Leger. Comparison of mathematically determined blood lactate and heart rate "threshold" points and relationship to performance. Eur. J. Appl. Physiol. 64: 309-317

8) Vachon JA, Bassett Jr DR and Clarke S. Validity of the heart rate deflection point as a predictor of lactate threshold during running. J Appl Physiol. 1999, 87: 452-459

9) Conconi, F., G. Grazze, I. Casoni, C. Guglielmini, C. Borsetto, E. Ballarin, G. Mazzoni, M. Patracchini, and F. Manfredini. The Conconi test: methodology after 12 years of application. Int. J. Sports Med. 1996, 17: 509-519

10) Yeh MP, Gardner RM, Adams TD, Yanowitz FG, Crapo RO. "Anaerobic threshold": problems of determination and validation. J Appl Physiol. 1983, Oct;55(4):1178-86

11) Gladden LB, Yates JW, Stremel RW, Stamford BA. Gas exchange and lactate anaerobic thresholds: inter- and intraevaluator agreement. J Appl Physiol. 1985 Jun;58(6):2082-9

12) Hughson RL, Weisiger KH, Swanson GD. Blood lactate concentration increases as a continuous function in progressive exercise. J Appl Physiol. 1987 May;62(5):1975-81

13) Campbell ME, Hughson RL, Green HJ. Continuous increase in blood lactate concentration during different ramp exercise protocols. J Appl Physiol. 1989 Mar;66(3):1104-7

14) Dennis SC, Noakes TD, Bosch AN. Ventilation and blood lactate increase exponentially during incremental exercise. J Sports Sci. 1993 Oct;11(5):371-5; discussion 377-8 

Friday
Jul292011

VO2 Max, Aerobic Power & Maximal Oxygen Uptake

By: Sports Advisor.
Site link: Sports Advisor.

VO2 max has been defined as:

"the highest rate of oxygen consumption attainable during maximal or exhaustive exercise" (3).

As exercise intensity increases so does oxygen consumption. However, a point is reached where exercise intensity can continue to increase without the associated rise in oxygen consumption. To understand this in more practical terms, take a look at the diagram below:

The point at which oxygen consumption plateaus defines the VO2 max or an individual's maximal aerobic capacity. It is generally considered the best indicator of cardiorespiratory endurance and aerobic fitness. However, as well discuss in a moment, it is more useful as an indicator of a person's aerobic potential or upper limit than as a predictor of success in endurance events.

Aerobic power, aerobic capacity and maximal oxygen uptake are all terms used interchangeably with VO2 max.

VO2 max is usually expressed relative to bodyweight because oxygen and energy needs differ relative to size. It can also be expressed relative to body surface area and this may be a more accurate when comparing children and oxygen uptake between sexes.

One study followed a group of 12-year-old boys through to the age of 20 - half of which were trained, the other half untrained but active. Relative to bodyweight no differences in VO2 max were found between the groups suggesting that training had no influence on maximal oxygen uptake. However, when VO2 max was expressed relative to body surface area, there was a significant difference between groups and maximal oxygen uptake did indeed increase in proportion to training (4).

VO2 Max In Athletes and Non Athletes

VO2 max varies greatly between individuals and even between elite athletes that compete in the same sport.

The table below lists normative data for VO2 max in various population groups:

Genetics plays a major role in a persons VO2 max (11) and heredity can account for up to 25-50% of the variance seen between individuals. The highest ever recorded VO2 max is 94 ml/kg/min in men and 77 ml/kg/min in women. Both were cross-country skiers (16).

Untrained girls and women typically have a maximal oxygen uptake 20-25% lower than untrained men. However, when comparing elite athletes, the gap tends to close to about 10% (3). Taking it step further, if VO2 max is adjusted to account for fat free mass in elite male and female athletes, the differences disappear in some studies. Cureton and Collins (29) suggest that sex-specific essential fat stores account for the majority of metabolic differences in running between men and women.

Training & VO2 Max

In previously sedentary people, training at 75% of aerobic power, for 30 minutes, 3 times a week over 6 months increases VO2 max an average of 15-20% (6). However, this is an average and there are large individual variations with increases as wide ranging as 4% to 93% reported (6).

Amongst groups of people following the same training protocol there will be responders - those who make large gains, and non-responders - those who make little or no gains (14,9). This was originally put down to a simple issue of compliance but more recent research suggests that genetics plays a role in how well any one individual responds to an endurance training program (13).

The extent by which VO2 max can change with training also depends on the starting point. The fitter an individual is to begin with, the less potential there is for an increase and most elite athletes hit this peak early in their career. There also seems to be a genetic upper limit beyond which, further increases in either intensity or volume have no effect on aerobic power (5). This upper limit is thought to be reached within 8 to 18 months (3).

Crucially, once a plateau in VO2 max has been reached further improvements in performance are still seen with training. This is because the athlete is able to perform at a higher percentage of their VO2 max for prolonged periods (2). Two major reasons for this are improvements in anaerobic threshold and running economy.

Resistance training and intense 'burst-type' anaerobic training have little effect on VO2 max. Any improvements that do occur are usually small and in subjects who had a low level of fitness to begin with (17). Resistance training alone does not increase VO2 max (30,31,32) even when short rest intervals are used between sets and exercises (33).

Considerable training is required to reach the upper limit for VO2 max. However, much less is required to maintain it. In fact peak aerobic power can be maintained even when training is decreased by two thirds (18). Runners and swimmers have reduced training volume by 60% for a period of 15-21 days prior to competition (a technique known as tapering) with no loss in VO2 max (19,20,21).

VO2 Max as a Predictor of Performance

In elite athletes, VO2 max is not a good predictor of performance. The winner of a marathon race for example, cannot be predicted from maximal oxygen uptake (15).

Perhaps more significant than VO2 max is the speed at which an athlete can run, bike or swim at VO2 max. Two athletes may have the same level of aerobic power but one may reach their VO2 max at a running speed of 20 km/hr and the other at 22 km/hr.

While a high VO2 max may be a prerequisite for performance in endurance events at the highest level, other markers such as lactate threshold are more predictive of performance (3). Again, the speed at lactate threshold is more significant than the actual value itself.

Think of VO2 max as an athletes aerobic potential and the lactate threshold as the marker for how much of that potential they are tapping.

Factors Affecting VO2 Max

There are many physiological factors that combine to determine VO2 max but which of these are most important? Two theories have been proposed:

Utilization Theory

This theory maintains that aerobic capacity is limited by lack of sufficient oxidative enzymes within the cell's mitochondria (3). It is the body's ability to utilize the available oxygen that determines aerobic capacity. Proponents of this theory point to numerous studies that show oxidative enzymes and the number and size of mitochondria increase with training. This is coupled with increased differences between arterial and venous blood oxygen concentrations (a-vO2 difference) accounting for improved oxygen utilization and hence improved VO2max.

Presentation Theory

Presentation theory suggests that aerobic capacity is limited not predominantly by utilization, but by the ability of the cardiovascular system to deliver oxygen to active tissues. Proponents of this theory maintain that an increase in blood volume, maximal cardiac output (due to increased stroke volume) and better perfusion of blood into the muscles account for the changes in VO2max with training.

So what plays the greater role in determining an athlete's VO2 max - their body's ability to utilize oxygen or supply oxygen to the active tissues?

In a review of the literature, Saltin and Rowell (7) concluded that it is oxygen supply that is the major limiter to endurance performance. Studies have shown only a weak relationship between an increase in oxidative enzymes and an increase in VO2 max (8,9,10). One of these studies measured the effects of a 6-month swim training program on aerobic function. While oxidative enzymes continued to increase until the end, there was no change in VO2 max in the final 6 weeks of the program (10). 

Determining VO2 Max

VO2 max can be determined through a number of physical evaluations. These tests can be direct or indirect. Direct testing requires sophisticated equipment to measure the volume and gas concentrations of inspired and expired air. There are many protocols used on treadmills, cycle ergometers and other exercise equipment to measure VO2 max directly.

One of the most common is the Bruce protocol often used for testing VO2 max in athletes or for signs of coronary heart disease in high risk individuals.

Indirect testing is much more widely used by coaches as it requires little or no expensive equipment. There are many indirect tests used to estimate VO2 max. Some are more reliable and accurate than others but none are as accurate as direct testing. Examples include the multistage shuttle run (bleep test), 12 minute walk test and 1.5 mile run.

VO2 Max at Altitude

VO2 max decreases as altitude increases above 1600m (5249ft) or about the altitude of Denver, Colorado. For every 1000m (3281ft) above that, maximal oxygen uptake decreases further by approximately 8-11% (3). Anyone with a VO2 max lower than 50 ml/kg/min would struggle to survive at the summit of Everest without supplemental oxygen.

The decrease is mainly due to a decrease in maximal cardiac output. Recall that cardiac output is the product of heart rate and stroke volume. Stoke volume decreases due to the immediate decrease in blood plasma volume. Maximal heart rate may also decrease and the net effect is that less oxygen is "pushed" from the blood into the muscles (2).

Effects of Aging on VO2 Max

VO2 max decreases with age. The average rate of decline is generally accepted to be about 1% per year or 10% per decade after the age of 25. One large cross sectional study found the average decrease was 0.46 ml/kg/min per year in men (1.2%) and 0.54 ml/kg/min in women (1.7%) (22,23).

However, this deterioration is not necessarily due to the aging process. In some cases the decease may be purely a reflection of increased body weight with no change in absolute values for ventilation of oxygen. Recall, that VO2 max is usually expressed relative to body weight. If this increases, as tends to happen with age, and aerobic fitness stays the same then VO2 max measured in ml/kg/min will decrease.

Usually, the decline in age-related VO2 max can be accounted for by a reduction in maximum heart rate, maximal stoke volume and maximal a-vO2 difference i.e. the difference between oxygen concentration arterial blood and venus blood (2).

Can training have an affect on this age-related decline?

Vigorous training at a younger age does not seem to prevent the fall in VO2 max if training is ceased altogether. Elite athletes have been shown to decline by 43% from ages 23 to 50 (from 70 ml/kg/min to 40 ml/kg/min) when they stop training after their careers are over (24). In some cases, the relative decline is greater than for the average population - as much as 15% per decade or 1.5% per year (27,28).

However in comparison, master athletes who continue to keep fit only show a decrease of 5-6% per decade or 0.5-0.6% per year (25,26,27,28). When they maintain the same relative intensity of training, a decrease of only 3.6% over 25 years has been reported (28) and most of that was attributable to a small increase in bodyweight.

It seems that training can slow the rate of decline in VO2 max but becomes less effective after the age of about 50 (3).

References

1) Baechle TR and Earle RW. (2000) Essentials of Strength Training and Conditioning: 2nd Edition. Champaign, IL: Human Kinetics

2) McArdle WD, Katch FI and Katch VL. (2000) Essentials of Exercise Physiology: 2nd Edition Philadelphia, PA: Lippincott Williams & Wilkins

3) Wilmore JH and Costill DL. (2005) Physiology of Sport and Exercise: 3rd Edition. Champaign, IL: Human Kinetics

4) Sjodin B, Svedenhag J. Oxygen uptake during running as related to body mass in circumpubertal boys: a longitudinal study. Eur J Appl Physiol Occup Physiol. 1992;65(2):150-7

5) Costill DL. (1986) Inside Running: Basics of Sports Physiology. Indianapolis: Benchmark Press

6) Pollock ML. (1973). Quantification of endurance training programs. Exercise and Sport Sciences Reviews. 1,155-188

7) Saltin B, Rowell LB. Functional adaptations to physical activity and inactivity. Federation Proceeding. 1980 Apr;39(5):1506-13

8) Gollnick PD, Armstrong RB, Saubert CW 4th, Piehl K, Saltin B. Enzyme activity and fiber composition in skeletal muscle of untrained and trained men. J Appl Physiol. 1972 Sep;33(3):312-9

9) Saltin B, Nazar K, Costill DL, Stein E, Jansson E, Essen B, Gollnick D. The nature of the training response; peripheral and central adaptations of one-legged exercise. Acta Physiol Scand. 1976 Mar;96(3):289-305

10) Costill DL, Thomas R, Robergs RA, Pascoe D, Lambert C, Barr S, Fink WJ. Adaptations to swimming training: influence of training volume. Med Sci Sports Exerc. 1991 Mar;23(3):371-7

11) Bouchard C, Dionne FT, Simoneau JA, Boulay MR. Genetics of aerobic and anaerobic performances. Exerc Sport Sci Rev. 1992;20:27-58

12) Pollock ML, Foster C, Knapp D, Rod JL, Schmidt DH. Effect of age and training on aerobic capacity and body composition of master athletes. J Appl Physiol. 1987 Feb;62(2):725-31

13) Bouchard C, Shephard RJ, Stephens T, Sutton JR and McPherson BD (Eds.), Exercise Fitness and Health (pp. 147-153). Champaign, IL: Human Kinetics

14) Green HJ, Jones S, Ball-Burnett M, Farrance B, Ranney D. Adaptations in muscle metabolism to prolonged voluntary exercise and training. J Appl Physiol. 1995 Jan;78(1):138-45

15) Energetics in marathon running. Medicine and Science in Sports. 1969 1(2):81-86

16) Astrand P-O and Rodahl K. (1986) The Textbook of Work Physiology: Physiological Bases of Exercise (3rd ed.). New York: McGraw-Hill

17) Kraemer WJ, Deschenes MR, Fleck SJ. Physiological adaptations to resistance exercise. Implications for athletic conditioning. Sports Med. 1988 Oct;6(4):246-56

18) Hickson RC, Foster C, Pollock ML, Galassi TM, Rich S. Reduced training intensities and loss of aerobic power, endurance, and cardiac growth. J Appl Physiol. 1985 Feb;58(2):492-9

19) Costill DL, King DS, Thomas R and Hargreaves M. Effects of reduced training on muscular power in swimmers. Physician and Sports Medicine. 1985; 13(2), 94-101

20) Houmard JA, Costill DL, Mitchell JB, Park SH, Hickner RC, Roemmich JN. Reduced training maintains performance in distance runners. Int J Sports Med. 1990 Feb;11(1):46-52

21) Houmard JA, Scott BK, Justice CL, Chenier TC. The effects of taper on performance in distance runners. Med Sci Sports Exerc. 1994 May;26(5):624-31

22) Jackson AS, Beard EF, Wier LT, Ross RM, Stuteville JE, Blair SN. Changes in aerobic power of men, ages 25-70 yr. Med Sci Sports Exerc. 1995 Jan;27(1):113-20

23) Jackson AS, Wier LT, Ayers GW, Beard EF, Stuteville JE, Blair SN. Changes in aerobic power of women, ages 20-64 yr. Med Sci Sports Exerc. 1996 Jul;28(7):884-91

24) Dill DB, Robinson S, Ross JC. A longitudinal study of 16 champion runners. J Sports Med Phys Fitness. 1967 Mar;7(1):4-27

25) Hagerman FC, Fielding RA, Fiatarone MA, Gault JA, Kirkendall DT, Ragg KE, Evans WJ. A 20-yr longitudinal study of Olympic oarsmen. Med Sci Sports Exerc. 1996 Sep;28(9):1150-6

26) Pollock ML, Mengelkoch LJ, Graves JE, Lowenthal DT, Limacher MC, Foster C, Wilmore JH. Twenty-year follow-up of aerobic power and body composition of older track athletes. J Appl Physiol. 1997 May;82(5):1508-16

27) Trappe SW, Costill DL, Goodpaster BH, Pearson DR. Calf muscle strength in former elite distance runners. Scand J Med Sci Sports. 1996 Aug;6(4):205-10

28) Trappe SW, Costill DL, Vukovich MD, Jones J, Melham T. Aging among elite distance runners: a 22-yr longitudinal study. J Appl Physiol. 1996 Jan;80(1):285-90

29) Cureton KJ, Sparling PB. Distance running performance and metabolic responses to running in men and women with excess weight experimentally equated. Med Sci Sports Exerc. 1980;12(4):288-94

30) Dudley GA, Fleck SJ. Strength and endurance training. Are they mutually exclusive? Sports Med. 1987 Mar-Apr;4(2):79-85

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