Armstrong's improvement 1992 - 1999

garnetstar

There was a thread on Armstorng's apparent improvement in power from 1999 - 2005, and whether this could have been achieved by legal means alone.

I don't know about that, but here's excerpt from a recently-published study on his improvement from 1992 - 1999. This subject isn't in my field, so I can't critically review it myself. But, it's published in a reputable, peer-reviewed journal, which means that between three and eight scientists in the field picked it apart and criticized it to death, and only allowed to be published what passed scrutiny as good science, and good conclusions drawn from good data. So, it does constitute scientific proof of whatever.

There's also two letters here dissenting from the study's conclusions (they sort of hint at doping? you can decide), and two replies from the study's author. As you'll see, even scientists get emotionally caught up in the Saint Lance/Demon Lance conflict! Some of it's pretty funny, too.


Here's the link to the paper: http://jap.physiology.org/content/vol98/issue6/ and to the dissenting letters: http://jap.physiology.org/cgi/content/full/99/4/1630

The study is free for anyone to download, and the letters will be free to download one year from the date of publiscation.

I've edited the wording a bit in these excerpts, and inserted my own comments in parentheses.

Note also that when a sentence contains a number in parentheses--like, (22)---that that is a citation to another published scientific paper. It means that the study's author isn't just stating an opinion, he's citing known facts proved by other scientific researchers.

The actual numbers that they found for Armstrong---Table 2 in the paper--are given after the text.


I can't tell if the improvements shown in this study could actually also have been caused by doping, since I don't know enough about it. But, you can take a look yourselves:


EXCERPT:


J Appl Physiol 98: 2191–2196, 2005.

Journal of Applied Physiology
June 2005


Improved muscular efficiency displayed as Tour de France champion matures

Edward F. Coyle
Human Performance Laboratory, Department of Kinesiology and Health Education, The University of Texas at Austin, Austin, Texas


First published March 17, 2005;this information is current as of October 1, 2005 .

Copyright © 2005 by the American Physiological Society.


This case study reports the physiological changes that occur in an individual bicycle racer during a 7-yr period spanning ages 21 to 28 years. The approach of this study will be to report results from standardized laboratory testing on this individual at five time points corresponding to ages:

21.1 years Novemver 1992 Training stage: Preseason

21.5 years January 1993 Training stage: Preseason

22.0 years September 1993 Training stage: Racing

25.9 years August 1997 Training stage:Reduced (8 mo after chemotherapy)

28.2 years November 1999 Training stage:Preseason



RESULTS
Training and medical history of the subject (not excerpted).

Anthropometry. Total body weight during laboratory testing ranged from 76 to 80 kg from 1992 through 1997 as well as during the preseason in 1999. However, when competing in the Tour de France in 1999–2004, body weight was reported by the subject to be 72–74 kg. Lean body weight was 70 kg during the period of 1992–1997 (Table 2). His height was 178 cm.
˙
VO2 max, maximal heart rate, and the blood LT. VO2 max during the preseason months of November through January generally ranged from 5.56 to 5.82 l/min during the period of 1992–1999.
VO2 max during the competitive season of 1993, soon after winning the World Road Racing Championships (September 1993), was 6.1 l/min and 81.2 ml/kg min1, results that were corroborated by the United States Olympic Committee (Colorado Springs, CO). Eight months after chemotherapy for cancer and during a period of inconsistent and reduced training (i.e., August 1997), VO2 max was 5.29 l/min and 66.6 ml_kg_1 _min_1. Furthermore, at this time of reduced training, maximal blood lactate concentration measured 4 min after exhaustion was 9.2 mM compared with previously recorded values in the range of 6.3–7.5 mM. Maximal heart rate declined from 207 to 200 beats/min from 1992 through 1999. The VO2 corresponding to the blood lactate threshold was 4.5– 4.7 l/min when measured in 1992–1993 and, as expected, it was reduced to 4.02 l/min during the period of reduced training in August 1997.


Mechanical efficiency. Gross efficiency and delta efficiency during the period from 1992 to 1999 are displayed in Fig. 1. These progressive increases in efficiency amount to an 8–9% improvement over the period. This improvement is also displayed in the measure of mechanical power generated when cycling at a given VO2 of 5.0 l/min, in that it increased from 374 to 403 W (i.e., 8%; Table 2). Given that success in the Tour de France is typically determined when cycling uphill on mountains, it is best to normalize power to body weight (i.e.,W/kg). Given this individual’s reduction in body weight from 78.9 kg (in 1992) to _72 kg during his victories in the Tour de France and given his increased muscular efficiency, his powerto-body weight ratio (i.e., power/kg) when cycling at 5.0 l/min is calculated to have increased by a remarkable 18% from 1992 to 1999 (i.e., 4.74 vs. 5.60 W/kg when VO2 is 5.0 l/min). In that his VO2 max remained at 6 l/min, this given VO2 of 5.0 l/min represents _83% max. Therefore, his “power per kilo-gram” at a given percentage of VO2 max (e.g., 83%) increased by 18%.



DISCUSSION

This case study reports that the physiological factor most relevant to performance improvement as he matured over the 7-yr period from ages 21 to 28 yr was an 8% improvement in muscular efficiency when cycling. This adaptation combined with relatively large reductions in body fat and thus body weight (e.g., 78–72 kg) during the months before the Tour de France contributed to an impressive 18% improvement in his power-to-body weight ratio (i.e., W/kg) when cycling at a given VO2 (e.g., 5.0 l/min or 83% VO2 max).

In the trained state, this individual possessed a remarkably high VO2 max of 6 l/min, and his blood lactate threshold (LT) occurred at a VO2 of 4.6 l/min (i.e., 76–85% VO2 max). These physiological factors remained relatively stable from age 21 to 28 yr. These absolute values are higher than what we have measured in bicyclists competing at the US national level (9), several of whom subsequently raced professionally in Europe during the period of 1989–1995.

The five-time Grand Champion of the Tour de France during the years 1991–1995 has been reported to possess a VO2 max of 6.4 l/min and 79 ml_kg_1 _min_1 with a body weight of 81 kg (28).

We estimate (Armstrong’s) VO2 max to have been at least 85 ml_kg_1 _min_1 during the period of his victories in the Tour de France. Therefore, his VO2 max per kilogram of body weight during his victories of 1999–2004 appears to be somewhat higher than what was reported for the champion during 1991–1995 and to be among the highest values reported in world class runners and bicyclists (e.g., 80–85 ml _kg_1 _min_1) (6, 15, 16, 28, 29)


It is generally appreciated that in addition to a high VO2 max, success in endurance sports also requires an ability to exercise for prolonged periods at a high percentage of VO2 max as well as the ability to efficiently convert that energy (i.e., ATP) into muscular power and velocity (5, 7, 8, 29). Identification of the blood LT (e.g., 1 mM increase in blood lactate above baseline) in absolute terms or as a percentage of VO2 max is, by itself, a reasonably good predictor of aerobic performance (i.e., time that a given rate of ATP turnover can be maintained) (7, 8, 14, 21), and prediction is strengthened even more when measurement of muscle capillary density is combined with LT (11). Capillary density is thought to be an index of the working muscle’s ability to clear fatiguing metabolites (e.g., acid) from muscle fibers into the circulation, whereas the LT is thoughtto reflect production of fatiguing metabolites in muscle fibers
(7, 8).


As expected, this individual possessed a high LT in the range of 76–85% VO2 max. However, the most unique aspect of this individual’s blood lactate profile was the extremely low lactate concentration measured 4 min after exhaustion during measurement of VO2 max.

Maximal blood lactate in the trained state was only 6.5–7.5 mM in the present subject. By comparison, all the competitive cyclists we have tested, including team mates training with this subject, possessed maximal blood lactate postexercise in the range of 9–14 mM (9, 11).

It should be noted that this individual indeed became exhausted during VO2 max testing, displaying the typical pattern for competitive cyclist, including a “plateau” of VO2 and heart rate at maximal values for 1–3 min, moderate hyperventilation, respiratory exchange ratio _1.05, and a progressive loss of pedal cadence at constant power during the 30–60 s before exhaustion.

Interestingly, when VO2 max and maximal blood lactate concentration were measured during the period of reduced training 8 mo after chemotherapy (age 25.9 yr), maximal blood lactate concentration was increased to 9.2 mM. This agrees with our previous observation that detraining in well-trained endurance athletes increases maximal blood lactate from 10 to 12.5 mM (12, 13, 24).

During this laboratory evaluation 8 mo after completing chemotherapy, this individual displayed no ill effects from his previous surgeries and chemotherapy. In particular, ventilatory volume during maximal exercise appeared typical, and his cardiovascular responses were normal at heart rates of 120–150 beats/min. Furthermore, maximal heart rate achieved the healthy level for this individual (i.e., 200 beats/min). However, as expected from his reduced training, VO2 max was lowered by 6–12% to 5.3 l/min and 67 ml_kg_1 _min_1. If this individual had no training for 3 mo, we predicted his VO2 max would stabilize at 5 l/min (e.g., 61–63 ml_kg_1 _min_1 for a body weight of 80 kg) based on our previous measurements in well-trained endurance athletes during detraining (13; see Fig. 1). A VO2 max in the range of 56–62 ml_kg_1 _min_1 is generally believed to
be the highest value that the average man who is not genetically endowed for endurance can achieve with prolonged and very intense endurance training (13, 23). As such, it appears that in the detrained state, this individual’s VO2 max is in the range of the highest values than normal men can achieve with training. (That’s depressing, isn’t it? Even when Armstrong is untrained, he’s got a VO2 max that’s as high as any normal man can achieve *with*training. Not fair!)




We previously reported from cross-sectional observation of competitive bicyclists that the percentage of slow-twitch muscle fibers of the vastus lateralis is directly and positively related to both efficiency measured either during bicycling or with the simple task of knee extension (10, 25). Therefore, one possible mechanism for increased efficiency is that this individual increased his percentage of slow-twitch muscle fibers during this 7-yr period of study.

We predict that he might have increased his percentage of slow-twitch muscle fibers from 60% to 80%. Interestingly, this magnitude of increase in percentage of slow-twitch fibers with 7 yr of continued endurance training in this individual is remarkably similar to our prediction made in 1991 based on cross-sectional observations of competitive cyclists (9; see Fig. 8).

During periods of extreme endurance training of rats (!! I’d just love to see the rats riding their little Trek bicycles over the mountain passes!), skeletal muscle appears to display conversion of slow-twitch to fast-twitch fibers (18).


It has been recognized for decades that endurance training of rats increases the (energy-making ability) of slow-twitch fibers while decreasing it in fast-twitch fibers (2). Therefore, intense endurance training performed for prolonged periods results in alterations in (energy-making ability) whereby fast-twitch become more like slow-twitch fibers and slow-twitch fibers (their energy-making ability) and alter muscle type and increase maximal velocity of shortening. These observations support the possibility that in the subject of the present study, 7 yr of extremely intense endurance training and improved muscular efficiency when cycling was related to altered muscle type that allowed more of the energy released during contraction to be converted to power production.


Muscle samples were not surgically obtained from this athlete to directly test the hypothesis that muscle fiber-type conversion contributed to the large increases in mechanical or muscular efficiency when cycling. (Why weren’t muscles surgically obtained? Lance, if you really want to clear this whole thing up, just donate one of your quadriceps to science!) Therefore, this hypothesis that the percentage of slow-twitch muscle fibers increased in this requires identification of other performance characteristics that clearly changed in this individual over that 7-yr period with discussion as to whether they are consistent with the hypothesis of increased percentage of slow-twitch muscle fibers.


Although during all laboratory measures of mechanical efficiency, cycling cadence was held constant at 85 rpm, this individual’s freely chosen cycling cadence during time trial racing of 30- to 60-min duration increased progressively during this 7-yr period from 85–95 rpm to 105–110 rpm. This increase in freely chosen revolutions per minute when cycling at high intensity is indeed consistent with increases in slow-twitch muscle fibers because cyclists with a higher percentage of slow-twitch fibers choose a higher pedaling cadence when exercising at high power outputs (22). Although this may initially seem paradoxical, higher cycling cadence serves to both bring muscle fiber contraction velocity closer to that of maximum power and reduce the muscle and pedaling force required for each cycling stroke. Keep in mind that when exercising at a given rate of oxidative metabolism, an 8% increase in mechanical efficiency will result in 8% more muscle power and force development on the pedals when cycling cadence is held constant.

As cycling efficiency increases due to increased percentage of slow-twitch muscle fibers, it is possible that increased power is manifested by increasing cycling cadence (i.e., velocity) rather than increasing the muscle forces directed to the pedals. This approach appears to produce less sensation of effort relative to muscular strength (27). Therefore, it is likely that the increases in freely chosen cycling cadence displayed over the years by this Tour de France champion reflect his increased mechanical efficiency, agreeing with the pattern expected to result from muscle fiber conversion from fast-twitch to slow-twitch.


This report has identified the physiological factor that improved the most from ages 21 to 28 yr in the bicyclist who has now become the six-time consecutive Grand Champion of the Tour de France as muscular efficiency. As a result, power production when cycling at an absolute VO2 of 5.0 l/min increased by 8%. Another factor that allowed this individual to become Grand Champion of the Tour de France was his large reductions in body weight and body fat during the months before the race. Therefore, over the 7-yr period, he displayed a remarkable 18% improvement in steady-state power per kilogram body weight when cycling at a given VO2 (e.g., 5 l/min). We hypothesize that the improved muscular efficiency might reflect alterations in muscle type stimulated from years of training intensely for 3–6 h on most days.

Clearly, this champion embodies a phenomenon of both genetic natural selection and the extreme to which the human can adapt to endurance training performed for a decade or more in a person who is truly inspired. (Saint Lance, ora pro nobis.)


Table 2. Physiological characteristics of this individual from the ages of 21 to 28 yr

Age, yr
21.1 21.4 22.0 25.9 28.2
Nov 1992 Jan 1993 Sept 1993 Aug 1997 Nov 1999
Preseason Preseason Racing Reduced Preseason

Anthropometry
Body weight, kg 78.9 76.5 75.1 79.5 79.7
Lean body weight, kg 70.5 69.8 70.2 71.6
Body fat, % 10.7 8.8 11.7

Maximal aerobic ability
Maximal VO2 uptake, l/min 5.56 5.82 6.10 5.29 5.7
Maximal VO2 uptake, ml_ kg_1 _min_1 70.5 76.1 81.2 66.6 71.5
Maximal heart rate, beats/min 207 206 202 200 200
Maximal blood lactic acid, mM 7.5 6.3 6.5 9.2

Lactate threshold
Lactate threshold VO2 uptake, l/min 4.70 4.52 4.63 4.02
Lactate threshold, % maximal VO2 uptake 85 78 76 76

Mechanical efficiency
Gross efficiency, % 21.18 21.61 22.66 23.05
Delta efficiency, % 21.37 21.75 22.69 23.12
Power at VO2 uptake of 5.0 l/min, W 374 382 399 404




J Appl Physiol 99: 1628-1629, 2005

Journal of Applied Physiology
October 2005

LETTER TO THE EDITOR

Has Armstrong's cycle efficiency improved?

David T. Martin
Marc J. Quod
Christopher J. Gore
Department of Physiology,
Australian Institute of Sport
Belconnen, ACT 2616, Australia
e-mail: david.martin@ausport.gov.au

To the Editor: The concept that extensive endurance training improves cycling efficiency is intuitively appealing but not well supported by the literature. Recently, Coyle (1) has published efficiency data from Tour de France Champion, Lance Armstrong. In this case study Coyle concluded that "the physiological factor most relevant to performance improvement as he matured over the 7-yr period from ages 21 to 28 yr was an 8% improvement in muscular efficiency when cycling" (1). Case studies documenting adaptations in truly elite endurance athletes are important (3); however, we believe Coyle’s case study is insufficient to support his conclusions because of limitations in study design and methodology.

Timing of testing sessions. Armstrong was tested five times over a period of 7 yr. Only the first and last test occurred during the same month (November), making it difficult to distinguish seasonal effects from maturation effects.

Accuracy and reliability of efficiency. Coyle does not present data documenting the accuracy and reliability of the techniques used to calculate cycling efficiency (oxygen uptake, carbon dioxide production, and power output).Were all tests performed on same ergometer?

Is efficiency responsible for success? It appears that conventional physiological adaptations to modifications in diet (loss in body mass) and training (gains in aerobic power) may be equally, if not more, important to Armstrong’s performance than the 9% improvements in cycling efficiency.

It appears that other more conventional explanations (like drugs, you mean? Get thee behind me, Demon Lance!) describing why Armstrong is such a successful cyclist may be equally tenable.



REPLY (Journal of Applied Physiology, October 2005)

Edward F. Coyle
Department of Kinesiology and Health Education
The University of Texas at Austin
Austin, Texas 78712
e-mail: coyle@mail.utexas.edu

To the Editor: I appreciate this opportunity to answer the four points....

1. Point 1: Timing of testing sessions. I agree that it is not possible to distinguish what aspects of Armstrong’s training over the 7-yr period were related to his improved gross efficiency. Thus it was not discussed (4). Again, it can only be pointed out that he continued to train and his efficiency improved. Because the first measure in 1992 and the last measure in 1997 were both made in November when Armstrong’s training was similar, the most appropriate design was indeed used to control for the possibility of seasonal variations in efficiency. The idea that cancer or chemotherapy might have improved Armstrong’s efficiency cannot be determined from these data (Ha ha. See, even scientists can be funny!)


2. Point 2: Accuracy and reliability of efficiency (not excerpted here. A long listing of every measurement they made and the accuracies and reliabilities of and error margin on all these measurements. Also how they calibrated and maintained all their equipment scrupulously, etc. Looks very convincing to me.)


3. Point 3: Were all test performed on the same ergometer? All the data presented on Armstrong in this manuscript (4) were indeed collected from the "same" ergometer (i.e., only one unit used). For what it is worth, the electronic circuitry of our 819 ergometer became nonrepairable as did our system for measuring indirect calorimetry. However, Armstrong is still going strong, albeit with a few repairs. (. Like I said, scientists are funny!)


4. Point 4: Is efficiency responsible for success? Improved mechanical efficiency and power (watts) accounted for approximately one-half of Armstrong’s improvement (i.e., 8–9%), and an 8–9% reduction of body weight (kilograms) accounted for the other one-half (4). Thus watts per kilogram increased by 18%.




J Appl Physiol 99: 1628-1629, 2005

Journal of Applied Physiology
October 2005

LETTER TO THE EDITOR


Scientific considerations for physiological evaluations of elite athletes
Yorck Olaf Schumacher, Stefan Vogt, Kai Roecker and Andreas Schmid

Department of Sportmedizin
Medizinische Universitaetsklinik Freiburg



REPLY (Journal of Applied Physiology, October 2005)

Edward F. Coyle
Department of Kinesiology and Health Education
The University of Texas at Austin
Austin, Texas 78712
e-mail: coyle@mail.utexas.edu



Not excerpted here. Pretty much the same objections as in the letter above, and the same reply from the study's author.

VeloFlash

Coyle's 1992-1999 work is an hypothesis on a 1991 hypothesis.

Without undertaking a biopsy he hypothesises LA has trained FT fibre to take on a slow twitch role to justify the improvement. He estimates LA to have, in 1999, only 20% FT fibre. Coyle admits there is no study to confirm that fast twitch fibre is convertible to slow twitch fibre. No biopsy and no reference support.

With only 20% FT you could not sprint out of a wet paper bag!

But in 2004 LA won a bunch sprint in Stage 3 of the Tour of Georgia displaying a classic bike throw against specialised sprinters, led out a USPS team mate, Van Heeswijk, to win the sprint in Stage 3 of the 2004 Tour of Murcia lead up race to the 2004 TdF and in the Alpe D'Huez a stage of the 2004 TdF (flat finish) dropped Floyd Landis in the sprint and sprinted down Kloden for the win.

Did LA recover some of his converted FT fibre by 2004?

This University of Texas paper has missing data in some tests to suggest there was no intent to prove the hypothesis in 1992-1999. Five tests. Three in one training/racing season (1992-1993), when he was in recovery and unfit (1997) and after the season in November 1999.

Only two tests are comparable - November 1992 and November 1999, both off season. November 1999 is missing vital comparable data as are two other tests which suggests from the outset and during the tests there was no scientific objective.

It must have remained gathering dust for the period 1999-2005 and was published in June 2005. LA was fighting damaging claims in LA Confidential and it has been noted in 2005 together with this "study" he had an interview with Playboy where he claimed his blood supply system to his legs is three times larger that "average" and Dr Michele Ferrari on 53x12.com made quite false claims about LA's extraordinary response to altitude training.

The altitude training response was normal and can be compared to numerous studies.

Some late spinning to support LA's freak of nature genetics, absent to 1999, against the Walsh and Ballester doping allegations.

I have never come across an exercise physiological study where the participants are identified or there are clues to identity. The Coyle study ensures that the article will garner attention through the title and would not be missed - Improved muscular efficiency displayed as Tour de France champion matures
.

__________________
VF

"Remember, even if you win the rat race, you are still a rat"

garnetstar

thanks for your thoughts, veloflash, as i have no cycling knowledge with with to judge this study.


btw, note that my shift key isn't working.

VeloFlash

Dr Michele Ferrari says:

“SaO2 reduction under effort in some athletes is more pronounced than in others, with remarkable differences between individuals.

”I could personally check an SaO2 value of 79% in a strong professional cyclist performing a very high intensity effort at sea level (at the end of an uphill time trial of approximately 17 minutes).

”Lance Armstrong never got below 92% in similar efforts, while at 2000m of altitude the same kind of high effort determined an SaO2 = 84%. At the end of a 2-week altitude training camp, Lance was able to bring this value up to 88%.”

92% is normal (refer to following articles). The body acclimatises to altitude for responders (about 40% are non responders) and an 84% to 88% improvement in Sa02 at altitude is within normal parameters. The strong implication is that Lance Armstrong is an exception.

Exercise induced hypoxemia (EIH)

Exercise induced hypoxemia (EIH) is where Sa02 (arterial oxygen saturation) falls below varying set limits. Studies are inconsistent for parameters and have been set at 4% reduction (of 96%), 90%, 91% and 92%.

About 50% of elite endurance athletes experience EIH as evidenced from these extracts.

Exercise-induced hypoxaemia in elite endurance athletes. Incidence, causes and impact on VO2max.

Powers SK, Martin D, Dodd S.

Department of Exercise and Sport Sciences, University of Florida, Gainesville.

Arterial oxygenation is well maintained in healthy untrained or moderately trained individuals during exercise. In contrast, approximately 40 to 50% of healthy elite endurance athletes (cyclists and runners) demonstrate a significant reduction in arterial oxygenation during exercise at work rates approaching VO2max.......

Incidence of exercise induced hypoxemia in elite endurance athletes at sea level.

Powers SK, Dodd S, Lawler J, Landry G, Kirtley M, McKnight T, Grinton S.

Applied Physiology Laboratory-School of HPERD, Department of Exercise and Sport Sciences, University of Florida, Gainesville 32611.

....... EIH was defined as a %SaO2 of less than or equal to 91% during exercise. EIH did not occur in any of the untrained subjects or the moderately trained subjects. However, EIH occurred in 52% of the highly trained endurance athletes tested and was highly reproducible (r = 0.95; P less than 0.05). These findings further confirm the existence of EIH in healthy highly trained endurance athletes and suggests a rather high incidence of EIH in this healthy population. Hence, it is important that the clinician or physiologist performing exercise testing in elite endurance athletes recognize that EIH can and does occur in the elite endurance athlete in the absence of lung disease.

Not only does LA maintain a 92% SaO2 at or near V02max but about 50% of elite endurance cyclists also maintain this level.

There are numerous other studies that support these conclusions.

In Coyle’s book, Lance Armstrong’s War (US title), in Chapter 9 “Isle of the Dogs” it states that LA and Michele Ferrari spent one week in March 2004 training at Tenerife in the Spanish Canary Islands.

“They stayed at the Parador Nacional hjotel on the crater, following the customary regimen of sleeping high and training low, which naturally boosts red blood-cell counts.”

I refer to these articles which prove that altitude training both at elevation or artificial do not boost hct. In a later post on that thread the manufacturers have conceded that there is no proven correlation between altitude hct boost and athletic performance. The manufacturer of the Wallace altitude tent also makes no guarantee.

http://www.cyclingforums.com/showpo...08&postcount=13

In relation to LA's annual decampment for one week to the Canary Islands for "atitude training" I refer to an interview with Doping Hunter Professor Frank Delbeke. He states in reference to microdosing of EPO to beat tests (pioneered by Michele Ferrari):

All professional cyclists have to list their staying addresses during the season. But anyway: they go abroad and when they’re there they take their big ‘shot’, so that they reach 47-48.

After their big shot carried out in a location where they are immune from testing for several days, they later maintain the level by microdosing.

__________________
VF

"Remember, even if you win the rat race, you are still a rat"

garnetstar

VeloFlash--Dr Michele Ferrari says:

“SaO2 reduction under effort in some athletes is more pronounced than in others, with remarkable differences between individuals.

”I could personally check an SaO2 value of 79% in a strong professional cyclist performing a very high intensity effort at sea level (at the end of an uphill time trial of approximately 17 minutes).

”Lance Armstrong never got below 92% in similar efforts, while at 2000m of altitude the same kind of high effort determined an SaO2 = 84%. At the end of a 2-week altitude training camp, Lance was able to bring this value up to 88%.”


so, did this ferrari guy publish this somewhere, or is this just a quote from the press, or what. actually, it doesn't matter, since coyle's j appl.phys. article says nothing about this subject. no matter what armstrong's sao2 is, or if it's normal or not, that wouldn't alter coyle's results.




'92% is normal (refer to following articles). The body acclimatises to altitude for responders (about 40% are non responders) and an 84% to 88% improvement in Sa02 at altitude is within normal parameters. The strong implication is that Lance Armstrong is an exception.


Exercise induced hypoxemia (EIH)

Exercise induced hypoxemia (EIH) is where Sa02 (arterial oxygen saturation) falls below varying set limits. Studies are inconsistent for parameters and have been set at 4% reduction (of 96%), 90%, 91% and 92%.

About 50% of elite endurance athletes experience EIH as evidenced from these extracts.



Exercise-induced hypoxaemia in elite endurance athletes. Incidence, causes and impact on VO2max.

Powers SK, Martin D, Dodd S.

Department of Exercise and Sport Sciences, University of Florida, Gainesville.

'Arterial oxygenation is well maintained in healthy untrained or moderately trained individuals during exercise. In contrast, approximately 40 to 50% of healthy elite endurance athletes (cyclists and runners) demonstrate a significant reduction in arterial oxygenation during exercise at work rates approaching VO2max.......'


'Incidence of exercise induced hypoxemia in elite endurance athletes at sea level.'

Powers SK, Dodd S, Lawler J, Landry G, Kirtley M, McKnight T, Grinton S.

Applied Physiology Laboratory-School of HPERD, Department of Exercise and Sport Sciences, University of Florida, Gainesville 32611.

'....... EIH was defined as a %SaO2 of less than or equal to 91% during exercise. EIH did not occur in any of the untrained subjects or the moderately trained subjects. However, EIH occurred in 52% of the highly trained endurance athletes tested and was highly reproducible (r = 0.95; P less than 0.05). These findings further confirm the existence of EIH in healthy highly trained endurance athletes and suggests a rather high incidence of EIH in this healthy population. Hence, it is important that the clinician or physiologist performing exercise testing in elite endurance athletes recognize that EIH can and does occur in the elite endurance athlete in the absence of lung disease.'


so are these quotes from journals or newspapers or what. got any links to the sources, or citations of the papers.




'Not only does LA maintain a 92% SaO2 at or near V02max but about 50% of elite endurance cyclists also maintain this level.'

it says that 'EIH was defined as a %SaO2 of less than or equal to 91%', and that it is eih that is found in elite endurance athletes. but you quote this ferrari as saying that armstrong's %SaO2 is 92%, out of the threshold value for this parameter. what's the error on the 91% or less number. why isn't 92% included. gotta see the data on this.


but, even so, if this ferrari said something wrong about armstrong's %SaO2 or how he got it, what's that got to do with coyle's data.




There are numerous other studies that support these conclusions.

please give links or citations.




In Coyle’s book, 'Lance Armstrong’s War' (US title), in Chapter 9 “Isle of the Dogs” it states that LA and Michele Ferrari spent one week in March 2004 training at Tenerife in the Spanish Canary Islands.

“They stayed at the Parador Nacional hjotel on the crater, following the customary regimen of sleeping high and training low, which naturally boosts red blood-cell counts.”

I refer to these articles which prove that altitude training both at elevation or artificial do not boost hct. In a later post on that thread the manufacturers have conceded that there is no proven correlation between altitude hct boost and athletic performance. The manufacturer of the Wallace altitude tent also makes no guarantee.'


this is the 'author's'--of Lance Armstrong’s War---statement of what he thinks that high altitude training does, not armstrong's or ferrari's. it is the author's error if that statement is wrong.

i see from the web that Lance Armstrong’s War was written by daniel coyle, who is not the same person as, and appears to be unconnected to, edward f. coyle, the author of the scientific paper that i posted excerpts from.




'In relation to LA's annual decampment for one week to the Canary Islands for "atitude training" I refer to an interview with Doping Hunter Professor Frank Delbeke. He states in reference to microdosing of EPO to beat tests (pioneered by Michele Ferrari):

'All professional cyclists have to list their staying addresses during the season. But anyway: they go abroad and when they’re there they take their big ‘shot’, so that they reach 47-48.'

'After their big shot carried out in a location where they are immune from testing for several days, they later maintain the level by microdosing.'


what's the evidence that this microdosing was pioneered by ferrari. 'Doping Hunter'--is that a title, or something. this is a press interview containing allegations against professional cyclists, not a peer-reviewed scientific publication. the difference in reliability could not be more enormous.

just as a completely tangential and unscientific aside, there is a heck of a lot of altitude in the canary islands--more than 230 volcanic craters just on the island of lanzarote alone. i had a nice hiking vacation there once, so i just had to throw in that quite irrelevant fact.


but, what's all this got to do with the published scientific study. are you saying that armstrong, or anyone else, could have gotten these 'improvements', as they're called, by doping. i'd be interested to know if you think that that data in the published paper could have come from epo use.

VeloFlash

On his website on 6 September 2005 about 2 weeks after L'Equipe allegations of LA EPO use in 1999..

http://www.53x12.com/do/show?page=article&id=54

The relevance is that in 2005 two scientific statements are issued about LA's superior physiology that are false (Ferrari) and highly questionable (Coyle) following on from Walsh & Ballester's presentation of circumstantial evidence of LA's illegal performance enhancement. Why did Dr. Edward Coyle release an old (1992-99) incomplete study in June 2005?

If you do a search on Pub Med (National Library of Medicine) you will find these studies plus numerous others.

See my first reponse.

The manuscript was approved by Armstrong prior to publication. LA has always promoted that altitude training/altitude tents promote the production of RBC's legally. You can see from the implication by his lack of denial in his Playboy interview:

PLAYBOY: Some cyclists train by sleeping in an "altitude tent" with thin air that helps thicken the blood. It's a legal way to make your blood more efficient. Have you got one?

ARMSTRONG: A tent's not big enough. I've got an altitude cubicle.

Correct. One (Daniel) is an author who was permitted access to the LA entourage during 2004 training and competition. The other (Edward) is an exercise physiologist at the University of Texas. They are not related.

The evidence of Fillipo Simeoni at the Italian sporting fraud trial of Ferrari. Armstrong was upset with Simeoni claiming he lied about Ferrari advising Simeoni on the use of EPO and how to avoid detection - microdosing. This was a breach of the rider's code of omerta. If Armstrong claims the advice given to him by Ferrari did not involve the use of illegal PED's how can Armstrong presume a practitioner with the notorious reputation as Ferrari was not advising other riders differently?

The Doping Hunter article gave some explanations on how rider's avoid detection and how they are ahead of the testers.

The paper provides information on LA's historical power output above anaerobic threshold. He was tested at 5.0l/min whereas 4.52 to 4.70l/min was his threshold level. His power output at this level above threshold ranged from 374 to 404 watts.

However in 2003 and 2004 (refer Daniel Coyle's book), Ferrari instituted pre training camp power measurements on LA on a 1km hill when he was 5.5 kgs overweight (2004). These results are a truer measurement of threshold but still less than the lab atmosphere. LA recorded 2003 = 440 watts; 2004 = 470 watts.

The last test prior to the TdF LA registered 2003 = 470 watts; 2004 = 493 watts.

Observers were amazed that LA had a 30 watt increase in one year (2003 to 2004) as disclosed in the Coyle book. You may note there is a thread here on this subject to which you have contributed. But the other Coyle now has revealed 1992 - 1999 figures which would make natural development of that power truly unbelieveable.

In Coyle's hypothesis for the improvement 1992-1999 he states:

Using our previously reported prediction of the percentage type I muscle fibers from our direct measurements of gross and mechanical efficiency in this individual, we predict that he might have increased his percentage of type I muscle fibers from 60 to 80%. and

Muscle samples were not surgically obtained from this athlete to directly test the hypothesis that muscle fiber-type conversion contributed to the large increases in mechanical or muscular efficiency when cycling. Therefore, this hypothesis that the percentage of type I muscle fibers increased in this individual requires identification of other performance characteristics that clearly changed in this individual over that 7-yr period with discussion as to whether they are consistent with the hypothesis of increased percentage of type I muscle fibers.

If improvement to LA's endurance performance 1992-1999 related to muscle fibre conversion from fast twitch to slow twitch leaving a predicted 20% of FT muscle, how would Coyle account for LA's phenomenal aerobic improvement to 2003 and 2004 and the fact he won sprints with 20% (and diminishing) FT fibre? There would be nothing left of the 20% FT fibre!

__________________
VF

"Remember, even if you win the rat race, you are still a rat"

VeloFlash

The study of LA covered the period November 1992 to November 1999 - 7 years. The study was allegedly to prove a hypothesis concluded from a study submitted/accepted 23 January 1991.

(Physiological and biomechanical factors associated with elite endurance cycling performance. Coyle EF, Feltner ME, Kautz SA, Hamilton MT, Montain SJ, Baylor AM, Abraham LD, Petrek GW.)

The hypothesis of Coyle et Al in that initial study was: "It appears that "elite-national class" cyclists have the ability to generate higher "downstroke power", possibly as a result of muscular adaptations stimulated by more years of endurance training."

But the results of the 7 year LA study were not submitted until February 2005 and accepted March 2005, over 5 years later when their was no collection of data post November 1999.

At the time of the studies LA was an elite international cyclist (TdF winner 1999 at end of study) but Coyle et Al suggested the muscular adaptations would occur to riders of "elite national class" level.

Though not referred, if muscle biopsies were a problem to LA then the only alternative to prove the hypothesis would be to recruit a young elite national class rider to participate in the study and undergo biopsies. The study still remains a hypothesis.
Disagree. He was out to prove his 1991 hypothesis and, in my opinion, did not.
PLAYBOY: Your coach, Chris Carmichael, has said you're not unique as a physical specimen but that you're pretty special. Isn't your heart 30 percent bigger than normal?

ARMSTRONG: It's bigger. And my muscles supposedly produce less lactic acid. But you know what's interesting? There's a big artery that runs from the middle of your body to your lower half, down to your legs. I had some scans done, and the doctors couldn't believe it: My artery is three times the size of a normal person's.

Every comment I have read about LA's superior genetic credentials compares him with "normal" or "average." Why is not he compared with his peer group?
These have been provided in another response.
The spin is in the timing plus you may note the Dr. Edward Coyle from the University of Texas is out doing the media rounds on this article. I find this unprecedented.
Why did Coyle wait until 2005 to publish conclusions that must have been attained in 1999? Why is vital performance measuring data missing from the September 2003 test? I will make a stab here. On 29 August 1993 LA won the World Championship, a single day event. He continued racing in September 2003 (Coyle describes this test as a "racing" period). I would suggest that LA was at his performance peak (peaks last about 6 weeks) and the data of higher power generation and AT would be inconsistent with the conclusion of gradual muscle fibre conversion over 7 years.

__________________
VF

"Remember, even if you win the rat race, you are still a rat"