Lance Armstrong through a physiological lens: hard training boosts muscle power 8%
A combination of long-term training, fat loss raises power gain to 18%: improvement aimed at Tour de France climbs. Winning combo: high maximum capacity, efficient sub-maximal capacity
[And yet…15 minutes intense training over 2 weeks boosts endurance capacity]*
BETHESDA, Md. (June 14, 2005) – Catch an athlete with clear potential early in his career, study his physiology over an incredibly eventful seven years including victory in the Tour de France, and you might uncover some incredibly important, indeed amazing facts about what training and dedication can accomplish.
What Edward F. Coyle of the University of Texas-Austin found out about Lance Armstrong was that from 1992-1999, the year of his first of now six consecutive Tour de France wins, "the characteristic that improved most (was) an 8% improvement in muscular efficiency and thus power production when cycling at a given maximal oxygen uptake." Combining the increased muscular efficiency with a planned 7% reduction in body weight and fat leading up to each Tour de France race, "contributed equally to a remarkable 18% improvement in his steady-state power per kilogram" output, the Coyle paper reported.
The study, "Improved muscular efficiency displayed as 'Tour de France' champion matures," appears in the June issue of the Journal of Applied Physiology, published by the American Physiological Society. The research was conducted by Edward F. Coyle, Human Performance Laboratory, Department of Kinesiology and Health Education, University of Texas at Austin.
*[Another study also appearing in the June issue of JAP reports on a different cycling approach: "Six sessions of sprint interval training increases muscle oxidative potential and cycle endurance capacity in humans," by Kirsten A. Burgomaster and Martin J. Gibala, et al., of McMaster University, Canada. See brief report after the Coyle-Armstrong study.]
"Amazing, quantified changes that get more guys off his wheel"
An independent physiologist familiar with the study commented: "This study shows that long term training has a lot bigger effects than we thought. They followed Armstrong – a well-known hard trainer – and the changes in his efficiency over seven years are really quite amazing. We wouldn't be surprised if some major physiological changes happened, but here's a real quantified example."
He added: "Generally there are two ways to improve efficiency: Train your maximum capacity to be very high, or train your sub-maximal capacity to be very efficient. In Armstrong's case, he did both. In the lab they measured his performance against standard oxygen consumption and by the end of the study he was much more efficient utilizing the same amount of oxygen. But on the road," he pointed out, "it means he can go faster and get more guys off his wheel."
Effect of cancer, therapy nil
The period that started when Armstrong was 21 and just turning professional and ending at age 28 with his first TdF victory, also included his cancer diagnosis, surgery, chemotherapy and recovery. About eight months after chemotherapy ceased (August 1997), Armstrong was tested in Coyle's laboratory in the same manner as in his other four visits. The results showed that he "displayed no ill-effects from his previous surgeries and chemotherapy" and were in line with measurements expected from highly trained athletes during periods of detraining, Coyle added later.
The study notes that these findings could be "important because it provides insight, although limited, regarding the recovery of 'performance physiology' after successful treatment for advanced cancer."
Muscular efficiency through possible fiber change: making it look easy
Coyle concedes in the study that the "physiological mechanisms responsible for the 8% improvements in (muscle) efficiency when cycling, as well as the stimuli that provided this adaptation, are unclear. The observation that both gross and delta efficiency improved to the same extent and also with the same time course suggests an improved efficiency of ATP turnover within muscle fibers during contraction." (ATP, or adenosine triphosphate, is a nucleotide present that serves as an energy source for many metabolic processes.)
"One possible mechanism for increased efficiency is that (Armstrong) increased his percentage of type I muscle fibers, (indeed) we predict that he might have increased his percentage of type I muscle fibers from 60% to 80%," the report said. "Interestingly, this magnitude of increase…is remarkably similar to our predictions made in 1991 based on cross-sectional observations of competitive cyclists."
This change in muscle type may account for the apparent ease with which Armstrong seems to be pedaling, albeit at a high cycling cadence.
Whereas the lab tests were held constant at 85 revolutions per minute (rpm) for comparison purposes, Armstrong's "freely chosen cycling cadence during time trial races of 30- to 60-minute duration increased progressively during this y-year period from about 85-95 rpm to about 105-110 rpm. This increase in freely chosen rpm when cycling at high intensity is indeed consistent with increase in type I muscle fibers because cyclists with a higher percentage of type I fibers choose a higher pedaling cadence when exercising at high power outputs," the report said. "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," it noted.
As body matures, it gets "smarter"
Coyle said increased muscle efficiency means that "for the same amount of cardiovascular and lung stress Armstrong is producing 8% more power, and yet producing less heat. These results have shown us how to improve already highly trained athletes by aiming at efficiency, which is a muscle phenomenon. But it's also nice to know," he added, "that as you get older that your body becomes wiser in how it does its job and less wasteful in energy usage."
Coyle added later: "There's no doubt that Armstrong started with a strong genetic makeup, but he maximized his abilities and got where his is through dedication and hard training."
The study, entitled "Improved muscular efficiency displayed as 'Tour de France' champion matures," appears in the June issue of the Journal of Applied Physiology, published by the American Physiological Society. The research was conducted by Edward F. Coyle, professor at the Human Performance Laboratory, Department of Kinesiology and Health Education, University of Texas at Austin.
Publisher's note: The research paper by Edward Coyle on Lance Armstrong is being made available at no charge to the public by the American Physiological Society, publisher of the Journal of Applied Physiology: http://jap.physiology.org/cgi/content/full/98/6/2191.
* McMaster study sees gains from different cycling training approach
Another study in the June issue considers at a different approach to training: "Six sessions of sprint interval training increases muscle oxidative potential and cycle endurance capacity in humans," by Kirsten A. Burgomaster, Martin J. Gibala et al., McMaster University, Hamilton, Canada.
In an editorial, Ed Coyle noted that the Burgomaster et al. study "reminds us of the 'potency' of very intense exercise, performed as 30-second sprints, for stimulating metabolic adaptations within skeletal muscle," in this case totaling as little as 15 minutes over 2 weeks.
The McMaster group "employed 'sprint interval training' on a bicycle ergometer, involving 30-second sprints performed 'all out,' with 4 minutes of recovery," Coyle summarized.
"Recreationally active college students performed only 2-4 minutes of exercise per session and just six sessions over 2 weeks. The remarkable find of this study was that this small total amount of very intense exercise training was sufficient to 'double' the length of time that intense aerobic exercise could be maintained (ie. from 26 to 51 minutes). Although peak oxygen uptake was not increased, aerobic adaptations did occur within active skeletal muscle as reflected by a 38% increase in activity of the mitochondrial enzyme citrate synthase," Coyle noted.
Mechanisms of physiological changes need further study
The Burgomaster et al. paper said the validity of their findings on the doubling of endurance time to fatigue "is bolstered by the fact that all subjects performed extensive familiarization trials before testing and that a control group showed no change in endurance performance when tested 2 weeks apart with no sprint training intervention." In addition, though previous studies showed increases in citrate synthase (CS) activity and glycogen content after several weeks of sprint interval training with equivocal data, "we show here that the total training volume necessary to stimulate these metabolic adaptations is substantially lower than previously suggested."
Nevertheless, they note: "We can only speculate on potential mechanisms responsible for the dramatic improvement in cycle endurance capacity, but it is plausible that a training-induced increase in mitochondrial potential, as measured by CS maximal activity, improved respiratory control sensitivity during exercise as classically proposed (by J Holloszy and E. Coyle)….We hope that the present observations will stimulate additional research to clarify the precise nature, time course, and significance of the physiological adaptations induced by short sprint interval training."
The study, "Six sessions of sprint interval training increases muscle oxidative potential and cycle endurance capacity in humans," by Kirsten A. Burgomaster, Scott C. Hughes, George J.F. Heigenhauser, Suzanne N. Bradwell and Martin J. Gibala, of McMaster University, Hamilton, Ontario, appears in the June issue of the Journal of Applied Physiology, published by the American Physiological Society. Except for Heigenhauser, researchers are with the Exercise Metabolism Research Group, Dept. of Kinesiology; Heigenhauser is in the Dept. of Medicine.
Editor's note: The media may obtain an electronic version of Burgomaster, Gibala et al., and interview members of the research team by contacting Mayer Resnick at the American Physiological Society, 301.634.7209, cell 301.332.4402 or email@example.com.
Source: Eurekalert & othersLast reviewed: By John M. Grohol, Psy.D. on 21 Feb 2009
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