Questioning the Fit

This is not the concept that has been cooking … rather a simple reflection on the research I’ve done over the past 20 years. I am estimating that I have about 75 or more experimental data sets lying around, likely to never be published. They are small and not so small experiments whose results got pushed to the back burner for too many reasons. They all shaped my thoughts on training and fitness and form the foundation of many of my answers to questions … maybe one day I’ll just write them all up in one tome, convert it to pdf, and put it all online. Probably more people would read it there than in an academic journal. I really don’t need peer-review approval anymore anyway. Just have to find the time … retirement?

Lots of stuff happening around here lately … a new post is festering in my brain, it will pop out soon.

http://news.yahoo.com/s/livescience/20100122/sc_livescience/humanscouldrun40mphintheory

Yes it’s sensationalism and misinformation at its best but it is what people read. Some coach out there is going to read either the news report or the original research report in the Journal of Applied Physiology (hugely unlikely) and will think that he needs to do more speed-work with his athletes. But the article isn’t about running fast, its just answering the question of whether the human body has the ability to tolerate forces larger than those encountered while sprinting. Any observant lay person could already answer that question … yes. The human body can tolerate huge forces, tremendously larger than those produced during sprinting. Wrestlers, football players, rugby players, powerlifters, weightlifters, gymnasts all tolerate joint and skeletal loading well beyond any experienced by a runner. That is already in the books.

The point that is proposed by the authors above is that the human can tolerate the forces that would be encountered at running 40mph. They point to the limitation in running speed to be muscle contractile velocity. What is implied, either intentionally or non-intentionally, is that we can magically train a muscle to improve its contractile velocity to a large degree.

Improving the speed of human movement is limited by simple physics. To move fast we have to apply force to the body very quickly and in large amounts. If we use low force we overcome inertia and accelerate slowly. If we apply the force slowly we accelerate slowly. Simple.

But training for speed is not so intuitive. There are two strategies possible, both derived from the simple equation for power:

Power = Work / Time

Strategy 1 for improving speed is to reduce the value of the denominator in the power equation. If I can apply the force faster (smaller denominator) then power output goes up. This approach is extremely limited in how much improvement is possible. To understand this let’s divide this strategy into two concepts.

(1)  Nerve conduction velocity is approximately 50 meters per second … or about 5 milliseconds per 10 inches. Some people might propose that we can improve the rate of neural conduction significantly by doing speed drills and random silliness. If we approach this objectively, without exercise professional conventional wisdom, we’ll see that this is not really productive over the long term.

Think of how close most muscles are to the vertebral column. Once a sensory nerve fires in the hip musculature, speeds to the spinal cord, then exits to the motor nerve and muscle, it takes about 20 maybe 30 milliseconds to make the trip. With weight training and sprint training (high loads and velocity) the motor end plates will adapt, and change structure as an adaptation, possibly to speed synapse. But the speed of conduction depends on the amount of myelination of the nerve axons not really on motor end plates. And with only 20-30 milliseconds of total travel time, can we significantly increase nerve conduction velocity enough to actually record a movement velocity change with a stopwatch or see a power output change with a barbell? Not likely.

(2)  Reaction time ranges from about 150 to 200 milliseconds (a simple stimulus yields a faster muscular response, a complex stimulus produces a slower muscular response).

We have to think consciously to make our bodies do what we want as a beginner. Think of the herky-jerky beginnings of you riding a bicycle as a kid. Wobbling every which way, your body was learning how to accomplish a complex movement task – your brain was trying to tell your body what to do but it couldn’t get the job done fast enough with you thinking and then reacting. As technique was honed through riding practice (this goes for any exercise movement), reaction time became faster as the body began to sense the movement as a simple task rather than a complex one. Essentially, after much practice the body treats the learned movement or skill as a simple reflex (I am simplifying).

You can improve quite a bit here with the maximum amount of improvement being on the order of about a 50 milliseconds or so reduction in reaction time BUT there is a bottom limit for reaction time of around 150 milliseconds. Once the bottom is hit there can be no more improvement on this side of neural adaptation.

This second approach above is the most applicable neural approach to all sport movement. Improve technical efficiency through repetition and speed in that movement will increase … to a limit specific to the individual. After that the only way to improve speed is to employ Strategy 2 – increase the numerator side of the power equation and increase force generation, i.e. work capacity – in other words get stronger. Stronger is ALWAYS better.

So will we see 40 mile an hour sprinting humans? With gene doping, I will not rule out anything. BUT in clean athletes we might see 30 mph before I finish my 10 decade tenure on earth (I’m optimistic). I think Bolt will break 28.

NBA
Francisco Garcia suffers a radial fracture, dislocation, and ligament tears.
Eddy Curry suffers from minor scrapes.

NCAA Basketball
Hudson Frickes suffers bilateral wrist fractures.

What do these three guys have in common? Swiss/Gym/Exercise Ball injuries. AND probably bad judgment on someones part.

Swiss balls are not a panacea for poor fitness. They have very few legitimate uses in strength and fitness training. They are OK for rehabilitation purposes when attempting to re-establish kinesthetic awareness and control. They are OK for relaxation and stretching during cool downs after exercise. BUT as the cases above suggest their common use, with weights, carries with it a degree of risk of injury higher than normal.

Swiss balls are designed for bodyweight support and bodyweight movements. They are rated to support a static load of approximately 300 to 600 pounds (depending on model and manufacturer). The manufacturers of the balls themselves do not even produce the balls with the intent for combined use with weighted apparatus (manufacturer’s spec sheet excerpt: “It is NOT recommended to use additional weights while performing exercises using this ball.”)

If we consider Garcia’s case, he is a 200 pound athlete, he was using two 80 pound dumbbells for bench pressing. So simple math, 200 + 80 + 80 = 360 pounds, suggests that his STATIC load may have exceed the load rating of the ball he was lying on. But the story does not end there. A bench press is dynamic and the amount of force at the bottom of the bench press, where the downward movement stops and changes direction, is increased significantly (a 10 pound plate lying on edge on your hand doesn’t hurt – drop it from 12 inches and it will). Even if Garcia was under the static load limit for his Swiss ball, adding movement to the system apparently did exceed it, resulting in the ball failure and injury.

So obviously the people at fault for these injuries are the coaches who prescribed the exercises to the athletes? Maybe. Maybe not. Obviously a professional coach should be cognizant of the limitations and proper use of the equipment he employs. However in this particular case, using weights on Swiss balls – without consideration of their physical limitations and potential risk – is heavily documented in the National Strength and Conditioning Associations coaching journal. One research article published in their research journal investigated barbell bench presses performed on a Swiss ball. Of course the subjects were much smaller than Garcia and used much less weight (the study was particularly inane in purpose). It would not be a stretch of the imagination that the NSCA’s publications would be perceived by less than critical coaches and trainers as endorsement of the use of Swiss balls in weighted exercise. So I guess I’m giving the coaches involved an out. I’m not giving the NSCA journal editorial staff the same. Allowing such articles to appear in their journals is irresponsible.

But then sometimes I can just be an opinionated bastard … with manners and at least a few synapsing neurons.

“Scientists should be cautious when giving training recommendations to runners and coaches based on the limited available scientific knowledge.”

Dr. Adrian Midgley, University of Hull

This absolutely true little nugget came out of Dr. Midgley’s paper evaluating the available science relative to improving VO2max – or in other words, improving aerobic fitness (Sports Med 2007; 37(10):857-80).

You might ask why this is important to me? It’s because it bugs me to have people – scientists, trainers, physicians, arm-chair coaches, web-thorities, or whomever – tell other people how to get aerobically fit without any actual data or experience to back it up.

Back in 2006, I wrote an article for the CrossFit Journal entitled “The Paradox of Aerobic Fitness Prescription: A Facultative Anaerobe Sucks the Air Out of VO₂max”. In that article I pointed out some flaws in conventional aerobic exercise wisdom and made some conjectures. One being that inducing hypoxemia (low blood oxygen content) with very intense exercise would disrupt O2 dynamics and induce a positive adaptation in VO2max. In essence, very short duration (20 minutes or less) exercise would outstrip the bodies ability to extract, deliver, and consume oxygen and that would set up a condition where the body would adapt to increase its ability to extract, deliver, and consume (increase VO2max).

Exercise induced hypoxemia is a phenomena of considerable interest to physiologists and clinicians. Frequently considered to be a negative result of excessive work, it is poorly understood although much research has focused upon it. Existing research lacks a systematic and interconnected approach to characterization of both its induction and its effects on human physiology and further has failed to link its presence to any harmful sequelae of transient low blood O2 in healthy individuals.

A basic flaw in approach of previous research is the failure to frame exercise induced hypoxemia within the context of Hans Selye’s theorization of the General Adaptation Syndrome, an ubiquitous and widely accepted conceptualization of how the body adapts to external stressors of any kind. Exercise induced hypoxia is manifested as a decrease in oxygen content of the blood as a result of exercise, expressed as a percent of saturation (O₂sat %). Normal blood O₂ saturations are 98% or greater. By convention, the exercise science community defines hypoxia as a reduction of O₂sat% of 4% or more (i.e., a reduction to 94%). O₂ saturations as low as 76% have been reported during mountaineering, so the 4% represents an arbitrary standard well within the range of human tolerance. It has been observed that 50% of males and 33% of females will not experience EIH during exercise. It has also been noted that it is most commonly experienced by well trained aerobic athletes. One very notable physician specializing in this area boldly states that humans cannot experience exercise induced hypoxemia unless the are at altitude.

This is absolutely true if your are running at speeds correlating to VO2max or below. But I don’t care about that particular training methodology. If you always run the same velocity, you will never get faster although you might be able to go longer. Going longer is about having enough fat and carbohydrate to provide power for the duration, not about VO2max.

In terms of the General Adaptation Syndrome, exercise induced hypoxemia represents the degree of overload required to disrupt endurance homeostasis (stage 1) and drive a positive adaptation in oxygen transport and utilization capacity,VO₂max (stage 2). Support for this belief comes from two studies; (1) a 1999 study by Roberts and Smith that demonstrated that reducing O₂sat% to or below 91% through high intensity exercise (110% of VO₂max) in well trained athletes induced an increase in erythropoietin concentrations. The implication of that study was that EIH, at levels well below the 4% drop used for diagnosis, induces a hormonal response that will ultimately increase erythrocyte concentrations and improve VO₂max, the primary indicator of aerobic fitness. (2) A study by Mucci and co-workers in 2004 demonstrated that repeated sprint training induced EIH as an effect of training and this led to significant increases in VO₂max. It must be noted here that while these two studies, along with a few other fairly well designed studies support this conjecture, the concept that sprint-type high intensity training driven by glycolytic metabolism may be the most efficient means of improving endurance is not widely understood nor is it intuitive. It is a commonly held belief that long duration, moderate intensity, and continuous exercise must be done in order to improve VO₂max. The two studies cited here and the my personal experiences challenge that belief.

Several studies have attempted with varying degrees of success to determine what type of exercise induces hypoxemia. The studies are frequently contradictory and fail to be representative of exercise training that would be used by the exercising public or athletes. An explanation of the contradictions found within existing research lies with:

1. Failure of studies to investigate the relevant populations, as untrained subjects will, by physiologic reality, respond to the any exercise stress in a positive manner whereas a trained individual requires not only a larger load but a degree of metabolic specificity in training to drive adaptation.
2. Failure to investigate similar training loads than those used in similar studies – it is hard to make a uniform interpretation of multiple experiments if none of the variables are similar.
3. Failure to select training modalities and training loads that would be considered, by practitioners, of utility and that could actually lead to an improvement in VO₂max.

An example of this last point can be found in the work of Galy et al who while using appropriate exercise modalities (cycling and running) used a workload of 75% of VO₂max. A 75% VO₂max workload would best be classified as a “recovery” or “light” workout, not one that any coach, personal trainer, or physical educator would consider, based on centuries of experiential knowledge, to be useful for improving fitness. The literature is ripe with similarly flawed studies that lack applicability in real-world application.

I propose a fundamental but important question – Can commonly used modalities and intensities of training, selected based on metabolic bias, induce exercise induced hypoxemia? A major assumption here is that an exercise intervention must establish a physiological state where cardio-respiratory oxygen supply cannot meet exercise demand from the working muscle. When this supply-demand mismatch occurs it represents the appropriate training load to disrupt homeostasis and subsequently drive adaptation. The adaptation being an improvement in the body’s ability to either extract O₂ from the atmosphere and deliver it to the working muscles or alternatively, and more likely, that the working muscles become more efficient at pulling O₂ from the blood and thus lowering O₂sat%. This latter point has a foundation in existing literature as it is frequently observed that well trained athletes can produce a lower O₂sat% than untrained individuals following training, an indication that exercise induced hypoxemia is a trainable entity.

I have been doing some pilot research on this topic with Justin Lascek for about a year. Early field data suggests that marked depression of O2sat% to as low as 89% is quite doable (through intense exercise) on a daily basis. Four weeks of five training sessions per week (monday through friday) for durations ranging from 9 minutes to 23 minutes yielded an increase in VO2max of 13ml/kg/min, hematocrit increased from 43 to 49, and hemoglobin went from 14 to 17 … all which correlated to more than a 2 minute drop in mile time. We are repeating the field study with more stringent laboratory measures presently. In April we will move the project completely into the lab with Dr. Frank Wyatt and Alissa Donaldson where we can tightly control things and add some more subjects.

About $12 Billion dollars are spent each year on running shoes. Each year we see the next generation of “high-tech” footwear supposedly representing the pinnacle of engineering applied to exercise. It’s is engineering and it is applied to exercise footwear but it is not a pinnacle of anything.

Performance – Even though athletic shoe companies have an ever growing menu of shoe features and shoe models, the shoes that win running races, sprints and up, have not changed much in concept or construction since the early 20th century. Look at Nike’s newest Zoom Miler and compare it to the Adidas shoe worn by Emil Zapotek in 1948. You will see similar structure; minimal heel, some support and cushioning, lightweight upper, laces, and that’s about it. One thing that is apparent to the attentive is that racers wear different shoes than runners.

For clarity we are using the Hunter S. Thompson definition of a racer and a runner from his description of Honolulu Marathon participants (The Curse of Lono):

“The racers run smoothly, with a fine-tuned stride like a Wankel rotary engine. No wasted energy, no fighting the street or bouncing along like a jogger. These people flow, and they flow very fast. The runners are different. Very few of them flow, and not many run fast. And the slower they are, the more noise they make. By the time the four-digit numbers came by, the sound of the race was disturbingly loud and disorganized. The smooth rolling hiss of the racers had degenerated into a hell broth of slapping and pounding feet”

Racers are in contention to win. Runners are in contention to finish.

Runners wear the heavily cushioned weird looking heel contraptions commonly advertised as running shoes. Racers don’t. Racers use a forefoot or midfoot strike running technique and runners use a heel strike technique. This is why Thompson perceived a “smooth rolling hiss” when the runners came by – the anatomy of the foot was doing what it was built for, absorbing and dissipating impact forces through its extensive network of bones, ligaments, muscles, and tendons. They don’t need anything more than a basic shoe. This is in stark contrast to the “hell broth” of runners using the heel strike method. Landing on the heel bone is jarring and the only thing the forefoot can do after the heel hits is to slap down too. The bottom line is that those big fluffy running shoes let people, rather, encourage people to run with inappropriate technique.

Learning correct running technique is more important than your shoes. How would I describe appropriate running technique? Remember arches are built to support our weight during all ambulation. Spend some money on learning how to run on the balls of your feet. If you are a fitness professional, learn how to teach running. Learn how to correct bad technique through apprenticing with EXPERT running coaches or attending their seminars. Learn how to teach a variety of running events by attending a USA Track & Field coaching course.

Injury - Learning how to run correctly will do more to reduce injury rate than any shoe modification.

Don’t believe me? The following is just the most recent in a line of research articles beginning to indict modern running shoes as a source of injury not protection.

PMR. 2009 Dec;1(12):1058-63.
The effect of running shoes on lower extremity joint torques.
Kerrigan DC, Franz JR, Keenan GS, Dicharry J, Della Croce U, Wilder RP.

OBJECTIVE: To determine the effect of modern-day running shoes on lower extremity joint torques during running. DESIGN: Two-condition experimental comparison. SETTING: A 3-dimensional motion analysis laboratory. PARTICIPANTS: A total of 68 healthy young adult runners (37 women) who typically run in running shoes. METHODS: All subjects ran barefoot and in the same type of stability running footwear at a controlled running speed. Three-dimensional motion capture data were collected in synchrony with ground reaction force data from an instrumented treadmill for each of the 2 conditions. MAIN OUTCOME MEASUREMENTS: Peak 3-dimensional external joint torques at the hip, knee, and ankle as calculated through a full inverse dynamic model. RESULTS: Increased joint torques at the hip, knee, and ankle were observed with running shoes compared with running barefoot. Disproportionately large increases were observed in the hip internal rotation torque and in the knee flexion and knee varus torques. An average 54% increase in the hip internal rotation torque, a 36% increase in knee flexion torque, and a 38% increase in knee varus torque were measured when running in running shoes compared with barefoot. CONCLUSIONS: The findings at the knee suggest relatively greater pressures at anatomical sites that are typically more prone to knee osteoarthritis, the medial and patellofemoral compartments. It is important to note the limitations of these findings and of current 3-dimensional gait analysis in general, that only resultant joint torques were assessed. It is unknown to what extent actual joint contact forces could be affected by compliance that a shoe might provide, a potentially valuable design characteristic that may offset the observed increases in joint torques.

NOTE: Anatomy Without a Scalpel includes a section about foot and ankle anatomy and how it interfaces with shoe anatomy. A detailed and surprising history of how heels and cushioning evolved is also included.

I have been dissatisfied with the standard definitions of fitness since I began studying and teaching to exercise professionals almost 20 years ago. As a junior faculty member I felt compelled to adopt the party (ACSM etc) stance and deliver that convention to my students. The longer I spent teaching the material, the more I questioned it. The available definitions were general, nebulous, unmeasurable and poorly stated. I started pointing out flaws in the accepted definition of fitness in my classes in 2001. By 2004 I had come up with what I propose are the three basic elements of fitness – strength, endurance, and mobility. My definition of fitness was as follows:

Possession of adequate levels of strength, endurance, and mobility to provide for
successful participation in occupational effort, recreational pursuits, and familial obligation.

I felt that these three simple and measurable entities were representative of everything exercise – a KISS approach. I ran that definition by Mark Rippetoe and being astute as always, he remembered a nice article by Frank Booth suggesting that inactivity results in a mal-expression of the human genome resulting in many of our modern disease states. Mark then penned the additional clause included in the published version of our definition:

Possession of adequate levels of strength, endurance, and mobility to provide for successful participation in occupational effort, recreational pursuits, familial obligation, and that is consistent with a functional phenotypic expression of the human genotype.

I then went on to construct the paper we would submit to the Journal of Exercise Physiology in 2005. Mark cleaned up my writing and added clarifications and commentary. It took until 2007 for the paper to get published (http://faculty.css.edu/tboone2/asep/JLKilgoreJEPonlineApril2007.doc).

Now, in 2010, I am wondering if I can do a better job. Physical fitness is about what our bodies can do in the real world. We have simple strength standards that can demonstrate functional capacity. We have simple endurance standards. We have a variety of mobility standards (however this area can stand further attention and focusing). But can we really measure a “a functional phenotypic expression” of genes in a meaningful way for the exercise professional and the exercising public? Can evaluating our performance according to defined standards be an adequate indicator of gene expression? Is there any viable measure of what a genotype will look and function like outside of the laboratory? If, as the following article implies, there is a different genotype for power athletes, and as previous researchers have found there is a unique profile for endurance athletes, can we expect the average Joe to look the same as any athlete when they are fit?

J Appl Physiol. 2009 Dec 31. [Epub ahead of print]

Can we identify a power-oriented polygenic profile?

Ruiz JR, Arteta D, Buxens A, Artieda M, Gomez-Gallego F, Santiago C, Yvert T, Moran M, Lucia A.

Karolinska Institutet.

I plan to add some little snippets about fitness and science as things occur to me … that might be occassionally or obsessively – Lon

PS – Don’t expect smooth flowing and well constructed prose, this is brain to keyboard writing with no editorial.