Monday, February 1, 2016

Biomechanical Fitness

So, it’s the New Year and you thought it would be wonderful to get it started with the “100 runs in 100 days challenge”. Sounds like a great idea to begin the season with a bang by establishing that super run base. But how do you avoid the common scenario of breaking out as the Chinese New Year super-stud and end up as the subsequent Easter train wreck?

You have to establish your biomechanical fitness. Biomechanical fitness, you might say? Biomechanical fitness is the ability of your musculoskeletal system (bones, tendons, muscles) to withstand the demands of increased training load and stress. But why is this any different than regular fitness? That, my friend, is the crux of the problem and the source of so many early spring aches and pains that derail or delay your training goals.

A healthy cardiovascular system rapidly adapts to new stress. The classic study by Saltin demonstrates that sedentary people have the ability to increase their VO2 max very rapidly, beginning within a few days of exercise. The majority of VO2 max change continues to occur within the first several weeks of training, and for the most part, is nearly complete within the first couple of months (Astrand & Bassett). This rapid, cardiovascular improvement is easily perceived as improved fitness and encourages us to swim, bike, and run faster. And most of us allow our cardiac fitness to regulate the increase in our training stress. As we become less winded with workouts, we continue to go faster and farther over a relatively short time span. Within weeks we ramp up our weekly training volume and intensity to mid-season goals. Then crash… plantar fascial pain drops us to our knees in the morning, the IT band is stabbing the outside our leg, our knees are aching and we are ready for an early, unplanned break in our training program.

The reason behind the crash is that our musculoskeletal system’s ability to respond to training stress can’t keep up with our cardiovascular system. The tissues that make up the bones, ligaments, and muscles respond to increases in training stress through a continual remodeling process. This system is a balancing act of resorption and subsequent repair monitored by cells that build (–blastic) and cells that clean (-clastic) away tissue. These cells respond to training stress in a linear fashion until a ceiling is reached. Beyond that point, increases in training stress have a detrimental effect and the cells tearing down the tissues win the ongoing battle. The result is stress fractures and multiple forms of tendonitis.

Training stresses come in a variety of flavors and affect each musculoskeletal tissue differently. Accordingly, the injuries of specific tissue affect our training uniquely…the microtears resultant from eccentric muscle contractions are a necessary injury to build durability to withstand downhill and fast running. Excessive stresses on our bones, however, result in increased resorption of bone creating stress fractures.

Interestingly, bone responds more favorably to intensity and frequency than to volume. In particular, each individual’s bones adapts up to a predetermined level of exercise intensity, but only to that amount, and no further. It must be stated that intensity measured from the standpoint of evaluating tissue response is quite different than intensity used in the context of triathlon training sessions. Simple, easy running applies forces that are many times greater than our body weight. In research terms, this is considered “intense” and capable of producing the positive adaptive responses in bone remodeling. This is in contrast to the “intensity” we commonly associate with VO2 max efforts when discussing training zones.

The difficulty in prescribing exact amounts of volume and intensity is the variability in each individual in regard to their past health and training history. Additionally, the individual traits from whom the information is gathered during scientific research is variable and often times different than those we are trying to apply the information towards. What we would like to know is real world scientific data that would guide us in delivering the appropriate training stress resulting in tissue remodeling instead of tissue breakdown. What we have to settle with is less than perfect studies that evaluate “snap-shots” in time. I’ve selectively chosen a few studies that look at aspects of training stress that result in the tissue remodeling response that may be applicable in endurance sport training.

The most interesting information in this regard is data on the volume of training and its affect on bone density. Karlsson studied soccer player’s bone mineral density in relation to their training volume. His research revealed a linear correlation of increased training volume to bone mineral density (BMD) up to 6 hours exercise/ week. Exercise beyond 6 hours demonstrated very little increase in BMD in elite level athletes.

In evaluating session frequency, short-term basic science research suggests that 3 sessions/wk were nearly as good as 5 sessions in increasing BMD, but there was a 50% increase in BMD when sessions were increased to 7/week (Umemura). This same study revealed no improvement in double daily sessions over single daily sessions. However, the data by Umemura was studied over the short time span of 8 weeks and begs the question of what the eventual outcome of continued high training stresses beyond two months would be. In real life, the risk of injury undoubtedly is much higher at 7 sessions/week and is likely what we see in most athletes who present with overuse injuries a few months after beginning training.

Muscles respond to training stress more favorably than bones and ligaments. It appears that skeletal muscle that has been immobilized and atrophied responds to concentric exercise immediately without untoward effects (Venojarvi et al). Eccentric muscle activity, though quite damaging to muscles as indicated above, is a healed by the body fairly rapidly. In fact, six weeks following an eccentric event creating severe muscle damage, the recovered muscle demonstrates far less damage to a second eccentric event of the same magnitude (Clarkson). This consistent and positive response by muscle tissue to high training stresses does not demonstrate the ceiling effect seen in bone. It is important to note that extreme muscular fatigue is felt to predispose one to stress fractures, as muscles can effectively reduce strain placed upon bones in shielding fashion (Milgrom, Yoshikawa). This fact again points to bone, and perhaps the linking tissue between it and the muscle,as the weak link in tissues responding to training stresses.

Tendons, as indicated above, are the tissues that connect the muscle to the bone. It is well documented that tendons in individuals who participate in endurance training develop qualitative, and to a lesser degree, quantitative positive tissue changes. However, tendon tissue is metabolically less active than muscle, and hence, slower to respond to biomechanical stresses. These changes take several weeks to months to occur. Therefore, the tendinous muscle insertion into bone is the source of many overuse injuries, as the tendons are not allowed adequate to remodel to the stresses placed upon them.

In summary, I believe that training below the limits of your musculoskeletal system, rather than your cardiovascular system, will lead to fewer overuse injuries. So, what should the initial training load be? The answer to that question isn’t a simple one. The rate at which your musculoskeletal system can safely adapt to change is highly variable and is dependent up your age, sex, nutritional status, years in the sport, individual limiters, and age in which you begin training for the sport. But, assuming the limiting factor is your musculoskeletal system, the approach should be long-term and allow your tissues time to remodel. This time is likely in the 6-8 week range.

Some basic guidelines to follow are:

  • Build your base slowly. If you are completely deconditioned and not doing some form of daily exercise, alternate run/bike days with swim days. If you are doing some form of daily weight bearing exercise, increase frequency before increasing volume.
  • Use a modest heart rate cap as a ceiling to training intensity. This will limit the forces placed upon the musculoskeletal system and give them time to remodel and make qualitative changes to withstand the new stresses.
  • In doubt, back off early. Add recovery modalities and technique work to facilitate improvement and reduce training stress.

Best of luck and healthy training.

Jeff “Dr. J” Shilt, M.D.

Jeff Shilt MD is an orthopedic surgeon based in Boise, ID. He is a father, husband and Kona-qualifier. Jeff uses his triathlon and medical backgrounds to assist EnduranceCorner.Com. He will be sharing his experience at the EC’s Spring Training Camp in Tucson, AZ. For more details check out the Endurance Corner website.

1. Earnest CP, Lavie CJ, Blair SN, Church TS (2008) Heart Rate Variability Characteristics In Sedentary Postmenopausal Women Following Six Months Of Exercise Training: The DREW Study. Plos ONE 3(6): E2288. Doi:10.1371/Journal.Pone.0002288
2. Haskell, William L.1; Lee, I-Min2; Pate, Russell R.3; Powell, Kenneth E.4; Blair, Steven N.3; Franklin, Barry A.5; Macera, Caroline A.6; Heath, Gregory W.7; Thompson, Paul D.8; Bauman, Adrian9 Physical Activity And Public Health: Updated Recommendation For Adults From The American College Of Sports Medicine And The American Heart Association[SPECIAL COMMUNICATIONS: Special Reports] Medicine & Science In Sports & Exercise:Volume 39(8)August 2007pp 1423-1434
3. Saltin, B., B. Blomquist, J. H. Mitchell, R. L. Johnson, K. Wildenthal, and C. B. Chapman. Response to submaximal and maximal exercise after bed rest and after training. Circulation 38(Suppl.7):1-78, 1968
4. Åstrand, P.-O. and K. Rodahl. Textbook of Work Physiology. New York: McGraw-Hill, 1970, pp. 279-430.
5. Bassett, D. R., Jr. and E. T. Howley. Limiting factors for maximum oxygen uptake and determinants of endurance performance. Med. Sci. Sports Exerc., Vol. 32, No. 1, pp. 70-84, 2000
6. M. Venojärvi et al. / Pathophysiology 11 (2004) 17–22
7. M K Karlsson, H Magnusson, C Karlsson, and E Seeman The duration of exercise as a regulator of bone mass. Bone. 2001 January; 28(1): 128–132.
8. Umemura et al. High-impact exercise frequency per week or day for osteogenic response in ratsJ Bone Miner Metab. 2008;26(5):456-60
9. Clarkson, P. M., Nosaka, K., & Braun, B. (1992). Muscle function after exercise-induced muscle damage and rapid adaptation. Medicine & Science in Sports & Exercise, 24, 512-520.
10. Milgrom, A. Finestone, Y. Levi, A. Simkin, I. Ekenman, S. Mendelson, M. Millgram, M. Nyska, N. Benjuya, and D. Burr. Do high impact exercises produce higher tibial strains than running? Br. J. Sports Med., June 1, 2000; 34(3): 195 – 199
11. T Yoshikawa, S Mori, AJ Santiesteban, TC Sun, E Hafstad, J Chen and DB Burr The effects of muscle fatigue on bone strain. Journal of Experimental Biology, Vol 188, Issue 1 217-233
12. Magnusson, S. P.; Hansen, P.; Kjaer, M Tendon properties in relation to muscular activity and physical training. Scandinavian Journal of Medicine & Science in Sports. 13(4):211-223, August 2003.