The key to running fast on race day: Muscle Tension

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The key to running fast on race day: Muscle Tension

Getting fit is rarely the problem. It does not take a genius to get an athlete in good physical shape. The problem arises when we need someone to be ready to race at a specific time. We’ve all experienced a race where we completely fell apart from the start of the race and felt completely off, despite going into the race with training going well. How does it happen?

High School workout: cruise 200's

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Below is a workout video of the High School guys.  It's a simple intermittent workout where the focus is on rhythm.  I really like these short intermittent workouts as ways to introduce faster work without going over the edge.  It's also a great wed. or thursday workout before a weekend meet.  For most distance kids, it's just enough work to raise muscle tension so that the runners feel good on race day.  I've briefly mentioned muscle tension before, but I'll devote a full post to it in the future.  It's basically getting your muscles to feel right and be at an optimal resting length.

I'll post some analysis video of the workout in the future too.  Enjoy.
Music in video is by a friend's band (Clairmont) because last time I got my video removed for using mainstream music.




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How hypoxia/altitude works

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Below is a paper I wrote for school on a hypothetical training situation.  I thought I'd share it because it gives the underlying science of how altitude/hypoxia works.  Remember that it's a hypothetical, so it doesn't mean that I think intermittent hypoxic training works.  Generally, the exposure is way too short for a lot of long term adaptations.  Enjoy:



Altitude training is increasingly being thought of as a necessity for performance in a variety of endurance sports. The interest extends from athletes and coaches to the research community. In recent years there has been an emphasis on living at high altitudes and training at lower altitudes. This process has proved to be highly beneficial to performance in many studies (Wilber et al. 2007). However, due to the challenge of finding an ideal place to follow such a procedure, or the costly and time consuming procedure of spending 10+ hours a day in a stimulated altitude tent, other researchers are trying to find a way around this. The two main options seem to be living and training at high altitude for periods of time before spending the next block of training at sea level, or performing some workouts in a simulated hypoxic environment. Both of these options require training in hypoxic environments. Therefore, in this paper, the goal will be to discern the mechanisms behind intense aerobic training (done around the lactate threshold) in a hypoxic environment on the major hypoxic induced change that seems to elicit improvements in performance, an increase in red blood cell (RBC) mass via an increase in EPO.


Going to a hypoxic environment, whether natural or artificial, puts a new stress on the body causing the various systems of the body to react and adapt to its new environment. Training, even at sea level, similarly causes numerous changes to occur within the body as it attempts to react to the stress of the particular training load. Therefore, when exercising at altitude, the body not only has to respond and adapt to one stimulus, it has to respond to two, a training and hypoxic one. When these two stressors combine, the body’s primary objective becomes insuring adequate oxygen delivery to the working muscles. It accomplishes this through a variety of mechanisms.


First, let’s look at some of the larger changes that occur when training in a hypoxic environment. Two main factors will determine the physiologic and metabolic response; the intensity of the exercise and the level of hypoxia. Both of these factors will affect the amount of oxygen delivered to the muscles through a variety of factors. The level of hypoxia will first affect the hemoglobin oxygen saturation due to the decrease in the pressure gradient which occurs because of the reduction in the partial pressure of oxygen at altitude (Rusko 2004). This greatly affects VO2max, as each 1% drop in oxygen saturation below 95%, decreases VO2max by 1-2% (Dempsey and Wagner, 1999). This drop in oxygen saturation even occurs at moderate to low intensities, as was demonstrated in well trained athletes seeing drops even when training at 60-85% VO2max (Peltonen 1999). The drop in oxygen saturation is linearly related to the drop in maximal heart rate that occurs at altitude (Rusko 2004). Due to this drop in HR max, cardiac output is reduced at altitude.
The nervous system also plays a role in controlling the response to hypoxic conditions. Due to the decrease in oxygen concentration, muscle activity is reduced in hypoxic conditions (Peltonen 1997). This reduction in muscle recruitment may be a way of the CNS governing performance. It has been suggested that the decrease in VO2max at altitude is the result of the CNS controlling exercise, instead of the decreased recruitment being a cause of the reduction in VO2max (Noakes et al. 2001). What the exact controlling mechanism of the response of the CNS to hypoxic conditions is remains unknown, but the CNS does play a role in the overall response to training in hypoxic conditions.


All of these changes that occur while training in hypoxic conditions lead to an eventual decrease in oxygen levels in the blood, and a decrease in the muscles themselves. This reduction in oxygen concentration in the blood and at the muscular level is the stimulus for the mechanisms behind our eventual desired outcome, an increase in RBC mass. A reduction in oxygen concentration of the blood activates the Hypoxia Inducible Factor-1 (HIF-1) pathway in tissues where EPO production can take place (i.e. kidney, liver, the brain) (Stockmann et al. 2006).




HIF-1 is a main oxygen homeostasis regulator in the body. Two subunits, HIF-1α and HIF-1β, make up the HIF-1 complex. Under normal conditions, HIF-1β is present, but HIF-1α is constantly being degraded by the proteasome (Dery 2005). When oxygen levels are lowered, the degradation of HIF-1α is inhibited, this stabilizes HIF-1α. The stabilization allows for HIF-1α to bind to transcriptional coactivators and enter the nucleus of the cell. Here, HIF-1α binds to HIF-1β, forming an HIF-1 transcriptional complex (Marzo et al. 2008). This HIF-1 complex then binds to the Hypoxia Response Element (HRE) on the EPO gene. This in turn leads to EPO expression (Stockmann et al. 2006).


EPO then needs to be transported to and bind with EPO receptors. EPO receptors can be found on erythroid stem cells in bone marrow (Marzo et al. 2008). The binding to the receptor on the cell membrane results in a signaling cascade that results in the activation of the transcription factor STAT-5 and two enzymes, PI3K and MAPK. These enter the nucleus and induce transcription of specific genes that result in the inhibition of apoptosis, programmed cell destruction (Marzo et al. 2008, Jelkmann 2004). The end result is that this prevention of destruction of developing RBC results in an increase in RBC.


A larger RBC mass means a larger oxygen carrying capacity, which ultimately results in increased oxygen delivery to the muscles. Oxygen delivery has been shown to be a major limiter of VO2max (Bassett & Howley 2000). In studies done on blood transfusion of RBC in elite endurance athletes, increases in endurance performance and in some cases VO2max have been significant (Calbet et al. 2006). In one particular study done on elite athletes with an average VO2max of 80 ml kg−1 min−1, time to exhaustion in an endurance test and VO2max were both significantly increased (Buick et al. 1980). Therefore, increased oxygen delivery results in increased aerobic capacity and the functional change of improved endurance.
This leads to reasoning behind the selection of the training intensity. The idea behind the selection of a training intensity around lactate threshold is due to our desired outcome. In order to elicit the reduction in oxygen levels in the blood and muscles, the intensity needs to be high enough that it will do this. As was stated earlier, Peltonen et al. found that oxygen saturation was reduced at even submaximal intensities of between 60-85% of VO2max (1999). In well trained individuals, this intensity corresponds well to that of LT. Secondly, the intensity has to be low enough to allow for a significant volume of training to take place. The duration spent training has to be long enough to allow for activation of the pathway responsible for the desired adaptations. The signaling of the HIF-1 pathway under hypoxic conditions has been shown to already show increases in HIF-1α in the first 2 minutes. However, maximum HIF-1α did not occur until 1 hour of hypoxia, with max half times occurring at between 12 and 13 minutes. In addition, the reduction of HIF-1α with reoxygenation occurred quickly, also within 2 minutes, and was back to normal within 32minutes (Jewell 2001). These results suggest that a sufficient duration is necessary to elicit maximum gains via the HIF-1 pathway. Lastly, in a study by Zoll et al. they found that training at an intensity that corresponded to the ventilatory threshold increased mRNA concentrations of the HIF-1α, giving credence to the theory discussed above (2005).


In looking at the research and the pathways involved in EPO production and RBC increase, it can be seen that in order for hypoxic training to increase RBC mass a sufficient intensity and duration is needed. The intensity must be high enough so that a drop in oxygen saturation occurs, while being low enough so that sufficient time can be spent training at that intensity for the pathway to be activated. The selection of intensity and duration of training, along with the level of altitude, might explain why mixed results have been seen in hypoxic training.



Bassett, D. R. & Howley, E. T. (2000). Limiting factors for maximum oxygen uptake and determinants of endurance performance. Medicine and Science in Sports and Exercise, 32, 70–84
Buick, F. J., Gledhill, N., Froese, A. B., Spriet, L., & Meyers, E. C. (1980). Effect of induced erythrocythemia on aerobic work capacity. J Appl Physiol, 48(4), 636-642.
Calbet, J. A., Lundby, C., Koskolou, M., & Boushel, R. (2006). Importance of hemoglobin concentration to exercise: acute manipulations. Respir Physiol Nerubiol, 151(2-3), 132–140.
Dempsey, J. A., & Wagner, P. D. (1999). Exercise-induced arterial hypoxemia. J Appl Physiol, 87(6), 1997–2006.
Dery, M. C., Michaud, M. D., Richard, D. E. (2005). Hypoxia-inducible factor 1: regulation by hypoxic and non-hypoxic activators. The International Journal of Biochemistry & Cell Biology, 37, 535–540.
Jelkmann, W. (2004). Molecular biology of erythropoietin. Internal Medicine, 43, 649–659.
Jewell, U. R., Kvietikova, I., Scheid, A., Bauer, C., Wenger, R. H., Gassmann, M. (2001). Induction of HIF-1 alpha is response to hypoxia is instantaneous. FASEB J, 15(7), 1312-1314.
Marzo, F., Lavorgna, A., Coluzzi, G., Santucci, E., Tarantino, F., Rio, T., Conti, E., Autore, C., Agati, L., & Andreotti, F. (2008). Erythropoietin in heart and vessels: focus on transcription and signalling pathways. J Thromb Thrombolysis, 26, 183–187.
Noakes, T. D., Peltonen, J. E., Rusko, H. K. (2001). Evidence that a central governor regulates exercise performance during acute hypoxia and hyperoxia. J Expl Biol, 204(18), 3225–3234.

Peltonen, J. et al. (1997). Effects of oxygen fraction in inspired air on force production and electromyogram activity during ergometer rowing. European Journal of Applied Physiology, 76, 495– 503.

Peltonen, J. E., Leppavuori, A. P., Kyro, K. P., Makela, P., & Rusko, H. K. (1999). Arterial haemoglboin oxygen saturation is affected by F(I)O2 at submaximal running velocities in elite athletes. Scand J Med Sci Sports, 9(5), 265-271.
Rusko, H. K., Tikkanen, H. O., & Peltonen, J. E. (2004). Altitude and endurance training. Journal of Sports Sciences, 22:10, 928 — 945.
Stockman, C. & Fandrey, J. (2006). Hypoxia induced erythropoietin production: a paradigm for oxygen-regulated gene expression. Clinical and Experimental Pharmacology and Physiology, 3, 968–979.
Wilber, R. L., Stray-Gunderson, J., Levine, B. D. (2007). Effect of Hypoxic "Dose" on Physiological Responses and Sea-Level Performance. Medicine and Science in Sports and Exercise. 39 (9):1590–1599
Zoll, J., Ponsot, E., Dufour, S., Doutreleau, S., Ventura-Clapier, R., Vogt, M., Hoppeler, H., Richard, R., & Fluck, M. (2006). Exercise training in normobaric hypoxia in endurance runners. III. Muscular adjustments of selected gene transcripts. J Appl Physiol, 100, 1258–1266.

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Learning how to run.

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I thought this was pertinent given the focus on running mechanics and barefoot running.  It's an article I wrote for Running Times online a couple years back.  It's a simple and practical look at how to run properly.

Running seems to come naturally, so why should we worry about our technique or form? Ask many coaches and they will tell you that distance runners should not worry about how they run. On the other hand there are books on running technique popping up everywhere. So what is the truth?

The truth can be found by studying the best distance runners in the world. If you look at frame by frame shots of world class runners, the majority of them run "correctly". Distance runners neglect working on their form it is difficult to change the way one runs. Recently, I sat down with two highly successful coaches and spent four nights watching 800m and 1500m Olympic or championship races. The similarities between almost all of the top runners were astounding.

Knowing how to run is the most difficult part. In the discussion below I will stick with what can be seen through analyzing elite runners and biomechanical knowledge. The following is based on the ideas of world renowned biomechanics expert and sprint coach Tom Tellez and I am much indebted for the information he provided.


The Drive Phase

The running stride can be divided into two phases, the recovery phase, and the support/drive phase. The drive phase causes the propulsion needed to get you moving and starts with when foot contact is made. Once foot contact is made you allow the foot to load up and extend the hip downwards and slightly back to create the force. The extension of the hip is where your power comes from. It is helpful to think of it as a crank device which you crank from the hip.

When coming off the ground you are trying to optimize the vertical and horizontal components of the stride. With too much horizontal movement you will flatten out and not come off the ground, thus losing air time and stride length. Too much vertical movement will leave you high up in the air for too long and you’ll bounce along with a very short stride length. Thus, it is important to optimize the angle and extend your hip so that you have a slight bounce in your stride. A good cue for this is to look at the horizon. If it stays flat, you are too horizontal. If it bounces a lot, you are too vertical. An analogy is to think back to your high school physics class and remember how to get the greatest distance when firing a cannon ball. The angle has to be optimized.


When the hip is extended correctly it will result in the working of a stretch/reflex mechanism. This is best thought of as a sling shot where you stretch it back and then let it go and it will shoot back to its original position. When you extend the hip you are putting it in a stretch position. Once the hip has extended, it is important not to try to do anything unnatural with your feet or toes. A common mistake is to try to push off at the end of this phase with your toes. This will likely result in too much horizontal momentum.

The Recovery Phase

With this mechanism, the recovery cycle of the leg will happen automatically. The lower leg will lift off the ground and fold so that it comes close to your buttocks (how close depends on the speed you are running) then pass under your hips with the knee leading. Once the knee has led through the lower leg will unfold and should touch down right underneath you.

Trying to actively move the leg through the recovery phase is a common mistake and will only result in more wasted energy. The leg won’t cycle through as quickly as it would if you allowed the stretch/reflex mechanism to work. A common mistake is to try to lift the knee at the end of the recovery cycle. The knee will lift enough if you stretch the hip sufficiently.

The knee should be allowed to cycle through and lift, but it should not be forced. The best example of this can be seen in assisted walking experiments with spinal cord injury patients. Since the spinal cord has been damaged, these people do not have use of their lower body. However, if they are put on a treadmill and someone actively pushes their leg back, extending the hip to initiate the stretch/reflex, the injured patient’s leg will cycle through the recovery part of walking without assistance! In addition it has been shown that the recovery phase of running constitutes less than 15% of the total energy used during running, further supporting the idea that most of the work is automatic because of the stretch/reflex. Trying to actively lift the knee or pull the leg through is a waste of time and energy.

Once the knee has cycled through, the lower leg should drop to the ground so that it makes contact close to under your center of gravity or your hips. When foot contact is made, it should be made when the lower leg is perpendicular to the ground. The leg does not extend outwards like is seen in many joggers and there should be no reaching for the ground. The leg should simply unfold and drop underneath the runner.

Initial foot contact is made on the outside of the foot, but you can not really feel this. For practical purposes, in distance running the foot should make contact flat footed, or on the forefoot with the heel touching the ground afterwards. Slamming the heel into the ground first is a braking action that also causes a high impact peak. By hitting forefoot/midfoot the braking action does not occur and the impact peak that shoe companies spend lots of money trying to eliminate does not occur. In addition to this, the Achilles tendon acts like a spring as it stores some of the energy that comes from the ground contact and releases it when the contact is broken.

If you remain up on your toes and never let the heel touch the ground or are too quick with the foot/ground contact, you lose this free energy because you don’t allow the foot and Achilles to properly store and then release the energy. This mechanism happens because of the elastic properties of the muscles and tendons. Once foot contact occurs, you allow the foot to load up, then extend the hip and start the cycle all over again.

Your arms are another integral part of the picture. They should work with you and be coordinated so that they swing in opposition with your legs and from the shoulder so that your shoulders do not turn or sway. When your left leg is forward, your right arm should be forward. On the upswing the arm angle should be slightly less than 90 degrees with the hands in a relaxed fist. In addition to this the arms should not swing across your body on the upswing. On the backswing they should swing back to just above and behind your hip joint.



Learning how to run properly is a very important aspect in maximizing your performance. It will make you much more efficient, meaning less energy is wasted during your race. Also, a major benefit is that it will decrease your likelihood of injuries. While these are good reasons to perfect your running, the best reason is that the majority of the world’s best run correctly and it is no coincidence that they seem to be able to race faster and train at very high volumes of work with very few injuries.

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