Let’s say you are a 20:00 minute 5k runner so, depending on how old you are, you are at least half decent and generally ‘in a good place’. The dread of an illness or injury knocking chunks from your hard fought5k time is evident to many.
2:22 marathoner, Jeff Gaudette, gives these estimates:
|Days of not running||Reduction in fitness||What this means for a 20 minute 5k runner|
|1-7 days||Negligible reduction in VO2 max and muscle power||Now running 20:10|
|10-14 days||6% reduction in VO2 max and minimal reductions in muscle power||Now in 21:05 shape|
|14-30 days||Estimated 12% reduction in VO2 max and decrease in muscle power||Now in 23:00 shape|
|30-63 days||19% reduction in VO2 max and significant decrease in muscle power||Now in 24:00 shape|
|63 days or more||25.7% reduction in V02 max and significant decrease in muscle power||Now in 25:30 shape|
So, he’s done some research into the science and then extrapolated from that. So it’s not his fault but I would suggest the falls he suggests are greater than what would happen reality.
I just can’t see how anyone who can do 20:00 would fall to 23:00 after 2-4 weeks. I just don’t see that.
And after 2 months of inactivity falling to 25:30 I just can’t see it. That’s a quantum change.
Still, for those of you worrying about Christmas over indulgence then you’ve probably only lost 10 seconds. I’ll buy that.
Certainly cross training (eg swimming, cycling) or mild aerobic activity (if possible) WILL halt the decline. I’ve found that myself.
Here’s my own personal take on whether or not swimming will help your efforts to a faster 5k. Or for that matter how much your swim training will better your other tri-related sports if instead you are training for more than just 5k. Or you might be injured and worried about getting worse at 5k when out of run-training due to injury.
I train for 3-4 hours a week in the pool. So. Less than some but maybe a bit more than many.
Swimming will help, for sure. It can’t ‘hurt’, surely?! It will help your CV system and also to some degree with specifically preparing your legs for running and cycling. However running and cycling are what you need to do to get good at running and cycling. They are FAR more focussed at what you want to get good at……running and cycling.
Swimming is a more upper bodily focussed activity. Because your weight is supported by the water it is also easier for your heart to do its job. So a 1 hour swim workout is MUCH easier than a one hour run workout.
Also the results of TSB or other measures of training load might be skewed because of the cross training effect of swimming. Eg your figures that include swimming might suggest you are more fatigued than you really are.
Then again the benefit of a swim might be that you won’t have much to recover from whereas running hard is quite hard on your body and requires recovery time/down time.
So don’t bother swimming to help your 5k or duathlon training
…but it WILL help….a bit.
The exceptions to ‘avoiding’ swimming might be
- You enjoy swimming
- You have lots of spare time (hmmm!)
- You are considering triathlon, one day
- You are injured – there are water based rehabilitative/maintenance exercises for running
- As an alternative for a recovery session – actually swimming is very good for getting the gunk out of your legs after a hard session, even the next day it helps. It can have a sports-massage type effect I guess.
- Core stabilisation – if you have a weak core then freestyle, done properly, will strengthen it.
- You have your own pool, etc. etc. If I’ve missed an important one please let me know.
Then again it depends on how much you can push yourself in the pool.
I swim for 3-4 hours a week…but I do triathlon. My run times have plateaud since taking swimming seriously as I can’t devote the time that I once did to running.
Personally, if you want more variety in your running and/or cycling, I would go for weights to build strength or spend more time on your technique.
I’d be particularly interested if anyone thinks they have got faster at running because they also swam. So, for example, you run 3 times a week and instead of doing 4 runs a week you did that 4th session in the pool. So in that example you would argue somehow that your pool session was better for your running than another run session would be. As I say the swimming WOULD help but you could spend the time better…running!
- Out With The Old… (chatterdoesfitness.wordpress.com)
- Improving my cycling speed (bobbyofbrunei.wordpress.com)
- My first blog in the run up to my first triathlon! (tanyaallen2014.wordpress.com)
- The First Steps (fromrunnertotriathlete.wordpress.com)
- 2013 Triathlon Season In Review: The Swim (chatterdoesfitness.wordpress.com)
- The first and only time I ever truly thought I was going to die. (farewelltooldky.wordpress.com)
- On Training: Simulate Race Conditions (metrorunwalkspringfield.wordpress.com)
- Fatter, Faster, Fitter, Broken: 2013 a retrospective (blindcider.wordpress.com)
OK, after a few mini posts full of flippant comments here is something you might want to put aside 10 minutes to digest. It’s a bit sciencey.
Basically Kirk describes in a bit of detail some of the energy production in the body. A key part of endurance sport.
He then goes on to suggest that to stimulate the body’s responses to better do this energy production requires some fairly high intensity intervals. He tempers that by also saying that ‘full race’ type energy expenditure should also be trained for.
He doubts that long slow rides (in this case but the same applies to any endurance sport) can achieve as much.
I’ve taken and re-published Kirk’s article verbatim (I don’t normally do that).
Mitochondria: The Aerobic Engines
Words by Kirk Willett
Aerobic metabolism provides nearly all the fuel we use to run our bodies. We can only live for a few minutes without the constant energy supply derived from aerobic respiration. It is why we have to breathe! Endurance sport performance places a premium on aerobic respiration and its ability to convert the energy in food into a form our body can use. It may not be intuitively obvious, but even maximal efforts as short as seventy-five seconds are primarily powered by aerobic energy systems (Gastin, 2001). As a result, a primary goal of any endurance sport training program involves the building of one’s aerobic engine. On the most basic level, mitochondria are our aerobic engines.
Mitochondria are the microscopic components of cells where aerobic respiration occurs. Aerobic respiration is nothing more than the use of oxygen’s affinity for electrons to drive the chemical conversion of the energy stored in organic molecules into adenosine triphosphate (ATP), which is the form of energy our cell’s molecular machinery needs to run our bodies. Aerobic respiration is not the only chemical pathway for ATP production, but it is in charge of producing the vast majority of the ATP necessary for our life-sustaining processes and the performance of endurance exercise. In this article, I’ll take a basic look at mitochondria, the signaling which induces their biogenesis, and the practical training application of this information to cycling performance.
So what are these mitochondria that take care of our needs for aerobic respiration? They are a bacterium sized organelle with its own genetic material found within the cytoplasm of our cells. The endosymbiotic theory states that mitochondria were likely at one point an independent aerobic bacterium which found a home within a larger eukaryotic cell (Alberts et al., 2002). This partnership was then favored by natural selection and resulted in a proliferation of larger organisms which required and could utilize the metabolic power of aerobic respiration. This symbiotic relationship has evolved to such an extent and economized so much that some of the mitochondrial genetic material has been transferred to our nuclear genome, and the function of both genomes have become greatly interdependent (Virbasius, 1994). As an aside, we inherit our mitochondria and our mitochondrial DNA from our mothers due to their residence in the cytoplasm.
Mitochondria have two membranes; an outer membrane and an inner membrane. The inner membrane is folded extensively into structures called cristae, which create a large surface area for the chemistry responsible for aerobic respiration. This chemistry occurs on both sides of, and within the inner mitochondrial membrane. ATP is eventually produced on the inner surface of this membrane and is then sent outside of the mitochondria to fuel the cell’s energy demands.
Endurance exercise is a strong stimulus for the proliferation of mitochondrial enzymes. The increase in mitochondrial density is associated with an increase in the duration one can perform endurance exercise and the ability to spare total body glycogen stores (Fittz et al., 1975). Generally, more lipids are used to generate ATP as a result of the increased mitochondrial density in response to exercise. A large body of research suggests that the enhancement of mitochondrial density in skeletal muscle is a key component in the development of performance in endurance sport. In a general sense, building more mitochondria allows an athlete to function closer to their potential.
How does one ramp up mitochondrial density? First, let’s take a quick look at what tells mitochondria to up-regulate. Recent research has begun to identify the signaling that initiates the chains of enzymatic reactions which turn on the combination of nuclear and mitochondrial genes responsible for mitochondrial biogenesis. It appears that at least two significant signals exist, and that potentially these signals work together. Cytosolic calcium concentrations are one of these signals.
Research suggests that simply an increase in the concentration of calcium within the cells of skeletal muscle, something which happens with each muscle contraction, is capable of inducing mitochondrial protein synthesis. This increase in calcium is suggested to activate an enzyme called calcium-calmodulin kinase (CAMK) which then plays a role in the expression of mitochondrial biogenesis associated proteins such as PGC-1, NRF-1, NRF-2, and mtTFA (Ojuka et al., 2003). However, it appears that not all of the proteins necessary for mitochondrial biogenesis are activated by calcium signaling alone (Devin, 2004).
The other apparently essential and dominant signal necessary to incur mitochondrial biogenesis appears to be a reduction in cellular concentrations of high energy phosphates such as ATP and phosphocreatine. Decreases in the concentrations of these molecules are generally associated with the inability of aerobic respiration to maintain them during high intensity exercise. Research in this area suggests that a reduction in the cellular concentrations of these high energy phosphates activates an enzyme called 5’-AMP activated protein kinase (AMPK), which is closely related to CAMK. Activation of this enzyme apparently plays a critical role in mitochondrial biogenesis (Winder et al., 2000; Zong et al., 2002). Interestingly, this enzyme also plays a role in the genetic expression of vascular endothelial growth factor (Ouchi et al., 2005), a key component in the induction of angiogenesis or the development of the new blood vessels needed to supply mitochondria with oxygen. The current knowledge regarding the genetic signaling necessary for overall mitochondrial up-regulation suggests that it may be necessary for mitochondrial uncoupling to occur, or when ATP consumption outpaces ATP production during intense exercise (Devin, 2004).
Research has also been done which investigated mitochondrial enzyme concentration responses to different exercise stimuli. It has been demonstrated that in all muscle fiber types, exercise durations longer than about sixty minutes at controlled intensities, do not result in significant, additional mitochondrial enzyme densities (Dudley et al., 1982). This research perhaps also supports the notion that calcium signaling has a limited role in the induction of mitochondrial biogenesis given the rapidly diminishing returns when muscle contractions are continued. Dudley et al. also demonstrated that very high exercise intensities (approaching and exceeding VO2max) performed as intervals with cumulative durations of less than thirty minutes per day increased mitochondrial enzymes similarly to longer durations at lower intensities in both slow twitch and fast twitch muscle. This result suggests that mitochondrial density adaptations can be achieved in a reasonably duration independent manner (Dudley et al., 1982). The overall higher mitochondrial densities associated with the higher intensities outlines the potential need for mitochondrial uncoupling and the AMPK signaling, at least beyond the completely untrained state. It is interesting to note that Dudley et al. also discussed in the cited research that a limiting factor in the slow twitch muscle fiber respiratory capacity development measured at the extremely high intensities tested was likely the mode of exercise and not the intensity of the exercise. The test subjects were running at very high speeds which required extreme muscle contraction velocities which may have been beyond the ability of the slow twitch fibers to produce sufficient tension. Therefore, the slow twitch fibers may not have been overloaded enough to fully adapt (Dudley et al., 1982). On a bicycle, muscle contraction speeds are essentially a non-factor due to the use of gears. Interestingly, research has also shown that extremely short but intense exercise bouts (~ 30 second all out sprints) can increase the respiratory capacity of whole muscle and overall endurance performance (Burgomaster et al., 2005).
So what does this all mean in terms of practical application to the development of cycling training programs? First of all, it means that rides over an hour in duration will not necessarily improve mitochondrial density and the respiratory capacity of skeletal muscle. These generally lower intensity rides, which are often suggested to be an essential part of building one’s aerobic engine, are not inevitably more productive than an hour long ride at the same intensity. Intuitively, this does make some sense. If one can already meet the rate of ATP demand with aerobic respiration, as suggested by already having the ability to sustain such intensities for that long or longer, there is not likely to be much, if any, effective stimulus for mitochondrial development. Additionally, intensities approaching or exceeding VO2max, or in cycling power terms above approximately 95% of one’s 20 minute maximal power (20MP), appear to be required in order to elicit the largest concentrations of total mitochondrial enzymes. This is likely a combined result of additional motor-unit recruitment with increasing intensity and mitochondrial uncoupling in the progressively oxygen limited environment found when closing in on the limits of oxygen delivery. Aerobic metabolism of a variety of organic molecules is not up to the job of energy production, and more mitochondria are needed to fill the demands.
In general, it appears that in order to push mitochondrial densities to their maximum when building one’s aerobic engine, it would be wise to regularly include intensities which approach VO2max or harder, or about 20MP or harder, on a regular basis within an overall training program. Perhaps, this can reasonably be broken down into 2-3, one or so hour rides per week with 20MP+ intervals as long as possible for a given intensity, accumulating 10-30 minutes per day. If time and weather permits, this can be augmented by 1-2 rides per week of event specific training. This generalization obviously does not require a large time investment, but it does require that one train intensely. Long, easy rides or larger volumes of moderate intensity (ie. tempo training) do not appear to be required for maximal mitochondrial adaptation. These types of training have a limited ability to induce the metabolic stresses required to elicit additional mitochondrial and vascular development with perhaps the exception of a very short period if beginning from a completely untrained state
In particular, long, exclusively easy rides do not appear to effectively promote mitochondrial development and/or bolster the size of one’s aerobic engine. The process of building a bigger aerobic engine appears to be skewed towards an accumulation of high intensity training over time. Eventually though, it is largely the ability to deliver oxygen to our mitochondria which limits the rate at which our mitochondria can generate ATP from the variety of organic molecules that can be oxidized. Without adequate oxygen, the chemical reactions involved in aerobic respiration are impaired. The primary reason our aerobic engines can only be so big is because our cardiac output and our blood’s oxygen carrying capacity can only be so good!
Once one gets beyond engine size, there are other factors which can influence performance. One cannot expect to have reached their performance potential in extremely long endurance events on a diet of exclusively one hour rides with high intensity intervals. The targeting of an event’s expected, more specific demands, such as a combination of the total work and the distribution of that work, is likely to be of benefit. In at least the weeks leading up to target events, an additional 1-2 rides per week can augment the 20MP+ training discussed above. It may be that these days are combined with the 20MP+ work. For example, if one is targeting an event expected to require 4000kj’s, it would be wise to include some training in preparation for the event which approximates those demands, even if such training is not likely to be helpful in building a larger aerobic engine.
The next time you are out there training, think about your mitochondria sucking up that oxygen and powering your body. They are your friends…diligently providing the matrix a portion of the enzymes responsible for the chemical reactions which power your muscles. It would also be a good idea to think about how to efficiently get more of them when trying to build your aerobic engine as big as it can be. Generally, you have to go hard to make them grow! The bigger the engine, the faster one can go! Train hard, rest hard, train hard again, and have fun along the way!
Alberts, Bruce, Alexander Johnson, Julian Lewis, Martin Raff, Keith Roberts, and Peter Walter. (2002). Molecular Biology of the Cell (4th ed.). New York: Garland Science.
Burgomaster, Kirsten A., Scott C. Hughes, George J.F. Heigenhauser, Suzanne N. Bradwell, and Martin J. Gibala. Six Sessions of Sprint Interval Training Increases Muscle Oxidative Potential and Cycle Endurance Capacity in Humans. J Appl Physiol. Jun; 98 (6): 1985-90.
Devin, Anne and Michael Rigoulet. (2004). Regulation of Mitochondrial Biogenesis in Eukaryotic Cells. Toxicology Mechanisms and Methods. 14: 271-279.
Dudley, G. A., W.M. Abraham, and R. L. Terjung. (1982). Influence of exercise intensity and duration on biochemical adaptations in skeletal muscle. J Appl Physiol. Oct; 53 (4):844-50.
Fitts, R. H., F. W. Booth, W. W. Winder, and J. O. Holloszy. (1975). Skeletal Muscle Respiratory Capacity, Endurance, and Glycogen Utilization. Am J Physiol. 1975 Apr; 228 (4): 1029-33.
Gastin, Paul B. (2001). Energy system interaction and relative contribution during maximal exercise. Sports Med. 2001;31(10):725-41.
Ojuka, Edward O., Terry E. Jones, Dong-Ho Han, May Chen, and John O. Holloszy. (2003). Raising Ca2+ in L6 myotubes mimics effects of exercise on mitochondrial biogenesis in muscle. FASEB J. Apr; 17(6):675-81.
Ouchi, Noriyuki, Rie Shibata, and Kenneth Walsh. (2005). AMP-activated protein kinase signaling stimulates VEGF expression and angiogenesis in skeletal muscle. Circulation Research. 96: 338-346.
Virbasius, Joseph and Richard Scarpulla. (1994) Activation of the human mitochondrial transcription factor A gene by nuclear respiratory factors: a potential regulatory link between nuclear and mitochondrial gene expression in organelle biogenesis. Proc Natl Acad Sci U S A. 1994 Feb 15; 91(4):1309-13.
Winder, W. W., B. F. Holmes, D. S. Rubink, E. B. Jensen, M. Chen, and J. O. Holloszy. (2000). Activation of AMP-activated protein kinase increases mitochondrial enzymes in skeletal muscle. J Appl Physiol. Jun; 88 (6): 2219-26.
Zong, Haihong, Jian Ming Ren, Lawrence H. Young, Marc Pypaert, James Mu, Morris J. Birnbaum, and Gerald I. Shulman. (2002). AMP kinase is required for mitochondrial biogenesis in skeletal muscle in response to chronic energy deprivation. Proc Natl Acad Sci U S A. December 10; 99(25): 15983–15987.
- 4×4 Minutes of HIIT Per Week That’s All It Takes For Already Well-Conditioned Individuals to Stimulate Mitochondrial Growth ➯ 15% Increase in VO2Max, Peak & Mean Power (titaniumprox.wordpress.com)
- Cellular Respiration (scienceoutlined.com)
You’ve been giving this 5k thing a really good shot for 2 to 3 years. Of course you’ve improved. Probably quite a lot. Maybe you’ve gone from 32 to 22 or from 24 to 19 minutes. But over the last 6 months you haven’t improved much. Yet you running mate, who is the same age but does less training, is noticeably faster on a regular basis. You have a sneaky suspicion that they might still be improving.
Why? Because it is really annoying and you really want to know his/her secret.
They may have trained more when they were younger or have some genetic component that makes them better. But after 3 years you would have thought that would have evened out. Maybe.
If they are broadly the same shape as you then it can’t be that either.
You could mix up your training for sure. That would help.
But it’s probably your running technique. It could be one of many aspects of your technique that reduce your running efficiency. Over striding, heel striking, landing ahead your body, bouncing a bit. Any of those and more besides.
You need to incorporate drills into your workouts. Every workout if you are so inclined. Personally I prefer some form of plyometrics which also have a warm up effect. Plyometrics will correct some of your technical flaws over time. But not all. Watch a video on evolution running or chi running or POSE…they all say the same thing pretty much. You could do the ‘running school’ which is good but expensive but you can pretty much get the drills from the internet quite easily.
Maybe now is the time to believe those strangely named methods? Your call. Must be annoying seeing that label on the back of your mate’s shorts all the time though.
- Improve Your Running with Fartlek Training (running.answers.com)
I’ve been doing a bit of research recently (talking with my physiotherapist and a nurse at A&E – so it must be true) and found that there are some things we should be aware of when ‘treating’ injuries with Nurofen/ibuprofen.
Apparently whilst ibuprofen does reduce swelling it also reduces the body’s ability to repair itself.
1. Do not have ibuprofen in the evening/night, it restricts the body’s ‘healing time’ overnight
2. Do not have ibuprofen within 72 hours of an injury.
So where does Mr Beckham come in? Well when he had his famous metatarsal injury he WAS treated with an ibuprofen-like substance. That subsequently stopped the healing and viola (spell check, not me) his forever-weak metatarsal. Apparently he tried to sue but no-one was at fault as there was no research. So, being the generally good chap that he appears to be, he paid for the research. So now we know.
Thank you Mr Beckham. When my Achiles flares up again I know what NOT to do.
Instead take paracetamol (http://www.patient.co.uk/medicine/Paracetamol.htm)
Injury seems to be inevitable for many of us. It can be bad luck, over-training, a lack of strength training or stretching…or many other things. Anyway if/when it happens what do you do? At least regarding missed training.
If someone’s done you a plan (hint, hint I do personalised coaching!) then tell that person. Typically your training load will be fairly high/close to optimum, week-on-week. So having some time off will free up a bit of extra capacity in your body BUT certainly not enough to cram in every missed session.
for a couple of sessions or 3 or 4 I would take the hit and then get back on the program as if you’d done the missed sessions.
Same would apply for a week or two’s missed training. For each of those missed weeks I would add in ONE longer session that you missed into the forthcoming week.
Any more than that and you need to drop back down a notch and start building up again.
It also depends during which part of your plan your injury happens. Closer to race day the bigger the problem.
A couple of years back leading up to a duathlon I got a week long injury right in the peak training week. I biked through it but really upped my speedwork into my taper. Result? Bad. Although a couple of weeks after my race I peaked rather nicely. Shame, really.
- 5 Tips to Quickly Whip You Into Shape (cfhugob.wordpress.com)
- Back to the Matter: Bodybuilding & Strength Training (iamchampionaire.wordpress.com)
- Why I Lift… (realistfit.wordpress.com)
- First session of Winter Training. (andyrutle82.wordpress.com)
- What first – strength or conditioning (barbellianfitness.wordpress.com)
If you are a marathon runner you will say “Doh! of course it does”. If you are a novice you will probably say, “What??!!????”. If you’ve read around on forums a bit and read some books on endurance sports you’ll probably say, “Yeah ,that’s right. I think. Everyone says that who seems to know what they’re talking about.”
Or do they?
“Surely though strong muscles make you go faster” Well, yes and no. Think “Arnold Schwarzenegger” and you think “muscles” but you most certainly don’t think “marathon runner”. Then think Mo Farah, Chris Froome or Alistair Brownlee and you certainly don’t think ‘muscle man’. (Though perhaps you might with Michael Phelps).
So to be excellent at triathlon or 5k you certainly DO NOT need big muscles and by extending and reversing that argument, proper endurance training won’t make you a muscle bound hunk. (Ladies and also weight-loss seeking people remember that please and keep exercising!)
Going fast builds speed too!
So then you think that these guys are light and that their lightness is why they are fast. Well that’s not true either. Sure you have to be very light to ride a bike very fast up a hill but you also have to be powerful (power to weight ratio is very important in that cycling respect).
So it’s not muscle mass that makes us fast per se. So what is it?
Well here are some of the training zones and what benefits you get from them. It’s equally applicable to any endurance sport.
These Zones are Wattbike zones – I would normally refer to Friel Zones which are a bit different but broadly the same.
Zone Recovery: Does what it says. this will not make you go faster. But it will help you recover better in time to push yourself harder in your next session. If you have to do one session a week it wont be this one!
Zone 1: This is your base endurance. It helps you metabolise fat. IE you get better at eeking energy out of your fat stores so all the other energy stores you have last longer. Obviously good for long stuff like a marathon or IronMan. You can also do stuff here that improves your technical efficiency at run/bike/swim. For middle distance events like a standalone 5k you will need some of this.
Zone 2: Improves body efficiency notably how oxygen is used. So if you train in this zone then you get better at doing X essentially for ‘less heart beats’. That’s good!
Zone 3: Improves metabolism around getting energy from carbs. Improves the power you can maintain. That sounds good for 5k. Creates more slow twitch muscles
Zone 4: As with Zone 3 but also develops your lactate threshold (look for LTHR on this blog). Too much time here can introduce ‘staleness’
Zone 5: Develops VO2 max and anaerobic systems. Good for TT. Perhaps you wouldn’t have too many of these in your IronMan training schedule?
Zone 6+above: Basically sprinting.
So there you have it. Zones 2-4 are probably where you want to be most of the time. Those long slow runs in Zone 1 will NOT MAKE YOU FAST much in themselves. OK they might improve technical efficiency (which will make you faster) and in a sense any exercise will make you faster…but the best zones to make you fast are 2, 3 and 4. That is pretty much the consensus of elite endurance training in the 21st century (I do NOT claim to be an elite trainer!)
So people who claim long slow runs make you faster are NOT strictly correct. First of all you probably aren’t talking about the same speed for the same distance event…their slow might be a tad faster than you think and they may well be referring to Zone 2 from above. And there I would agree with them. But you can’t just throw the ‘slow’ word around without clarifying it otherwise a lot of people will ‘waste’ a lot of training time (well under-utilise, anyway). Secondly long slow runs won’t make you slower but other zones will make you faster, quicker.
The other issue is that speed gains from slower speed training take longer to come by but, on the positive side, they stay for much longer (hence base building). So when you peak, say, 3 weeks before your race you will be doing fast stuff that has a quick payback but which you will lose relatively quickly. You can do that fast stuff because you have already done the base building work which gives your bod the capacity to do the fast stuff better.
Another issue is that the longer the event the more important the slower training zones become.
That’s it really. Train smart.
Way before your race you would still do the odd Zone 4 session; close to your race you would probably not bother too much with Zone 2 stuff.
Too complicated?: I can produce a customised training plan for you.
- Trying To get in shape? hither’s How (brendafulcher13.wordpress.com)
- Better Fitness for Faster Running! (stephanbel.wordpress.com)
- Why going slow builds speed (the5krunner.com)
- Muscle Performance – Genetic Factors (23andme.com)
- Trying To pay back inch Shape? Here’s How (brendafulcher13.wordpress.com)
- Periodization: you can’t train the same way all of the time. (marciaruns.wordpress.com)
- Marathon Running (drumstutor.wordpress.com)
- The perfect sports massage (mahisolomou.wordpress.com)
- The Difference Between Fast & Slow Twitch Muscle Fibers (toddpetersonblog.wordpress.com)
According to USA Triathlon, an athlete must meet one of six criteria to apply for elite status: finish within 8 percent of the winning elite time in three USA Triathlon-sanctioned events; finish in the top 10 and within 8 percent of the winner’s time at the International Triathlon Union Age Group World Championships; finish in the top 10 in the amateur field at the Ironman World Championship; finish in the top five and within 8 percent of the winning time at the USAT Age Group National Championships; finish in the top five and within 8 percent of the winning time at the USAT Collegiate National Championships; or finish in the top three in the amateur field at an Elite Qualifying Race.
So in the UK
1. Finish in the top 10 and within 8 percent of the winner’s time at the ITU AG Group World Championships
2. Finish in the top 5 and within 8 percent of the winning time at the ETU AG European Championships
3. Top 3 in the National Championships AND within 5% of winning time of your AG’s elite winner (as defined by above 2 criteria).
Thoughts? I invented the last one! but it seems reasonable.
- Again a Brownlee is triathlon champion (utsandiego.com)
You’ve been running a while right?
OK, good. Go get an old pair of running-only shoes. Not day-to-day shoes.
Turn ‘em upside down and look where they wear out. If the heel is wearing out then you heel strike. If the bit under where your toes start is wearing out then you strike mid-foot or forefoot.
So no argument there please. I don’t care what the video analysis might say about you. The evidence is literally staring you in the face from your shoes.
Note we pretty much ALL heel strike whilst walking.
There are undoubtedly great runners who heel strike.
However if you heel strike then your foot has to roll down from the heel and onto the front of the foot before you push off. That takes time. Not a lot of time. But time nevertheless. If you heel strike you cannot escape that obvious fact. That wasted time multiplied by the number of steps you take is a LOT of wasted time. Heel striking is slower.
IT might be faster for you now. But it IS slower than it otherwise could be. It is slowing you down.
There are also other factors at play where heel striking acts as a cushioning brake as the mass of your body move from behind the heel to in front of it. This weight transfer process also take its toll on the knee. It’s probably why you get knee or hip injuries.
Fore-foot or mid-foot (flat-foot) striking requires less contact time with the ground. It more naturally has more of the weight further forwards and more naturally engages more muscles groups better. It puts a bit more strain on your calves. So you can’t change overnight without building up your calf muscles.
You’ve probably got little calf muscles as well right? Yep. That’s because you heel strike (often!). More proof.
Start to use those poxy calf muscles for midfoot running too much too soon and you WILL have all sorts of calf, soleus, achillees problems. And these can take a LONG time to heal.
It might take a year to gradually transition. At the end of that you will probably be no faster but you will be in a good place to GET FASTER WITH LESS INJURIES.
Go for it.
- Barefoot Running Injury Risk (bodyactive-nation.co.uk)
- I-phone, android, barefoot, blue shorts (monkeyraces.wordpress.com)
- Thoughts on minimalist running (areweanycloser.wordpress.com)
- Foot strike, thinking backwards? (camfordclinic.wordpress.com)
- Running (onthegofitness.wordpress.com)
- Shoes for Happy Feet (teambrioche.wordpress.com)