January 2018

Monthly Archives

Metabolic Testing – Now Available!

The evolution of training is such a fast moving topic the last few years its fun to watch. Smarter software analysis tools keep arriving to help coaches and athletes see a more comprehensive view of their training and, increasingly, individualized physiology. One of the smarter and more interesting, to me at least, programs comes from INSCYD. They have a testing protocol and some serious computational back end heft to support in depth analysis via models for things like lactate clearing curves, optimal recovery power, as well as physiological profiles expected from power based training.

Among their development partners has been Bora Hansgroh, home of World Champion Peter Sagan, and a few others.
Their goal was to create an accurate map of the physiological systems based on a couple of notable variations in the data collection protocol and a proprietary algorithm that they say tests above 95% for accuracy vs lab testing and invasive protocols. This is really inventive stuff in that it allows for a complex and comprehensive profile of you as an athlete via non-invasive, power based testing!

I’m pretty happy to be working with these guys as I think they bring a new approach that fits nicely with the research. To that end I’m doing a start up special on the testing package for $150.00. Normally it’s $225.00.

There are 10 spots a day available at this rate thru Feb 4th. I’d be so pleased if you shared this information with those you think might find it worth doing.

SIGN UP HERE!

or share the link: https://www.eventbrite.com/e/personal-metabolic-testing-special-launch-pricing-tickets-42650139716)

Here is a partial sample of the data sets:

And some insight from the report:

“All graphs above visualize important endurance metrics, in steady state condition, in relation to the intensity (power or speed).The upper left graph shows the metabolic demand and oxygen uptake (in steady state). The oxygen demand (also named VO2tot – dark blue curve) increases with the intensity (speed or power). The oxygen demand is similar to the energy demand needed at a certain intensity. However it is converted into ml/min/kg of oxygen instead of using kJ or a similar unit of energy. Therefore the increment of oxygen demand in relation to the intensity shows the efficiency. The light blue curve shows the actual oxygen uptake (VO2) in steady state conditions. The unit is ml/min/kg – oxygen normalized to the body weight. As can be seen, at lower intensities, the actual oxygen uptake almost matches the oxygen demand, thus the needed amount of energy is almost completely covered by aerobic metabolism.At higher intensities however, a gap is opening up and the oxygen uptake cannot match the demand. This gap is shown as the light blue area, and shows the amount of energy (or more precisely oxygen) which needs to be covered by glycolytic metabolism. The lower left graph shows: Gross lactate clearance rate (blue), the lactate production rate (red) and the lactate concentration (yellow).During exercise lactate is be cleared from the muscle cell by aerobic metabolism (oxidation). Simplified, lactate gets burned and acts as a fuel in the aerobic metabolism. Therefore, the rate at which lactate can be cleared is directly related to the actual oxygen uptake. You will notice that the shape of the blue lactate clearance curve looks similar to the oxygen uptake curve above.The red curve shows the actual lactate production. As lactate clearance, the unit here is mmol/l/min. Look for the crossing point of the lactate production (red) and the lactate combustion (blue) – this is intensity of anaerobic threshold. At any intensity below, it can be seen the possible combustion of lactate is higher then the actual production. At any intensity above this crossing point, the lactate production rate is higher then the possible combustion rate, which results in an accumulation of lactate.The yellow line shows the lactate concentration in steady state conditions – this is a result of the production and clearance rates described above. Steady state means that time is infinite, and therefore shows the concentration that lactate concentration (in mmol/l) would reach. At anaerobic threshold – also known as maximum lactate steady state, the curve increase to infinite as no steady state can be reached anymore. The top right graph shows the lack of pyruvate (or lactate, grey line) and the actual lactate accumulation (purple). If you look back to the lactate production and lactate combustion, you can identify the gap between both at intensities below anaerobic threshold (below the crossing point of both). The gap between gross production and gross clearance is the lack of pyruvate. Or in other words: the amount of lactate that could be cleared additionally to the gross production. Lack of pyruvate curve is shown in mmol/l/min of lactate clearance. It shows the ability to recover from lactate accumulation in relation to the intensity (speed or power). At anaerobic threshold it runs to zero – the aerobic metabolism is saturated with lactate and no additional lactate can be combusted.The purple curve shows the rate of lactate accumulation. This occurs at intensities higher than anaerobic threshold. The steeper the curve, faster lactate accumulation at any given intensity.”

Thanks!

Matt


Busy

Having a plate full of things to do is invigorating and terrifying!

District CX is tomorrow and I still have to get the set-up set up, glue a tire, charge the battery, and I’m sure a dozen other small things that I’ll forget til the last minute.
Early Birds start on Sunday morning; Always a full day of fun in Fremont, you should come out!

National CX is next Thursday in the midst of a run of mayhem that is typical for a January, albeit a bit different this year…

Monday night team meeting – really important, lots to cover – better get started on that.
Tuesday head to Reno for Nationals (presuming I manage to dodge jury duty), set up tents, prep bikes, hang with teammates, pre ride, eat, rest and recover
Wednesday – Nationals race support, pre riding again, etc
Thursday race like the dickens, party like a rock start Thursday night
Friday rally down to Santa Maria for VeloSport Junior camp.
Saturday / Sunday Work junior camp Saturday and Sunday, rail home for..
Monday Team Ride
Tuesday – finally reset into the training year with my personal training clients

I love my job!

Another archive article today, stepping all the way back to October 2014 for this look at Anaerobic Power and W’

This past weekend the Cyclo-cross World Cup kicked off in Valkenburg with a commanding win by Lars Van der Haar, after a typically audacious start for the young gun. The ability to sprint for the hole shot by LVdH and other young stars like Mathieu Van der Poel are impressive and, surely, taxing, but how taxing are they?

One of the critical aspects of success in cyclocross is the ability to repeatedly hit the gas in short and crisp efforts. Ranging from the charge off the line to the myriad of 5 and 10 pedal stroke punches out of corners, and on out to those 10-60 second efforts that define cross racing, you are tapping your anaerobic capacity, or W’ (pronounced W prime) from the start of the race, so let’s learn a little bit more about it.

What Is W’
Over the past decade or so, lactate threshold, and the mechanisms therein, has risen to be the de facto gold standard of performance coaching and analysis. It is often discussed in both lay and scientific literature, and has been written about time and again by myself and others in the Toolbox family. Consider that a high lactate threshold power (or functional threshold power (FTP), maximal lactate steady state (MLSS), or critical power (CP)) really sets the entry point for success in racing, if yours isn’t sufficiently high, you probably won’t be in the pack to make the final selection.

Conversely, anaerobic efforts – those short and demanding 20-90 s efforts – while often discussed as to their importance, have been a bit of a black box. Thankfully, it is coming more and more to the front of the discussion of what drives performance. This makes sense, really, when you think about racing. After all, rare is the breakaway where you ride everyone off your wheel while doing a steady threshold effort. Whether on the road or in CX, eventually you need to make one or more supra-threshold effort to free yourself from the pack for that winning break or sprint.

The “Match”
Watching the first 5 minutes of a pro cyclocross race, it’s easy to believe that they sprint the entire time. And while their pace is likely a sprint to you and I, the reality is that an individual’s true capacity for those supra-threshold efforts is fairly limited. Often referred to as Anaerobic Work Capacity or more currently W’ (W prime), it is a short term energy source that uses non-aerobic (non oxygen) pathways that fills the gap when you hit the gas.

Essentially, anaerobic glycolysis is a 10 step process that very quickly produces energy to meet the demands of exercising muscles at a rate that aerobic metabolism simply cannot match. We typically speak of efforts in the 20 s – 2 minute range as being primarily ‘anaerobic’.

Indeed, in the nomenclature of power based training we often have an “anaerobic” zone that is generally greater than 120% of your threshold power, and this zone of training is used to try and raise both the absolute size of this reserve, and your ability to recover from those efforts. It’s a very useful system, unfortunately, the trade off is that there isn’t very much of it. You’ve likely heard this in recent coaching parlance as your “box of matches” in terms of saving those matches during races and increasing the number and burn power of those matches during training.

How Many Matches?
In 2012 Skiba et al, sought to model W’ use during bouts above Critical Power (roughly equivalent to the functional threshold power you likely have heard about – the power you can sustain for about an hour*), followed by recovery at different workloads. Each effort involved a 60 s hard interval followed by a 30 s recovery interval, with each recovery phase at a different intensity ranging from easy (20 Watts) to moderate, then hard, then severe.

They established a few notable observations:

• The absolute size of W’ in their subjects ranged between 14 and 28 Kilojoules, with a mean of 21 Kj. Recall that a Kilojoule is simply a thousand joules, and a joule is equal to watts x seconds (J= W x s). So when you are doing 333W for 3 seconds you’ve used 999 joules, or roughly 1 Kj! That’s not a very big basket, about a minute all-out!

• They affirmed that W’ began to be immediately depleted once power rose above Critical Power and that reconstitution of W’ did not start until subject power was under CP.

• The time of reconstitution (Tw) was impacted by the intensity of the recovery. Indeed at the 20W recovery level, reconstitution ranged between 370-380 seconds, while it was 452 seconds for the “medium” recovery effort and averaged 580 seconds for the “hard” recovery interval. The “severe” recovery constant averaged over 7000 s, indicating no W’ reconstitution within the 30 s recovery phase of the trial.

Building Your Matchbox
So how can you use this information in your daily training and racing? First, recognize that your stores of anaerobic energy are likely smaller than you thought they were. This again highlights the critical strategy of conserving your energy as much as possible while racing. Easier said than done, but that should always be your overriding goal until you make your decisive move.

When you, or your coach, are designing “AWC/W’” workouts, maximize your recovery! If your workout goal is to truly emphasize your W’ stimulus, then it makes no sense to start your next interval until you are recovered from the previous one. Recall that, even at the 20 watt recovery level, it still took roughly 6 minutes for your W’ system to reset itself. On the other side of the coin, when you are doing W’ work, the key is to go hard enough to tax the system, and mix the durations – remember it’s a range of effort.

Finally, focus on threshold! Skiba et al demonstrated that those with a higher VO2max had significantly faster reconstitution than those with lower aerobic capacities. They surmised that this was due to the larger “gap” between their critical power and recovery power, essentially they had a bigger tank to draw from for their recovery. So work to get your threshold up as high as possible.

A final observation from the studies was the idea that fiber type and creatine phosphate levels may have a significant role in recovery, possibly indicating a different recovery mechanism between the two fiber types. That is a compelling tidbit and I hope to see more research on that.

Summary
Anaerobic level efforts, those twenty to one hundred and twenty second efforts that hurt so much, can be viewed as the crucible in which results are derived. While functional threshold power gets you to the party, ability to deliver supra-threshold efforts during crunch time keeps you in for the win.

Unfortunately, each of us possess a relatively small amount of W’ and the reconstitution of it takes a very long time. On average, in the Skiba study, participants had less than 25 Kilojoules of available anaerobic capacity, and a 30 second all out sprint took an average of 333 seconds to recover from even when power was exceptionally low (20 watts). Higher recovery power took even longer.

The practical applications of this are notable when you begin to look at your performance in events like cyclocross, with a high anaerobic demand profile. Train the systems you need in a manner that will maximize your return, and don’t neglect your threshold power.

References
Gastin, PB. Energy system interaction and relative contribution during maximal exercise” Sports Medicine, 2001: 31(10): 725-41

Noordhoof et al. “Determining Anaerobic Capacity in Sporting Activities” Intl Journal of Sports Physiology and Performance, 2013, 8, 475-482

Skiba,et al. Modeling the Expenditure and Reconstitution of Work Capacity Above Critical Power” Medicine & Science in Sport and Exercise, 2012; 1526 – 1534

*It is important to note that although each method results in a similar estimation of W’ capacity, they go about it from very different approaches and shouldn’t necessarily be used interchangeably as the protocols are unique.


On belt buckles and archives

When I was in ninth grade I lived in a little tiny town in Southern Colorado.

La Veta was all of 600 people, zero stoplights and only a couple of paved streets. It sits at the base of the Wahatoya, two 13,000 foot peaks just south of town.

We played 8-man football against teams like Simla, Sierra Grande, and Aguilar. Most everyone played both ways. I was the 105 pound freshman running back and defensive end who was mostly used as fodder for the varsity on practice days.

Wrestling was a better fit and my coach was also my history teacher. I spent the last couple of months of school that spring living with Mr Denton, his wife and two kids, a few miles outside of town where the wind seemed nearly always on. My mom and step-dad had moved to Colorado Springs for a new job, but didn’t want to take me out of school. I remember having elk steak, going to the Southern Baptist church on Sundays and helping with finish work on Rodeo belt buckles. I learned to rope hay bales in anticipation of roping calfs sometime and I burned the crap out of my index finger and thumb grabbing a hot muffler off of a lawn mower or splitter.

Mr Denton had a side business making custom order belt buckles. He was actually quite an artist, quintessential cowboy painter. His buckles were sought after far and wide, which meant lots of finish work on buckles. In total I probably did less than 8 hours in those weeks, but it was memorable in that I saw real craftsmanship on display, and man I wanted a buckle! Thing is, you gotta earn a buckle. His kids had a slew of buckles for barrel riding, roping, etc, I’m sure. He didn’t offer and passed before I could order one as an adult. I still want a buckle.

Cowboy Legend Jim Shoulders Championship buckle is amazing. Don’t know the artist, but Mr Denton was on par I know.

I have written a bunch of stuff over the last 10 years or so, this is an archive post – a combination of two articles from PezCyclingNews (1, 2) a few years back. Interesting to see some of the current iterations of training metrics and analysis options coming on line. Analysis stuff like INSCYD and WKO4, Best Bike Split, etc…then mix in the rise of aerodynamics/biomechanics on the fly and more telemetry to boot!
This looks at some of the science behind the terminology and factors influencing “fatigue”.

Part 1 –

Lactate and Lactic Acid production are routinely offered as the seemingly natural cause and effect parameters that cause fatigue and decrease in performance, but are they really the source of the problem?

By Matt McNamara

If you’ve read anything about training in the last ten years you’ve probably come across the idea of Lactate Threshold and a discussion of how lactic acid production limits performance. The argument often goes something like this:

“As exercise intensity increases lactic acid production rises at a rate that, eventually, overwhelms the bodies ability to buffer this build-up and a decrease in performance naturally follows.”

Heck, I’ve repeated the mantra myself time and again over the years, despite KNOWING that it was an incomplete explanation of what actually happens. The truth is it provides a simple, though not wholly inaccurate, way to explain the well-documented trends of decreasing performance with increasing lactate concentrations. The idea of cause and effect just sort of fit well. So rather than perpetuate mediocre understanding, let’s jump in and learn a bit more:

A Brief, Albeit Incomplete, History
Lactic Acid was first isolated by Swedish researcher Carl Wilhelm Scheel from a batch of sour milk in 1780 (hence the commonly used term “lactic” instead of the far sexier formal name of 2-hydroxypropanoic acid, but I digress). Otto Meyerhoff and Archibald Hill, Nobel Prize winners in 1922, demonstrated that Lactic Acid was actually produced as a side reaction of Glycolysis, a primary metabolic pathway that converts carbohydrate/glucose into pyruvate, in the process converting energy into ATP through a 10-step set of reactions. In the absence of oxygen this conversion is sustained with Lactic Acid. This anaerobic process releases a proton (H+).

This was a key finding as it seemed to offer a cause and effect relationship between lactate production (lactate is, essentially, the salt or base of Lactic Acid) and the extended concept of Lactic Acidosis, or a decrease in pH that results from the release of protons in the system (cell or bloodstream).

This cause and effect relationship was taken as fact by researchers throughout the 20th and into the 21st century. However, in reviewing past and current research, Robergs et al (2004) have shown that there was no actual empirical evidence to support the cause/effect relationship; rather it was largely based on statistical correlation and the reputation of the Nobel Laureates Meyerhoff and Hill (which was richly deserved, I might add).

So, if the cause and effect nature of lactate production and acidosis is not an accurate portrayal of the role of Lactate in the onset of acidosis, and therefore performance, what is?

Debunking Lactic Acidosis
In 2004 Roberg, et al wrote an extensive review of the literature that sought to debunk the long-standing cause and effect relationship between lactate production and metabolic acidosis. Their sixteen page review takes an exhaustive, and somewhat intimidating, look at the true biochemistry of metabolic acidosis.

For example they detail the role of the phosphagen, glycolytic and mitochondrial systems in producing ATP and the differences in how each manages any released protons. They also note the difference in the nature of the proton release in glycolysis depending on whether the carbohydrate was derived from blood glucose or muscle glycogen. Glycogen is less acidifying to muscle during intense exercise.

Roberg then goes on to detail the many benefits derived from lactate production including the alkalizing effect of LDH, Lactate Dehydrogenase, or that it then circulates away the lactate to other areas that need it including the kidney, liver, and heart, for use as a substrate.

Finally, they looked at the role of nonmitochondrial ATP production, via research by Gevers in 1977 and 1979. Gevers established that metabolic processes other than LDH might contribute to the removal of protons in the form of the turnover of ATP via glycolysis. In other words that non-mitochondrial ATP production was likely responsible for metabolic acidosis.

But here’s where lactate threshold based training comes in

Training Threshold
Lactate threshold based training is a great tool. More specifically using the combination of a powermeter and a threshold based training approach is a highly effective way to manage your training.

Andy Coggan recently hosted a webinar on Lactate Threshold via USA Cycling. In addition to a comprehensive look at the establishment, definitions, and relationships of training around one’s lactate threshold. Among the cool takeaways

The first is to see terminology like Lactate Threshold, Maximal Lactate Steady State, Onset Blood Lactate Accumulation, etc as talking about roughly the same range of intensity. It’s likely going to be between about 80-90% of your VO2max for sustained periods of time. This will raise your general metabolic fitness. Further specialization is ideal for targeting specific race preparation

Coggan also noted that it has been shown in a wide array of studies that many other factors and processes contribute to fatigue. Things like epinephrine/norepineprine (adrenaline/noradrenalin), plasma potassium, and cortisol level, etc. often show a similar threshold type profile to that of lactate.

Abiss and Laursen did a comprehensive look at fatigue in 2005. Models to Explain Fatigue During Prolonged Endurance Cycling looked at no fewer than 10 different models of fatigue including the cardiovascular/anaerobic model, neuromuscular biomechanical, thermoregulatory models, and several others. Their net conclusion is that any number of systems may contribute to fatigue in a specific way for a specific situation, but in general the limitation of the system is derived from oxygen delivery to the muscles. Since we established above that metabolic acidosis is not derived from lactic acid, but that lactate production is an important contributor to oxygen delivery, it time to embrace those burning quads and get to work improving that lactate tolerance.

References:

1.Abbiss, Chris, Laursen, Paul – Models to Explain Fatigue During Prolonged Endurance Cycling. School of Exercise, Biomedical and Health Sciences, Edith Cowan University, Australia. 2005
2.Coggan, Andy – Explaining Lactate Threshold. Webinar Presentation. 2010
3.Robergs, Robert A., Ghiasvand, Farzenah, Parker, Daryl – Biochemistry of exercise-induced metabolic acidosis. Am J Physiol Regul Integr Comp Physiol 287: R502–R516, 2004

Part 2 – Lactic Acid Explained
It is a common misnomer that Lactic Acid is the cause of fatigue and cessation of high intensity exercise, yet training plans built around your individual Lactate Threshold are highly effective despite the debunking of the “Lactic Acidosis” rationale. Let’s learn why…

By Matt McNamara

Last month we looked at the intricacies of Lactic Acid/Lactate production and its role in limiting performance. The short summary of that article is to say that Lactic Acid production is NOT the limiter in high intensity exercise, and the science behind that belief was founded on an inferred cause and effect relationship between lactate production and cessation of exercise that, ultimately, proved to be untrue.

While lactate production may not be a limiter, it is clearly a marker of overload and does play a role in athletic development and performance. Lactate Threshold based training, when paired with use of a powermeter, is seen as the gold standard for endurance based performance improvement. So let’s explore the real meaning and value of Lactate Threshold based training.

What Does Lactate Threshold Really Mean?
First off, Lactate Threshold is commonly defined as “the exercise intensity at which lactate production exceeds lactate removal, and thus begins to accumulate in muscle and hence in the blood.” Unfortunately, the definition of what constitutes “Lactate Threshold” is highly variable.

Many researchers establish threshold as the point when lactate concentration rises 1 mmol above an exercise baseline. Others use a fixed value, for example 2.5 mmol per liter, as the threshold point. Still another approach is to use D-max which takes the mid-point between the baseline and maximal lactate concentrations. In the end the most important consideration isn’t the way threshold was determined, so much as the concept of Lactate Threshold (and associated terms) as illustrating the non-linear relationship between lactate concentration and exercise intensity.

It is also important to acknowledge that terms like Maximal Lactate Steady State (MLSS), Onset Blood Lactate Accumulation (OBLA), Ventilatory Threshold (VT), Individual Anaerobic Threshold, Critical Power, etc are talking about roughly the same range of intensity. Each of these, MLSS and OBLA in particular, correlate well with the power training concept of Functional Threshold Power (FTP), which is itself defined as your maximal sustained power output for approximately 60 minutes.

Now that we have a clearer idea of what is meant by Lactate Threshold, and we know that Lactic Acid is not the cause of fatigue, let’s look at other factors that might play a role.

Other Causes of Fatigue
In 2005 researchers from Edith Cowan University in Western Australia set out to do just that. Models to Explain Fatigue During Prolonged Endurance Cycling, Chris Abbiss and Paul Laursen’s comprehensive review of fatigue literature, looked at no fewer than ten different explanations of fatigue.

Abiss and Laursen point out that fatigue is usually defined by the type of research being done. For example, if one is looking into psychological causes then they will tend to classify fatigue as “a sensation of tiredness,” while a biomechanist might look more at changes in force output to qualify fatigue. Fatigue research is also driven by a reductionist approach; those doing the research tend to look for a single ‘answer’ to the question of fatigue.

Among the different paradigms and models explored were the anaerobic/cardiovascular model, the energy supply/depletion model, neuromuscular fatigue, biomechanical, thermoregulatory, and muscle trauma models. In addition the psychological/motivational model, central governor, and complex systems models were also reviewed. A quick summary of characteristics might demonstrate that:

Neuromuscular fatigue tends to be divided into a question of where along the neuromuscular pathway inhibition occurs, while the muscle trauma model seeks to explain fatigue as coming from damage to the muscle itself, or to alterations in the chemical homeostasis.

The biomechanical paradigm seeks to define fatigue as the result of decreased efficiency of motion, where increasing efficiency lowers the production of metabolites (like lactate) and energy consumption, helping attenuate increases in core temperature. This segues nicely into the thermoregulatory model which looks at the role of core temperature and the increased demands on the physiological systems brought about as a result of increased core temperature towards critical points at which exercise capacity is reduced or terminated.

While psychologically no single variable appears to be responsible for motor output alteration due to afferent (outgoing) signals, it is thought that numerous mechanisms are responsible for the subconscious perception of fatigue and alterations in central activation and perceived exertion.

The central governor and complex systems theories seek to explain fatigue as a function of oversight by an as-yet-undefined central mechanism, or through the complex inter-relationship of multiple feedback loops seeking to maintain homeostasis, respectively.

Their net conclusion is that any number of systems may contribute to fatigue in a specific way for a specific situation, but in general the limitation of the system is derived from oxygen delivery to the muscles, especially at high intensity.

To further clarify in the Abiss and Laursen article fatigue was defined as “tiredness and associated decrements in muscular performance and function.” This is an important point as much research has looked at performance to exhaustion. The relevance comes when we look at how to best apply some of the factors above into the creation of a responsible training program. Many of the changes we seek are built around the optimization of oxygen delivery and increasing metabolic efficiency during the training year, so how does Lactate Threshold help?

Threshold As Proxy
An individual’s Lactate Threshold is the single most important physiological determinant of endurance exercise performance. It is trainable, reliable, and a sort of proxy for other important metabolic processes that underlie performance.

For example hormone production, like epinephrine/norepinephrine, shows a similar curvelinear relationship with increasing exercise intensity. Plasma potassium concentration, catecholamine concentration, plasma ammonia concentrations, growth hormone, cortisol and many other elements also demonstrate the same threshold type trends as lactate.

Power at Threshold
Now that we’ve established what Lactate Threshold is, how it is determined, and what processes it parallels, let’s spend a little bit of time on what advantages threshold level training can bring to your performance.

For untrained athletes the Lactate Threshold benefits of training can be seen at a wide range of intensities. Simply getting on the bike regularly will bring about many changes including increased mitochondrial density, blood lactate response, and reductions in lactate concentration at a given intensity.

For the trained athlete however, continuous training at intensities around Lactate Threshold has been shown to be beneficial since the time of the fabled East German sports machine in the twentieth century. The East Germans were famous for doing extended hours of training at OBLA!

In a similar vein, Gorostiaga et al in 1991 compared a continuous training group at circa-threshold intensity to one that did only structured high intensity VO2max type intervals (of the type that are all the rage today) and found some compelling differences. While the VO2max group did show a two fold increase in percentage change in VO2max (16% increase v 8% increase), the continuous training group had a ten fold increase in citrate synthase production compared to the VO2max group (25% increase v 2.5% increase). Citrate synthase is one of the main markers for muscle mitochondrial capacity, and is a good reference for total metabolic efficiency.

Both of these examples (the first decidedly anecdotal) serve to illustrate the value of continuous training at an intensity around Lactate Threshold. This has most recently been termed ‘sweet spot’ training, but the idea has been advocated by Lydiard, Coggan, and others in various forms or years. Typically “sweet spot” is defined as approximately 88-93% of your Lactate Threshold power, however the true measure of intensity should be determined by your ability to repeat them over multiple days in a training block.

These circa-threshold efforts should be at least twenty minutes in length, but can last up to two hours or more for advanced athletes. A key determinant of the duration and intensity is your ability to replicate the workout intensity/duration again the next day. A well prepared, motivated athlete doing 60 minutes at 88-93% of threshold power (FTP), should be able to replicate that workload again the second and third days. If you can’t then you probably went too hard, too long, or don’t have a good estimate of your FTP and need to adjust. My suggestion is to start doing some field testing to establish your FTP and then see what you can do. Have fun and let me know how it goes…

References:

1. Abbiss, Chris, Laursen, Paul – Models to Explain Fatigue During Prolonged Endurance Cycling. School of Exercise, Biomedical and Health Sciences, Edith Cowan University, Australia. 2005
2. Coggan, Andy – Explaining Lactate Threshold. Webinar Presentation. 2010
3. Robergs, Robert A., Ghiasvand, Farzenah, Parker, Daryl – Biochemistry of exercise-induced metabolic acidosis. Am J Physiol Regul Integr Comp Physiol 287: R502–R516, 2004


January

Is proving harder and harder to sit down and postulate on.

Too many balls in the air and too few hours to lock em down.

Fun projects from 30,000 feet, occasionally less so in the trenches. Hopefully the outcome gets a smile.

Sorta felt like riding on a hot air balloon over 24/36 months or so. Fortune and dumb luck often colliding in fetes of fun that, thankfully, have pictures. Belgian legends, Irish legends-to-be. Points in between. Sometimes a blur, always always a blast. The future still to book one plows ahead hoping a moments pivotal silence sneaks up again soon.