Physiological Model of Training- Why it and "zone training" are outdated

Physiological vs connection model.

(This is going to be a long one…heads up…..)

                I hate zone training.  It’s a pet peeve of mine.  I hate the idea and the concept behind it.  But so many coaches out there use it, and in actuality we all tend to classify workouts into different zones.  I’ve wrestled with trying to explain my hatred for zone training and what I’d call the alternative method for a while, but it’s a difficult thing to wrap your head around.  I knew I hated it, but I couldn’t effectively explain why to outsiders.  I’d dance around the why’s but never had a satisfactory answer.  Part of the reason was I didn’t have a simple way to explain the alternative.  I could throw a bunch of information and examples to describe it, but there was no easy descriptor. Before getting into what the alternative is, lets look at what exactly the physiological model is and how we got there.

Defining a model:

                The physiological model of training is one that relies on the premise that there are a few big physiological parameters that govern performance.  The big ones mentioned in research and the literature are VO2max, Running Economy (RE), Lactate Threshold (LT), and sometimes lactate tolerance or anaerobic capacity/tolerance depending on publication.  The idea is that these four things combine to create performance.

The central premise of the physiological model is that IF we improve one of these parameters, then performance improves. 

But how does this relate to training?  The model takes another step and says that there are certain intensities or zones that will improve X parameter.

So the full model really states that IF we do X training, Y parameter will improve and thus performance improves.

If this was a logic class it would look something like this:  X->Y=↑ P

Sounds reasonable right?  Well, hold your horses…

A bunch of Scientific research from ACSM conference

Last week was the big American College of Sports Medicine annual meeting.  I wasn’t in attendance as I was at the Prefontaine classic. So instead I had the pleasure of browsing through the 3,500+ abstracts that were presented at the conference.  There were a lot of interesting studies to pop up, so I figured I’d share my highlights of the abstracts.  In the coming weeks, I’ll go through some of the more intriguing studies to come out and give their real life impacts.

(Some are more in depth than others because I was taking hand written notes as my computer broke…So, if you want to search the abstracts, I’ve included the authors when I remembered.  Also, remember that experimental procedure and subjects matter.  So just because I say X did Y, it doesn’t apply to everyone..)

My comments on the studies will be in blue.

(Full abstracts can be seen here: http://acsmannualmeeting.org/wp-content/uploads/2012/04/12AMFinalProgramCombined.pdf )

Exercise Induced Arterial Hypoxemia:

·         -The higher the VO2max, the more likely for oxygen saturation to be less than 91% at sea level.  71% of well trained reached low oxygen saturation levels (Chapman)

·         -Mechanical ventilator constraints are a contributor

·         -Faster runners- pulmonary diffusing capacity of nitric oxide is limited

·         -Aveolar-capillary membrane conductance is a limiter (Lavin et al.)

Impact: Limiters and physiology change as you deal with people futher outside the norm.  For highly trained athletes, O2 saturation drops might play a role.  This might be the reason various interventions in terms of respiratory training are successful.  It depends on the population you are addressing.  It’s simple to test if an athlete has EIAH.  Simply buy a pulse oximiter for $60 and then test during a really hard workout.