Got Built?

I’m fiddling with an interesting cardio protocol I read about earlier this year. In a nutshell, it’s 8-second sprints with 12-second recovery periods. I’m nicknaming it “8 seconds of glory” and you build up to doing these 20-second cycles for 15 minutes in total. I started with three. I’m at eight right now. Trust me, by the 6th minute, you hate your life.

Method:
Set up on an upright or recumbent bike (I prefer recumbent for the quad pump, plus it’s easier on my back but either is fine) and start pedaling at a tension that you COULD keep up for at least 20 minutes. Start watching the clock.

1. When it hits the 20-second mark, pedal like mad for 8 seconds
   Then pedal as slowly as you like for 12 seconds.
2. Repeat as many times as you can. I would suggest 3 minutes if you’re in reasonable shape. Build it up to as many as 10 minutes of these little intervals.
3. Cool down for the rest of your 20-minute session. In other words, if you warmed up for a minute, then did 3 minutes of intervals (ie 9 complete 20-second cycles), you have used up 4 minutes - spin it out at a moderate intensity for 16 more minutes. As you do more intervals, your cool-down gets shorter, until you are doing 10 minutes of each. At this point, increase the tension on the bicycle to make the interval work harder rather than doing more and more intervals, k?

Observations:
It’s clearly a variant of HIIT, and one of the problems inherent in HIIT was demonstrated by Romijn, Coyle, Sidossis, Zhang and Wolfe: 5 minutes after high intensity cardio there’s an overshoot of blood FFA levels, probably from a removal of the inhibition of release. This is because anything over about 8 seconds involves going beyond ATP for energy, and that means lactate.

I’ll explain where I’m going with this:

ATP (adenosine triphosphate - that means three phosphates, folks) fuels muscle cells by breaking off a phosphate, forming ADP (adenosine diphosphate - two phoshpates are left) as the ATP is used to provide energy. Simple math will tell you ADP increases as ATP is broken down for energy.

This increase in relative ADP concentration activates AMPk, an enzyme that stimulates both fatty acid oxidation and glucose uptake in skeletal muscle.

Acute activity induces a sudden energy-need at the cellular level. The energy produced from phosphate breaking off ATP is useful for extremely short bursts - say under 10 seconds.

When ATP is high enough, and excess energy is available, it is stored (through the phosphate) as CP. The phosphate in CP is not immediately available to the cell as energy, but it is a compact energy storage unit for phosphate which is required to regenerate (from ADP and phosphate) ATP - which is the only available energy source to the cell.

My thinking is that ATP is the energy handler. CP is the non-user-friendly storage space for P. ATP hands off P for energy, then picks up P from CP so it has it available for the next energy request. At least, that’s how it makes sense in my little brain. This is very fast food for the muscle cell - but there isn’t very much of it. Activity lasting longer than 8 or 10 seconds is going to need a different fuel source. Enter pyruvate.

Glycolysis is the process through which glucose becomes available for fuel, resulting in the production of both pyruvate and ATP.

In the presence of oxygen, pyruvate is ultimately fully oxidized to carbon dioxide and water. That’s what happens when you go for a walk, where oxygen availability keeps up with demand. Contrast this with what happens when you sprint: here we have anaerobic respiration, where oxygen is in short supply. In this situation, because oxygen is still required to create ATP, oxygen debt builds as pyruvate reduces to lactate, the accumulation of which is responsible for “the burn” that eventually forces you to rest. (As an aside this oxygen debt is behind EPOC, but that’s a whole ‘nother story…)

For the 8-seconds sprinting, 12 seconds of recovery sprint protocol, we’re stopping short of glycolysis. The acute energy need of the cell increase the ratio of ADP to ATP, which activates AMPk. In doing so, fatty acid oxidation is increased. Because the sprints are so short (ie under the 10-second threshold), glycogen is spared. This is a “pure” ATP protocol.

Now, the sprinting stimulates catecholamine release, promoting lipolysis. ADP:ATP increases, AMPk is activated, promoting fatty acid oxidation.

Marriage made in heaven, right?

Sooo… you do the sprint, you stimulate catecholamine. This promotes lipolysis of peripheral stores. If you go beyond 10 seconds, you go into the glycolytic pathway, producing lactate as a byproduct of the incomplete (ie anaerobic) combustion of glucose. But we don’t go this far - and it appears that it’s the lactate that prevents the FFAs mobilized through catecholamine-induced lipolysis from hitting the blood-stream. This was the part Romjin et al discovered in their ground-breaking research a few years back, and which is why Lyle has people sit on their asses and wait five minutes after doing stubborn fat loss protocol before doing the SS cardio which follows.

I may have bits of this wrong. I’m still working it out.

My friend Linnaete offers this:

ATP is broken down to form ADP, and CP is another reservoir in which ADP can resynthesize back into ATP. There’s more CP in the body than ATP, and ATP can’t just be replenished by blood or tissues when depleted, it must be resynthesized in the mitochondria - which requires a food source (limitations of ATP)

In order for fats to be used as energy, a certain amount of carbohydrates must be broken down in order to ensure that the Krebs cycle (which is how fats catabolize) can continue. My brain thinks that this is why we have the short high energy bursts (carbs) followed by the moderate recovery (fats) to promote the highest amount of lipid catabolism possible. This instead of a purely steady state which uses both carbs and fats but at a possibly lower level of fatty acid manipulation. So yeah, I think you’re on target!

Or maybe I’m crazy.

Oh and the theory of lactate prohibiting FFA metabolism could be right… I know that it inactivates certain enzymes. And lactic acid is stored with pyruvate until a later time when oxygen is available to break it down, which directly affects FFA breakdown because they require oxygen. Hence, that 5 minute break which allows the respiratory cycle to regulate and oxygen to become available again.

Oh, and I might be on crack. For an opposing viewpoint read here.