Sprints increase fat mobilisation

I've linked to the research before about the 8 second on 12 second off sprint programme being studied at the University of New South Wales. Gail Trapp's whole PhD is available but she has just had another article published on the same area:


Metabolic response of trained and untrained women during high-intensity intermittent cycle exercise

The metabolic response to two different forms of high-intensity intermittent cycle exercise was investigated in young women. Subjects (8 trained and 8 untrained) performed two bouts of high-intensity intermittent exercise: short sprint (SS) (8-s sprint, 12-s recovery) and long sprint (LS) (24-s sprint, 36-s recovery) for 20 min on two separate occasions. Both workload and oxygen uptake were greater in the trained subjects but were not significantly different for SS and LS. Plasma glycerol concentrations significantly increased during exercise. Lactate concentrations rose over the 20 min and were higher for the trained women. Catecholamine concentration was also higher postexercise compared with preexercise for both groups. Both SS and LS produced similar metabolic response although both lactate and catecholamines were higher after the 24-s sprint. In conclusion, these results show that high-intensity intermittent exercise resulted in significant elevations in catecholamines that appear to be related to increased venous glycerol concentrations. The trained compared with the untrained women tended to show an earlier increase in plasma glycerol concentrations during high-intensity exercise.

The longer sprint (24 on 36 off) appeared to be more effective, but I'd need to read the whole article to comment any further. however both were effective in elevating catecholamines.

Why are catecholamines signficant? My knowledge of this really comes from Lyle McDonald's Ultimate Diet 2.0 (Which is an excellent book that I would recommend to anyone) (I hope he doesn't mind me quoting at length)

The first step in burning off bodyfat is getting it out of your fat cells. You might even argue that this is the most important step since, if you can't get it out of the fat cell, you can't burn it off. Recall from last chapter that bodyfat is primarily stored triglyceride, with a small amount of water and some enzymatic and cellular machinery. Mobilizing bodyfat requires that we first break down the stored triglyceride into three fatty acids and a molecule of glycerol. The rate limiting step in this process is an enzyme called hormone sensitive lipase (HSL).

So what regulates HSL? Although a number of hormones such as testosterone, cortisol, estrogen, and growth hormone have modulating effects on HSL activity (mainly increasing or decreasing total levels of HSL in the fat cell), the only hormones that we need to be concerned with in terms of HSL activity are insulin and the catecholamines.

The primary inactivator of HSL is the hormone insulin and it only takes very tiny
amounts (depending on insulin sensitivity) to have an effect. Even fasting insulin levels are sufficient to inactivate HSL by nearly 50%. Small increases in insulin (from either protein or carbohydrate intake) inactivate HSL further. Additionally, the mere presence of triglycerides in the bloodstream (via infusion or by just eating dietary fat by itself) also inhibits HSL activity so this isn't as simple as just blaming insulin. One way or another, any time you eat, HSL is going to be inactivated, either by the increase in insulin from protein or carbs or the presence of fat in the bloodstream from eating fat.

The primary hormones which activate HSL are the catecholamines: adrenaline and noradrenaline. Adrenaline is released from the adrenal cortex, traveling through the bloodstream to affect numerous tissues in the body. This means that blood flow to fat cells has an impact on how much or how little adrenaline will reach fat cells. Noradrenaline is released from nerve terminals which interact directly with the cells.

More technically, both insulin and the catecholamines affect levels of cyclical AMP (cAMP) in the fat cell which is what really determines how active HSL is. When cAMP levels are low, HSL activity is also low and fat breakdown is low. When cAMP levels are high, HSL activity is high and fat breakdown increases.

Insulin lowers levels of cAMP and the catecholamines, in general, raise levels of cAMP (I'll explain this statement in a second). The higher the level of cAMP, the more active HSL is and the more bodyfat that gets broken down and released from the fat cell. It should be clear that, from a fat loss standpoint, we want high levels of cAMP