Why a Fast Start Makes You Suffer – Runner’s World

Why a Fast Start Makes You Suffer  Runner’s World

Start of a sprint.

Oscar Rethwill via Flickr and licensed under Creative Commons Attribution (CC BY) 2.0 License

When you’re starting on the start line, your muscles aren’t burning much energy. Then the gun fires, and suddenly they’re burning a whole lot.

Your heart, lungs, and muscles respond—but they can’t ramp up to full capacity instantly. It takes two or three minutes for the heart and lungs to speed up, blood vessels to dilate, and perhaps most importantly, for the oxygen-processing enzymes in the muscles themselves to get fully activated.

In the meantime, you’re running on borrowed energy, powering your muscles with quick but unsustainable anaerobic metabolism, which produces byproducts that ultimately lead to muscle fatigue. So the faster you can ramp up to full aerobic energy production, the better.

Interestingly, that ramp-up rate, known as oxygen uptake kinetics (which I’ve written about previously, such as here and here), varies from person to person. In a bit of tragic irony, middle-distance runners, whose fast race starts incur the greatest oxygen deficits, tend to have relatively slow oxygen kinetics. That may be because middle-distance runners need to have exceptional anaerobic capacities, so their bodies have learned to rely more on anaerobic energy.

Marathoners, in contrast, are aerobic monsters with lightning-quick kinetics, even though their more leisurely starting pace means they don’t really need it. Marathon world record-holder Paula Radcliffe, for example, was reportedly able to reach an aerobic steady state within about 35 seconds when going from rest to running at 6:00 per mile pace, which is an extremely rapid transformation.

In theory, then, runners (and other endurance athletes) who have quick oxygen kinetics should experience less muscle fatigue than those with slower oxygen kinetics if they both start out at a similar effort. In practice, though, that idea had never been tested—so that’s what Guillaume Millet and his colleagues at the University of Calgary did in a new study that appears in the European Journal of Applied Physiology.

They took 10 subjects, and first tested their oxygen kinetics, by measuring how quickly oxygen uptake increased when going from a standstill to a relatively rapid pace on an exercise bike. Then they had the subjects do a very hard six-minute cycling trial, and tested their muscle function before and after using various techniques (maximal efforts, electrical stimulation).

One of the key advances in the study was the use of a specially built exercise bike that allowed the subjects to pedal as normal, but could also have the pedals instantly locked into position for maximal strength tests. In studies of this kind, it usually takes a minute or two to transfer the exhausted subject from the bike to the force-measuring equipment—a gap that distorts the measurements of fatigue, since some forms of muscle fatigue begin recovering within seconds.

Anyway, the headline result was as expected: Subjects who had slower oxygen kinetics tended to also have greater muscle fatigue (i.e., greater loss of strength) after the six-minute cycling test, independent of their overall fitness levels or VO2 max. Presumably their slow aerobic kinetics forced them to go more anaerobic, which produced more nasty byproducts that produced muscle fatigue.

So what are these “byproducts” that cause fatigue? That’s still very much an open area of research. According to the paper, the two main candidates are inorganic phosphates, produced by the use of the instant-but-shortlived stores of phosphocreatine in the muscle; and protons, produced by the anaerobic breakdown of glucose.

The study can’t determine whether one or both of these byproducts dominated, but the particular pattern of fatigue observed suggests the result was a failure of “excitation-contraction coupling.” That means, in essence, that a given electrical signal from your brain isn’t producing as big a contraction in the muscle, thanks to changes at the nerve-muscle junction.

All of this, of course, raises the question of what you can do to improve your oxygen kinetics. There are two major things you can do.

One is to train. In one 2009 study from Andy Jones and his colleagues, two weeks of sprint intervals produced a big improvement in kinetics (e.g., 28 to 21 seconds for the time constant on one measure of kinetics), while steady efforts didn’t produce any changes. That makes intuitive sense: To ramp up more quickly, you should do some abrupt zero-to-max transitions in training. The study used four to seven all-out 30-second reps with four minutes rest.

The other thing you can do, on a more acute level, is warm up properly. You can get your blood vessels dilated and oxygen-processing enzymes activated by making sure your warm-up includes a priming effort that reaches threshold intensity or a little higher—and then, crucially, allowing enough time to ensure your anaerobic energy stores have recovered before the race. These days, for example, I like to do a couple of 45- to 60-second efforts at around 5K pace, finishing 10 minutes before a race starts.

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