Speed Gene

The summary of this study seems to be: the number of people who are predisposed to speed is low, and the number of people with a gene that blocks full development of speed is high, therefore evolution favours endurance running.

Is it just me, or does this seem like somewhat of a stretch? When the span of physical activities of our species is considered, the importance of combat and/or sport in various societies throughout history, and the role of speed in the success of these, it seems counter-intuitive to say that those who achieve greatly are being bred out.

It strikes me as being akin to saying that because physical beauty (in an extreme) is such a rare trait that we’re evolving past it, or have left it behind. There’s something off about using rarity of occurrance as the root of a theory – if I’m reading this correctly.

Additionally, there’s the notion of our own history to examine: the claim is that this shift away from speed and toward endurance – if indeed such a shift has really occurred – has happened only recently in human evolutionary history.

Yet when you look at the past couple thousand years of our history, for the most part travel became very limited once domestication of livestock and crops became commonplace. What need is there for long-distance endurance running when people make little to no use of that ability?

If such a need existed, it would be more valuable in pre-agricultural times when a nomadic lifestyle may have existed without the aid of horses or other riding and pack animals to depend upon. Yet even then hunting would be more favourable for those who are capable of generating greater speed and power, much like other predatory animals.


[QUOTE]Born to run: Gene clue to athletic endurance
[SIZE=“1”]Sun Sep 9, 1:31 PM[/SIZE]

PARIS (AFP) - If you were a prehistoric human, would you prefer to able to sprint very fast for short distances? Or to jog comfortably for kilometres (miles)?

That’s one of the questions thrown up by the so-called “gene for speed,” known as ACTN3.

One of the most intriguing genes discovered, ACTN3 encodes a protein that governs metabolism in “fast twitch” muscle fibres, which generate force at high speed.

Around 18 percent of the world’s population has a truncated variant of the gene which blocks this protein. The stubby variant, called R577X, is common among successful endurance athletes, previous research has found.

On the other hand, elite sprinters, who need explosive speed, are likelier to have the reverse – a functioning variant of ACTN3.

Keen to find out more, researchers led by Kathryn North, a professor at the Children’s Hospital at Westmead, in Sydney, Australia, created a batch of mice that had been engineered to lack ACTN3.

The “knockout” mice and ordinary mice with a functioning ACTN3 gene were put on a motorised treadmill, which spun ever faster until the luckless rodents were exhausted.

The easy winners in this endurance test were the knockout mice, which were able to run on average a third further than their counterparts.

The apparent reason for this: the loss of ACNT3’s protein was compensated by a different protein, called alpha-actinin-2, which shifted muscle metabolism towards a smoother, more efficient, aerobic pathway.

As a result, fast-twitch leg muscles could be contracted again and again, without tiring.

North’s team also looked through genetic profiles from individuals of European and East Asian descent and found that there was remarkably little sign of mutation in the wider stretch of genetic code in the vicinity of R577X.

Such similarity is a telltale sign of what evolutionary experts call positive selection. Genes which help the fight for survival get lastingly incorporated in the human genome, whereas those that encumber it get weeded out.

In other words, the ability to run longer distances became a preferential trait that became incorporated into a wide swathe of Homo sapiens.

If so, the incorporation happened recently, on the long scale of human history.

According to North’s calculations, R577X took root among populations in central Europe around 15,000 years ago and in East Asia around 33,000 years ago.

The variant has not been incorporated in all of us, either because so little time has elapsed for this to happen or is being countered by selective pressures in favour of other genes, they speculate.

The study is published on Sunday in the specialist journal Nature Genetics.[/QUOTE]