Platelet-rich plasma doesn’t work for rotator cuff (shoulder) tendons

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As of September 2017, new Sweat Science columns are being published at www.outsideonline.com/sweatscience. Check out my bestselling new book on the science of endurance, ENDURE: Mind, Body, and the Curiously Elastic Limits of Human Performance, published in February 2018 with a foreword by Malcolm Gladwell.

- Alex Hutchinson (@sweatscience)

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Yet another salvo in the ongoing debate about whether platelet-rich plasma (PRP) therapy — sometimes known as “blood spinning” — is a miracle tendon healer or an expensive placebo. At an American Orthopaedic Society for Sports Medicine conference in San Diego, researchers presented the results of a new study of PRP for rotator cuff tendon repair — and the results weren’t encouraging.

The study involved 79 patients who all received standard surgical rotator cuff repair and post-operation rehab; half of them were randomized to receive a form of PRP treatment. There were “no real differences” between the groups:

“In fact, this preliminary analysis suggests that the PRFM [the form of PRP used in the study], as used in this study, may have a negative effect on healing. However, this data should be viewed as preliminary, and further study is required” said study author Scott Rodeo, MD, of New York City’s Hospital for Special Surgery.

Right now it’s just a conference presentation; the study will presumably be published eventually, at which point we’ll get some more details on the design and specific results of the study. But the scientists still seem optimistic:

Researchers think there may be several reasons for a lack of response in healing, including variability in the way platelets are recovered, platelet activation and the mechanisms for the way the PRFM reacts with the tendon cells. The study was also unable to document the number of platelets actually delivered to patients who received the PRFM…

“Additional research needs to be performed to figure out the mechanisms for why PRP is successful in healing certain areas of the body and not others…” said Rodeo.

I’m not really sure which areas of the body he’s talking about. I only know of one properly controlled clinical trial that came to a positive conclusion, on tennis elbow — but even that study was subject to criticism. So far PRP is one of those ideas that makes perfect sense in theory, but hasn’t yet proven itself in practice.

More about stride length, rate, and “cruise control” for runners

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As of September 2017, new Sweat Science columns are being published at www.outsideonline.com/sweatscience. Check out my bestselling new book on the science of endurance, ENDURE: Mind, Body, and the Curiously Elastic Limits of Human Performance, published in February 2018 with a foreword by Malcolm Gladwell.

- Alex Hutchinson (@sweatscience)

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I posted last week about a newly invented “cruise control” device for runners, which controls pace by cueing stride frequency with a metronome. That ignited an interesting discussion about how we change pace while running: do we take quicker strides, longer strides, or a combination of both?

For starters, Pete Larson send me a paper with some nice clear data that shows how the two factors interact (at least in one physically active group of 24 men and nine women between 18 and 34 years old):

The x-axis runs from 0 to 12 m/s, so the data runs from 2.5 to just over 9 m/s, which is 6:40/km to under 2:00/km — i.e. sprinting). Sure enough, stride length is a much bigger factor than stride frequency at typical jogging/running speeds, but the frequency curve is never perfectly flat.

I also exchanged a few e-mails with Max Donelan, one of the co-inventors of the cruise control, who explained a little more about how the device works and what sort of interactions between stride rate, length and running speed they saw in their testing. His answers were very interesting and well-explained, so with his permission I’m going to post them here rather than trying to summarize them. One of the most interesting points, I think, is that when his metronome cues runners to increase their stride rate, they also automatically increase stride length to arrive at the pace they’d naturally associate with the new cadence. Makes sense, but that hadn’t occurred to me.

Q: I’m also curious (as you saw in my blog entry) about how effective cadence is at controlling pace.

A: We have tested a number of subjects running at a range of speeds. It is absolutely true that some runners increase speed predominantly by increasing stride length. In fact, I would say that most runners that we have tested increase stride length more than frequency. However, all the runners we have tested also increase their frequency when they increase speed. We have yet to find a runner that only increases stride length or only increases stride frequency. For our purposes, it doesn’t matter whether people increase speed predominantly with increasing stride length as long as the relationship between speed and frequency is not perfectly flat (and we have yet to find a subject like that).

Of equal importance is a second phenomenon which is less intuitive. When someone is running at a particular cadence and you ask them to match a faster cadence, they not only increase their stride frequency but also their stride length.They alter both frequency and length to converge on the speed that they normally prefer at the new cadence. For example, a 10% increase in frequency might yield a 40% increase in length to get a 54% increase in speed. This allows us to use frequency to have control authority over speed.

Q: What sort of testing did you do?

A: We initially determined how frequency and length change with increases in speed by having subjects run at different steady state speeds on a treadmill. We carefully calibrated the treadmill speed and we measured step frequency with pressure sensitive foot switches. Stride length is simply speed divided by stride frequency.

To study how runners change both speed and step length when you give them an increase in cadence to match, we had them run overground with a metronome beeping in their ear. After a few minutes, the metronome frequency would rapidly increase to a new frequency. Subjects were instructed to match the beat. They were free to choose whatever speed they liked and, in principle, they could have stayed at the same speed. We measured step frequency with the same pressure sensitive foot switches. We measure and record overground running speed using a high-end GPS designed for quantifying acceleration in race cars.

We test our cruise control algorithm also during running overground. When we implement cruise control, we get runners within 0.5% of their desired average speed. This compares well with recreational athletes who average an 8% error, and collegiate runners who average a 4% error:

Green et al. Pacing accuracy in collegiate and recreational runners. Eur J Appl Physiol (2010) vol. 108 (3) pp. 567-572 http://dx.doi.org/10.1007/s00421-009-1257-5

For the recreational runners, an 8% error means that they will only be within 4 minutes of their target time for a 50 min 10 K. Running 4 minutes too fast may mean a surprisingly fast personal best, but it may also mean crashing and burning.

Very interesting stuff — both from a practical point of view (i.e. the cruise control), and for understanding more about how we run. Thanks to both Max and Pete for their contributions.

What do we actually KNOW about running injuries?

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As of September 2017, new Sweat Science columns are being published at www.outsideonline.com/sweatscience. Check out my bestselling new book on the science of endurance, ENDURE: Mind, Body, and the Curiously Elastic Limits of Human Performance, published in February 2018 with a foreword by Malcolm Gladwell.

- Alex Hutchinson (@sweatscience)

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I’m a couple of weeks behind the curve on this, but I just wanted to highlight an excellent post by Pete Larson of Runblogger. He recently attended a conference/course on running injuries taught primarily by Blaise Dubois, and took the opportunity to write up a succinct list of 16 things we know about running injuries, ranging from the very basic to the fairly technical.

Part of the reason I liked it so much was that it was very balanced — not promoting big shoes, little shoes, or no shoes as the panacea that will cure everything. In fact, his fourth point is:

Most running injuries are overuse injuries that can be attributed to stubborn and obsessive runners doing too much too soon. In doing this, runners exceed their body’s stress threshold and something gives. The end result is an injury.

Just for kicks, though, I’ll quibble with one point. He writes:

One of the things that also came through loud and clear is that barefoot running is our default. It is how we evolved, and modern shoes are a change from that default. Thus, the burden of proof should be to prove that we are better off running in big, bulky shoes. People often seem to think that the notion that we should run in a way that emulates the barefoot gait is radical (whether actually barefoot or in minimal shoes), but in reality it’s what our species has done for nearly 2 million years prior to about 1970.

I understand the point, of course. But let me make a competing point: in the U.S. alone, according to Running USA, there were 25.559 million people who ran at least 50 times in 2009. Some 10.29 million of them finished a road race. They bought a total of 39.76 million pairs of running shoes. How many of those people went barefoot, or in minimalist shoes? I really don’t know — I wish I had the data. But I think it’s fair to say that the overwhelming majority of people who have grown up in a modern, western, convenience-filled, concrete-covered society and have taken up running without having relied on it as a primary form of transport throughout their childhood have done so wearing conventional running shoes. Does that mean barefooting or minimalism or forefoot striking is bad? Definitely not. But since we don’t have any answers yet, let’s be circumspect about applying the “burden of proof.”

Anyway, I’m just quibbling here. Pete’s post is great, and a must-read for anyone interested in the topic!

Carbo-loading with a “hyperglycemic-hyperinsulinemic glucose clamp”

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As of September 2017, new Sweat Science columns are being published at www.outsideonline.com/sweatscience. Check out my bestselling new book on the science of endurance, ENDURE: Mind, Body, and the Curiously Elastic Limits of Human Performance, published in February 2018 with a foreword by Malcolm Gladwell.

- Alex Hutchinson (@sweatscience)

***

In search of the ultimate carbo-loading protocol, I stumbled across a paper in the European Journal of Applied Physiology that was posted online a few weeks ago. Researchers at Liverpool John Moores University in Britain investigated the use of a “hyperglycemic-hyperinsulinemic glucose clamp” as a sort of super-accelerated way of stuffing your muscles full of glycogen (the form in which carbs are stored in the body).

What the heck does that mean, you ask? Basically, the subjects spent two hours the day before the big exercise test, lying around with needles stuck in their arm delivering elevated levels of glucose and insulin. (The “clamp” means they picked a specific level of blood sugar and infused exactly enough glucose to maintain the subjects at that level for the two hours.) Glucose is carbohydrate, and insulin is one of the signals that initiates the storage of carbohydrate in your muscles, so the subjects were able to pack about 198 grams of carbohydrate into storage during the two-hour protocol.

The next day, the subjects did a 90-minute steady-state bike ride following by a 16K time trial — and sure enough, the clamp improved time-trial performance by 3.3% (49 seconds over ~24 minutes) compared to when the subjects received a placebo saline infusion. So yes, you can carbo-load in two hours the day before a race without any special dietary or training intervention (though it doesn’t show whether this method is better or worse than standard carbo-loading protocols). Of course, this really doesn’t have much practical significance. I suppose you could imagine Tour de France riders having the resources and incentive to undertake a protocol like this, but insulin is banned by WADA. (Oh wait…)

The most interesting part of the paper is buried near the very end, and it’s written very confusingly — it sounds very much as if the paper’s peer reviewers have insisted on a bunch of caveats and rephrasings, which wouldn’t be surprising as the topic is Tim Noakes’s highly controversial “central governor” theory. It relates to a somewhat confusing quirk in the data:

[D]espite the evidence of alterations in substrate availability (higher glucose and insulin), the patterns of substrate oxidation were no different.

In other words, carbo-loading makes more carbohydrate available, but it doesn’t seem to change how much carbohydrate (versus fat) is actually burned. A number of other studies have found similar anomalies, which has made some researchers question whether we really understand why carbo-loading works to improve performance:

The essence of this theory, supported by appropriate findings, is that muscle glycogen may have a signalling function that influences pacing strategy. Subjects who start exercise with elevated levels of muscle glycogen would be able to exercise at a higher pace due to signalling between muscle and the brain than when in a glycogen depleted state.

In this picture, carbo-loading is just another version of the carbohydrate mouth wash, whose function is to convince your brain that you have enough fuel. It’s hard to imagine that this is always the limiting factor, but it’s an interesting area of research.

New explanations for runner’s high

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As of September 2017, new Sweat Science columns are being published at www.outsideonline.com/sweatscience. Check out my bestselling new book on the science of endurance, ENDURE: Mind, Body, and the Curiously Elastic Limits of Human Performance, published in February 2018 with a foreword by Malcolm Gladwell.

- Alex Hutchinson (@sweatscience)

***

Gretchen Reynolds has an article in the New York Times about recent research into the origins of “runner’s high,” suggesting that endocannabinoids rather than endorphins might be responsible — in other words, the body’s internal version of marijuana instead of morphine:

But perhaps the most telling experiment was published last year by researchers in France who had bred mice with no functioning endocannabinoid receptors. Mice usually love to run, but the genetically modified animals, given free access to running wheels, ran about half as much as usual.

Reynolds is usually an excellent reporter, but I was a bit disappointed in the lack of context offered in this article. She dismisses the role of endorphins as follows:

Endorphins, however, are composed of relatively large molecules, “which are unable to pass the blood-brain barrier,” said Matthew Hill, a postdoctoral fellow at Rockefeller University in New York. Finding endorphins in the bloodstream after exercise could not, in other words, constitute proof that the substance was having an effect on the mind.

This is true, but German researchers published a study back in 2008 that was very widely reported (including in the Times by Reynolds’s colleague Gina Kolata) that directly measured the increase of endorphins in the brain after a two-hour run. Both Reynolds and Hill are undoubtedly familiar with this study, so it seems disingenuous to pretend that we don’t know anything about the link between exercise and endorphins in the brain.

Ultimately, the runner’s high is such a nebulous, ill-defined thing, meaning different things to different people, that it’s probably a combination of several different effects — endorphins, endocannabinoids, and perhaps other factors, including some straightforward psychological ones. So it seems silly to dismiss the “old” theory in favour of a new one when there’s no reason the two can’t coexist.