Why the hell did Dinosaurs get so big?  How could they?  Wouldn’t it be impossible given Galileo’s square-cube law?

In what has become known as the dinosaur paradox, a few key issues have plagued scientists.

1. Inadequate bone strength to support the largest dinosaurs
   
2. Inadequate muscle strength to lift and move the largest dinosaurs
   
3. Unacceptable high blood pressure and stress on the heart of the tallest dinosaurs
   
4. Aerodynamics principles showing that the pterosaurs should not have flown

I’m only going to focus on number two, as this is the most relevant to what we do here on this blog.  (If you want to read more about why dinosaurs were able to get so big, you can read my post at my other blog: sapien games.)

Sometimes (often) in science, something that at first appears to be a “paradox” is in fact not one at all.  Instead, the original facts of that case were simply misunderstood.  And once the facts become clear, the one-time paradox fades away.

In worst cases, these facts were misunderstood simply because scientists in different fields don’t pay nearly any attention to what others scientists are doing in other fields.  Something of that sort is happening here.

Here is a paragraph from the article on the dinosaur paradox at dinosaurtheory.com:

The relative bone strength and the relative muscle strength are grouped together because they are similar scaling problems. For both, strength is function of the cross-sectional area. If we look at the longest length of a bone or muscle and then imagined cutting this length in half, the newly exposed area is the cross-sectional area. The strength of either a bone or a muscle is directly proportional to this cross-sectional area, so both bone and muscle strength are two dimensional attributes. Yet body mass is a function of volume, a three dimensional attribute. In accordance to the Square-Cube, as we look at increasing larger animals the mass of each animal increases at a faster rate than the cross-sectional areas of either the bone or the muscle. Thus, larger animals have less relative muscle strength and less relative bone strength than that of smaller animals.

The bold is mine – these statements are false.

Any undergrad in exercise science would know that strength is NOT directly proportional to muscle cross-sectional area, but a professional paleontologist might not.  This is not to disparage the paleontologist (there is plenty of info in their field that exercise sci people wouldn’t know).  But, sometimes this lack of understanding can lead to paradoxes that aren’t paradoxes. 

To most people, when they see a big bodybuilder, they assume that they must be one of the strongest men on the planet.  After all, they LOOK strong.  They are so big; they have so much muscle.  The top pro bodybuilders are literally the most muscular men to have ever walked the earth.  But, they are decidedly NOT the strongest.

The cold-hard truth is that the size of muscle is NOT directly proportional to strength and is therefore not a 2-dimensional attribute. (That is, when size goes up strength goes up and vice versa – think of a simple Cartesian graph.)  It IS true that as mass goes up it becomes harder to be as relatively strong.  But, does that mean that dinosaurs weren’t strong enough to hold themselves up?  No. 

When it comes to building strength, we can call muscle size (it’s cross sectional area) the “weak” force.  And we can call motor unit activation and fiber types the “strong” forces.  All of which are more complex than you might expect.

The statements above are predicated on a single fallacy of both science and logic.  It goes something like this:

Statement A:  Strength goes up if and only if muscle size goes up

This statement is really the conjunction of two statements:

A1:  If Strength goes up, then muscle size goes up.

A2:  If muscle size goes up, then strength goes up.

Let’s start with A2.

It IS true in a weak sense that if muscle size goes up, then strength goes up.  But, not as much as one would think.

The size of muscle is dictated by a lot of things, among them being contractile proteins and sarcoplasm.   Contractile proteins are the little guys that actually do the mechanical work of moving your body around.  The sarcoplasm is the fluid in your muscle cells.  Believe it or not, the size of your muscle has as much to do with how much “water weight” you’re carrying as it does with how many contractile proteins you have.  Yes, more sarcoplasm does correlate with more strength, but not as highly as with more contractile proteins. 

Even with a “maximum” amount of both of these, this still doesn’t mean you will be as strong as someone half your size.

Which leads me to A1.

The first of the strong forces is much more complicated, and it is at least part of what accounts for the fact that top middleweight powerlifters and olympic weightlifters are SIGNIFICANTLY stronger than the worlds top bodybuilders, in spite of the fact that they are half their size.

Just because you have (for the sake of argument) 10 muscle fibers, doesn’t mean that you use all 10 every time you do something.  In fact, most people won’t be able to activate all 10 even in their moments of greatest need (like when lifting a really heavy weight).  The reason is that the body is all about efficiency.  Using all of your muscle fibers all at once is taxing as hell.  This is why the more advanced you get in strength sports, the longer your rest periods have to become, because you’ve literally worked harder than someone who is just beginning can possibly work.

What we’re saying here is that it is perfectly possible to get a whole lot stronger without ever getting much bigger, simply by training your muscles to actually work at the top of their capacity. 

OK …  is that it?  Nope.

We also have the difference in fiber types.  There are lots of them (and the list seems to get bigger every decade), but to keep things simple as all hell, we’ll just go with two groupings of them: fast twitch fibers and slow twitch fibers.

The fast twitch fibers are the ones you use when you want to go … fast (surprised?), and the slow twitch fibers are better at going the distance.  The fast ones are more efficient at bursts of energy that result in both speed and strength.  The slow twitch ones are more efficient at avoiding burnout. 

So if you go for a long hike up a mountain, you’d better hope you have an abundance of slow twitch fibers in your legs so that it doesn’t burn the whole way! (Trust me, I hate hiking for a reason …)

Now imagine two ladies, each with identical cross-sectional area of muscle in their thighs.  But one has an over abundance of fast twitch fibers and the other has an over abundance of slow twitch fibers.  They are the same size, but the first is going to be a ton stronger. 

There’s more to all of this, of course, including the neuromuscular coordination problem and the importance of leverage as dictated by limb-length, tendon and ligament attachment points, etc;  but, I’m not even going to get into that.

The “paradox” regarding dinosaur size includes statements about the lack of muscle strength adequate enough to support their weight.  But, this assessment is based solely on the myth of Statement A, above.  Clearly, that statement is false.

OK, I know what you’re thinking, “Nick, for heaven’s sake!  You’re talking about mammals, and humans particularly.  The author above is talking about dinosaurs!  OMG!”

True.

But, hear me out. 

We have NO fossilized evidence of what the muscles of dinosaurs were like.  So, speculation based upon available current animals is all we have.  Further, we DO know that dinosaurs are closest related to modern-day birds, and bird muscles function in the same way as ours.  That is, among animals, a muscle is a muscle in the broad sense, and species “pick” which configuration they can most use from the available options (as discussed above).  (Well, natural and sexual selections “pick” for them.)

We also know that these beasts DID exist, and they WERE huge.  So, clearly they were able to stand up and hold their own weight.  Part of the many reasons (see here for more) that they were able to do this is likely because of a muscle-configuration-distribution that made that possible.  We know that Statement A is false with regards to mammals, and by Occam’s Razor, it was probably false for dinosaurs.

They had big legs, but they also must have had strong legs – not the same thing.

Ice Cream Sushi!

Great news for Athletes trying to pack on muscle mass.  A new study has shown that eating saturated fat can increase your appetite and trick you into thinking you need more food.

Since THE major factor holding back athletes who are looking to add large amounts of muscle (or even to maintain what they have–marathon runners, I’m looking at you!) is their inability to eat enough, this fact may come in handy.

My suggestion? Eat ice cream.  It’s high calorie and loaded with saturated fat which will apparently make you hungrier.  You get two for the price of one!

Of course, the article I found this tid-bit on was most worried about the implications of saturated fat on our overall health profiles.  But, that isn’t your problem.  You’re too skinny, and you need to muscle up.  That takes more calories than you can eat comfortably.   Science (and Ice Cream) to the rescue!

Below is the abstract to the  actual study (I hate that most articles don’t do this, especially when they are on the web).

Insulin signaling can be modulated by several isoforms of PKC in peripheral tissues. Here, we assessed whether one specific isoform, PKC-θ, was expressed in critical CNS regions that regulate energy balance and whether it mediated the deleterious effects of diets high in fat, specifically palmitic acid, on hypothalamic insulin activity in rats and mice. Using a combination of in situ hybridization and immunohistochemistry, we found that PKC-θ was expressed in discrete neuronal populations of the arcuate nucleus, specifically the neuropeptide Y/agouti-related protein neurons and the dorsal medial nucleus in the hypothalamus. CNS exposure to palmitic acid via direct infusion or by oral gavage increased the localization of PKC-θ to cell membranes in the hypothalamus, which was associated with impaired hypothalamic insulin and leptin signaling. This finding was specific for palmitic acid, as the monounsaturated fatty acid, oleic acid, neither increased membrane localization of PKC-θ nor induced insulin resistance. Finally, arcuate-specific knockdown of PKC-θ attenuated diet-induced obesity and improved insulin signaling. These results suggest that many of the deleterious effects of high-fat diets, specifically those enriched with palmitic acid, are CNS mediated via PKC-θ activation, resulting in reduced insulin activity.

Normally your bodies cells are told to stop demanding food by a couple of hormones, leptin and insulin. This study suggests that certain saturated fats, particularly palmitic acid tell your brain to send signals to your bodies cells instructing them to ignore leptin and insulin.  And therefore, you can be “objectively” full, but not feel like you are.  So, you keep eating.

Clearly, if you want to lose weight, this is bad news.  Keep your saturated fats down, and stick to unsaturated fats if you can like fish oils and olive oil.

But, if you are trying to gain size, this is GREAT.  More ice cream, fried chicken, bacon, and even more ice cream!

(The image above is from SushiGallery.net.  Very cool.)

References

Benoit, Stephen C, Christopher J Kemp, Carol F Elias, William Abplanalp, James P Herman, Stephanie Migrenne, Anne-Laure Lefevre, et al. 2009. Palmitic acid mediates hypothalamic insulin resistance by altering PKC-theta subcellular localization in rodents. The Journal of Clinical Investigation 119, no. 9 (September): 2577-2589. doi:10.1172/JCI36714.

Research at the Seoul National University has suggested that the inorganic phosphates in a whole host of processed foods can increase the growth of lung cancer tumors.

According to Dr. Myung-Haing Cho, D.V.M., Ph.D who (along with his colleagues) conducted the research:

“Lung cancer is a disease of uncontrolled cell proliferation in lung tissue, and disruption of signaling pathways in those tissues can confer a normal cell with malignant properties,” Dr. Cho explained. “Deregulation of only a small set of pathways can confer a normal cell with malignant properties, and these pathways are regulated in response to nutrient availability and, consequently, cell proliferation and growth.

“Phosphate is an essential nutrient to living organisms, and can activate some signals,” he added. “This study demonstrates that high intake of inorganic phosphates may strongly stimulate lung cancer development by altering those (signaling) pathways.”

Read here about why this gene is NOT likely a major factor in his outstanding performance.  Primarily in the fact that (in all likelyhood) ALL of his competitors have it too.

Rather, my point is that an excessive emphasis on ACTN3 as a major explanation for Jamaican success does a grave disservice to the complex interplay of genetic and environmental factors required for top-level athletic performance. This suggestion goes against everything we’ve learnt about the genetics of complex traits from recent genome-wide association studies, which have revealed that quantitative traits (like height and body weight) are frequently influenced by dozens to hundreds of genes, each of small effect; if anything, it’s likely that athletic performance will be even more genetically complex than these traits. The ACTN3-centred argument also dismisses the importance of Jamaica’s impressive investment in the infrastructure and training system required to identify and nurture elite track athletes, the effects of a culture that idolises local track heroes, and the powerful desire of young Jamaicans to use athletic success to lift themselves and their families out of poverty.

That last point is one of the explanations as to why the Japanese have been so crappy at Sumo in the last number of years–They’re too rich!  And why Sumo players from poorer countries are dominating.

Peak Power Output and Muscle Metabolism in Sprinters

For more, See my new post on Usain Bolt SMASHING the world record in Berlin!

Usain Bolt, the enigmatic 21 year old sprinter from Jamaica, has taken Olympic track and field by storm being the first person in 24 years to win gold in both the 100 meter and the 200 meter sprints. His successes in both were definitive. He broke the 100 meter world record with a 9.69 (seconds). And his 200 meter was another world record at 19.30. In both races he was able to sprint at top speed for nearly the entire race, only losing a bit of speed near the end of the 200 meters.

In contrast to Bolt, Sonya Richards, the American favorite in the women’s 400 meters, ended up barely getting the bronze. She started out strong, way ahead in the first 200 meters sprinting at top speed. She still had a solid lead at the beginning of the last 100 meter stretch. But, then, suddenly, and dramatically, she ran “out of gas”. She struggled just to stay in third place. She didn’t have the energy to keep up, and she lost her chance at a gold medal.

It is rare for a runner to run out of gas at the end of a 100 or 200 meter dash. But, it happens a lot in the 400. Why the discrepancy? What does it say about the limits of human sprinting ability? And how long can a person, even an elite athlete, maintain maximal speed?

At the elite level, a 100 meter dash lasts about 10 seconds; a 200 meter lasts about 20 seconds; and the 400 takes about 1 minute. It is interesting to note that the 200 meter time is about double that of the 100 meter time, but the 400 meter is six times the 100 meter.

Insight into why it is that after about the 200 meter mark, or after about 20 seconds, the human body can’t keep up its maximal speed can be found at the cellular level: it comes down to ATP (the body’s preferred fuel source) production and the ATP turnover rate (Katz, 1986). The ATP turnover rate refers to your body’s speed-ability to produce ATP. But, to use ATP, the body first has to make it. There are three primary sources of ATP production. The fastest is the phosphocreatine (PCr) system that relies on creatine phosphate. This is used primarily for the shortest bouts of energy, like lifting a maximum weight for one repetition or a 20 meter dash. The second fastest is glycolysis that relies on sugar metabolism used for repetitions at a maximum power output, such as sprinting up to 200 meters. And the slowest is aerobic metabolism that relies on oxygen, primarily used at sub-maximal thresholds. Marathon runners rely primarily on aerobic metabolism.

According to a study by Bogdanis (1996), PCr is highly important to maximum power output for the first 10 seconds of sprinting, but declines rapidly thereafter. Peak power output, the highest level of power that a sprinter can produce, occurs at approximately 3 seconds (Bogdanis, 1998).

It has become widely accepted that PCr provides up to 25-30% of ATP production in a 30 second sprint, the rest coming primarily from glycolysis. In another study, also by Bognanis (1998), PCr stores were found to drop by nearly 60% after the first 10 seconds of sprinting. And after 20 total seconds of sprinting PCr levels have dropped to as low as 25% of the resting value. This means that in a sprint lasting longer than 10 seconds, there just isn’t enough PCr to do the job. But, power output doesn’t slow to a crawl.

Glycolysis generally works right along side the PCr system. Glycolysis uses glucose to form ATP. The glucose is stored in both the liver and in the muscle cells themselves. Glycolysis can operate in an anoxic (without oxygen) environment which makes it ideal for sustained maximal power output situations like a 100 to 200 meter dash because at that speed, the aerobic (oxygen) pathway can’t keep up. But, it has its drawbacks. The primary drawback of glycolysis is that when it is performing without oxygen the system backs up and produces an excess flood of lactic acid (Klapcinska) that builds up to high levels fairly quickly after the first 200 meters.

Aerobic metabolism is the way that our bodies generate ATP while we’re simply waking around, watching TV, or reading papers about metabolic reactions. It is slow, but it creates a large abundance of ATP. The trouble is that at top speed the aerobic pathway just isn’t fast enough to keep up. But, aerobic metabolism isn’t completely out to lunch in an all-out sprint. Remember that Usain Bolt and his competitors all ran the 200 meter sprint at close to full speed throughout the race, and it took most of them about 20 seconds to do it. They slowed down a bit near the end, but not much. If their PCr stores were used up, and their glycogen levels were down one would suspect that their speed would drop considerably as their ability to maintain maximum power output would be severely compromised. But, while their speed did drop near the end, it didn’t drop that dramatically (barely noticeable in fact). There must be some help coming from a different source. Bognanis (1998 ) found that some of that help may be coming from aerobic pathways, though more study is needed to examine why and how this happens.

But the aerobic pathway is too slow to help out for too long. For Sonya Richards, her all out effort for the first 200 meters of her 400 meter sprint left her completely lacking in power by the end of the race. She’d used up all her PCr, she’d depleted her glycogen, and the aerobic pathways just weren’t sufficient to replenish the amount of ATP she needed to win the gold. Her competitors, however, relied more on a combination of their aerobic pathways and glycolytic pathways in the first part of the race and saved their maximal power output for the end where they were able to overtake her.

Human beings are able to do amazing things when they train hard for them. Usain Bolt is a shining example of that. But there are limits to what our species can accomplish. After 10 to 20 seconds, it becomes exponentially harder to maintain the same average power output that one was able to achieve up to that point in an all out sprint. It just so happens that the fastest people in the world sprint the 200 meters in almost exactly 20 seconds, and the 100 meters in under 10 seconds. But, for 400 meter runners, an all out maximal sprint is not a good strategy. The body simply can’t maintain that pace for long. A lesson Sonya Richards will likely never forget.

References:

1. Bogdanis, G (1996). “Contribution of phosphocreatine and aerobic metabolism to energy supply during repeated sprint exercise”. Journal of applied physiology (1985) (8750-7587), 80 (3), p. 876.

2. Bogdanis, G (1998). “Power output and muscle metabolism during and following recovery from 10 and 20 s of maximal sprint exercise in humans”. Acta physiologica Scandinavica (0001-6772), 163 (3), p. 261.

3. Gaitanos, G (1993). “Human muscle metabolism during intermittent maximal exercise”. Journal of applied physiology (1985) (8750-7587), 75 (2), p. 712.

4. Katz, A (1986). “Muscle ATP turnover rate during isometric contraction in humans”. Journal of applied physiology (1985) (8750-7587), 60 (6), p. 1839.

5. Klapcinska, B (2001). “The effects of sprint (300 m) running on plasma lactate, uric acid, creatine kinase and lactate dehydrogenase in competitive hurdlers and untrained men”. Journal of sports medicine and physical fitness (0022-4707), 41 (3), p. 306.