11/07/2009 1:42pm, #271
- Join Date
- Aug 2009
- Oakland, CA (East Bay Area)
Noob question: why do we want to slow down the digestion of fats, proteins, vitamins?
11/07/2009 7:59pm, #272
-If stuff in your digestive tract is in too much of a hurry (think diarrhea, for example), you don't have a chance to absorb it before it's gone.
-If, on the other hand, stuff in your digestive tract is readily digestible but not stored by your body (whey or hydrolyzed protein, for example), it'll get absorbed, processed and excreted in fairly short order.
In short, I want to be providing my body with food to keep it in an anabolic state even when I'm asleep and thus not stuffing my face. I suspect that a slow protein (casein, from milk protein) + fats (slow digestion) + soluble fiber (slow absorption) = a nice slow, steady flow of nutrients overnight.
11/08/2009 3:10am, #273
- Join Date
- Aug 2009
- Oakland, CA (East Bay Area)
Hmm. Does this same principle apply to giving you a steady source of energy during activity like a race or a fight? I hear about people carbo-loading to achieve the same effect, is this just a different way of doing it?
11/08/2009 11:26am, #274
Fights and most races are short and intense enough that you're running off of energy you've already absorbed (typically muscular/liver glycogen). In the case of marathons and long bike races, you'll see people taking sports drinks, carb gels, etc. while on the hoof, but those are actually designed to get out of your digestive tract and into your bloodstream as quickly as possible (with the expectation that you'll have another once it's depleted).
This is because the other effects of having stuff in your digestive tract during exertion ranges from "I don't really notice it" to "oh man, I just shat/puked/peed myself" depending on the volume, location and constitution of it.
11/20/2009 1:18am, #275
Question: Does anyone here know much about the risk of head trauma in collegiate wrestling? This paper (PDF, p.156) seems to indicate it's about as risky as cheerleading in that regard. Anecdotal evidence is welcome.
Also, who wants to be my study buddy for introductory organic chemistry?
11/25/2009 12:13am, #276
I didn't want to bump a five-year-old thread, so I decided I'd flog my own instead.
Antagonists of myostatin, a blood-borne negative regulator of muscle growth produced in muscle cells, have shown considerable promise for enhancing muscle mass and strength in rodent studies and could serve as potential therapeutic agents for human muscle diseases. One of the most potent of these agents, follistatin, is both safe and effective in mice, but similar tests have not been performed in nonhuman primates. To assess this important criterion for clinical translation, we tested an alternatively spliced form of human follistatin that affects skeletal muscle but that has only minimal effects on nonmuscle cells. When injected into the quadriceps of cynomolgus macaque monkeys, a follistatin isoform expressed from an adeno-associated virus serotype 1 vector, AAV1-FS344, induced pronounced and durable increases in muscle size and strength. Long-term expression of the transgene did not produce any abnormal changes in the morphology or function of key organs, indicating the safety of gene delivery by intramuscular injection of an AAV1 vector. Our results, together with the findings in mice, suggest that therapy with AAV1-FS344 may improve muscle mass and function in patients with certain degenerative muscle disorders.
Fulltext is on Scribd.
What does this mean? It means that five or ten years from now, the kid with muscular dystrophy will be the most popular kid in school.
11/25/2009 12:36am, #277
I was just reading about this a few weeks ago and wondering when I could get my hands on some...
11/30/2009 1:31am, #278It was early observed that lactic acid appears in stimulated muscles, or in muscles which have been allowed or caused to go into rigor mortis, and for many years it was thought that this lactic acid represents a waste product formed as a result of the stimulation of the muscle. The work of Fletcher and Hopkins and later of Meyerhof and A.V. Hill has shown that this formation of lactic acid is rather to be regarded as an essential part of the cycle of processes which occur during contraction, while its removal constitutes recovery.
Here's the thing... that article is from 1924. I'm pretty sure this is saying that we've known lactate isn't just a waste product for eighty-five years now, yet people are still surprised by this.
12/01/2009 2:25am, #279
Omalu has set his sights on curing CTE. And why not? “You pop a pill before you play, a medicine that prevents the buildup of tau,” he says. “Like you take an aspirin to prevent heart disease.” Why not? “This is how we now need to talk. Not this back-and-forth of human selfishness. Not this NFL politics and meanness. Anybody still denying the disease is out of his mind. The issue now is treatment. That is my next step, now that I understand the pathology.”
I'm not sure that blocking tau protein formation will necessarily solve the problem, but it's at least worth trying.
On stuff I see in literature that does not make a lick of fucking sense:
If ATP produced by oxidative phosphorylation and ATP coming from glycolysis are similar molecules, intracellular architecture and complex metabolic networks favor a channeling of energetic metabolism. Several lines of evidence do suggest that numerous membrane enzymes (including the Na+/K+-ATPase) electively consume glycolytic ATP.
Since when is there any difference between ATP from different sources?
Can anyone explain this?
12/05/2009 12:22am, #280
It's liable to be six months before I get my MRI, but I'm going to Quebec for Christmas, and they have private clinics there. Tempting.
As noted earlier in this thread, what "makes sense" isn't always correct. Example, from a NYT Blog called "Phys Ed: Why Doesn’t Exercise Lead to Weight Loss?"...
People will read this:
The cycling was deliberately performed at a relatively easy intensity (about 55 percent of each person’s predetermined aerobic capacity). It is well known physiologically that, while high-intensity exercise demands mostly carbohydrate calories (since carbohydrates can quickly reach the bloodstream and, from there, laboring muscles), low-intensity exercise prompts the body to burn at least some stored fat.
Calories are largely fungible - a surplus or deficit in one source will tend to distribute itself to others, because your body can interconvert between fat and carbohydrate. Think about it - if you eat ten pounds of sugar a day, you aren't consuming any fat, but you're sure going to pack on the pounds.
And what's more, this poor reasoning led them to sabotage the experiment:
To their surprise, the researchers found that none of the groups, including the athletes, experienced “afterburn.” They did not use additional body fat on the day when they exercised. In fact, most of the subjects burned slightly less fat over the 24-hour study period when they exercised than when they did not.
After a 5 week conditioning period on a recumbent cycle, The High Intensity Interval Training (HIIT) group perform sprints while the Endurance Training (ET) group performed a more traditional aerobic protocol, throughout the remaining 15 weeks. Both groups progressed in intensity. At the conclusion of the study, the HIIT group lost over 3 times as much subcutaneous fat as the ET group despite expending less than half as many calories. For every calorie expended during HIIT, there was a nine fold loss of subcutaneous body fat, as compared to the ET group.
I would have expected the study's authors to know stuff like this. Disappointing.