MITOCHONDRIA QUESTION for phoenix, tinman and others

My take on this is two-fold. First, sometimes sudden deteriorations in aerobic ability happen at times during your season, though you have done everything right, per se. Second, don't do any hard training in the last 10 days before an important race. Rather, do maintenance work. Also, aside from this and related to previous discussions, consider doing the types of training that keep your body at the same level as during your intelligently applied buildup as long as you aren't tired. Otherwise, decrease the stress on your body, but still do the aerobic work. Also, do some quality, but make sure not to do anaerobic endurance work int the peaking phase, especially if you are tapering out mileage because you will have decreased aerobic enzymes available to process O2 and maintian substrate utilization (burn fats, especially). Small amounts of max VO2 may be your personal ticket. Otherwise, do some longer running because it will keep you body in tune. Do keep in mind that it takes 75% of Max VO2 to stimulate the two aerobic muscle cells that contribute to racing performance: slow twitch and fast oxidative glycolytic. So, you may have to do some marathon pace running in your taper to keep your mitochondria up to snuff. If you are not doing max VO2 work in your taper, then the marathon paced running will be critical. For those who are fat marathoners (2:30 or less) then you can run a tad slower than marathon pace in about 1/3rd of your runs in the last 10-14 days because the 3-hour racing mark is what correlates to 75% of max VO2. (fast marathoners run at closer to 80% of max VO2, i.e.. The good part about being a marathoner and using peaking runs at 75% of max VO@ instead of tapering down mileage a lot and doing faster interval work to maintain mitochondrial density and volume is the mere fact that 75% is really close to the pace you need to race at in the marathon...meaning you are maintaining or improving your marathon running economy while you are peaking. Plus, by reducing the quantity of hard intervals you may have been doing prior to the 10-14 days pre-race window, you also gain back neural muscle power and your legs wont be sore. Remember, 10 days is the length of time it takes to recover from eccentric contraction abuse caused by hard speed, downhills, or really long runs.

honest question. what is a simple definition of mitochondria.

aerobic powerhouse of a cell

My previous post was supposed to read "fast" maratoners (2:30 and under), not fat marathoners. Ha ha ha! Sorry!

Just found this thread.

This is great stuff. Thanks tinman.

It explains a lot on why runners/athletes will inexplicably have a couple bad days in the middle of a season. And why I've never done well with a low intensity taper.

Most of your suggestions I've sort of found out through trial and error over the years, but I will definitely use this info on my current training cycle.

Anyway, thanks.

It appears that Tinman might be plagiarizing the Peak Performance website.

http://www.pponline.co.uk/encyc/0129.htm

How about it Tinman, can you explain anything you've cut-and-pasted in plain English? I'd like you to go over that part about mitosis again? I'm having trouble with it.

You're an exercise physiologist or a coach right? What is it you do for a living Tinman? Who do you coach? Where did you go to school?

Tinman did not plagiarize. A careful reading of the PPO article reveals that it is quite complentary to what Tinman has posted.

Additionally, Anderson's ultimate conclusion on PPO is wrong. Tinman is correct.

An intelligent cytologist would have noticed that.

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Interesting info about the "short" and "long" mitochondria. At a conference I attended last year an expert on mitochondrial energetics show some confocal fluorescent micrographs of muscle mitochondria:

"Mitochondria are not mitochondria are not mitochondria," he said.

They also are not shaped like little beans in muscle. They form more of a reticulum. They look a lot like the end of a neuron with dendrites splaying out everywhere. It is interesting to note that the mitochondria in type I fibers

are located closer to the edge of the fiber while those in IIb fibers are more in the center. Type II fiber are generally large in diameter than type I fibers which really puts a diffusion distance strain on IIb fibers and larger IIa fibers.

Mitochondrial half-life decay is the same as that for production with a lag time of a couple of 2-3 days before they start to crash. Glut-4 level go back to baseline 36 hours after glycogen repletion.

To be correct, the half-life numbers refers to increases and decreases in mitochondrial enzyme activites which are more transient than increases and decreases in mitochondrion size and number.

The flat feeling from a taper more likely comes from crashing levels of stress hormones that have been elevated with hard training. Coming down off of a "stress high" will always leave you tired.

Cytologist wrote:

JonnyO you need to take some beginning life sciences courses before you post. Mitochondria don't live or die anymore than any other cellular structures (cell walls, ribosomes,plasma, etc..) live or die.

Wrong Cytologist. Before you belittle someone else, at least make sure you are right.

75% of the proteins comprising mitochondria are coded for by chromosomal DNA but the other 25% are coded for by mitochondrial DNA which is in circular plasmid form. Thus, mitochondria have their own DNA separate and apart from chromosomal DNA. This is the mitochondrial DNA inherited from the maternal line. They divide to increase in number and apoptose to to die.

Evolutionarily mitochondria derive from bacteria forming a symbiotic relationship with eukaryotes. Ribosome, lysozomes, etc. come strictly from chromosomol DNA and are not self-replicating in the least. Neither to they apoptose and die.

Mitochondrial density is maxed out in normal cardiac muscle such that cardiac muscle is ~8% mitochondria by volume. Training does not increase mitochondrial density in the heart. Untrained skeletal muscle is ~1% mitochondria by volume while fully trained skeletal muscle is ~2% mitochondria by volume.

Activation of the enzyme AMPK (cellular energey status) signals for mitochondrial increases. A transgenic experiment also showed that CAMK (calcium signaling) signals for mitochondrial increases as well.

Phoenix:

Thanks for the excellent info. I did not know that dimensions of mitochonrions are not bean-shaped as portrayed in nearly every textbook on the subject I've seen over the years. Like dendrites? Cool image! It makes me wonder.

Thank you for the support on the previous post. I have not looked at an Owen Anderson prose in quite awhile. I simply tired of his ambling from one panacea to another. However, several years ago I did enjoy reading about certain topics that I had no access to until I attended a university that had a nice physiology library. No harm intended to Dr. Anderson!

I have much to learn, like anyone who has an interest in ex. science. What you offer, Phoenix, I read carefully because I know that I will learn a little more each time. Thank you.

By the way for the person accusing me of plagarizing, how dare you! I am plenty sharp enough and industrious enough to postulate, theorize, and formulate for myself. I did cite the posts I wrote earlier. Dr. Bob Treffene wrote that article I put in quotes. It was published in a swimming publication entitled "Lactate Transporters." I take credit for only piecing together information in pragmatic ways for athletes' to use. Every athlete I know wants to figure out the mystery. I simply enjoy thinking about what has been researched by scientists and relating it to my personal experiences as a competitor and coach. Sure, I studied ex. physiology in grad school and did a bunch of lab testing, but consider the world of sport and fitness a bigger lab. Like anyone who enjoys science and spends hours thinking about it, I have figured out things that others are wondering about. Soon thereafter, some research from around the world clarifies the point or at least brings to light more possibilities. Any good coach or athlete who has studied in the ex. science domain will tell you that at one time or other they figured out something that could put one more piece in the puzzle. Ask Jack Daniels, Jack Wilmore, David Costill, Bengt Saltin, etc. if they had theoretical answers to questions people had wondered about for you years and they will say "Yes, of course I did, but I just needed time." or "I was doing another project at the time, so I could not get to it yet, but it was in the back of my mind." I claim to not be on the same stage as the masters listed, but rather waiting for my expertise and experience to grow so that one day I may face the lights, the audience, and the stares of those wanting to see, feel, hear the truth.

For those of you out there who do like to question reality, feel free to share your thoughts and experiences with me and people like Phoenix (who obviously loves the unravelling the mystery too...and is darn good at it!). Again, thanks for the support and encouragement, Phoenix. tinman

mito info wrote:

I don't post here but some interesting facts about mitochondria:

1. mitochondrial density is governed by hereditary factors

Yes but not in the conventional sense that most may think, mitochondrial DNA is entirely maternally inherited, your mtDNA is identical with your mother's. It is the energy producing part of the cell that is believed to have been a separate organism that adapted to living in a symbiotic relationship in our cells. Consequently there are multiple copies of it within each cell and it reproduces by dividing independantly inside the cell, (there can be 1000's of copies/cell).

tinman wrote:

Phoenix:

Thanks for the excellent info. I did not know that dimensions of mitochonrions are not bean-shaped as portrayed in nearly every textbook on the subject I've seen over the years. Like dendrites? Cool image! It makes me wonder.

The reticular shape of skeletal muscle mitochondria offers a tremendously greater surface area to volume ratio than a bean shape would. This has implications for O2 diffusion into the mitochondria as well as the number of ATP producing H+ channels.

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As far a mitochondrial DNA and mitochondria, there is a bit of confusion here:

"Mitochondrial DNA" or mtDNA is ~100% inherited from ones mother. A true statement.

However, the proteins that mitochondrial proteins are composed of are coded for by both mtDNA and chromosomal DNA--75% of the mitochondrial proteins by number are actually coded for by chromosomal DNA which is inherited from the maternal AND paternal line, while only 25% come from mtDNA.

Thus, while mtDNA is strictly from the maternal line, whole mitochondria are from the maternal and paternal line.

Tinman, Phoenix:

What can you tell us about the mitochondiral condition that LeMond and other endurance athletes are reported to have experienced later in their careers? Noakes talks about this condition as being induced by many, many years of inducing muscle damage in training. Any new insights here?

Please post what Dr. Noakes said and we can respond to the statement. Thanks.

tinman, phoenix,

What is your take on mitohonrial development with multi-tier/pace training. Specificly, would some of the higher end training decrease your ability to develope aerobically, and logically not be as effective as perodization.

Secondly, Lydiard said something to the effect that, high amounts of lactate from anaerobic training causes a change in your blood ph and destroys aerobic enzymes.(do you know an actual study that indicates this). Do you think it's possibly the decrease in aerobic ability/performance following some high end training was actually the mitochondria going through a change

On-hand, I don't have a research paper to cite which discusses degradation of aerobic enzymes due to muscle fiber acidosis or blood acidosis. Peter Janssen, MD, sports scientist in Holland mentions that aerobic enzymes do degrade when too much lactic acid training takes place. I think Mader and Madsen, old-school East German scientists mentioned the same thing in journal articles published in the 70s and early 80s. Maybe we can do some searching for it.

It is my general observation that lactic acid training ruins economy. I have tested athletes before and after a typical middle distance runner's workout of repeat 400s at race pace or faster with short recoveries and found that economy had eroded by around 7-8% three days later at paces up to 80% of race pace speed. I did not test at faster than 80% of 1500m race pace speed. So, if a guy had run 4:00 for the 1500m (64 per 400 ave.) then he maxed out on the treadmill at a tad over 11.2 mph (about 80.467 per 440 yds). The interesting thing was that we tested guys and gals (from the track team and from a local triathlon club) who rated their extertions on the Borg scale as being even higher than the 7-8% might have indicated. If, for example, a guy ran at 10 mph before the lactic acid workout and rated the effort at 10mph as a 14 out of 20, when he returned after the workout for the retest he would claim the effort was a 15-17 out of 20. We measured their heart rates too and they were a little higher, but not a lot; perhaps 3-4 beats on ave., but most had no change in heart rates, statistically which indicates to me that heart rate might not be a good indicator in some circumstances of accute fatigue.

My freind and I tested the heck out of each others running and biking abilities in the human performance lab. Although we are just two subjects which would limit the applicability and validity of juxtaposing our data on a broader population, our lactic acid levels were higher at sub-threshold paces following workouts that brought our heart rates above 90% of max. For example, my buddy, a grad student in human performance too and a darn good triathlete, might have shown a blood lactate level two days after a repeat 800m workout at 5k pace of 4.0 mmols at 8 mph on the treadmill whereas before the workout he showed a 3.2 mmol level. His heart rate would be within the same range as before. His RPE would be higher by 1 or 2 too. I personally experienced even greater differences in my blood lactat levels and RPE levels two days after the same workout, though we were about the same racing fitness level. We concluded that he recovers faster than I do. It would take me a good 5 days to recover and have either equal blood lactate levels or RPE levels at the same 8mph pace or slightly better. I mentioned this to Jack Daniels once and wondered if he had noticed recovery rates being differnt for runners. We talked about doing a joint study to determine recovery rates, but it did not materialize due to the fact that I was running out of money. Regardless, I have noticed since those testing days in the late 80s that their is a wide range of recovery abilities, especially when high intensity training is concerned. Some runners are wiped out for several days after and intense workout or race, though they are well-conditioned athetes, while others recover in 2-3 days just fine. I have wondered about the enzymatic effects of high intensity training on certain individuals. Does lactic acid exercise cause erosion of their mitochondrial enzymes such as cytochrome c and cytrate sythase more for some people than others? Do all people erode their aerobic effieciency (economy) as the athetes we tested before and after intense workouts? I suspect that many people do erode their economy level, at least in the short term. But, what if said athletes do frequent intense workouts? Would their economy levels erode even further and what is happening to their mitochondrial enzymes which facilitate aerobic metabolism?

On the ultramarathonworld.com home page there is a link to a report on a South African study on "premature aging" in ultra athletes; the report mentions the study's finding of mitochondrial abnormalities.

Mitochondria density might maynot be improved after 8-12 weeks, but maximum VOLUME (as in total number) of them can take years to acheive, right?

I really don't know for sure. I do think that the number of years has less to do with it the the density of the stimulus. Is the stimulus multiplied by the duration divided by time high enough is the key. Then, how often does a person go to far or too fast and destroy that which they built up?

I think one of the big reasons that some people seemingly pop up from nowhere and run at elite levels in a matter of 3-4 years is that had both gentics and dense training that was uninterrupted by injuries, burn-out, or excessive fatigue. How many people who run 120 miles per week should run 100 and benefit more? How many do the right mileage but not enough intensity? How many go for long periods without intensity in their training yet expect to raise to higher levels of fitness each year and it never happens? Why can some guy or gal who quits running because they hate the abuse they received by their coaches in high school or college return to running and change their approach, balancing all the key elements, and surpass everyone around them, though they appeared to be mediocre in their prior running life?

Because they learned their lessons in the abuse years, and

applied that knowledge when they were not injured.