Mitochondria are ancient bacteria that merged into the eukaryotic cell, accordinga to a theroy. They have a distinct DNA from the rest of the human body and are inherited via the mother. The amount of mitochondria can change, if you exercise more and eat less sugar, the number of mitochondria in your body grows!
Mitochondria are involved in aerobic energy production in the cell, using O2 (oxygen) and some energy substrate to produce ATP (adenosyne tri-phosphate), the "energy currency of the cell".
"exercise more" means "higher energy needs", and growing the amount of mitochondria would be adaptive.
"eat less sugar" means less anaerobic energy production, I guess. Thus more aerobic energy production in exchange.
Interesting - I guess there is some sort of balance there, given the radical biochemistry that is seen with Mitochondria. “The more [mitochondria] the merrier” …?
The more the merrier, yes. I’m an amateur road cyclist and most of my training is spent in the lower heart-rate “zones” trying to train my mitochondria. The theory is that for endurance sports the key variable is your mitochondria’s capacity to use oxygen and fuel to produce ATP.
Further, if the mitochondria is being asked to make more ATP than it can aerobically, then it will skip the final respiratory step and respire without oxygen (anaerobically). This causes a build up of lactate in the cells that is not tolerated above a certain level, I believe due to it raising acidity levels in the cell.
You’ll often hear athletes and coaches talk about lactate threshold and Functional Threshold Power (FTP). This is all to do with mitochondria function.
If I'm rowing for 20-30 minutes in a HF range of 150-160, that should fall into your parameters, right? This is a very interesting fact - I have been sedentary for a couple of years and I'm fighting a kind of fatigue. Maybe this is a way to work against the symptoms. Do you know of a way to tell if the effects are taking hold?
It also applies selective pressure on your population of mitochondria which can reduce the prevalence of deleterious mutations and make them more efficient on a population basis.
that theory doesn't seem to encompass all that is know.
> Wallace notes: “The mitochondrial theory of aging holds that as we live and produce ATP, our mitochondria generate oxygen free radicals that inexorably attack our mitochondria and mutate our mitochondrial DNA.”1
if aging is killing the mitochondria, why then the mother passing mitochondria to the offspring give them a blank state if they got dna-damaged mitochondria to begin with?
The mitochondria that mothers pass down are from a special group of cells that already existed when the mother was born and they are kept in a special, protected state that minimizes damage.
My understanding is that only happens to a point, then new fat cells are generated, which will then just deflate/inflate when weight is lost and regained again. I think it's one of the reasons that losing fat is so much harder than gaining fat.
The obvious benefit is having a greater ability to produce cellular energy, in principle also having the feeling and experience of having more energy. When you gain weight your overall energy expenditure does go up a lot, but not really in a useful way- you are just supporting the maintenance and physical movement of the extra weight. It’s more useful to think of energy expenditure in proportion to bodyweight.
