September 20, 2011
Exercise Increases Mitochondria In Brain Cells
At least in mice exercise increases the number of energy-generating mitochondria in brain cells.
Bethesda, Md. (Sept. 16, 2011)—Researchers have long known that regular exercise increases the number of organelles called mitochondria in muscle cells. Since mitochondria are responsible for generating energy, this numerical boost is thought to underlie many of the positive physical effects of exercise, such as increased strength or endurance. Exercise also has a number of positive mental effects, such as relieving depression and improving memory. However, the mechanism behind these mental effects has been unclear. In a new study in mice, researchers at the University of South Carolina have discovered that regular exercise also increases mitochondrial numbers in brain cells, a potential cause for exercise’s beneficial mental effects.
What I would like to know: Would a before-and-after exercise regimen test of willpower (see Roy Baumeister and John Tierney's excellent book Willpower for a survey of the current state of scientific research on the subject) show that exercise increases one's ability to sustain resistance to temptation and sustain other acts of will? Also, does exercise increase one's ability to sustain concentration on complex tasks?
Does exercise late in life merely add more poorly functioning mitochondria?
Is there a way to increase the efficiency of existing and added mitochondria?
And would a quantum leap in energy levels be detrimental to older people?
Perhaps if I exercised I could answer these questions.
without a doubt consistent hard exercise has beneficial mental effect. seems temporary though. stop exercise, beneficial brain effects soon disappear.
researchers at the University of South Carolina have discovered that regular exercise also increases mitochondrial numbers in brain cells
No shit, Sherlock. It has been known since the late 80's that body building exercise (resistive weight training) increases the natural production of IGF-1, which is necessary for muscle growth. What has also been known since the mid 90's is that the closely related growth factor, IGF-2, is necessary for neurogenesis. Since IGF-1 and IGF-2 are very similar, it is reasonable to assume that the mechanism that produces them would also be similar. Thus, it is reasonable to expect that exercise will increase neurogenesis and protect brains from aging.
Now, can someone remind me why the FDA will not approve therapies to cure aging and why we need such a bureaucracy in the first place? Its our tax dollars at work.
Because they think it's more politically feasible to make sure we die, than to raise the age at which people get social security.
I don't see great physicists and other important scientists being bodybuilders, so it's obvious that whatever the exercise is making, is not making people smarter.
Well, no, we start out with enough mitochondria in the brain, the number just diminishes with time, leaving us with less mental endurance. A bright person who gets mentally fatigued fast is still bright, even if it's not as much use to them. And restoring numbers in a dull person just makes them an alert dull person.
You're still better off being alert than being mentally fatigued all the time, even if it won't transform you from Forrest Gump to Steven Hawking.
I can totally believe this based on first hand experience. I'm 50, and had let my physical condition lapse. Just about 6 weeks after I started running regularly again, I can think more clearly without getting foggy so early in the day.
I also started taking quercetin & dihydroquercetin, not sure if that's had any effect or not...
@Lou P. - the answer is "yes" that the effects are synergistic. Also, Quercetin is particularly suitable for improving immune response among people undergoing extreme physical challenges (a friend of mine at ASU did the original research in this area). Large doses have also been shown to be protective against cancer. I am *not* big on supplements but this is one that I can recommend without reservation.
@fb0252 - umm, yes, if you stop exercising, you'll stop enjoying the benefits of exercise. First, why is that surprising? Second, why would you stop exercising? It is a lifestyle, not a magic pill.
The data on Quercetin is interesting and peek my interest some time ago. But, as is par the course for this area, it's just one university study of modest size being done on a molecule that is a flavonol with several hydroxyl groups hanging off it. Beware such products which are promiscuous and binds to many, many targets.
MDBritt and Vince,
A quick web search indicates that a typical diet provides about 30 mg/day of quercetin.
My guess is that this means vegans probably consume 60-100 mg/day
- so would taking 200 mg/day be reasonable?
I'm not going to speculate on the plasma levels needed to recapitulate the in-vitro results in-vivo, if even possible, but in terms of tolerability the following is taken from: 'A critical review of the data related to the safety of quercetin and lack of evidence of in vivo toxicity, including lack of genotoxic/carcinogenic properties' by Harwood et al., 2007. (http://www.ncbi.nlm.nih.gov/pubmed/17698276)
"In humans, total plasma quercetin levels (i.e., quercetin, quercetin glycosides, glucuronides, and sulfates) between 29 and 248 ng/mL were attained following ingestion of single meals consisting of quercetin-rich foods (∼50 mg quercetin) ( [Hollman et al., 1996] , [de Vries et al., 1998] and [McAnlis et al., 1999] ); however, daily ingestion of 114 mg quercetin from onions for 7 continuous days resulted in total quercetin plasma levels of 453 ng/mL (Janssen et al., 1998). While in earlier human trials the unconjugated quercetin aglycone was not identified in plasma samples following oral administration of the flavonol ( [Manach et al., 1998] , [Erlund et al., 2000] , [Walle et al., 2000] and [Graefe et al., 2001] ), more recent trials utilizing improved detection methods have demonstrated trace quantities of the aglycone in the plasma of one subject ingesting fried onions (Mullen et al., 2004) and mean plasma levels of up to 8 ng/mL in another study in which participants were provided 500 mg quercetin three times daily (t.i.d.) for a period of 5 days (120–350 ng/mL of total quercetin) (Wang and Morris, 2005). Following single-dose administration of 10 mg quercetin per 70 kg of body weight dissolved in different beverages (i.e., vegetable juice, white wine, or grape juice), mean plasma aglycone levels of up to 25 ng/mL were identified, with the highest plasma levels observed when quercetin was provided in wine (Goldberg et al., 2003). Some variability in plasma concentrations of the quercetin aglycone, as observed between the [Wang and Morris, 2005] and [Goldberg et al., 2003] studies, is expected as a result of differences in methods of analysis. Also, the food matrix in which quercetin is administered appears to play a significant role in the bioavailability of the free aglycone following ingestion (Goldberg et al., 2003).
While both animal and human studies have demonstrated that following oral consumption of quercetin as much as 60% of the dose is absorbed (as total quercetin), extensive metabolism as a result of the first-pass effect ensures that the free unconjugated quercetin aglycone circulates in plasma at extremely low concentrations.
There were no reported significant adverse health effects following oral administration of quercetin to humans at doses up to 1000 mg/day for up to 12 weeks. Although nephrotoxicity was reported in a phase I intravenous injection trial, the parenteral route of administration is inappropriate for assessing the safety of orally administered quercetin, because bioavailability of the dietary quercetin aglycone is low or negligible as a result of extensive metabolism. Based on the most recent study demonstrating human plasma aglycone levels of 8 ng/mL following oral administration of 1500 mg quercetin/day (Wang and Morris, 2005), an unrealistically high oral dose (i.e., ∼28 kg of quercetin) would be required in order to attain a plasma quercetin level comparable to that following intravenous administration of 722 mg quercetin (∼150 mg/L), the dose level above which nephrotoxicity occurred in some study subjects. It should be noted that the study group consisted of subjects with compromised health (i.e., cancer patients non-responsive to traditional therapy), and not unlikely a somewhat incapacitated detoxification system. In addition to the controlled clinical trials, a number of epidemiological reports were reviewed which unequivocally support the absence of any relationship between flavonoid consumption from the diet and an increased risk of cancer. The results of the human clinical trials, corroborated by the epidemiological data, together with a safe history of use as a dietary supplement, support findings from oral toxicity studies in animals that the consumption of quercetin at levels proposed for use in foods would not be expected to cause any adverse health effects.
The dose levels in the long-term animal studies at which no toxicologically significant adverse effects were reported support the addition of food-grade quercetin to foods at levels resulting in exposure estimates approximating intakes of naturally-occurring quercetin from the diet by consumers with a high fruit and vegetable intake (i.e., 200–500 mg/day)."
@PacRim Jim Maybe AL carnitine+lipoic acid www.juvenon.com
Does rutin have a similar effect?
It would be good if there were RSS updates for each post comments.
In Uruguay they are working in a liposomal quercetin (so that it reaches the brain) for the treatment of strokes
More papers from Uruguay
Since my Spanish lessons were years ago, I cannot read these reports without great difficulty.
Is the liposome delivery meant to bypass the digestive system or to bypass the blood-brain-barrier?
BTW, according to the reference at http://www.ncbi.nlm.nih.gov/pubmed/19902180, quercetin may make methymercury more toxic.
Rutin looks like it may have potential also.
Sorry Lou, I lost track of this. I wish there were RSS for the comments.
The first article reads they developed a liposomal solution that crosses the cellular barrier and allowed the product to act on the neurons affected by the stroke.
Anyway, what I know from different sources is that it acts on the brain. I should contact the author and ask about the state of development.
The article you link: "Quercitrin (10 microg/mL) and quercetin (10 microg/mL) protected mitochondria from MeHg (5 microM)-induced changes. In contrast, rutin did not afford a significant protective effect"
I don´t know what to think about it. It seems protective in vitro and bad in vivo?. Also why there is methylmercury in the brain? is it normal or an intoxication condition? I would not worry if the latter.