Tiny Cells. BIG Problems.
The Fountain of youth has been discovered.
And no it’s not in some far away paradise, or some mountain spring buried under a mountain.
In fact, the exact location is closer than you can possibly imagine.
And your body holds the key to unlocking the greatest mystery of aging.
YOU have the POWER to unlock this mystery just by looking INSIDE of you.
Give me a minute to explain this wonderful discovery…
Mitochondria and Youth
Inside each of your cells, you hold the key to longevity.
They are small, round and control ALL of your energy needs and demands.
I would be referring to your mitochondria.
The “mighty” mitochondria, just happens to be the powerhouse of ALL your everyday energy needs.
Through different chemical reactions that occur in your mitochondria every second, these reactions create that controls your muscles contractions.
Without this tiny little reactor your CELLS may not function correctly
The problem: when you age, the number and efficiency of your mitochondria dwindle.
This may create greater oxidative stress which might cause damage to the DNA in your mitochondrial cells.
Let me explain…
Through normal metabolism of nutrients, your mitochondria release reactive oxygen species (ROS).
These species may have the ability to create tremendous stress to the rest of your cells and your body.
A lack of efficiency may result in more ROS leaking out of your cells
This may create EVEN MORE damage to the DNA in your mitochondria, possibly DAMAGING IT FOREVER.
The damage may cause mutations to the DNA, possibly creating a GREATER NUMBER of Reactive Oxygen Species.
This viscous cycle may bring on a further decline in efficiency.
Let me back up for just a second.
The Mighty Mitochondria
Mitochondria are located in ALL your cells.
And this tiny powerhouse has a TREMENDOUS amount of responsibility.
Your mitochondria not only produce ATP through aerobic metabolism, but it may also cause cell death, steroid synthesis, heat production (like in brown fat) and the regulation of your calcium levels.
So as you can see, without your mitochondria you may have EVEN BIGGER PROBLEMS in the future.
Low mitochondria numbers may lead to sarcopenia
But what is sarcopenia?
Sarcopenia is the degenerative loss of muscle tissue as you age.
It may cause weakness and frailty which may result in pain and broken bones as you get older.
When you age, you may first see a decrease in muscle size.
And this decrease in size may lead to the weakness.
In some cases, you may see FAT replacing
YOUR MUSCLE TISSUE
One reason for sarcopenia may be caused by atrophy of the mitochondria in your MUSCLE TISSUE.
You may be asking: how can you turn back the hands of time?
And the answer is…
Exercise and YOUR Mitochondria
The easiest way to possibly turn back time, and REVERSE the aging process, is through exercise.
Or at least when talking about the HEALTH of your mitochondria.
You know that exercise may prevent muscle atrophy.
And that exercise may increase the amount of muscle fiber and may increase your strength.
And you also know that you may lose strength and endurance during aging.
Unless you continue to exercise, that is!
Researchers may have determined that exercise may reverse the aging process in your mitochondria.
These researchers determined, damage to your mitochondria may be RESPONSIBLE for muscle atrophy, weakness and functional impairment.
They took biopsies from healthy older adults and younger adults.
What they found was SHOCKING.
The older adults were 59% WEAKER than the younger adults.
So they put BOTH GROUPS through a six-month resistance training program.
After ONLY six months of exercise, those same older adults were only 38% weaker than the younger adults!
The research showed a significant INCREASE in strength and a very interesting change in their mitochondria.
They showed that exercise possibly REVERSED mitochondrial function- matching that of the YOUNGER ADULTS.
Older adults had tremendous mitochondrial
impairment and weakness
But with regular exercise this damage may be REVERSED due to decreased mutation in the DNA of the mitochondria.
In a similar study, exercise dramatically improved in the efficiency of the mitochondria in mice.
They stated that endurance exercise may reduce the risk for chronic diseases and may extend life expectancy.
However, they wanted to see if exercise improved the efficiency of the mitochondria of mice programmed to die younger.
The results were AMAZING!
They showed that five months of endurance exercise stimulated mitochondrial biogenesis, prevented mtDNA depletion and mutations, and increased mitochondrial oxidative capacity.
They also saw restored mitochondrial morphology and a decrease in mitochondrial programmed death.
They concluded that endurance exercise PREVENTED premature mortality by increasing mitochondria numbers and the efficiency of the mitochondria.
Harnessing the Power of Youth
When you age, your muscles may slowly become smaller and weaker from muscle atrophy.
Lack of efficiency of your mitochondria may stimulate the destruction of muscle tissue resulting in more muscle atrophy.
Exercise may the FOUNTAIN of YOUTH
Performing strength and endurance exercise, you may be able to REVERSE or partially REVERSE the aging process.
Exercise may also prevent chronic diseases and possibly extend your life.
Exercise may increase the number of mitochondria, which might prevent premature death in some tissue.
So when you get out of bed with creaky joints or an aching back it finally may be time to participate in regular exercise.
Everyone ages, but now YOU may have the ability to SLOW THE PROCESS, keeping you FOREVER young at heart.
NEXT: Get Your Body Back Here >>
Melov, S. Tarnopolsky, M. Beckman, K. Felkey, K. Hubbard, A. Resistance Exercise Reverse Aging in Human Skeletal Muscle. PLoS ONE. 2007. Vol. 2(5): e465. Doi:10.1371/journal.pone.0000465.
Safdar, A. Bourgeois, J. Ogborn, D. Little, J. Hettinga, B. Akhtar, M. Thompson, J. Melov, S. Mocellin, N. Kujoth, G. Prolla, T. Tarnopolsky, M. Endurance exercise rescues progeriod aging and induces systemic mitochondrial rejuvenation in mtDNA mutator mice. PNAS. 2011. doi: 10.1073/pnas.1019581108.