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Here's How Muscle Memory Works | Outside Online
The most significant adaptation to endurance training is an increase in the amount of mitochondria in your cells. When you stop training, the amount of mitochondria declines again. But the extra nuclei, which stick around, contain the genetic information that controls the formation of new mitochondria. As a result, the Temple researchers demonstrated that when you start training again, your cells are already primed to ramp up mitochondria production more rapidly if you’ve been fit before.
Crunched for time? High-intensity exercise gives same cell benefits in fewer minutes: Mitochondrial changes similar in short sprint exercise versus longer moderate-intensity workouts -- ScienceDaily
In addition, the research team found that fewer minutes of higher-intensity exercise produced similar mitochondrial responses compared to a longer moderate-intensity activity. "A total of only two minutes of sprint interval exercise was sufficient to elicit similar responses as 30 minutes of continuous moderate-intensity aerobic exercise," the researchers wrote. "This suggests that exercise may be prescribed according to individual preferences while still generating similar signals known to confer beneficial metabolic adaptions. These findings have important implications for improving our understanding of how exercise can be used to enhance metabolic health in the general population."
Heat therapy boosts mitochondrial function in muscles: Increased capability of cells' energy centers could help treat heart disease, diabetes -- ScienceDaily
Mitochondria, the "energy centers" of the cells, are essential for maintaining good health. A decrease in the number or function of mitochondria may contribute to chronic and potentially serious conditions such as heart disease, chronic obstructive pulmonary disease and type 2 diabetes. Exercise has been shown to create new mitochondria and improve function of existing mitochondria. However, some people with chronic illnesses are not able to exercise long enough -- previous research suggests close to two hours daily -- to reap the benefits. Rodent studies have suggested that heat exposure may also induce the production of more mitochondria.
Researchers from Brigham Young University in Utah studied 20 adult volunteers who had not participated in regular exercise in the three months prior to the study. The research team applied two hours of shortwave diathermy -- a type of heat therapy generated by electrical pulses -- to the thigh muscles of one leg of each person every day. The researchers based the six-day trial of heat on the minimum amount of exercise needed to measure changes in muscle, or about two hours each day. They designed the treatment to mimic the effects of muscle heating that occurs during exercise. The therapy sessions increased the temperature of the heated leg by approximately 7 degrees F. Each participant's other leg served as a control, receiving no heat therapy or temperature change. The researchers looked at mitochondria content in the muscles on the first day of therapy and 24 hours after the last treatment.
Mitochondrial function increased by an average of 28 percent in the heated legs after the heat treatment. The concentration of several mitochondrial proteins also increased in the heated legs, which suggests that "in addition to improving function, [repeated exposure to heat] increased mitochondrial content in human skeletal muscle," the research team wrote.
How Mitochondria Keep Our Brains and Minds Moving – Association for Psychological Science
Although the exact mechanisms through which mitochondria may contribute to such a range of disorders is still poorly understood, the authors wrote, studies suggest that the path to mitochondrial health is a familiar one: Exercise, getting enough sleep, eating a nutrient rich diet, and engaging in stress-reducing activities like yoga and meditation can all have a positive influence.
In one study, rats who swam for 10 to 30 minutes a day for 20 weeks were found to have fewer mutations in their mitochondrial DNA than those who did not. Some research suggests that eating a ketogenic diet high in fat and low in carbohydrates and sugar may improve energy production.
Our circadian clock sets the rhythm for our cells’ powerhouses -- ScienceDaily
Countless genetically controlled clocks tick inside different parts of our bodies, such as the liver, kidneys and heart. Among other things, they initiate many metabolic processes, ensuring that these occur at the optimal time of day.
Mitochondria -- small organelles that exist in almost all our cells and supply them with energy -- play an important role in these cellular processes. Until now, it was unclear how exactly the 24-hour circadian rhythm regulated energy metabolism.
Fission protein sets the rhythm
In most cells, mitochondria connect in a constantly changing network that can adapt to various conditions. Mitochondria can thus fuse together and then divide again. Disruption of this fission-fusion dynamic can lead to health problems.
Researchers have now investigated exactly how the mitochondrial network interacts with our internal biological clock by using a combination of in vitro models and clock-deficient mice or mice with impaired mitochondrial fission.
Their results show that the mitochondrial fission-fusion cycle is controlled by the fission protein Drp1, which is in turn synchronized by an internal biological clock. This rhythm is integral to determining when and how much energy the mitochondria can supply.
"The time of day determines the design of the mitochondrial network, and this, in turn, influences the cells' energy capacity," explains study leader Professor Anne Eckert from the University of Basel's Transfaculty Research Platform Molecular and Cognitive Neurosciences MCN.
Vitamin stops the aging process of organs: Nicotinamide riboside rejuvenates stem cells, allowing better regeneration processes in aged mice -- ScienceDaily
This is why the researchers wanted to "revitalize" stem cells in the muscles of elderly mice. And they did so by precisely targeting the molecules that help the mitochondria to function properly. "We gave nicotinamide riboside to 2-year-old mice, which is an advanced age for them," said the researcher. "This substance, which is close to vitamin B3, is a precursor of NAD+, a molecule that plays a key role in mitochondrial activity. And our results are extremely promising: muscular regeneration is much better in mice that received NR, and they lived longer than the mice that didn't get it."
