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60 minutes of endurance training is enough to shift body clock in mice -- ScienceDaily

This means that exercise is a cue for setting the clocks in muscles. The researchers determined this by studying mice that ran in different phases of the day: in the middle of their rest phase, an hour before starting their active phase, and in the middle of their active phase. Active and rest phases in mice are equivalent to day and night in humans. They then looked at how the amount of a primary clock protein changed over the course of multiple days following muscle contractions. Their results showed that depending on the timing of contractions the clocks shifted about an hour to either an earlier or later time and that this does not require circulating hormones or the central clock.

Muscles support a strong immune system -- ScienceDaily

"If the T-cells, which actively fight the infection, lose their full functionality through continuous stimulation, the precursor cells can migrate from the muscles and develop into functional T-cells," said Jingxia Wu, lead author of the study. "This enables the immune system to fight the virus continuously over a long period." So could regular training strengthen the immune system? "In our study, mice with more muscle mass were better able to cope with chronic viral infection than those whose muscles were weaker. But whether the results can be transferred to humans, future experiments will have to show," explains Guoliang Cui.

How to Make Your Strength Routine Evidence-Based | Outside Online

Put all these results together, shake them around, and you emerge with some fairly simple guidelines for people who want to get stronger but aren’t planning to enter any bodybuilding competitions. Pick a range of exercises covering the body’s major muscle groups (here’s a good place to start, courtesy of Brad Stulberg). Do at least one set of each, several times a week, aiming for about 8 to 12 reps, and be consistent about your routine. If you use lighter weights, push close to failure on each set. To maximize size gains, do more sets.

Vitamin D deficiency is associated with poor muscle function in adults aged 60+ -- ScienceDaily

The prevalence of muscle weakness was twice as high among older adults with vitamin D deficiency (40.4%) compared with vitamin D adequacy (21.6%). Similarly, impaired 'muscle performance' was 3 times higher in older adults with vitamin D deficiency (25.2%) compared with vitamin D adequacy (7.9%). Based on more complex statistical analysis, the study showed that vitamin D deficiency significantly increased the likelihood of impaired muscle strength and performance. The study confirmed the associated benefits of physical activity. Older adults partaking in regular moderate physical activity had significantly lower likelihood of poor muscle strength and physical performance.

One or the other: Why strength training might come at the expense of endurance muscles -- ScienceDaily

This remodeling of the neuromuscular synapses during strength training results in the body developing more strength muscle fibers. "However, strength muscle growth occurs at the expense of the endurance fibers. More precisely, through the release of BDNF, the endurance muscles are transformed into strength muscles," clarifies Handschin. This makes BDNF a factor proven to be produced by the muscle itself and to influence the type of muscle fibers formed.

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.

How do muscles know what time it is? -- ScienceDaily

In collaboration with Italian and Austrian colleagues (from the Venetian Institute of Molecular Medicine and the Universities of Padua, Graz, and Trieste) the researchers identified certain processes that are switched on at night by the regulators of the internal clock: "They include, for example, fat storage, glucose metabolism and insulin sensitivity," explains Henriette Uhlenhaut. At the same time, opposing processes such as fatty acid oxidation and protein breakdown are throttled down, according the authors. These patterns are especially pronounced in the hours before awakening and are thought to prepare the muscles for the day ahead. In the final step, the scientists investigated possible ways to intervene in these processes. To this end, they examined mice lacking these master regulators. Without a circadian clock, the animals were leaner, with less fat and more muscle mass. "Taken together, our work has revealed an entire metabolic network at multiple levels," Uhlenhaut explains. "Another biologically exciting finding is that, contrary to expectations, the key regulator is not centrally located in the brain, but is in fact the internal clock of the muscle cells themselves." In the long term, the authors will investigate the mechanisms also in humans and try to find a way for therapeutic interventions. Their hope is that it might be possible to counteract insulin resistance in type 2 diabetes or to stimulate energy use to combat obesity.

Effects of eight weeks of time-restricted feeding (16/8) on basal metabolism, maximal strength, body composition, inflammation, and cardiovascular risk factors in resistance-trained males

After 8 weeks, the 2 Way ANOVA (Time * Diet interaction) showed a decrease in fat mass in TRF compared to ND (p = 0.0448), while fat-free mass, muscle area of the arm and thigh, and maximal strength were maintained in both groups. Testosterone and insulin-like growth factor 1 decreased significantly in TRF, with no changes in ND (p = 0.0476; p = 0.0397). Adiponectin increased (p = 0.0000) in TRF while total leptin decreased (p = 0.0001), although not when adjusted for fat mass. Triiodothyronine decreased in TRF, but no significant changes were detected in thyroid-stimulating hormone, total cholesterol, high-density lipoprotein, low-density lipoprotein, or triglycerides. Resting energy expenditure was unchanged, but a significant decrease in respiratory ratio was observed in the TRF group.

When muscles weaken with age -- ScienceDaily

Working with our colleagues from the University of Aachen, we first systematically surveyed the changes taking place in the peripheral nerves of people aged between 65 and 79," Rudolf Martini describes his team's approach. During this, the researchers encountered an increased number of macrophages in the samples. Macrophages are cells of our body's immune system that engulf, digest and dispose microbes, foreign substances, cellular debris, aging cells etc. They set inflammatory responses in motion, help heal wounds and cleanse the tissue. Unfortunately, however, they also cause damage in some diseases. To find out whether this also applies to age-related nerve degeneration, the scientists performed an experiment on mice. "For this purpose, we looked more closely at the nerves of 24-month-old mice which is an advanced age for mice," Rudolf Martini explains. It turned out that the age-related changes in the mice's peripheral nerves are very similar to those in humans. As in their human counterparts, the number of macrophages was increased in the mice. Also, the older animals had less strength than their younger siblings and their motor endplates, the synapses connecting nerves and muscle fibres, were also less intact.