Our muscles evolved a clever way to keep us warm, even when they’re doing nothing: ScienceAlert

When Mercury drops, mammals like us have an advantage over so-called cold-blooded creatures; Our muscles can act like ovens, generating the heat needed to keep our body temperature stable by converting fuel into motion.

But even when you’re relaxed, our muscles can still produce heat—a trick called muscle-based thermogenesis.

As you sit quietly reading this article, realize that the development of muscle-based thermogenesis was a key step in your evolution, making it possible for your ancestors to spread out in less tropical environments around the world.

Now, Australian researchers have identified a specific way in which mammalian muscle tissue develops from that of cold-blooded or “exothermic” animals.

“Cold-blooded animals, such as frogs and toads, and warm-blooded mammals, such as humans, use the same basic muscle structures to generate force for posture and movement,” said one of the authorsUniversity of Queensland biomedical scientist Bradley Launikonis.

But mammals achieved their geographic freedom by altering the way the concentration of calcium ions is regulated in their muscles at rest, setting them on a different path than our exothermic relatives. This adaptation allows mammalian muscle cells to tolerate higher concentrations of calcium in the surrounding fluid, which requires the muscles to expend energy in order to expel the calcium.

Calcium ion pumps in skeletal muscles stabilize calcium ion levels. previous search Pump activity has also been shown to influence the amount of heat that skeletal muscles give off when they are at rest.

Even the small amounts of heat generated build up in each muscle fiber when you have enough of the skeletal muscles covering your body, allowing your internal temperature to remain constant in cold environments. Add some insulation, and that heat energy can go a long way.

The researchers studied the muscle fibers of mammals and those of outdoor animals and compared how they functioned under the same conditions, finding that each counteracted the effects of increased concentrations of calcium ions in different ways.

They analyzed dissolved calcium in muscle fibers from frogs, mice, and people with malignant hyperthermia, a condition often caused by a mutation in ryanodine receptors that makes calcium channels more likely to open when exposed to a stimulus.

ryanodine receptors (RyR) are intracellular calcium channels in animal tissues such as muscle and nerve cells, through which calcium ions flow. Calcium ion pumps work in the opposite direction, pumping calcium the other way, restoring intracellular homeostasis.

A type called RyR1 is expressed in skeletal muscles in mammals, while exogenous animals express two types of receptors in their skeletal muscles, namely αRyR and βRyR.

The results of this study show that in mammals, sudden increases in calcium in the fluid surrounding relaxed muscle fibers cause ions to accumulate in a membrane-wrapped intracellular compartment called the sarcoplasmic reticulum, rather than to be rapidly released.

Normally, an influx of calcium ions into muscle cells stimulates RyR channels to release more calcium into the cell’s cytoplasm, which triggers a cascade that leads to muscle contraction. However, it appears that mammals have developed some resistance to elevated levels of calcium within their muscle cells.

This is important because it allows for a steady leakage of calcium ions from the sarcoplasmic reticulum, which forces the calcium ion pump to work harder, producing more heat.

Loss of one form of RyR appears to have helped mammalian muscles become less sensitive to calcium ion stimuli, which in addition to metabolism supports them. endothermic.

The research adds detail to our understanding of not only mammalian evolution, but our own health as well, laying an important foundation for understanding how our muscles burn energy even while they are relaxed. Read another amazing article in ScienceAlert.

This research has been published in the journal Proceedings of the National Academy of Sciences.

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