When the mercury drops, mammals like us have an advantage over so-called cold-blooded critters; our muscles can act as furnaces, generating the heat needed to keep our body temperature stable by turning fuel into movement.

But even when relaxed, our muscles can continue to produce heat – a trick called muscle-based thermogenesis.

As you sit quietly reading this article, appreciate that the development of muscle-based thermogenesis was a key step in your evolution, making it possible for your ancestors to spread into less tropical environments all over the globe.

Now, Australian researchers have identified a specific way that mammalian muscle tissue evolved from those of cold-blooded or 'ectothermic' animals.

"Cold-blooded animals, like 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 authors, University of Queensland biomedical scientist Bradley Launikonis.

But mammals have achieved their geographical freedom by changing the way the concentration of calcium ions is regulated in their resting muscles, setting them on a different course from our ectothermic relatives. This adaptation allows mammalian muscle cells to tolerate higher calcium concentrations in the surrounding fluid, requiring the muscle to expend energy in order to flush the calcium out.

The calcium ion pumps in skeletal muscles work to keep the level of calcium ions steady. Previous research has shown the pump's activity also has an effect on how much heat skeletal muscle makes when it is at rest.

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

The researchers looked at the muscle fibers of mammals and those of ectothermic animals and compared how they worked under the same conditions, finding each resisted the effects of increasing concentrations of calcium ions in different ways.

They analyzed dissolved calcium in muscle fibers from cane toads, mice, and people with malignant hyperthermia, a condition which is often caused by a mutation in a ryanodine receptor that makes calcium channels more likely to open when exposed to a stimulant.

Ryanodine receptors (RyR) are intracellular calcium channels in animal tissue like muscles and neurons, through which calcium ions flow. Calcium ion pumps work in the opposite direction, pumping calcium back the other way, to restore the balance inside cells.

A type called RyR1 is expressed in skeletal muscle in mammals, whereas ectothermic animals express two types of the receptor in their skeletal muscle, αRyR and βRyR.

The results of this study showed that in mammals, abrupt increases in calcium in the fluid surrounding resting muscle fibers cause the ions to accumulate in a membrane-wrapped compartment inside cells called the sarcoplasmic reticulum, rather than be rapidly released.

Usually, an influx of calcium ions into muscle cells triggers RyR channels to release more calcium into the cell's cytoplasm, setting off a cascade that leads to muscle contraction. However, mammals appear to have developed some resistance to rising calcium levels inside their muscle cells.

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

It seems that losing one form of RyR helped mammals' muscles become less sensitive to calcium ion triggers, which in addition to metabolism supports their endothermy.

The research adds details to our understanding of not just mammalian evolution, but our own health, laying important groundwork in understanding how our muscles burn energy even while we're simply chilling out, reading another amazing ScienceAlert article.

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