The theoretical notion of a ‘quantum heat engine’ has been around for several decades. It was first introduced around sixty years ago by Scovil and Schulz-DuBois, two physicists at Bell Labs who drew an analogy between three-level masers and thermal machines.

In the years that followed, other researchers have developed a variety of theories building on the ideas of Scovil and Schulz-DuBois, introducing proposals of thermodynamic cycles at the quantum scale. Very recently, physicists have started testing some of these theories in experimental settings.

One of these experiments was carried out by a team of researchers at the University of Waterloo, Universidade Federal do ABC and Centro Brasileiro de Pesquisas Físicas, who successfully demonstrated a spin quantum heat engine in a laboratory setting. Their paper, published in Physics Review Letters, outlines the implementation of a heat engine based on a spin-1/2 system and nuclear magnetic resonance techniques.

“The so-called ‘quantum thermodynamics’ are currently under development,” Roberto Serra, one of the researchers who carried out the study, told Phys.org. “This emerging field is also associated with developments in quantum technology, which promises a kind of new industrial revolution at the nanoscale with disruptive devices for computation, communication, sensors, etc.”

In their experiment, Serra and his colleagues successfully implemented a proof-of-principle quantum heat engine using a nuclear spin placed in a chloroform molecule and nuclear magnetic resonance techniques. The researchers specifically manipulated the nuclear spin of a Carbon 13 isotope using a radiofrequency field, ultimately producing an Otto cycle (i.e., the thermodynamic cycle used in most common motors).

“The energy difference between the two possible nuclear spin states (let as say up and down) was increased and decreased similar to a piston expansion and compression in a car engine,” Serra explained. “Under some conditions, the nuclear spins in the molecule can absorb and release heat from/to radio waves.”

Energy fluctuations play a crucial role in the quantum scenario that Serra and his colleagues focused on. Measuring these fluctuations in a thermodynamic cycle, however, is an extremely challenging task, which the researchers were surprisingly able to complete. They found that when performing a quantum Otto cycle at maximum power, their quantum heat engine could achieve an efficiency for work extraction of η≈42%, which is very close to its thermodynamic limit (η=44%).

“In the present experiment, we were able to characterize all energy fluctuations in work and heat, besides the irreversibility at the quantum scale,” John Peterson one of the co-authors of the study, told Phys.org. “Fast operation of our molecular machine produces transitions between the spin energy states, which are related to what we call ‘quantum friction’ that reduces performance. This kind of friction is also associated with an increase in entropy. On the other hand, a very slow operation (that decreases quantum friction) will not deliver a considerable amount of extracted power. So, the best scenario is to conciliate some amount of power with low levels of quantum friction or entropy production, in a similar way to what modern engineering does in cars’ engines.”

The study carried out by Serra and his colleagues is among the first to experimentally demonstrate a proof-of-concept spin quantum heat engine. This proof-of-concept heat engine could ultimately inform future studies exploring the functioning and potential of quantum thermal machines.

“In our experiment, the tiny spin engine reaches an efficiency close to its thermodynamic limit at maximum power, which is much better than what car engines can do nowadays,” Serra said. “The quantum spin engine would not be very useful in practice since the work produced would supply a very small amount of energy to radio waves. It would only be sufficient to alter another nuclear spin. We are more interested in measuring how much energy it uses, how much heat it dissipates, and how much entropy is produced during operation.”

In their future work, Serra and his colleagues also hope to identify ways to optimize the operation of small quantum thermal machines, demonstrating their effectiveness in real experiments. This could ultimately help to build more advanced quantum refrigerators that could be implemented in new quantum computers.

Grizzly bears spend many months in hibernation, but their muscles do not suffer from the lack of movement. In the journal Scientific Reports, a team led by Michael Gotthardt reports on how they manage to do this. The grizzly bears’ strategy could help prevent muscle atrophy in humans as well.

A grizzly bear only knows three seasons during the year. Its time of activity starts between March and May. Around September the bear begins to eat large quantities of food. And sometime between November and January, it falls into hibernation. From a physiological point of view, this is the strangest time of all. The bear’s metabolism and heart rate drop rapidly. It excretes neither urine nor feces. The amount of nitrogen in the blood increases drastically and the bear becomes resistant to the hormone insulin.

A person could hardly survive this four-month phase in a healthy state. Afterwards, he or she would most likely have to cope with thromboses or psychological changes. Above all, the muscles would suffer from this prolonged period of disuse. Anyone who has ever had an arm or leg in a cast for a few weeks or has had to lie in bed for a long time due to an illness has probably experienced this.

A little sluggish, but otherwise fine

Not so the grizzly bear. In the spring, the bear wakes up from hibernation, perhaps still a bit sluggish at first, but otherwise well. Many scientists have long been interested in the bear’s strategies for adapting to its three seasons.

A team led by Professor Michael Gotthardt, head of the Neuromuscular and Cardiovascular Cell Biology group at the Max Delbrueck Center for Molecular Medicine (MDC) in Berlin, has now investigated how the bear’s muscles manage to survive hibernation virtually unharmed. The scientists from Berlin, Greifswald and the United States were particularly interested in the question of which genes in the bear’s muscle cells are transcribed and converted into proteins, and what effect this has on the cells.

Understanding and copying the tricks of nature

“Muscle atrophy is a real human problem that occurs in many circumstances. We are still not very good at preventing it,” says the lead author of the study, Dr. Douaa Mugahid, once a member of Gotthardt’s research group and now a postdoctoral researcher in the laboratory of Professor Marc Kirschner of the Department of Systems Biology at Harvard Medical School in Boston.

“For me, the beauty of our work was to learn how nature has perfected a way to maintain muscle functions under the difficult conditions of hibernation,” says Mugahid. “If we can better understand these strategies, we will be able to develop novel and non-intuitive methods to better prevent and treat muscle atrophy in patients.”

Gene sequencing and mass spectrometry

To understand the bears’ tricks, the team led by Mugahid and Gotthardt examined muscle samples from grizzly bears both during and between the times of hibernation, which they had received from Washington State University. “By combining cutting-edge sequencing techniques with mass spectrometry, we wanted to determine which genes and proteins are upregulated or shut down both during and between the times of hibernation,” explains Gotthardt.

“This task proved to be tricky—because neither the full genome nor the proteome, i.e., the totality of all proteins of the grizzly bear, were known,” says the MDC scientist. In a further step, he and his team compared the findings with observations of humans, mice and nematode worms.

Non-essential amino acids allowed muscle cells to grow

As the researchers reported in the journal Scientific Reports, they found proteins in their experiments that strongly influence a bear’s amino acid metabolism during hibernation. As a result, its muscle cells contain higher amounts of certain non-essential amino acids (NEAAs).

“In experiments with isolated muscle cells of humans and mice that exhibit muscle atrophy, cell growth could also be stimulated by NEAAs,” says Gotthardt, adding that “it is known, however, from earlier clinical studies that the administration of amino acids in the form of pills or powders is not enough to prevent muscle atrophy in elderly or bedridden people.”

“Obviously, it is important for the muscle to produce these amino acids itself—otherwise the amino acids might not reach the places where they are needed,” speculates the MDC scientist. A therapeutic starting point, he says, could be the attempt to induce the human muscle to produce NEAAs itself by activating corresponding metabolic pathways with suitable agents during longer rest periods.

Tissue samples from bedridden patients

In order to find out which signaling pathways need to be activated in the muscle, Gotthardt and his team compared the activity of genes in grizzly bears, humans and mice. The required data came from elderly or bedridden patients and from mice suffering from muscle atrophy—for example, as a result of reduced movement after the application of a plaster cast. “We wanted to find out which genes are regulated differently between animals that hibernate and those that do not,” explains Gotthardt.

However, the scientists came across a whole series of such genes. To narrow down the possible candidates that could prove to be a starting point for muscle atrophy therapy, the team subsequently carried out experiments with nematode worms. “In worms, individual genes can be deactivated relatively easily and one can quickly see what effects this has on muscle growth,” explains Gotthardt.

A gene for circadian rhythms

With the help of these experiments, his team has now found a handful of genes whose influence they hope to further investigate in future experiments with mice. These include the genes Pdk4 and Serpinf1, which are involved in glucose and amino acid metabolism, and the gene Rora, which contributes to the development of circadian rhythms. “We will now examine the effects of deactivating these genes,” says Gotthardt. “After all, they are only suitable as therapeutic targets if there are either limited side effects or none at all.”