What’s Up: November 2026 Skywatching Tips from NASA

 

Meteor Showers, a Spacecraft Milestone, and a Supermoon

Catch Taurid and Leonid meteors, spot Mars near Jupiter, celebrate Voyager 1's light-day milestone, and watch November's supermoon.

Skywatching Highlights

• Around Nov. 5: Southern Taurids peak; occasional bright fireballs
• Around Nov. 12: Northern Taurids peak; around five meteors per hour under ideal conditions
• Nov. 15-16: Mars and Jupiter appear 1.2 degrees apart before sunrise
• Nov. 17: Shine Bright for Voyager’s Light-Day activation
• Nov. 17-18: Leonids before dawn after moonset; up to around 15 meteors per hour under ideal conditions
• Nov. 24: Full supermoon; first in a series of three consecutive supermoons

A full Moon rises over Vasquez Rocks Natural Area and Nature Center north of Los Angeles, California, on June 24, 2021.

Credit: NASA/Preston Dyches

Transcript

A month of meteor showers ... a close pairing of Mars and Jupiter ... and a supermoon!

That’s What’s Up for November.

November offers a buffet of opportunities to see a meteor streak across the sky!

The Southern Taurids peak around November 5th, followed by the Northern Taurids around November 12th.

Those names refer to the two areas in the constellation Taurus, where the meteors appear to originate.

Each Taurid shower produces only a handful of meteors per hour—around five, under ideal conditions—but an occasional bright fireball can make the wait worthwhile.

A sky chart showing where to look for the Leonids in November 2026.

NASA/JPL-Caltech

Next up are the Leonids. For the best viewing times, try the early morning hours of November 17th and 18th, after the Moon sets. Under ideal conditions, the shower could produce around 15 meteors per hour, though most viewers will see fewer.

To level up your viewing experience, you will want to find a dark location, give your eyes about half an hour to adjust, and take in as much sky as you can.

Around mid-month, there’s another reason to head outside early. On the mornings of November 15th and 16th, look southeast before sunrise to see Mars and Jupiter close together.

A sky chart showing Mars and Jupiter close in the night sky.

Credit: NASA/JPL-Caltech

They’ll appear about 1.2 degrees apart—a little more than the width of two full Moons side by side. Jupiter is the brighter point of light, with reddish Mars nearby.

Both planets are easy to see with the unaided eye. They’re still far apart in space, but from Earth, they appear almost side by side.

Watch over several mornings to see them draw closer together - and then go their separate ways.

Artist's rendering of a NASA Voyager spacecraft traveling through interstellar space.

Credit: NASA/JPL-Caltech

This month, NASA’s Voyager 1 spacecraft will reach a historic milestone, becoming the first human-made object to travel one light-day from Earth.

That means a signal traveling at the speed of light takes 24 hours to reach the spacecraft - and another 24 hours for us to hear back from it!

If you want to imagine where Voyager 1 is currently traveling, look in the direction of the constellation Ophiuchus, the Serpent Bearer.

A night sky chart highlights the location of Voyager 1 within the constellation Ophiuchus on November 17 around 5 p.m., looking toward the western horizon.

Credit: NASA/JPL-Caltech

And on November 17th, join us in celebrating this milestone by participating in our Shine Bright for Voyager’s Light-Day activation. Learn more at nasa.gov/voyager.

On November 24th, the evening sky will be lit by a supermoon.

Because the Moon’s orbit is slightly oval, its distance from Earth changes. When it’s closer, the full Moon appears larger and brighter than average - though the difference can be subtle.

This kicks off a series of three consecutive supermoons in November, December, and January.

Look east around sunset to watch it rise. It may look even bigger near the horizon, but that’s the Moon illusion —a common effect with any full Moon.

Here are the phases of the Moon for November:

Moon phases for November 2026, showing the dates for Third Quarter, New Moon, First Quarter, Full "Supermoon," and a concluding Third Quarter in Pacific Time.

Credit: NASA/JPL-Caltech

You can stay up to date on all of NASA's missions exploring the solar system and beyond at NASA Science.

Raquel Villanueva 

Source: What's Up: November 2026 Skywatching Tips from NASA - NASA Science

Why Aging Muscles Trade Strength for Protection

Muscles weaken as we get older, and the mitochondria inside them, the structures that produce much of their energy, become less efficient. That part is expected. What has puzzled researchers is that ageing muscle also shifts toward slow-twitch fibres, the type that depends most heavily on mitochondria. Why would a muscle lean harder on an energy system that is failing? A study from the University of Copenhagen, published in Nature Aging, proposes an answer: the shift is a trade, giving up power in exchange for protection.

Fast fibres, slow fibres and a paradox

Muscle is built from bundles of fibres with different jobs. Fast-twitch fibres deliver powerful, rapid movements but tire quickly. Slow-twitch fibres support sustained activity and contain more mitochondria. With age, the proportion of slow-twitch fibres rises, which looks paradoxical given that their mitochondria are the part that is deteriorating. Similar shifts have been seen in several conditions that cause muscle wasting.

A fat molecule in the spotlight

The team focused on cardiolipin, a specialised lipid found almost exclusively in the inner membrane of mitochondria, where it helps maintain the membrane’s folded structure. Without enough of it, mitochondria struggle to produce energy and the other materials and signals cells need.

The researchers report that cardiolipin levels in muscle mitochondria fall with age and disease in both mice and humans, alongside structural abnormalities and loss of function. To test whether the drop is a cause rather than a bystander, they lowered cardiolipin in young mice. The muscles of these animals moved away from fast-twitch toward slow-twitch fibres, resembling the pattern seen in older mice and people.

Restoring cardiolipin to roughly two-thirds of its normal level began to reverse the muscle wasting in these mice and fully prevented the early deaths seen in the affected animals.

Power traded for protection

Why would the muscle switch fibre type? The proposed explanation runs through reactive oxygen species (ROS), reactive molecules that can damage cell structures but also act as warning signals. When cardiolipin is low, damaged mitochondria produce much more ROS. In muscle cells lacking cardiolipin, an antioxidant reduced the fibre-type transition, suggesting that ROS help trigger it. A protein called ERRγ appears to coordinate the response, telling cells to reorganise their mitochondria and change fibre type. When ERRγ was blocked in cultured muscle cells, the transition stopped entirely.

The remodelled fibres then defend themselves in a specific way. Mice with too little cardiolipin took up considerably more glucose from the blood, but their muscles did not mainly burn it for energy. Tracing labelled glucose showed that it was being diverted toward making the cells’ own antioxidants.

First author Fabian Finger put it this way: the muscle is trading power for protection. That also explains a counterintuitive result. When the mice were given antioxidants to mop up ROS, their muscles did worse, not better, presumably because the signal that triggers the protective adaptation was being removed.

Possible routes to treatment, and the limits

The authors see two potential targets: raising cardiolipin in ageing muscle, or influencing ERRγ to promote healthy adaptation. Cardiolipin can already be targeted in one setting: the FDA recently granted accelerated approval to elamipretide, a drug designed to stabilise cardiolipin, for Barth syndrome, a rare inherited disorder. Whether it would help ordinary age-related muscle loss is unknown. ERRγ belongs to the nuclear receptor family, which is the target of roughly 10 to 15 percent of FDA-approved small-molecule drugs, and drugs that activate ERRγ are being explored in preclinical research for other uses.

·         The protective mechanism and the reversal of muscle wasting were shown in mice and lab-grown cells. Human muscle samples were used only to show that cardiolipin declines with age in people.

·         The results do not show that antioxidant supplements harm muscle in people. The backfiring effect was observed in mice in this specific experimental setting.

·         No treatment for age-related muscle loss based on this work exists yet. Whether raising cardiolipin or targeting ERRγ would work and be safe in older people has not been tested.

The research involved scientists from more than 20 institutions, led by the Novo Nordisk Foundation Center for Basic Metabolic Research at the University of Copenhagen together with the Center for Adipocyte Signaling at the University of Southern Denmark. Funding came from the Novo Nordisk Foundation, the European Research Council, the Lundbeck Foundation, the US National Institutes of Health and other organisations. This post summarises a research finding and is not medical advice.

Sources and further reading

·         Original press release: Hidden Switch Behind Aging Muscle’s Biggest Paradox (University of Copenhagen release, as republished by Mirage News, 29 September 2026)

·         Paper: Finger F, Frost M, Watanabe S, et al., Gerhart-Hines Z. Mitochondrial membrane lipid cardiolipin controls fiber-type adaptations in aging muscle via estrogen-related receptor γ. Nature Aging, 2026. DOI: 10.1038/s43587-026-01227-7

·         Open-access full text of the paper: PubMed Central

Source: Why Aging Muscles Trade Strength for Protection