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The Science of Exercise for Cancer | Kerry Courneya, PhD

For decades, exercise was considered an optional part of cancer care—something beneficial for general health but not essential. The evidence is now overwhelming: exercise is not just supportive—it’s a therapeutic intervention that recalibrates tumor biology, enhances treatment tolerance, and improves survival outcomes.

With over 600 peer-reviewed studies, Dr. Kerry Courneya’s work has fundamentally reshaped our understanding of how structured exercise—whether aerobic, resistance training, or high-intensity intervals—can mitigate treatment side effects, enhance immune function, and directly influence cancer progression.

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CHAPTERS:
00:00:00 Introduction.
00:01:47 Why exercise should be effortful.
00:02:33 How to meaningfully reduce risk of cancer.
00:06:22 What type of exercise is best?
00:07:59 How exercise reduces risk—even for smokers and the obese.
00:10:48 Weekend-only exercise.
00:13:49 150 vs. 300 minutes per week (more is better—up to a point)
00:16:03 Why pre-diagnosis exercise matters.
00:19:09 Why resilience to cancer treatment starts with exercise.
00:21:01 Why low muscle mass drives cancer death.
00:23:58 Why BMI fails to measure true obesity.
00:27:51 Why daily activity isn’t enough (structured exercise matters)
00:29:34 Breaking up sedentary time—do ‘exercise snacks’ help?
00:31:50 Supplements vs. exercise.
00:32:32 Where exercise fits with chemo and immunotherapy.
00:35:30 Why rest is not the best medicine.
00:41:20 Aerobic vs. resistance.
00:42:11 How chemotherapy patients were able to put on over a kilogram of muscle.
00:42:13 How weight training improves ‘chemo completion’
00:44:41 Why exercise creates vulnerability in cancer cells (limitations do apply)
00:47:09 Why exercise might be crucial for tumor elimination.
00:53:03 Why cardio may be better at clearing tumor cells.
00:56:18 When cancer spreads quickly—and when it doesn’t.
00:57:43 Why liquid biopsies may prevent over-treatment.
01:02:56 Exercise-sensitive vs. exercise-resistant cancers.
01:06:06 Prostate cancer therapy—why strength training matters.
01:08:10 When exercise is the only therapy—does it work?
01:09:26 Why HIIT reduces PSA in prostate cancer.
01:11:40 Avoiding over-treatment—can exercise buy you time?
01:12:00 Why high-intensity exercise boosts anti-cancer biology.
01:13:11 Turning a diagnosis into a wake-up call.
01:16:11 Why oncologists are rethinking exercise.
01:18:50 Why exercise eases anxiety about cancer—proven psychological benefits.
01:25:00 Before, during, and after treatment.
01:27:02 Why exercise is unique among cancer therapies.
01:28:16 Why cancer patients stop exercising—the risky mistake almost everyone makes.
01:30:41 How to get sedentary cancer patients exercising (realistically)
01:33:15 The $1 million case for including exercise.
01:34:56 Why recurrence trials haven’t convinced doctors—yet.
01:37:36 The bottom-line message.
01:37:55 The myth of a cancer panacea (exercise included)
01:44:07 What’s the best $50 investment for staying active?
01:44:40 Only 15 minutes per day—what’s the best anti-cancer exercise?

A quick cautionary note: Always consult a qualified healthcare provider—presumably an oncologist if your questions involve cancer treatment—particularly if you’re considering actions based on or inspired by our conversation today. This episode should not be construed as a substitute for qualified medical advice.

*Kerry Courneya, PhD*

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Nanoscale tweaks help alloy withstand high-speed impacts

Researchers across 14 medical centers in China, including Peking University People’s Hospital, have found that an investigational drug, berberine ursodeoxycholate (HTD1801), significantly lowered blood sugar levels and improved metabolic and liver health in patients with type 2 diabetes (T2D). The findings and an invited commentary, both published in JAMA Network Open, suggest that HTD1801 could serve as a new oral treatment option for T2D and its related complications.

‘Jumping gene’ caught in the act: Advanced imaging provides new insights into retrotransposons

An arms race is unfolding in our cells: Transposons, also known as jumping genes or mobile genetic elements as they can replicate and reinsert themselves in the genome, threaten the cell’s genome integrity by triggering DNA rearrangements and causing mutations. Host cells, in turn, protect their genome using intricate defense mechanisms that stop transposons from jumping.

Now, for the first time, a retrotransposon has been caught in action inside a cell: Refining cryo-Electron Tomography (cryo-ET) techniques, scientists imaged the retrotransposon copia in the egg chambers of the fruitfly Drosophila melanogaster at sub-nanometer resolution. The paper is published in the journal Cell.

Among the international team of scientists achieving this detailed visualization are three scientists with Vienna BioCenter ties: Sven Klumpe, currently in the laboratory of Jürgen Plitzko at the Max Planck Institute of Biochemistry in Martinsried, will join IMBA and IMP to build a group as a Joint Fellow; Julius Brennecke, a Senior Group Leader at IMBA, the Institute of Molecular Biotechnology of the Austrian Academy of Sciences; and Kirsten Senti, staff scientist in the Brennecke group. Also involved in this collaboration is the group of Martin Beck at the Max Planck Institute of Biophysics in Frankfurt.

New gene switch activates with simple skin patch and could help treat diabetes

ETH researchers have developed a new gene switch that can be activated using a commercially available nitroglycerine patch applied to the skin. One day, researchers want to use switches of this kind to trigger cell therapies for various metabolic diseases.

The body regulates its metabolism precisely and continuously, with specialized cells in the pancreas constantly monitoring the amount of sugar in the blood, for example. When this blood sugar level increases after a meal, the body sets a signal cascade in motion in order to bring it back down.

In people suffering from diabetes, this regulatory mechanism no longer works exactly as it should. Those affected therefore have too much sugar in their blood and need to measure their blood sugar level and inject themselves with insulin in order to regulate it. This is a relatively imprecise approach compared to the body’s own mechanism.

Scientists Successfully Rejuvenate a 53-Year-Old Woman’s Skin Cells by 30 Years

The fields of regenerative medicine and cellular biology are advancing rapidly, demonstrating that some aging-related processes may be more reversible than previously thought.

Recent research has shown that it is possible to rejuvenate the skin cells of a 53-year-old woman by 30 years, a groundbreaking scientific achievement that could redefine modern approaches to treating age-related diseases.

Cellular aging is a complex process marked by gradual changes in cell structure and function. Over time, alterations in gene expression, DNA damage accumulation, and reduced tissue regeneration capacity occur.

Biological Age, Age At Menopause, And Longevity (4 Studies)

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Scientists Just Discovered an RNA That Repairs DNA Damage — And It’s a Game-Changer

Genome Instability and Disease Risk

Every time a cell divides, its DNA is at risk of damage. To complete division, the cell must copy its entire genetic code — billions of letters long — which can lead to occasional errors. But cell division isn’t the only threat. Over time, exposure to factors like sunlight, alcohol, and cigarette smoke can also harm DNA, increasing the risk of cancer and other diseases.

Fortunately, cells have built-in repair systems to counteract this damage. This process, known as the DNA damage response (DDR), activates specific signaling pathways that detect and fix errors. These mechanisms help maintain genetic stability and ensure the cell’s survival.

From classical to quantum: Navier–Stokes equations adapted for 1D quantum liquids

Although Navier–Stokes equations are the foundation of modern hydrodynamics, adapting them to quantum systems has so far been a major challenge. Researchers from the Faculty of Physics at the University of Warsaw, Maciej Łebek, M.Sc. and Miłosz Panfil, Ph.D., Prof., have shown that these equations can be generalized to quantum systems, specifically quantum liquids, in which the motion of particles is restricted to one dimension.

This discovery opens up new avenues for research into transport in one-dimensional quantum systems. The resulting paper, published in Physical Review Letters, was awarded an Editors’ Suggestion.

Liquids are among the basic states of matter and play a key role in nature and technology. The equations of hydrodynamics, known as the Navier–Stokes equations, describe their motion and interactions with the environment. Solutions to these equations allow us to predict the behavior of fluids under various conditions, from the and the in blood vessels, to the dynamics of quark-gluon plasma on subatomic scales.

Inflammation identified as a potential cause of multiple sclerosis progression

For the first time, researchers have identified that inflammation—long associated with multiple sclerosis (MS)—appears to cause increased mutations linked to MS progression.

MS is a progressive neurological disease that affects 33,000 Australians and three million people worldwide. About one-third of people living with MS have progressive disease, which current treatments do not address effectively.

The researchers studied MS brain lesions, visible as spots on MRI scans, which are areas of past or ongoing brain inflammation. They found located in MS brain lesions have a that is two-and-a-half times faster than in normal neurons.

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