Tadej Debevec retweeted
You train to protect your mitochondria from aging. And it works. Exercise preserves mitochondrial energy production into your 90s. But a 2025 study by @GGouspillou and colleagues reveals there's a second mitochondrial function that declines with age no matter how much you nd his colleagues at Université du Québec à Montréal divided 139 men aged 20 to 93 into active and inactive groups. They measured physical performance, muscle composition, and three critical mitochondrial functions: energy production, free radical generation, and calcium handling capacity.
The conventional wisdom says mitochondria wear out with age, becoming a leaky metabolic engine that produces more oxidative stress and becomes less capable of taking nutrients and converting them into ATP.
Direct measurement across 73 years of aging shows that's not necessarily correct.
Mitochondrial energy production stayed completely stable in active participants from their 20s through their 90s.
A 90-year-old who stayed active had mitochondria that produced energy like a 20-year-old. Inactive individuals showed declining energy production, but it tracked with how little they moved, not how many years they'd lived.
When normalized to mitochondrial content, the differences disappeared entirely. The study suggests that aging doesn't break energy production. Physical inactivity reduces how many mitochondria you maintain. Each individual mitochondrion works just as well at 90 as at 20.
Free radical production, blamed for decades as an aging driver, showed no increase with age. Active participants actually produced more free radicals than inactive individuals while displaying superior strength and performance. The free radical theory of muscle aging didn't hold.
The study had some interesting headlines:
• Physical activity protects performance across the lifespan but doesn't completely prevent age-related decline
• Mitochondrial energy production depends on activity level, not chronological age
• Free radical production remains stable with aging and reflects mitochondrial health, not damage
• Mitochondrial calcium handling capacity drops sharply after age 60 in both active and inactive individuals
• Reduced calcium handling correlates with lower muscle mass, strength, and performance
• Deterioration accelerates dramatically after 60 rather than declining gradually
The calcium handling finding represents the first mitochondrial function that deteriorates with aging regardless of exercise. Mitochondria normally act as calcium buffers, absorbing excess calcium to keep cells functioning properly. When this buffering capacity fails, a protective channel called the permeability transition pore opens too easily.
Think of it like a circuit breaker that's supposed to trip only during emergencies but starts tripping at lower and lower thresholds. When the pore opens prematurely, stored calcium floods back into the cell, triggering a cascade of damage.
This calcium release activates pathways that break down muscle protein faster than the body builds it back up. It generates bursts of oxidative stress that damage cellular components. It releases mitochondrial DNA that the immune system mistakes for bacterial invasion, triggering inflammation.
Each pathway drives muscle loss without requiring energy failure. The mitochondria still produce ATP normally. They've just lost the ability to prevent calcium from activating destructive programs that eat away at muscle tissue.
The study measured calcium handling by exposing muscle mitochondria to calcium loads and tracking retention. Both active and inactive participants showed declining capacity, but the pattern matters. Calcium handling remained relatively stable from ages 20 to 60, then dropped sharply after 70.
Calcium retention capacity correlated with thigh muscle mass, knee strength, walking distance, and mobility performance. It also correlated with GDF15, a stress molecule that rises with aging and predicts worse health outcomes. This suggests calcium handling directly influences muscle health and systemic aging markers.
Physical activity protected functional performance. Active participants outperformed inactive individuals on strength and mobility tests across all age groups. But both groups showed age-related declines. Exercise delays deterioration but doesn't eliminate it.
Muscle fiber composition revealed how activity and aging affect muscle differently. Active young adults had more type I endurance fibers that stayed stable across decades. Inactive individuals showed fiber type changes suggesting nerve disconnection from muscle that active individuals avoided.
Intermuscular fat, the marbling that accumulates in muscle tissue, increased with aging in both groups. But physical activity provided protection in later decades. Older active individuals had less fat infiltration than older inactive individuals, though the protective effect only emerged after years of consistent activity.
The implications challenge decades of research direction. Drug development targeting mitochondrial energy production in aging muscle produced zero effective treatments. This study suggests those efforts addressed the wrong problem. Energy production itself doesn't decline with healthy aging.
Calcium handling deterioration appears to be the actual mechanism driving muscle loss.
Restoring calcium buffering capacity or preventing the permeability transition pore from opening prematurely may represent more effective intervention points than trying to boost energy production or mitochondrial numbers.
There are some limitations that stand out when you read the paper:
First, only men participated. So findings may not apply equally to women.
Participants were relatively healthy community-dwelling adults, not people with severe muscle wasting. The design prevents establishing whether calcium handling failure causes muscle loss or just accompanies it.
With that being said, the data fundamentally reframe what aging does to muscle. Energy failure on per mitochondria level isn't the driver in healthy aging. Inactivity reduces mitochondrial numbers while aging leaves energy production intact. The exception, calcium handling deterioration occurring regardless of activity, appears to be where aging actually operates.
The conventional wisdom says mitochondria wear out with age, becoming a leaky metabolic engine that produces more oxidative stress and becomes less capable of taking nutrients and converting them into ATP.
Direct measurement across 73 years of aging shows that's not necessarily correct.
Mitochondrial energy production stayed completely stable in active participants from their 20s through their 90s.
A 90-year-old who stayed active had mitochondria that produced energy like a 20-year-old. Inactive individuals showed declining energy production, but it tracked with how little they moved, not how many years they'd lived.
When normalized to mitochondrial content, the differences disappeared entirely. The study suggests that aging doesn't break energy production. Physical inactivity reduces how many mitochondria you maintain. Each individual mitochondrion works just as well at 90 as at 20.
Free radical production, blamed for decades as an aging driver, showed no increase with age. Active participants actually produced more free radicals than inactive individuals while displaying superior strength and performance. The free radical theory of muscle aging didn't hold.
The study had some interesting headlines:
• Physical activity protects performance across the lifespan but doesn't completely prevent age-related decline
• Mitochondrial energy production depends on activity level, not chronological age
• Free radical production remains stable with aging and reflects mitochondrial health, not damage
• Mitochondrial calcium handling capacity drops sharply after age 60 in both active and inactive individuals
• Reduced calcium handling correlates with lower muscle mass, strength, and performance
• Deterioration accelerates dramatically after 60 rather than declining gradually
The calcium handling finding represents the first mitochondrial function that deteriorates with aging regardless of exercise. Mitochondria normally act as calcium buffers, absorbing excess calcium to keep cells functioning properly. When this buffering capacity fails, a protective channel called the permeability transition pore opens too easily.
Think of it like a circuit breaker that's supposed to trip only during emergencies but starts tripping at lower and lower thresholds. When the pore opens prematurely, stored calcium floods back into the cell, triggering a cascade of damage.
This calcium release activates pathways that break down muscle protein faster than the body builds it back up. It generates bursts of oxidative stress that damage cellular components. It releases mitochondrial DNA that the immune system mistakes for bacterial invasion, triggering inflammation.
Each pathway drives muscle loss without requiring energy failure. The mitochondria still produce ATP normally. They've just lost the ability to prevent calcium from activating destructive programs that eat away at muscle tissue.
The study measured calcium handling by exposing muscle mitochondria to calcium loads and tracking retention. Both active and inactive participants showed declining capacity, but the pattern matters. Calcium handling remained relatively stable from ages 20 to 60, then dropped sharply after 70.
Calcium retention capacity correlated with thigh muscle mass, knee strength, walking distance, and mobility performance. It also correlated with GDF15, a stress molecule that rises with aging and predicts worse health outcomes. This suggests calcium handling directly influences muscle health and systemic aging markers.
Physical activity protected functional performance. Active participants outperformed inactive individuals on strength and mobility tests across all age groups. But both groups showed age-related declines. Exercise delays deterioration but doesn't eliminate it.
Muscle fiber composition revealed how activity and aging affect muscle differently. Active young adults had more type I endurance fibers that stayed stable across decades. Inactive individuals showed fiber type changes suggesting nerve disconnection from muscle that active individuals avoided.
Intermuscular fat, the marbling that accumulates in muscle tissue, increased with aging in both groups. But physical activity provided protection in later decades. Older active individuals had less fat infiltration than older inactive individuals, though the protective effect only emerged after years of consistent activity.
The implications challenge decades of research direction. Drug development targeting mitochondrial energy production in aging muscle produced zero effective treatments. This study suggests those efforts addressed the wrong problem. Energy production itself doesn't decline with healthy aging.
Calcium handling deterioration appears to be the actual mechanism driving muscle loss.
Restoring calcium buffering capacity or preventing the permeability transition pore from opening prematurely may represent more effective intervention points than trying to boost energy production or mitochondrial numbers.
There are some limitations that stand out when you read the paper:
First, only men participated. So findings may not apply equally to women.
Participants were relatively healthy community-dwelling adults, not people with severe muscle wasting. The design prevents establishing whether calcium handling failure causes muscle loss or just accompanies it.
With that being said, the data fundamentally reframe what aging does to muscle. Energy failure on per mitochondria level isn't the driver in healthy aging. Inactivity reduces mitochondrial numbers while aging leaves energy production intact. The exception, calcium handling deterioration occurring regardless of activity, appears to be where aging actually operates.
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Females exercised at a higher relative intensity and derived relatively more energy from blood glucose. M & F had similar leg metabolic responses to hypoxia, with the lower power output and metabolic rate in hypoxic TTs primarily regulated by reduced estimated glycogen oxidation.
New great work by Anders Aagaard Hansen, @Skattebo_Oyvind et al in @JPhysiol
Leg glucose uptake and substrate utilisation during time trial exercise: Effects of acute hypobaric hypoxia and biological sex
physoc.onlinelibrary.wiley.com/doi/full/10.11…
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New great work by Anders Aagaard Hansen, @Skattebo_Oyvind et al in @JPhysiol
Leg glucose uptake and substrate utilisation during time trial exercise: Effects of acute hypobaric hypoxia and biological sex
physoc.onlinelibrary.wiley.com/doi/full/10.11…
Leg glucose uptake and substrate utilisation during time trial exercise: Effects of acute hypobaric hypoxia and biological sex
physoc.onlinelibrary.wiley.com/doi/full/10.11…
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Great work Ben Hunter, @naotofuj et al!
Durability of Physiological Determinants of Distance-Running Performance in Warm and Temperate Environments
onlinelibrary.wiley.com/doi/full/10.11…
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Durability of Physiological Determinants of Distance-Running Performance in Warm and Temperate Environments
onlinelibrary.wiley.com/doi/full/10.11…
onlinelibrary.wiley.com/doi/full/10.11…
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Ketone monoester intake attenuates exercise performance decline in normobaric hypoxia: A post-hoc subgroup analysis of 5 young male adults without acute mountain sickness
physoc.onlinelibrary.wiley.com/doi/10.14814/p…
physoc.onlinelibrary.wiley.com/doi/10.14814/p…
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Tadej Debevec retweeted
Anatomy of the G.O.A.T. - documentary about Tadej Pogačar's incredible way of "playing" with the bicycle starts and finishes in Slovenia 💚
#ifeelsLOVEnia
#ifeelsLOVEnia
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Indeed and unfortunately, the glaciers in the Slovenian mountains are essentially extinct!
Only 2 glaciers remained in Slovenia, Triglav and Skuta! 🧊🔥
The Triglav Glacier can now be considered extinct after the 2026 summer! ✝️
📷 by Bine Mekina on 3rd Sept. 2026
slovenia.si/this-is-sloven…
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Great to see this nice work by my friends from @JSI_SLO and their colleagues published in @PNASNews
Dissociation of gravity and limb dynamics in motor control
pnas.org/doi/10.1073/pn…
Dissociation of gravity and limb dynamics in motor control
pnas.org/doi/10.1073/pn…
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Tadej Debevec retweeted
1/10 🚴 My first PhD paper is out in @JSportsSci
How can cyclists track fitness without frequent maximal tests?
Most submaximal tests use power or HR targets, often based on maximal testing. What if RPE guided intensity instead?
Here's what we found 🧵
tandfonline.com/doi/full/10.10…
How can cyclists track fitness without frequent maximal tests?
Most submaximal tests use power or HR targets, often based on maximal testing. What if RPE guided intensity instead?
Here's what we found 🧵
tandfonline.com/doi/full/10.10…
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Tadej Debevec retweeted
📢 New paper! Among 303 Polish S&C coaches, 31.7% reported clinically relevant depressive symptoms and 34% anxiety symptoms — significantly higher than reported in Polish Olympic coaches and support staff. Coach mental health deserves attention:
doi.org/10.1177/174795…
doi.org/10.1177/174795…
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Tadej Debevec retweeted
少し前は、暑熱順化の効果や適応の進み方には男女差がある、という論が強かった気がします。が、近年ではそうでもないよ、という論文もこのように出てきております
個人的にも、暑熱順化の男女差は、あったとしても大きくない気がします
性差関係なく適応の個人差は大きいので、そっちのほうをより気にすべきかと
個人的にも、暑熱順化の男女差は、あったとしても大きくない気がします
性差関係なく適応の個人差は大きいので、そっちのほうをより気にすべきかと
暑熱順化は、鍛錬した男女持久系ランナーの体温調節・循環機能を同程度改善する！
ことを示すJ Appl Physiolの研究
鍛錬したランナー18名（女性10名）を対象に、全員が40℃と22℃の両環境で、それぞれ10日間にわたり60分間のランニング（最大酸素摂取量到達時の走速度の50%）を計7回実施。両環境で走速度を統一
40℃では22℃と比べて、運動中の体温・心拍数の低下や発汗量の増加（暑熱順化）が大きかった一方、これらの適応の大きさや進み方に明確な男女差は認められなかった
普段からトレーニングしているランナーでも、暑熱順化の効果は男女にかかわらず十分期待できそうです
journals.physiology.org/doi/abs/10.115…
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Tadej Debevec retweeted
tandfonline.com/doi/full/10.10… first "full-text paper" from our Icarus project aiming at better understanding of individual heat vulnerability - who gets dizzy, makes mistakes... when the environmental thermal stress is elevated
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Tadej Debevec retweeted
暑熱順化は、鍛錬した男女持久系ランナーの体温調節・循環機能を同程度改善する！
ことを示すJ Appl Physiolの研究
鍛錬したランナー18名（女性10名）を対象に、全員が40℃と22℃の両環境で、それぞれ10日間にわたり60分間のランニング（最大酸素摂取量到達時の走速度の50%）を計7回実施。両環境で走速度を統一
40℃では22℃と比べて、運動中の体温・心拍数の低下や発汗量の増加（暑熱順化）が大きかった一方、これらの適応の大きさや進み方に明確な男女差は認められなかった
普段からトレーニングしているランナーでも、暑熱順化の効果は男女にかかわらず十分期待できそうです
journals.physiology.org/doi/abs/10.115…
ことを示すJ Appl Physiolの研究
鍛錬したランナー18名（女性10名）を対象に、全員が40℃と22℃の両環境で、それぞれ10日間にわたり60分間のランニング（最大酸素摂取量到達時の走速度の50%）を計7回実施。両環境で走速度を統一
40℃では22℃と比べて、運動中の体温・心拍数の低下や発汗量の増加（暑熱順化）が大きかった一方、これらの適応の大きさや進み方に明確な男女差は認められなかった
普段からトレーニングしているランナーでも、暑熱順化の効果は男女にかかわらず十分期待できそうです
journals.physiology.org/doi/abs/10.115…
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Supporting physiological resilience to climate change through anthropology, environmental exercise physiology and sport science: are we doing enough?
link.springer.com/article/10.100…
link.springer.com/article/10.100…
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New in @JSportsSci
Effects of exogenous ketones on post-exercise recovery: A systematic review and meta-analysis
tandfonline.com/doi/abs/10.108…
Effects of exogenous ketones on post-exercise recovery: A systematic review and meta-analysis
tandfonline.com/doi/abs/10.108…
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Tadej Debevec retweeted
Our special issue on 'Integrative regulation of cerebral blood flow in response to exercise and environmental extremes' is now live! 🧠
Read the introductory Editorial by @DamianMBaileyEP and Shigehiko Ogoh 👇️
buff.ly/odswByJ
Read the introductory Editorial by @DamianMBaileyEP and Shigehiko Ogoh 👇️
buff.ly/odswByJ
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