How movement activates the body’s longevity pathways

We also examine how mitochondrial health can be assessed through biomarkers and what evidence-based strategies support healthy ageing at the cellular level.

What are mitochondria and why are they important for health?

Mitochondria are specialised structures found inside nearly every cell in the human body. Their primary role is producing energy in the form of adenosine triphosphate (ATP), which powers essential biological processes including muscle contraction, brain activity and immune function.

However, mitochondria do far more than generate energy. They also regulate:

• Cellular metabolism
• Oxidative stress
• Inflammatory signalling
• Apoptosis and cell repair
• Calcium homeostasis

Because of these functions, mitochondrial dysfunction has been identified as one of the central hallmarks of biological ageing (López-Otín et al., 2013).

As mitochondrial efficiency declines with age, cells produce less energy and accumulate damage from reactive oxygen species. This contributes to a range of age-related diseases including cardiovascular disease, metabolic syndrome and neurodegeneration (Sun, Youle and Finkel, 2016).

For this reason, maintaining mitochondrial function is increasingly recognised as a cornerstone of healthy longevity.

What happens when mitochondrial health declines?

When mitochondria become dysfunctional, the effects can be felt across multiple biological systems.

Common consequences include:

Reduced energy production

Cells generate less ATP, leading to fatigue and reduced physical capacity.

Metabolic dysfunction

Impaired mitochondrial oxidation can contribute to insulin resistance and metabolic disease.

Increased oxidative stress

Damaged mitochondria produce higher levels of reactive oxygen species, which accelerate cellular ageing.

Chronic inflammation

Mitochondrial stress can activate inflammatory pathways associated with ageing, sometimes referred to as inflammaging.

These processes collectively contribute to biological ageing and increased risk of chronic disease.

Why exercise is one of the most powerful longevity interventions

Modern geroscience research suggests that exercise influences ageing through mechanisms that extend far beyond cardiovascular fitness.

A review published in the BMJ highlights that physical activity stimulates the release of signalling molecules known as exerkines, which influence metabolic, immune and neurological health across the body (Kaeberlein et al., 2025).

Rather than affecting only muscles, exercise initiates systemic biological signalling that can improve mitochondrial function and cellular resilience.

What are exerkines and myokines?

During physical activity, contracting muscles release signalling proteins called myokines. When combined with signalling molecules released from other tissues in response to exercise, they are collectively referred to as exerkines.

These molecules act as biological messengers that coordinate communication between organs such as the brain, liver, adipose tissue and immune system (Safdar et al., 2016).

Key examples include:

Interleukin-6 (IL-6)
Regulates glucose metabolism and inflammatory responses.

Brain-derived neurotrophic factor (BDNF)
Supports neuronal function, brain plasticity and mitochondrial activity.

Irisin
Promotes metabolic adaptations and may stimulate mitochondrial biogenesis.

These exercise-induced molecules allow skeletal muscle to function as a powerful endocrine organ that influences whole-body physiology.

How exercise improves mitochondrial function

One of the primary ways exercise supports mitochondrial health is through activation of PGC-1α (peroxisome proliferator-activated receptor gamma coactivator 1-alpha), a transcriptional coactivator that regulates mitochondrial biogenesis.

PGC-1α acts as a master controller of mitochondrial production and function, which acts as a transcriptional coactivator that stimulates the formation of new mitochondria inside cells.

When activated during exercise, it promotes:

• Formation of new mitochondria
• Increased oxidative capacity
• Improved metabolic efficiency
• Enhanced endurance capacity

Research has demonstrated that endurance training significantly increases mitochondrial density in skeletal muscle through this pathway (Wu et al., 1999). This process, known as mitochondrial biogenesis, is one of the primary reasons regular physical activity improves metabolic health.

Exercise also activates AMP-activated protein kinase (AMPK), a key cellular energy sensor that stimulates mitochondrial maintenance and fatty acid oxidation (Hardie, 2015).

Together these pathways improve the ability of cells to produce energy efficiently.

AMPK signalling: the cellular energy sensor

AMP-activated protein kinase (AMPK) functions as a metabolic energy sensor within cells.

When cellular energy levels fall, AMPK becomes activated and initiates processes that restore energy balance.

These include:

• Increased glucose uptake
• Enhanced fatty acid oxidation
• Stimulation of mitochondrial biogenesis
• Suppression of energy consuming pathways

Exercise is one of the strongest natural activators of AMPK signalling (Hardie, 2015).

Through this pathway, physical activity improves mitochondrial function and metabolic efficiency.

AMPK activation is also thought to interact with longevity related pathways including sirtuin signalling and autophagy, linking energy metabolism with cellular maintenance

VO₂ max: One of the strongest predictors of longevity

Cardiorespiratory fitness is frequently measured using VO₂ max, the maximum amount of oxygen the body can utilise during intense exercise.

VO₂ max reflects the combined efficiency of the heart, lungs, circulation and mitochondria.

Large cohort studies show that higher cardiorespiratory fitness is strongly associated with lower risk of cardiovascular disease and mortality (Blair et al., 1996).

In fact, VO₂ max has been described as one of the most powerful predictors of long term health outcomes.

Because mitochondrial function determines how efficiently cells use oxygen to generate ATP, improvements in VO₂ max often reflect improved mitochondrial capacity.

Fasting and metabolic switching

Periods of reduced caloric intake can trigger metabolic switching, where the body shifts from glucose metabolism toward fatty acid and ketone utilisation.

This shift activates pathways associated with mitochondrial efficiency and cellular stress resistance.

Fasting states have been shown to stimulate:

• AMPK signalling
• Autophagy (cellular clean-up processes)
• Mitochondrial repair mechanisms

These processes help maintain cellular energy systems and may contribute to improved metabolic resilience (Longo and Mattson, 2014).

However, fasting strategies should be approached cautiously and tailored to individual health conditions.

Why wearables alone cannot measure mitochondrial health

Wearables can provide useful information about activity levels, heart rate variability and sleep patterns.

However, they do not measure internal metabolic processes.

Understanding mitochondrial health requires biomarker data, which provides insight into inflammation, metabolic regulation and nutrient status.

Combining wearable data with blood biomarkers offers a more complete picture of physiological health and biological ageing.

Exercise and the biology of inflammation

Ageing is often associated with chronic low-grade inflammation, sometimes referred to as inflammaging.

Persistent inflammatory signalling contributes to cardiovascular disease, metabolic dysfunction and cognitive decline.

Exercise helps counteract this process.

Regular physical activity has been shown to reduce circulating inflammatory markers and improve immune regulation (Gleeson et al., 2011).

Myokines released during exercise suppress pro-inflammatory cytokines and promote anti-inflammatory signalling, helping protect mitochondrial function.

Can exercise influence telomeres and biological age?

Telomeres are protective DNA structures located at the ends of chromosomes. Each time a cell divides, telomeres shorten slightly.

Over time this shortening contributes to cellular ageing.

Research suggests regular physical activity may help preserve telomere length through multiple mechanisms including:

• Improved metabolic regulation
• Reduced oxidative stress
• Increased telomerase activity

Several studies have shown that physically active individuals tend to have longer telomeres compared with sedentary individuals of the same age (Denham and Sellami, 2021).

These findings suggest exercise may influence cellular ageing pathways directly.

The systemic loop between exercise, mitochondria and ageing

When viewed together, these mechanisms form a biological feedback loop.

1. Muscle contraction stimulates release of exerkines and myokines.
2. These signalling molecules circulate throughout the body.
3. They influence mitochondrial activity, metabolic function and immune regulation.
4. Improved mitochondrial function supports cellular energy production and repair.

This integrated signalling network helps explain why regular movement is associated with lower risk of chronic disease and improved longevity.

How common is physical inactivity in the UK?

Despite the clear biological benefits of exercise, physical inactivity remains common.

Data from the UK Government indicates that around 22 percent of adults in England are physically inactive, meaning they perform less than 30 minutes of moderate activity per week (UK Government, 2024).

A sedentary lifestyle reduces the release of exercise-induced signalling molecules and weakens the biological pathways that support mitochondrial health.

Over time this may contribute to metabolic dysfunction and accelerated biological ageing.

What biomarkers reflect mitochondrial and metabolic health?

Mitochondrial health cannot be measured directly with a single test, but several biomarkers provide insight into the metabolic systems that support mitochondrial function.

Examples include:

C-reactive protein (CRP)

A marker of systemic inflammation that can influence mitochondrial function.

HbA1c

Reflects long-term blood glucose regulation and metabolic health.

Fasting insulin

Elevated levels may indicate insulin resistance and impaired mitochondrial metabolism.

Vitamin B12 and folate

Important cofactors for cellular energy production and mitochondrial function.

Ferritin and iron status

Iron is required for mitochondrial electron transport and oxygen utilisation.

Tracking these markers over time can provide valuable insight into metabolic health and biological ageing processes.

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Evidence-based strategies to support mitochondrial health

Research consistently shows that several lifestyle factors support mitochondrial function.

Regular aerobic exercise

Improves mitochondrial density and oxidative capacity.

Resistance training

Helps maintain muscle mass and mitochondrial function during ageing.

Adequate sleep

Supports mitochondrial repair and metabolic regulation.

Nutrient-dense diet

Provides essential cofactors required for mitochondrial energy metabolism.

Maintaining metabolic health

Reducing insulin resistance and chronic inflammation protects mitochondrial function.

These strategies represent the most well supported interventions for supporting cellular energy systems.

The key takeaway

Exercise does far more than improve physical fitness + Healthy ageing is not driven by a single molecule or supplement.

It activates a network of biological signals that regulate metabolism, inflammation, mitochondrial health and cellular ageing.

Through the release of exerkines and activation of mitochondrial pathways, movement acts as a powerful regulator of longevity biology.

For this reason, physical activity remains one of the most evidence-based strategies for supporting healthy ageing.​​​​​​​

By stimulating mitochondrial biogenesis, regulating inflammation and improving metabolic flexibility, regular movement acts as a biological signal that supports cellular health across the lifespan.

FAQ

What are mitochondria?

Mitochondria are organelles within cells that produce energy in the form of ATP and regulate several important metabolic and signalling pathways.

What are exerkines?

Exerkines are signalling molecules released during exercise that influence metabolic, immune and neurological functions across the body.

Does exercise slow ageing?

Exercise may influence biological ageing by improving mitochondrial function, reducing inflammation and supporting telomere stability.

Can mitochondrial health be measured?

Mitochondrial health cannot be measured directly, but biomarkers such as inflammation markers, glucose metabolism indicators and nutrient levels can provide insight into metabolic systems that support mitochondrial function.