Mitochondrial Dysfunction Testing: What You Can Measure in 2026

The term “mitochondrial dysfunction” is everywhere. In scientific research, it is considered an important mechanism in ageing and many diseases. In the longevity space, it is also frequently used to explain fatigue, declining performance and chronic symptoms. At the same time, a growing industry is offering “mitochondrial tests” and supplements that promise to improve cellular energy production.

But what does mitochondrial dysfunction actually mean medically? Which symptoms can genuinely point toward a problem? And most importantly: what can meaningfully be measured in 2026, and where does the marketing begin?

This article provides a sober, evidence-based perspective. We separate established diagnostics from speculative approaches and explain how to build a useful picture of your metabolic and functional health without relying on a supposed single “mitochondrial marker”.

What mitochondrial dysfunction actually means

Mitochondrial dysfunction describes impaired mitochondrial processes. This can include reduced oxidative energy production, abnormalities within the respiratory chain, impaired regulation of reactive oxygen species, or problems with mitochondrial quality control.

Mitochondrial dysfunction is not one single disease. It describes a cellular mechanism that can occur across very different conditions.

In rare genetic mitochondrial disorders, a primary defect in mitochondrial function sits at the centre of the disease. Changes in mitochondrial biology are also studied in relation to ageing, metabolic disease, neurodegenerative disorders and many chronic conditions.

Mitochondria: more than cellular power plants

Mitochondria are often described as the “power plants of the cell”. That captures one of their major roles, but it is an oversimplification.

A large proportion of cellular energy is generated in the form of adenosine triphosphate, or ATP, through oxidative phosphorylation inside mitochondria.

Their functions go well beyond ATP production. Mitochondria are involved in:

• fatty acid oxidation
• cellular calcium regulation
• multiple metabolic pathways
• regulation of programmed cell death
• production and regulation of reactive oxygen species
• several steps involved in steroid hormone synthesis

Mitochondria also contain their own DNA, known as mitochondrial DNA or mtDNA.

This complexity already highlights an important diagnostic problem: there is no single measurable entity called “mitochondrial health”.

The respiratory chain: energy production and signalling

A central component of mitochondrial energy production is the respiratory chain within the inner mitochondrial membrane.

Electrons derived from carbohydrate and fat metabolism are transferred through several protein complexes. The resulting energy creates a proton gradient, which is ultimately used to generate ATP.

Reactive oxygen species, or ROS, are also produced during this process.

ROS are often described purely as harmful “free radicals”. That is too simplistic. At physiological concentrations, they play important roles in cellular signalling.

Problems arise when ROS production and cellular protective systems become imbalanced.

Depending on the underlying cause, mitochondrial dysfunction may involve:

1. reduced oxidative ATP production
2. altered oxygen utilisation
3. impaired ROS regulation
4. abnormalities in mitochondrial dynamics and quality control

Which of these processes is affected depends strongly on the underlying condition.

Why there is no single “mitochondrial blood marker”

Overall mitochondrial function cannot be captured by one blood test.

A single marker cannot simultaneously tell you:

• how efficiently the respiratory chain is working
• how high the oxidative capacity of skeletal muscle is
• how efficiently fatty acids are being oxidised
• whether mitochondrial DNA is intact
• how mitochondria respond to exercise
• how effectively damaged mitochondria are removed and replaced

Specialised research laboratories can directly assess certain aspects of mitochondrial function.

For example, they can measure oxygen consumption in living cells under different conditions. These techniques can provide detailed information about cellular bioenergetics.

However, they are technically demanding, heavily influenced by cell type, sample processing and laboratory protocol, and are currently not established screening tools for healthy individuals.

That distinction matters.

Being able to measure something does not automatically mean that the result improves clinical decision-making.

Non-specific symptoms: fatigue, reduced performance and exhaustion

Chronic fatigue, unexplained reductions in performance, concentration problems or poor recovery are frequently linked to mitochondrial dysfunction.

The biological reasoning initially sounds plausible: if cellular energy production is impaired, overall performance may also decline.

The problem is that these symptoms are highly non-specific.

Similar symptoms can occur with:

• iron deficiency or iron-deficiency anaemia
• vitamin B12 deficiency
• thyroid disease
• insufficient sleep
• sleep disorders
• infections
• medication side effects
• psychological stress
• insufficient calorie or nutrient intake
• cardiovascular disease
• pulmonary disease
• overtraining or insufficient recovery

Fatigue alone is therefore not evidence that your mitochondria are “not working properly”.

Before considering specialised cellular testing, structured medical baseline diagnostics are usually far more useful.

Mitochondrial disease: which symptoms are actually relevant?

Primary mitochondrial diseases often present with several symptoms at the same time. Tissues with high energy demands are particularly vulnerable, including skeletal muscle, the nervous system and the heart.

Neuromuscular symptoms

Possible manifestations of mitochondrial disease include:

• muscle weakness
• marked exercise intolerance
• rapid muscular fatigue
• muscle pain or cramps
• ptosis, or drooping eyelids
• impaired eye movement
• neurological abnormalities
• certain forms of hearing loss

When these symptoms raise clinical suspicion, diagnosis is not based on a simple commercial “mitochondrial test”. It requires specialist medical assessment.

Depending on the clinical question, this may include genetic testing, biochemical diagnostics, imaging, muscle investigations and functional exercise testing.

ME/CFS and mitochondrial changes

Changes in energy metabolism and muscle metabolism are also being studied in myalgic encephalomyelitis/chronic fatigue syndrome, or ME/CFS.

Several studies describe metabolic and bioenergetic abnormalities.

However, the disease cannot be reduced to a single mitochondrial problem.

ME/CFS is a complex multisystem condition. Immunological, autonomic, vascular, neurological and metabolic mechanisms remain under investigation.

Referring to “the mitochondrial cause” of ME/CFS would therefore go beyond what the current evidence supports.

Metabolic and cardiovascular disease

Changes in mitochondrial processes are also observed in many common conditions, including:

• insulin resistance
• type 2 diabetes
• metabolic dysfunction-associated steatotic liver disease
• certain cardiomyopathies
• neurodegenerative diseases

It is important, however, to separate cause from consequence.

The presence of mitochondrial changes within a disease does not automatically mean that primary mitochondrial dysfunction is the sole cause of that disease.

Why laboratory markers alone are rarely diagnostic

Traditional laboratory parameters can provide clues, but they usually cannot confirm a mitochondrial disorder on their own.

Lactate is one example.

Lactate can be elevated in certain mitochondrial diseases. However, elevated lactate has many other potential causes and is strongly influenced by sample collection, recent exercise, circulatory status and sample handling.

The lactate-to-pyruvate ratio can also provide useful information in specific contexts. It is primarily meaningful when lactate itself is elevated.

A fixed threshold on its own does not diagnose mitochondrial disease.

When there is a genuine clinical suspicion, diagnosis depends on the overall picture, including:

• symptoms
• family history
• physical examination
• laboratory findings
• functional testing
• genetic diagnostics where appropriate
• additional specialist investigations

For preventive medicine, however, another question is often more useful:

How well do your metabolism, cardiovascular system and muscles actually function in everyday life and under stress?

What can actually be measured in 2026?

The question “Can you test mitochondria?” cannot be answered with a simple yes or no.

Certain aspects of mitochondrial function can be measured directly in laboratory settings.

For healthy individuals, however, these tests are not currently established as routine preventive diagnostics.

In clinical practice, other measurements are often more useful because they show how well the physiological system actually performs.

Research: direct measurement of cellular bioenergetics

One scientific approach is to measure mitochondrial respiration in living cells.

For example, immune cells can be isolated and their oxygen consumption assessed.

Under controlled conditions, parameters can include:

• basal respiration
• ATP-linked respiration
• maximal respiratory capacity
• respiratory reserve

Composite measures such as the Bioenergetic Health Index, or BHI, have also been proposed based on these measurements.

These methods are scientifically interesting.

For broad preventive use, however, there are still important limitations:

• sample handling can influence results
• different cell types can produce different findings
• protocols are not universally standardised
• reference ranges are not broadly established
• the additional clinical value in healthy people remains unclear
• they are not part of routine preventive diagnostics

Direct cellular measurements are therefore mainly research tools and may be useful for selected medical questions.

They should not be confused with an established general “mitochondrial health check”.

Functional assessment: VO₂max and cardiopulmonary exercise testing

If you want to know how well your overall aerobic energy system performs, cardiopulmonary exercise testing, or CPET, is one of the most informative established methods.

VO₂max, or VO₂peak, describes how much oxygen your body can take up and utilise during intense or maximal exercise.

The result depends on several systems working together:

• ventilation and lung function
• cardiac output
• oxygen transport in the blood
• blood flow to working muscle
• oxygen extraction in the tissues
• oxidative capacity of muscle cells

Mitochondria play a central role in this process, but CPET does not measure them in isolation.

A reduced VO₂max can have many causes. It may be influenced by training status, cardiac function, pulmonary disease, oxygen transport, circulation or muscle abnormalities.

A low VO₂max is therefore not specific evidence of mitochondrial dysfunction.

This integration of several organ systems is precisely what makes CPET so useful in preventive medicine.

It does not tell you how one isolated cellular pathway performs. It shows how well the entire oxygen transport and aerobic energy system functions under stress.

Cardiorespiratory fitness is also one of the best-studied functional health parameters.

Large observational studies consistently show a strong inverse association between cardiorespiratory fitness and long-term mortality risk.

Cardiopulmonary exercise testing with measurement of VO₂peak or VO₂max is therefore a central component of the YEARS Core® check-up.

Indirect markers within the YEARS Core® programme

Mitochondria do not operate independently from the rest of the body.

Metabolic health, inflammation, nutrient status, training status and cardiovascular performance all influence the biological environment in which cellular energy production takes place.

Within the YEARS Core® programme, we therefore assess a range of established parameters that reflect relevant parts of this wider system.

Glucose metabolism and insulin sensitivity

Insulin resistance is one of the most important metabolic risk factors for many chronic diseases.

Markers of glucose metabolism can help identify impaired metabolic regulation before overt diabetes develops.

Depending on the assessment, relevant measurements may include fasting glucose, HbA1c, insulin or calculated indices.

These markers do not directly measure mitochondrial function.

They do, however, provide important information about metabolic health.

Heart rate variability

Heart rate variability, or HRV, describes variation in the time intervals between heartbeats and provides information about autonomic cardiovascular regulation.

It is influenced by training status, stress, sleep, illness, age and many other factors.

HRV is not a marker of mitochondrial health.

It can, however, provide additional information about autonomic regulation and physiological load.

Omega-3 Index

The Omega-3 Index reflects the proportion of certain omega-3 fatty acids within red blood cell membranes.

Omega-3 fatty acids are components of biological membranes and are associated with several cardiovascular and inflammatory processes.

Again, the same principle applies:

The Omega-3 Index is not a test of mitochondrial function.

hs-CRP

High-sensitivity C-reactive protein, or hs-CRP, is a marker of systemic inflammatory activity.

Chronic low-grade inflammation is associated with many metabolic and cardiovascular diseases.

Inflammatory pathways and mitochondrial processes can also influence each other biologically.

An elevated hs-CRP level does not, however, tell you whether mitochondrial dysfunction is present.

Ferritin and selected micronutrients

Iron is essential for oxygen transport and many enzymatic processes.

Significant iron deficiency can therefore lead to fatigue, reduced performance and impaired exercise tolerance.

Ferritin is one of the key markers used to assess iron stores, although it must be interpreted within the clinical context because inflammation can also affect ferritin concentrations.

Other micronutrient deficiencies can likewise impair relevant metabolic processes when a genuine deficiency is present.

The key message remains:

None of these markers directly measures mitochondrial function.

Together, however, they provide a far more useful picture of systemic health than overinterpreting a single supposed “mitochondrial marker”.

What helps, and what the evidence does not support

When it comes to maintaining healthy mitochondrial function, the most effective interventions are relatively unremarkable.

Physical activity in particular is a very strong stimulus for adaptations in mitochondrial energy metabolism.

Exercise and training

Endurance training produces numerous adaptations in skeletal muscle.

These include:

• increased mitochondrial capacity
• changes in mitochondrial enzymes
• improved oxidative energy production
• improved use of fats and carbohydrates
• increased capillarisation
• improved cardiorespiratory fitness

Signalling pathways such as PGC-1α and AMPK play important roles in these adaptations.

Both moderate endurance training and high-intensity interval training can increase mitochondrial content and oxidative capacity in skeletal muscle.

The magnitude of these changes varies substantially between studies and depends on training status, training protocol, duration and measurement method.

Fixed statements such as “six weeks of training increase mitochondrial density by 40%” are therefore too general for the broader population.

Resistance training

Resistance training also has positive effects on muscle metabolism.

Some adaptations differ from those seen with traditional endurance training. For long-term health, physical performance and function, both training modalities are relevant.

A sensible combination of endurance and resistance training therefore targets more physiological systems than either form alone.

Sleep

Sleep influences nearly every major regulatory system in the body.

Chronic sleep restriction can:

• impair insulin sensitivity
• affect inflammatory processes
• alter hormonal regulation
• reduce training performance and recovery
• alter metabolic processes

Mitochondrial processes and cellular quality control are also influenced by sleep-wake rhythms.

However, the exact role of individual processes such as mitophagy in humans cannot be reduced to the statement that “mitochondria are repaired during deep sleep”.

For most adults, professional guidelines generally recommend regularly getting at least seven hours of sleep per night, although individual needs vary.

Metabolic health

Good metabolic health also supports the physiological conditions required for efficient cellular energy production.

More important than trying to avoid individual short-term “glucose spikes” are longer-term factors such as:

• energy balance
• body composition
• fibre intake
• overall diet quality
• physical activity
• insulin sensitivity
• blood pressure
• blood lipids
• sleep

Metabolism should therefore be assessed as a wider system.

NAD+, CoQ10 and other “mitochondrial supplements”

A growing part of the longevity market is built around products that claim to improve mitochondrial function.

These include:

• coenzyme Q10
• nicotinamide riboside, or NR
• nicotinamide mononucleotide, or NMN
• alpha-lipoic acid
• various antioxidants

Many of these molecules have biologically plausible roles.

That alone is not evidence that supplementation produces meaningful health benefits.

Coenzyme Q10

Coenzyme Q10 plays an important role within the mitochondrial electron transport chain.

Supplementation can be useful in selected medical situations.

That does not automatically mean that taking additional CoQ10 improves mitochondrial performance or extends lifespan in every healthy person.

NAD+ precursors

NAD+ is an important coenzyme involved in many metabolic and cellular processes.

NR and NMN can increase NAD+-related metabolites in humans.

That does not yet show that long-term supplementation in healthy people:

• prevents cardiovascular disease
• reduces cancer risk
• extends lifespan
• meaningfully slows human ageing

Many promising findings still come from animal models, cell studies or relatively small human trials.

The evidence for hard clinical outcomes remains far less convincing.

The limits of lifestyle interventions

Exercise, sleep and metabolic health can substantially influence mitochondrial metabolism and physical performance.

They are not treatments for every form of mitochondrial disease.

Primary genetic mitochondrial disorders are rare, sometimes severe diseases that require specialist medical care.

It would be medically incorrect to suggest that a respiratory-chain disorder can simply be “fixed” with exercise, fasting or supplements.

For preventive medicine, a different approach makes more sense.

Rather than diagnosing a difficult-to-measure “mitochondrial dysfunction” whenever someone reports fatigue or reduced performance, the first step should be to identify established risk factors, functional limitations and medical causes that can actually be assessed.

Conclusion: what you can actually do

Mitochondrial dysfunction is a real biological phenomenon.

The term is used far more often, however, than it is actually demonstrated diagnostically in individual people.

There is currently no simple blood test that can reliably tell you:

“Your mitochondria are 73% healthy.”

For most people, a different approach is more useful.

1. Take symptoms seriously without jumping to one explanation

Fatigue, reduced performance or poor recovery can be medically relevant.

They can also have many possible causes.

Structured baseline diagnostics should therefore come before highly specialised testing.

2. Measure function rather than isolated mechanisms

Cardiopulmonary exercise testing does not directly measure mitochondria.

It does, however, show how well your overall aerobic system performs under stress.

That includes the oxidative capacity of skeletal muscle.

This is exactly why it is so useful in preventive medicine.

3. Assess metabolic and cardiovascular risk

Blood pressure, blood lipids, glucose metabolism, body composition and other established risk factors often provide more clinically relevant information than experimental “mitochondrial scores”.

4. Start with the best-supported interventions

Regular endurance exercise, resistance training, sufficient sleep, a balanced diet and treatment of established risk factors have much stronger evidence behind them than most so-called mitochondrial supplements.

How we assess this at YEARS

At YEARS, we do not perform an isolated “mitochondrial test”.

Instead, we assess the systems that are central to metabolism, oxygen transport, physical performance and long-term health.

One particularly important component is cardiopulmonary exercise testing.

This allows us to measure the functional performance of the entire aerobic system. That includes the heart, lungs, circulation, oxygen transport, skeletal muscle and oxidative energy production within muscle cells.

Mitochondrial capacity contributes to this performance, but it is not measured in isolation.

We then interpret these findings alongside relevant metabolic, cardiovascular and functional parameters.

Within the YEARS Core® check-up, this forms part of a broad preventive medical assessment with more than 87 markers and examinations.

These include:

• cardiopulmonary exercise testing
• metabolic laboratory diagnostics
• cardiovascular risk factors
• body composition
• lung function
• functional performance testing
• additional individually relevant assessments

The results are then reviewed together with a physician.

The goal is not to measure as many unusual biomarkers as possible.

It is to collect the data that actually helps identify risk, understand functional performance and derive meaningful next steps.

References

• Chacko, B. K., Kramer, P. A., Ravi, S., Johnson, M. S., Mitchell, T., & Darley-Usmar, V. M. (2014). The Bioenergetic Health Index: a new concept for evaluating mitochondrial bioenergetic function in human patient samples. Redox Biology, 2, 280–282. DOI: 10.1016/j.redox.2014.02.007
• Germain, A., Ruppert, D., Levine, S. M., & Hanson, M. R. (2017). Metabolic profiling of a myalgic encephalomyelitis/chronic fatigue syndrome discovery cohort reveals disturbances in fatty acid and lipid metabolism. Journal of Translational Medicine, 15, 164. DOI: 10.1186/s12967-017-1261-5
• Mandsager, K., Harb, S., Cremer, P., Phelan, D., Nissen, S. E., & Jaber, W. (2018). Association of Cardiorespiratory Fitness With Long-term Mortality Among Adults Undergoing Exercise Treadmill Testing. JAMA Network Open, 1(6), e183605.
• Parikh, S., Goldstein, A., Koenig, M. K., et al. (2015). Diagnosis and management of mitochondrial disease: a consensus statement from the Mitochondrial Medicine Society. Genetics in Medicine, 17, 689–701.
• Granata, C., Jamnick, N. A., & Bishop, D. J. (2018). Training-induced changes in mitochondrial content and respiratory function in human skeletal muscle. Sports Medicine, 48, 1809–1828.