Quick Answer: Why Exercise Is Such an Important Clue in MOTS-c Research
Exercise is more than a test of cardiovascular fitness. At the cellular level, exercise creates a controlled metabolic challenge: ATP demand rises, substrate availability changes, mitochondrial respiration increases, redox conditions shift and skeletal muscle must rapidly adapt to energetic stress.
That makes exercise an unusually informative environment for studying MOTS-c, a 16-amino-acid mitochondrial-derived peptide encoded within the mitochondrial 12S rRNA region.
Researchers have investigated MOTS-c in the context of acute exercise, endurance training, skeletal-muscle metabolism and mitochondrial function. Human studies have reported exercise-associated changes in circulating MOTS-c, while newer experimental work has connected MOTS-c with skeletal-muscle mitochondrial bioenergetics and the AMPK/PGC-1α network.
But the most important scientific point is also the easiest to miss: exercise research does not prove that exogenous MOTS-c improves athletic performance. Instead, it provides clues about how mitochondrial stress may interact with peptide signaling and cellular adaptation.
Key Takeaways
- Exercise creates a measurable mitochondrial and metabolic stress environment in skeletal muscle.
- MOTS-c is one of several mitochondrial-derived peptides being investigated as part of the cellular response to metabolic stress.
- Human research has examined changes in circulating MOTS-c after endurance and resistance exercise.
- A 2024/2025 study reported an association between endurance training, circulating MOTS-c, aerobic capacity and skeletal-muscle mitochondrial function, although the mechanistic and translational interpretation requires caution.
- A 2026 experimental study found that exogenous MOTS-c improved intrinsic skeletal-muscle mitochondrial bioenergetic function in mouse models through mechanisms involving AMPK and PGC-1α.
- The same 2026 study found no measurable arterio-venous difference in MOTS-c across exercising human skeletal muscle, suggesting that skeletal muscle may not simply be the source of circulating MOTS-c during exercise.
- Exercise intensity matters: high-intensity and sprint exercise can produce substantial metabolic and mitochondrial stress, but different exercise prescriptions can generate different molecular adaptations.
- MOTS-c should therefore be viewed as a research signal within exercise biology—not as a validated substitute for training adaptation.
Introduction: What Happens Inside Muscle During a Hard Ride or Run?
For cyclists, runners and athletes in Da Nang, exercise is usually described in practical terms: pace, power, heart rate, cadence, distance, recovery and performance.
At the cellular level, however, every hard training session is also an experiment in energy management.
As skeletal muscle contracts repeatedly, ATP is consumed. Mitochondria increase oxidative metabolism to help regenerate ATP. Glucose and fatty acids are mobilized. Redox balance changes. Reactive oxygen species can transiently increase. Intracellular signaling pathways respond to changes in energy availability and metabolic stress.
These signals are not necessarily harmful. In appropriate amounts, they can become part of the stimulus that drives adaptation.
This concept is central to modern exercise physiology: the stress created by exercise can become the signal that tells muscle to adapt.
MOTS-c is interesting because researchers are investigating whether a mitochondrial-derived peptide participates in this communication between mitochondrial metabolism and broader cellular responses.
That makes exercise one of the most useful contexts in which to study MOTS-c.
Exercise Is a Biological Stress Test for Mitochondria
Mitochondria have to respond rapidly when exercise intensity increases.
During endurance exercise, oxygen consumption rises substantially as skeletal muscle increases oxidative ATP production. During intervals, hill climbs and sprint efforts, the energetic demand can increase even faster.
Research in human skeletal muscle shows that exercise can alter mitochondrial respiration, reactive oxygen species production and multiple stress-signaling pathways.
For example, studies comparing high-intensity interval exercise with continuous endurance exercise have demonstrated acute changes in mitochondrial respiration, hydrogen peroxide release and metabolic signaling.
More recent human research has shown that sprint-interval exercise can produce a distinct mitochondrial stress signature involving mitochondrial structural changes, the integrated stress response and mitochondrial quality-control pathways.
This is important for understanding MOTS-c because a mitochondrial-derived peptide should not be studied independently of the environment in which mitochondria are being challenged.
A temporary rise in metabolic stress, reactive oxygen species or mitochondrial signaling during exercise does not automatically indicate injury. These signals can be part of the adaptive process. The key biological question is how the cell resolves the stress and remodels itself afterward.
Where Does MOTS-c Enter the Exercise Story?
MOTS-c belongs to the mitochondrial-derived peptide family. Its sequence is encoded by a short open reading frame within the mitochondrial 12S rRNA region.
This origin is particularly relevant to exercise research because mitochondria are central to endurance metabolism.
Researchers therefore began asking whether MOTS-c changes when exercise increases mitochondrial demand.
There are several distinct questions:
- Does acute exercise change circulating MOTS-c?
- Does endurance training alter baseline MOTS-c?
- Does skeletal muscle produce or release MOTS-c during exercise?
- Does MOTS-c influence mitochondrial function?
- Could MOTS-c participate in the adaptation to repeated exercise-induced metabolic stress?
These questions should not be treated as interchangeable. Evidence that exercise changes circulating MOTS-c does not automatically demonstrate that MOTS-c causes training adaptation.
What Human Exercise Studies Have Actually Found
One of the important early human studies examined acute endurance and resistance exercise and measured both circulating MDPs and skeletal-muscle responses.
Participants completed either endurance exercise involving cycling or resistance exercise. Researchers collected blood and skeletal-muscle samples before exercise and during recovery.
The study found exercise-related molecular responses in skeletal muscle, including changes in genes associated with exercise adaptation. Circulating MDP responses were also investigated.
The researchers observed a tendency toward increased MOTS-c following endurance exercise, whereas the response differed following resistance exercise. This suggested that MDP responses may depend on the type of exercise stimulus rather than simply reflecting “exercise” as a single biological condition.
That distinction matters for athletes. A two-hour endurance ride and a short maximal sprint session may create completely different combinations of energetic demand, oxygen flux, substrate utilization and mechanical stress.
MOTS-c signaling should therefore be studied in the context of exercise mode, intensity, duration and recovery.
Endurance Training Adds Another Layer
Acute exercise is one event. Training is repeated exposure.
Repeated endurance exercise can increase mitochondrial content, alter respiratory capacity and improve the ability of skeletal muscle to oxidize substrates.
A recent study investigated the relationship between MOTS-c, endurance exercise and skeletal-muscle mitochondrial function in humans and experimental animals.
The researchers reported an association between serum MOTS-c and aerobic exercise capacity in human participants. In mice, long-term endurance training was associated with enhanced skeletal-muscle mitochondrial respiratory function and increased MOTS-c-related signaling, including activation of the AMPK/PGC-1α pathway.
These findings are scientifically interesting because they connect three areas that are usually studied separately:
↓
MOTS-c signaling
↓
AMPK / PGC-1α network
↓
Mitochondrial adaptation
However, the mouse findings and human associations should not be treated as equivalent evidence. An association between serum MOTS-c and aerobic capacity in humans does not demonstrate that increasing MOTS-c would increase aerobic capacity.
The 2026 Study: A Closer Look at Muscle Mitochondrial Bioenergetics
A particularly relevant 2026 study investigated whether MOTS-c directly affects skeletal-muscle mitochondrial function.
The researchers used two transgenic mouse models to investigate mitochondrial bioenergetics following MOTS-c administration. They reported improved intrinsic mitochondrial bioenergetic performance and identified dependence on both AMPK and PGC-1α.
The study also reported reduced mitochondrial reactive oxygen species emission and reduced markers of oxidative protein damage. RNA-sequencing suggested changes across multiple mitochondrial processes, including redox handling, mitochondrial integrity and oxidative-phosphorylation efficiency.
This is important because it moves the MOTS-c discussion beyond a generic “metabolic peptide” concept.
The study asks a much more specific question:
Can MOTS-c alter how efficiently skeletal-muscle mitochondria perform their work?
In the experimental mouse models, the answer was promising.
But the human component produced an equally important caution. During one-legged knee-extensor exercise, researchers did not observe an arterio-venous difference indicating net release of MOTS-c from the exercising skeletal muscle. Their interpretation was that skeletal muscle may not be the primary source of circulating MOTS-c in response to exercise.
That finding prevents an overly simple story in which “working muscle releases MOTS-c into the blood.”
The biology appears more complicated.
The newest exercise-focused evidence does not simply strengthen the claim that muscle releases MOTS-c during exercise. It raises a more interesting question: if circulating MOTS-c changes with exercise but exercising muscle does not show a clear net release, which tissues or compartments contribute to the circulating signal, and how is that signal regulated?
Why Exercise Intensity May Matter
Not all exercise creates the same mitochondrial stress.
Moderate continuous cycling, threshold work, high-intensity intervals and maximal sprinting produce different metabolic environments.
High-intensity exercise can generate substantial perturbations in ATP turnover, glycolytic flux, redox balance and mitochondrial signaling.
Human studies have shown that low-volume high-intensity exercise can produce strong mitochondrial biogenesis-related transcriptional responses when metabolic stress is sufficiently high.
More recent work has demonstrated that sprint-interval exercise can produce a distinct mitochondrial stress response involving mitochondrial structural remodeling and the mitochondrial unfolded protein response.
This gives MOTS-c research a broader framework:
- Acute stress: What happens to MOTS-c during or immediately after exercise?
- Recovery: How quickly do circulating or tissue-associated signals return toward baseline?
- Repeated stress: Does repeated exercise exposure change the baseline MOTS-c system?
- Adaptation: Does MOTS-c contribute causally to improved mitochondrial function?
The fourth question is the hardest—and the most important for translating exercise biology into therapeutic research.
MOTS-c and AMPK: The Exercise Connection
AMPK is one of the major energy-sensing pathways activated by energetic stress in skeletal muscle.
During exercise, changes in cellular energy status can activate AMPK. This contributes to increased glucose transport, fatty-acid oxidation and broader metabolic adaptation.
MOTS-c has been linked to AMPK through a proposed pathway involving folate metabolism and AICAR/ZMP signaling.
The 2026 mitochondrial bioenergetics study adds another layer by reporting that MOTS-c-mediated improvements in muscle mitochondrial function were dependent on AMPK and PGC-1α in experimental models.
This creates a scientifically coherent hypothesis:
↓
Energy-sensing pathways
↓
AMPK / PGC-1α signaling
↓
Mitochondrial remodeling and metabolic adaptation
MOTS-c may intersect with this network rather than functioning as an isolated “energy” molecule.
The PGC-1α Connection: Why Endurance Athletes Should Pay Attention
PGC-1α is one of the most important transcriptional coactivators in skeletal-muscle mitochondrial adaptation.
Exercise can stimulate PGC-1α-related signaling, contributing to mitochondrial biogenesis and changes in oxidative metabolism.
This is one reason endurance training can gradually increase the oxidative capacity of skeletal muscle.
The relationship between MOTS-c, AMPK and PGC-1α is therefore particularly interesting for endurance research. If MOTS-c can influence this network, it could provide one possible link between mitochondrial-derived signaling and the cellular adaptations observed after repeated endurance exercise.
But again, pathway involvement is not the same thing as clinical performance enhancement.
Cycling, Running and the Da Nang Athlete
Da Nang provides a particularly interesting environment for this research lens.
The city’s coastal roads, surrounding hills and outdoor lifestyle attract runners, cyclists, triathletes and other endurance-oriented athletes. Training can involve long rides, repeated climbs, interval sessions and high-volume aerobic work.
For these athletes, mitochondrial adaptation is not an abstract concept. It is directly related to how skeletal muscle handles repeated oxidative demand.
That makes MOTS-c interesting as a research signal because its biology sits at the intersection of mitochondria, metabolic stress and exercise adaptation.
But the appropriate scientific question is not “Can MOTS-c replace training?”
It is:
This framing is considerably more useful for athletes because it keeps the peptide within the biology that originally made it interesting.
Exercise Does Not Simply “Boost Mitochondria”
One of the common simplifications in fitness content is that exercise “improves mitochondrial health.”
That statement is directionally correct but biologically incomplete.
Different exercise stimuli can produce different mitochondrial responses.
For example, a systematic review of human exercise-training studies found that training can increase skeletal-muscle mitochondrial and capillary adaptations, but the magnitude and pattern depend on training characteristics and participant factors.
High-intensity exercise may generate a strong acute stress signal, while longer-duration endurance training provides repeated oxidative stimuli that promote remodeling over time.
Mitochondrial adaptation is therefore a process of stress, signaling, recovery and remodeling.
MOTS-c is interesting precisely because researchers are investigating whether it participates somewhere within that chain.
Mitochondrial Stress: The Signal That Starts the Adaptation
A useful way to understand exercise-induced mitochondrial stress is to distinguish between the stimulus and the adaptation.
The stimulus can include increased ATP demand, altered redox state, changes in calcium handling, metabolic intermediates and transient reactive oxygen species production.
The adaptation includes changes in gene expression, mitochondrial quality control, respiratory capacity and substrate utilization.
This concept is supported by human exercise research showing that metabolic stress can influence mitochondrial biogenesis-related transcriptional responses.
In this model, mitochondrial stress is not simply an unwanted side effect of exercise. It can function as information.
MDPs such as MOTS-c are interesting because they may be part of the molecular language through which mitochondria communicate that information.
What About Reactive Oxygen Species?
Reactive oxygen species, or ROS, are another important part of exercise signaling.
During exercise, mitochondrial electron transport and other metabolic processes can alter ROS production. Transient increases in ROS can participate in adaptive signaling, while excessive or poorly resolved oxidative stress can contribute to molecular damage.
Human ultra-endurance research has demonstrated that prolonged exercise can increase mitochondrial hydrogen peroxide production, with the response returning toward baseline during recovery.
The distinction between signal and damage is therefore essential.
Interestingly, the 2026 MOTS-c mitochondrial study reported lower mitochondrial ROS emission and reduced oxidative protein damage following MOTS-c treatment in experimental models.
This raises an intriguing hypothesis: MOTS-c may influence not only energy production but also how mitochondria manage oxidative stress.
However, these findings remain experimental and should not be translated into claims that MOTS-c prevents exercise-induced oxidative damage in humans.
Why the Circulating MOTS-c Question Is Still Unresolved
One of the most interesting unresolved questions is where circulating MOTS-c comes from during exercise.
If blood MOTS-c changes after exercise, it is tempting to assume that working skeletal muscle is releasing the peptide.
The 2026 study complicates that assumption. Despite increased interstitial MOTS-c levels, researchers did not observe a clear arterio-venous difference across exercising human skeletal muscle.
This means the circulating signal may involve other tissues, altered production elsewhere, redistribution between compartments or mechanisms that are not captured by a simple muscle-release model.
That uncertainty is scientifically valuable because it identifies a specific research gap rather than allowing a convenient but unsupported explanation.
Acute Exercise vs Long-Term Training
These two concepts should always be separated.
| Dimension | Acute Exercise | Long-Term Training |
|---|---|---|
| Primary question | What changes immediately? | What adapts after repeated exposure? |
| Mitochondrial state | Transient metabolic stress | Remodeling and functional adaptation |
| MOTS-c research | Circulating and tissue responses | Relationship with mitochondrial function and endurance adaptation |
| Interpretation | Signal | Adaptation |
A single post-exercise increase in a biomarker does not demonstrate improved fitness. Likewise, a chronic training association does not prove that the biomarker caused the adaptation.
MOTS-c Is Not a Substitute for Exercise
This distinction deserves its own section because the exercise connection can easily be misinterpreted.
Exercise activates hundreds of interacting pathways simultaneously. These include AMPK, PGC-1α, calcium-dependent signaling, mechanical signaling, redox pathways, inflammatory mediators and mitochondrial quality-control mechanisms.
MOTS-c represents one research variable within this much larger system.
Even if future studies establish that MOTS-c contributes causally to mitochondrial adaptation, that would not mean that a peptide can reproduce every benefit of endurance training.
Training creates mechanical, metabolic, cardiovascular, neuromuscular and systemic adaptations simultaneously.
A peptide-mediated molecular effect should therefore never be treated as biologically equivalent to the complete exercise stimulus.
Injection Pen Format vs Exercise Biology
The MOTS-c injection pen is a product format. The exercise literature concerns biological signaling.
These are different layers of the research question.
Exercise studies can tell us how endogenous MOTS-c or related mitochondrial-derived peptides respond to physiological stress. Experimental administration studies can investigate what happens when MOTS-c is supplied exogenously.
Neither automatically validates the other.
For research-oriented readers, this distinction is especially important because an injection pen does not demonstrate that the peptide reproduces the spatial, temporal or concentration profile of endogenous MOTS-c released during exercise.
The scientifically responsible approach is therefore to keep exercise physiology, endogenous signaling and exogenous peptide pharmacology as separate but related questions.
Statistics & Evidence Snapshot
| Research Finding | Study Context | What It Means |
|---|---|---|
| 45 min cycling at approximately 70% estimated VO₂max | Human acute exercise study | Provided a controlled endurance-exercise model for studying circulating MDP responses |
| n=10 endurance + n=10 resistance + n=10 control | Acute human MDP study | Small mechanistic human sample; useful but not sufficient for clinical conclusions |
| 2026 experimental mouse study | Skeletal-muscle mitochondrial bioenergetics | MOTS-c improved mitochondrial bioenergetic performance through AMPK/PGC-1α-dependent mechanisms |
| Human knee-extensor experiment | 2026 MOTS-c study | No clear arterio-venous release of MOTS-c from exercising skeletal muscle |
| Endurance-trained human and animal research | Long-term endurance training | MOTS-c associated with aerobic capacity and mitochondrial adaptation, but causality remains under study |
What Cyclists and Runners Should Take From the Research
The strongest takeaway is not that athletes should try to manipulate MOTS-c.
It is that exercise itself is a powerful mitochondrial signaling experiment.
Every demanding ride, run or interval session changes cellular energy demand. Repeated exposure creates an adaptive program involving mitochondrial remodeling, substrate utilization, redox regulation and transcriptional responses.
MOTS-c is interesting because researchers are beginning to understand how a mitochondrial-derived peptide may fit into that adaptive network.
For athletes, this provides a useful conceptual model:
- Training creates metabolic stress.
- Metabolic stress activates cellular signaling.
- Signaling changes gene expression and mitochondrial function.
- Recovery allows remodeling and adaptation.
- Repeated cycles produce longer-term physiological changes.
MOTS-c research is investigating where mitochondrial-derived peptide signaling belongs within that sequence.
Frequently Asked Questions
Exercise creates a controlled physiological challenge involving increased ATP demand, mitochondrial respiration, metabolic stress and cellular signaling. This makes it an informative environment for studying mitochondrial-derived peptides such as MOTS-c.
Human studies have reported exercise-associated changes in circulating MOTS-c, particularly in endurance-exercise contexts, but responses vary by exercise type and study design. The biological meaning of these changes remains under investigation.
This remains unresolved. A 2026 study found increased interstitial MOTS-c but no clear arterio-venous difference across exercising human skeletal muscle, suggesting that muscle may not simply be the source of circulating MOTS-c during exercise.
In experimental mouse models, MOTS-c improved intrinsic skeletal-muscle mitochondrial bioenergetic performance through mechanisms involving AMPK and PGC-1α. The study also reported reduced mitochondrial ROS emission and oxidative protein damage.
There is not enough clinical evidence to make that claim. Associations between MOTS-c and aerobic capacity are scientifically interesting, but association does not establish that administering MOTS-c improves endurance performance.
AMPK is a major energy-sensing pathway activated by energetic stress during exercise. MOTS-c has also been linked experimentally with AMPK signaling, making the pathway an important area of investigation.
PGC-1α is a transcriptional coactivator strongly involved in skeletal-muscle mitochondrial adaptation. Exercise can stimulate PGC-1α-related signaling, and recent MOTS-c research has identified PGC-1α as part of the peptide’s experimental mitochondrial mechanism.
Not necessarily. Transient metabolic and oxidative stress can act as adaptive signals. Problems arise when stress is excessive, poorly resolved or accompanied by inadequate recovery. Exercise physiology therefore distinguishes signaling stress from sustained molecular damage.
Not necessarily. Different exercise modes produce different combinations of energetic demand, metabolic perturbation and mitochondrial stress. Human MDP studies already suggest that endurance and resistance exercise can produce different responses.
MOTS-c is more appropriately described as a mitochondrial-derived peptide. Although muscle and exercise are important contexts for its study, current evidence does not justify assuming that skeletal muscle is the sole or primary source of circulating MOTS-c during exercise.
No. Exercise produces a broad combination of cardiovascular, neuromuscular, metabolic and mitochondrial adaptations. Investigational peptide signaling cannot be assumed to reproduce the complete physiological stimulus of training.
Endurance cycling places substantial repeated demands on oxidative metabolism. Mitochondrial respiratory capacity, substrate utilization and muscle metabolic adaptation are therefore central to endurance physiology, making mitochondrial-derived signaling scientifically relevant to cyclists.
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Scientific References
- Lee C, Zeng J, Drew BG, et al. The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance. Cell Metabolism. 2015;21(3):443-454. PMID: 25738459. DOI: 10.1016/j.cmet.2015.02.009.
- Woodhead JST, Merry TL. Mitochondrial-derived peptides and exercise. BBA – General Subjects. 2021;1865(12):130011. PMID: 34520826.
- Acute endurance exercise stimulates circulating levels of mitochondrial-derived peptides in humans. PMID: 34351816.
- Endurance training enhances skeletal muscle mitochondrial respiration by promoting MOTS-c secretion. 2024/2025. PMID: 39706498.
- Gudiksen A, Hansen CC, van der Stede T, et al. MOTS-c improves intrinsic muscle mitochondrial bioenergetic health and efficiency in a PGC-1α/AMPK-dependent manner. Free Radical Biology and Medicine. 2026;246:682-696. PMID: 41520850. DOI: 10.1016/j.freeradbiomed.2026.01.002.
- Trewin AJ, et al. Acute HIIE elicits similar changes in human skeletal muscle mitochondrial H2O2 release, respiration, and cell signaling as endurance exercise even with less work. American Journal of Physiology-Regulatory, Integrative and Comparative Physiology. 2018;315:R1003-R1016. PMID: 30183338.
- Wadley GD, et al. Metabolic stress-dependent regulation of the mitochondrial biogenic molecular response to high-intensity exercise in human skeletal muscle. Journal of Physiology. 2018. PMID: 29727016.
- Botella J, et al. Sprint interval exercise disrupts mitochondrial ultrastructure driving a unique mitochondrial stress response and remodelling in men. Nature Communications. 2025. PMID: 41326383.
- Mølmen KS, Almquist NW, Skattebo Ø. Effects of Exercise Training on Mitochondrial and Capillary Growth in Human Skeletal Muscle: A Systematic Review and Meta-Regression. Sports Medicine. 2025;55:115-144. PMID: 39390310. DOI: 10.1007/s40279-024-02120-2.
- Ultraendurance exercise increases the production of reactive oxygen species in isolated mitochondria from human skeletal muscle. 2010. PMID: 20110545.
- Mitochondrial-derived peptides in healthy ageing and therapy of age-related diseases. 2023. PMID: 37437978.
- Mitochondrial-derived peptides: Antidiabetic functions and evolutionary perspectives. 2024. PMID: 38160808.
Conclusion
Exercise may be one of the most revealing environments in which to study MOTS-c because it creates precisely the type of biological challenge that makes mitochondrial signaling interesting.
When a cyclist climbs a steep road or a runner completes a hard interval, skeletal muscle experiences increased ATP demand, altered substrate use, changes in redox balance and mitochondrial stress. The resulting signals help determine how the muscle adapts.
MOTS-c sits within this research conversation as a mitochondrial-derived peptide whose relationship with exercise, metabolic stress and mitochondrial function is increasingly being investigated.
The evidence is becoming more interesting. Human studies have demonstrated exercise-associated changes in circulating MOTS-c. Experimental endurance-training work has connected MOTS-c with mitochondrial respiration and AMPK/PGC-1α signaling. Most recently, 2026 research reported improved intrinsic skeletal-muscle mitochondrial bioenergetics following MOTS-c administration in experimental models.
Yet the same 2026 study also highlighted an important unresolved question: exercising human skeletal muscle did not show clear net release of MOTS-c into the circulation.
That is exactly what makes the field scientifically interesting.
The story is not finished.
Mitochondria sense the challenge.
Cellular signaling converts stress into adaptation.
MOTS-c may be one part of that signaling conversation.
For cyclists, runners and athletes in Da Nang, that is a more useful way to understand MOTS-c than viewing it simply as another performance or fat-loss peptide. Its scientific value lies in what it may reveal about the molecular language of exercise adaptation.
Quick Answer
Core Questions: Does exercise increase MOTS-c? What happens to MOTS-c during endurance exercise? Does skeletal muscle release MOTS-c? How does MOTS-c relate to mitochondrial adaptation? What did the 2026 MOTS-c mitochondrial study find? How are AMPK and PGC-1α connected to MOTS-c? Why are cyclists and runners interested in MOTS-c research?
Evidence Level: Human exercise studies provide emerging observational and mechanistic evidence; animal experiments provide stronger causal evidence for mitochondrial effects; clinical performance benefits of exogenous MOTS-c remain unestablished.