Preterm BirthNCT06334107
Mitochondrial DNA Signatures of Poor Aerobic Exercise Trainability in Young Adults Born Preterm
A study testing Exercise in people with Preterm Birth, run by Texas Tech University at 1 site in United States.
Trial summary
Young adults born very preterm (32 weeks gestation or earlier) do not respond well to aerobic exercise training, meeting the recommendations set by the Physical Activity Guidelines for Americans, where they do not increase their fitness level (or cardiorespiratory fitness). Read more about this study
- Who is it for?
- Ages 18 to 35 yearsHealthy volunteers can take part
- Conditions the study is for
- Preterm Birth
- What is being tested?
- Exercise
- Type of treatment
- Lifestyle or therapy programme
- Could I receive a placebo?
- No, everyone receives an active treatment
- How many people
- 60 participants
- Where
- 1 siteUnited States
- Study dates
- 1 May 2024to 31 Dec 2026
- Phase
- Interventional
- Are there results?
- Not yet: the study is under way
Key requirements
Who can take part, as listed by the sponsor. Only the study team can confirm whether you are eligible, so take this list to your doctor.
- Ages 18 to 35 years
- All sexes
- Healthy volunteers accepted
- Adult
Who may be able to join
- Preterm born (PTB)young adult group: Participants must be inactive (reported exercise \< 150 mins/week; See IPAQ Attachment), males and females aged 18-35 years born preterm with a gestational age \<37 weeks.
- Normal term-born (NTB) young adult control group: Participants must be inactive (reported exercise \< 150 mins/week) and will be age- and sex-matched and born at term (37 gestational age).
- The biological mother of PTB participants: The PTB biological birth mother must be the one who gave birth to the participant and the one from whom the child inherited half of its genetic background (i.e., DNA).
- PTB and NTB young adults must pass the PAR-Q+ Questionnaire assessment, indicating readiness to begin a moderate-intensity exercise training program. We will follow the American College of Sports Medicine\'s aerobic exercise training program participation guidelines. Subjects who are cleared via the PAR-Q+ assessment will be permitted to participate in the training program.
Who cannot join
- PTB and NTB young adults only: Having a diagnosed bronchopulmonary hyperplasia, cardiovascular (cardiac or peripheral arterial disease), metabolic (Diabetes Mellitus Type 1 or 2), or renal or liver disease, and signs or symptoms of these conditions, including pain: discomfort in the chest, neck, jaw, arms, or other areas that may result from ischemia; shortness of breath at rest or with mild exertion; dizziness or syncope; orthopnea or paroxysmal nocturnal dyspnea; ankle edema; palpitations or tachycardia; intermittent claudication; known heart murmur; unusual fatigue or shortness of breath with usual activity.
Trial locations and contacts
1 site in 1 country. Contact the study team or a site near you to ask about taking part.
United States1 site, 1 recruiting
- Recruiting
Texas Tech University | Kinesiology and Sport Management Building
Lubbock, Texas, 79409
Heather L Vellers, Ph.D., 806-834-8554, heather.l.vellers@ttu.edu
Heather L Vellers, Ph.D., 9792194343, heather.l.vellers@ttu.edu
About this study
Young adults born very preterm (32 weeks gestation or earlier) do not respond well to aerobic exercise training, meeting the recommendations set by the Physical Activity Guidelines for Americans, where they do not increase their fitness level (or cardiorespiratory fitness). Thus, they do not receive the health benefits of exercise. Achieving physical fitness through aerobic exercise training is the most cost-effective method for preventing and treating many diseases. Young adults born very preterm also have a higher risk of these conditions. Thus, their inability to respond to increase their fitness is a major problem.
One likely explanation for poor exercise trainability and increased heart disease risk in young adults born very preterm is the effect of the early birth on the major energy producers in all our cells: Mitochondria. During late-stage gestation, mitochondria change from relying on sugar as a major fuel source to fat. Unfortunately, individuals born very preterm miss this transition in fuel source reliance, which causes significant stress and damage to mitochondria. Mitochondria are critical for post-natal organ development; thus, it is thought that preterm birth-induced mitochondrial dysfunction is the underlying cause of poor trainability and high disease risk in young adults born very preterm. Indeed, mitochondrial dysfunction is evident in these individuals.
Read more
To date, there is not a way to help young adults born preterm improve their fitness level. One likely target is in the mitochondria: it's DNA. Mitochondrial DNA helps determine how mitochondria function and can be damaged under stress. Our goal in this proposed work is to determine the role of mitochondrial DNA in mitochondrial dysfunction and its link to their poor trainability.
Questions:
- Are there mitochondrial DNA markers linked to mitochondrial dysfunction and poor exercise trainability in young adults very born preterm?
- Do mitochondrial DNA in young adults born very preterm respond differently to aerobic exercise training than those born at term?
The investigators expect this work will show mitochondrial DNA changes linked to mitochondrial dysfunction and poor trainability, which can be used for future targets to improve health. This work supports AHA mission by helping to identify a marker in individuals born very preterm linked to their higher heart disease risk and death early in life.
Read the detailed description
Young adults born very preterm (VPTB; ≤ 32 weeks gestational age) have an impaired response to aerobic exercise training (AET), often characterized by no change in aerobic capacity (VO2max) following AET. This diminishes the potential of AET to offset their elevated cardiovascular disease risk early in life VPTB\&#39;s poor trainability is linked to their known mitochondrial dysfunction, thought to occur due to blunted mitochondrial maturation with early birth. Currently, no therapeutics are available to improve VO2max trainability for this population.
Data from our lab in humans and mice demonstrate that mitochondrial DNA (mtDNA) variants and other mitochondrial genomic aspects have a role in VO2max trainability. In humans, the investigators found that individuals with the largest increase in VO2max following AET had a higher occurrence of mitochondrial heteroplasmy (a shift in sequence across mtDNA). In contrast, heteroplasmy decreased in those with little-to-no change in VO2max. The reduction in heteroplasmy correlated with higher mtDNA lesions, suggesting exercise was inflicting excessive oxidative stress on mitochondria in these individuals. The investigators also identified 13 mtDNA variants in those with poor trainability, possibly linked to their lowered heteroplasmy response after exercise training. These data indicate that genetic diversity characterized by the response of mtDNA heteroplasmy with AET is an important factor determining the adaptability of VO2max with AET. To date, VPTB mitochondrial genomes have not been characterized. An onset of variants in their mitogenomes due to early birth would be easily identifiable compared to their birth mother, given that mtDNA is maternally inherited. Importantly, these mitogenome variants may inform the effect of AET on heteroplasmy and their low trainability. Thus, there is a critical need to characterize VPTB mitochondrial genome characteristics and how AET influences these dynamics.
Our long-term goal is to improve mitochondrial function and VO2max trainability in VPTB young adults facing disproportionately higher disease risk where exercise is known to be beneficial as a treatment and preventative measure. Accordingly, the overall objectives of this application are to i) characterize VPTB-induced mtDNA changes in sequence, heteroplasmy, and damage, and ii) determine the effect of AET on these mtDNA traits and mitochondrial function in cells known to correlate with heart mitochondrial oxidative capacity: namely peripheral blood mononuclear cells (PBMCs). Our central hypothesis is that VTPB young adults will have unique mtDNA variants/mutations and that AET will significantly decrease PBMC mtDNA heteroplasmy and copies alongside lowered mitochondrial oxidative capacity compared to normal-term birth (NTB) adults. The rationale for this project is that characterizing unique VPTB mtDNA aspects and the heteroplasmy response to AET might reveal an underlying mechanism for their poor trainability that can be targeted for future work. To meet these objectives, the investigators will assess these two specific aims: Aim 1: Assess for informative mtDNA variants in VPTB young adults. The investigators hypothesize there will be de novo mtDNA variants in VPTB offspring compared to their birth mothers.
Aim 2: Determine the effect of AET on mitochondrial oxidative capacity and mtDNA heteroplasmy, copy number, and lesions in isolated PBMCs in VPTB and NTB young adults. The investigators hypothesize VPTB adults will exhibit decreased mtDNA heteroplasmy and increased lesions following AET compared to age-matched NTB adults.
After completing the proposed research, our expected outcome is identifying a unique signature of mtDNA variants and heteroplasmy responses to AET in VPTB adults that will explain their low trainability. These results are expected to have a positive impact for researchers because it will provide a foundation for future research to target mtDNA as a strategy to help VPTB adults reduce their risk for cardiovascular disease and improve their quality of life.
- Conditions
- Preterm Birth
- Being tested
- Exercise
- Keywords
- Preterm birth, Aerobic capacity trainability, mitochondrial DNA, heteroplasmy, mitochondrial oxidative capacity
- Medical subject headings
- Premature Birth
What participants receive
What participants receive. In a randomised study each person is assigned to one group by chance.
ExerciseBehavioural
Participants will be asked to follow a moderate-intensity aerobic exercise training program for 4-5 days per week for 40-60 minutes each session.
| Study group | Role | What they receive |
|---|---|---|
| Aerobic Exercise Training | Experimental | Participants will be asked to complete a 16-week aerobic exercise training program. Receives: Behavioral: Exercise |
| Mitochondrial DNA Sequencing | No intervention | Participants will be asked to provide a blood or saliva sample for mitochondrial DNA sequencing analysis to assess for variants unique to individuals born prematurely. |
What is being measured
The primary outcome is the main question the study is designed to answer.
Mitochondrial DNA heteroplasmy
The full-length mitochondrial DNA sequence will be analyzed and assessed for heteroplasmic sites in the mitochondrial genome. Briefly, mitochondrial DNA exists in many copies, and heteroplasmy is noted when the amino acid sequence changes from the major read 2% or more across the DNA copies. The change in the mean heteroplasmy frequency and the mean number of sites with heteroplasmy with aerobic exercise training by comparing these changes in young adults born preterm to those born at term.
Measured: Immediately after aerobic exercise training intervention; change in pre- to post-frequency
Mitochondrial DNA sequence variants
The full-length mitochondrial DNA sequence will be determined in participants who report being born prematurely, which will be compared to their biological birth mother. In this comparison, we will assess for variants. We deem a site as an 'informative' mitochondrial DNA variant in young adults born prematurely as a change in amino acid sequence from the biological birth mother.
Measured: Immediately after visit 1
Change in maximal aerobic capacity
The change in maximal aerobic capacity will be assessed via the modified Balke-graded exercise test before and after the aerobic exercise training program.
Measured: Immediately after aerobic exercise training intervention; change in pre- to post-frequency
Change in mitochondrial oxidative capacity in peripheral blood mononuclear cells
Mitochondrial maximal respiration (i.e., oxidative capacity) will be measured in isolated peripheral blood mononuclear cells.
Measured: Immediately after aerobic exercise training intervention; change in pre- to post-frequency
Secondary outcomes (1)
Daily sleep habits
Daily sleep data will be collected from the Fitbit Charge via the Fitabase software program during the experimental period. Subjects will be instructed to create a habit of wearing their Fitbit Charge each night of the training period. At the completion of the study, the research team will collect daily sleep data that includes the estimated time spent (i.e., minutes or seconds) in each stage (awake, rapid eye movement, light, and deep).
Measured: Daily for 16 weeks.
Timeline
From the start of the study to its completion; the mark is today. Estimated dates are the sponsor’s plan.
- First posted27 Mar 2024
- Study start1 May 2024
- Primary completion1 Dec 2026 (estimated)
- Study completion31 Dec 2026 (estimated)
Resources
- Official record on ClinicalTrials.govThe registry entry this page is built from, with its full change history.
- Other trials for Preterm BirthStudies of the same condition, open and under way.
- What the trial phases meanHow a treatment moves from first tests in people to approval.
More details
For doctors and researchers: how the study is designed, who runs it, and its registry IDs.
Study design
- Study type
- Interventional
- Phase
- Phase N/A
- Primary purpose
- Basic science
- Allocation
- Non-randomised
- Intervention model
- Parallel groups
- Masking
- Single blind
- Who is masked
- Participant
- Enrolment
- 60 participants (estimated)
Sponsor and investigators
- Lead sponsor
- Texas Tech University
- Sponsor type
- University, hospital or other
- Responsible party
- Sponsor
IDs, dates and publications
- ClinicalTrials.gov ID
- NCT06334107
- Sponsor's protocol ID
- 24AIREA1191995
- Status last verified
- Dec 2025
- First submitted
- 18 Mar 2024
- Last updated
- 18 Dec 2025
- Results posted
- No
- Data monitoring committee
- No
- FDA-regulated drug
- No
- FDA-regulated device
- No
- Individual data sharing
- No
Study at a glance
From the registry record, last updated by the sponsor on 18 Dec 2025. Recruitment status is as the sponsor reported it: confirm with the study team.
- Official title
- Mitochondrial DNA Signatures of Poor Aerobic Exercise Trainability in Young Adults Born Preterm
- ClinicalTrials.gov ID
- NCT06334107
- Acronym / sponsor ID
- 24AIREA1191995
- Conditions
- Preterm Birth
- Keywords
- Preterm birth, Aerobic capacity trainability, mitochondrial DNA, heteroplasmy, mitochondrial oxidative capacity
- Study type
- Interventional
- Recruitment status
- Recruiting
- Enrolment
- 60 participants (estimated)
- Lead sponsor
- Texas Tech UniversityUniversity, hospital or other
- Study start
- 1 May 2024 (actual)
- Primary completion
- 1 Dec 2026 (estimated)
- Study completion
- 31 Dec 2026 (estimated)
- First posted
- 27 Mar 2024 (actual)
- Results
- Not posted in the source record
Clinical summary
The research question as the sponsor registered it. This describes what the study plans to test, not what it found.
Young adults born very preterm (32 weeks gestation or earlier) do not respond well to aerobic exercise training, meeting the recommendations set by the Physical Activity Guidelines for Americans, where they do not increase their fitness level (or cardiorespiratory fitness). Thus, they do not receive the health benefits of exercise. Achieving physical fitness through aerobic exercise training is the most cost-effective method for preventing and treating many diseases. Young adults born very preterm also have a higher risk of these conditions. Thus, their inability to respond to increase their fitness is a major problem.
One likely explanation for poor exercise trainability and increased heart disease risk in young adults born very preterm is the effect of the early birth on the major energy producers in all our cells: Mitochondria. During late-stage gestation, mitochondria change from relying on sugar as a major fuel source to fat. Unfortunately, individuals born very preterm miss this transition in fuel source reliance, which causes significant stress and damage to mitochondria. Mitochondria are critical for post-natal organ development; thus, it is thought that preterm birth-induced mitochondrial dysfunction is the underlying cause of poor trainability and high disease risk in young adults born very preterm. Indeed, mitochondrial dysfunction is evident in these individuals.
To date, there is not a way to help young adults born preterm improve their fitness level. One likely target is in the mitochondria: it's DNA. Mitochondrial DNA helps determine how mitochondria function and can be damaged under stress. Our goal in this proposed work is to determine the role of mitochondrial DNA in mitochondrial dysfunction and its link to their poor trainability.
Questions:
- Are there mitochondrial DNA markers linked to mitochondrial dysfunction and poor exercise trainability in young adults very born preterm?
- Do mitochondrial DNA in young adults born very preterm respond differently to aerobic exercise training than those born at term?
The investigators expect this work will show mitochondrial DNA changes linked to mitochondrial dysfunction and poor trainability, which can be used for future targets to improve health. This work supports AHA mission by helping to identify a marker in individuals born very preterm linked to their higher heart disease risk and death early in life.
Detailed description
Young adults born very preterm (VPTB; ≤ 32 weeks gestational age) have an impaired response to aerobic exercise training (AET), often characterized by no change in aerobic capacity (VO2max) following AET. This diminishes the potential of AET to offset their elevated cardiovascular disease risk early in life VPTB\&#39;s poor trainability is linked to their known mitochondrial dysfunction, thought to occur due to blunted mitochondrial maturation with early birth. Currently, no therapeutics are available to improve VO2max trainability for this population.
Data from our lab in humans and mice demonstrate that mitochondrial DNA (mtDNA) variants and other mitochondrial genomic aspects have a role in VO2max trainability. In humans, the investigators found that individuals with the largest increase in VO2max following AET had a higher occurrence of mitochondrial heteroplasmy (a shift in sequence across mtDNA). In contrast, heteroplasmy decreased in those with little-to-no change in VO2max. The reduction in heteroplasmy correlated with higher mtDNA lesions, suggesting exercise was inflicting excessive oxidative stress on mitochondria in these individuals. The investigators also identified 13 mtDNA variants in those with poor trainability, possibly linked to their lowered heteroplasmy response after exercise training. These data indicate that genetic diversity characterized by the response of mtDNA heteroplasmy with AET is an important factor determining the adaptability of VO2max with AET. To date, VPTB mitochondrial genomes have not been characterized. An onset of variants in their mitogenomes due to early birth would be easily identifiable compared to their birth mother, given that mtDNA is maternally inherited. Importantly, these mitogenome variants may inform the effect of AET on heteroplasmy and their low trainability. Thus, there is a critical need to characterize VPTB mitochondrial genome characteristics and how AET influences these dynamics.
Our long-term goal is to improve mitochondrial function and VO2max trainability in VPTB young adults facing disproportionately higher disease risk where exercise is known to be beneficial as a treatment and preventative measure. Accordingly, the overall objectives of this application are to i) characterize VPTB-induced mtDNA changes in sequence, heteroplasmy, and damage, and ii) determine the effect of AET on these mtDNA traits and mitochondrial function in cells known to correlate with heart mitochondrial oxidative capacity: namely peripheral blood mononuclear cells (PBMCs). Our central hypothesis is that VTPB young adults will have unique mtDNA variants/mutations and that AET will significantly decrease PBMC mtDNA heteroplasmy and copies alongside lowered mitochondrial oxidative capacity compared to normal-term birth (NTB) adults. The rationale for this project is that characterizing unique VPTB mtDNA aspects and the heteroplasmy response to AET might reveal an underlying mechanism for their poor trainability that can be targeted for future work. To meet these objectives, the investigators will assess these two specific aims: Aim 1: Assess for informative mtDNA variants in VPTB young adults. The investigators hypothesize there will be de novo mtDNA variants in VPTB offspring compared to their birth mothers.
Aim 2: Determine the effect of AET on mitochondrial oxidative capacity and mtDNA heteroplasmy, copy number, and lesions in isolated PBMCs in VPTB and NTB young adults. The investigators hypothesize VPTB adults will exhibit decreased mtDNA heteroplasmy and increased lesions following AET compared to age-matched NTB adults.
After completing the proposed research, our expected outcome is identifying a unique signature of mtDNA variants and heteroplasmy responses to AET in VPTB adults that will explain their low trainability. These results are expected to have a positive impact for researchers because it will provide a foundation for future research to target mtDNA as a strategy to help VPTB adults reduce their risk for cardiovascular disease and improve their quality of life.
Study design
- Primary purpose
- Basic science
- Allocation
- Non-randomised
- Intervention model
- Parallel groups
- Masking
- Single blind (participant)
- Number of arms
- 2
| Arm | Type | Receives |
|---|---|---|
| Aerobic Exercise Training | Experimental | Behavioral: ExerciseParticipants will be asked to complete a 16-week aerobic exercise training program. |
| Mitochondrial DNA Sequencing | No intervention | –Participants will be asked to provide a blood or saliva sample for mitochondrial DNA sequencing analysis to assess for variants unique to individuals born prematurely. |
Who may qualify
- Ages
- 18 to 35 years
- Sex
- All
- Healthy volunteers
- Accepted
- Age groups
- Adult
Key inclusion criteria (4 listed)
- Preterm born (PTB)young adult group: Participants must be inactive (reported exercise \< 150 mins/week; See IPAQ Attachment), males and females aged 18-35 years born preterm with a gestational age \<37 weeks.
- Normal term-born (NTB) young adult control group: Participants must be inactive (reported exercise \< 150 mins/week) and will be age- and sex-matched and born at term (37 gestational age).
- The biological mother of PTB participants: The PTB biological birth mother must be the one who gave birth to the participant and the one from whom the child inherited half of its genetic background (i.e., DNA).
- PTB and NTB young adults must pass the PAR-Q+ Questionnaire assessment, indicating readiness to begin a moderate-intensity exercise training program. We will follow the American College of Sports Medicine\'s aerobic exercise training program participation guidelines. Subjects who are cleared via the PAR-Q+ assessment will be permitted to participate in the training program.
Key exclusion criteria (1 listed)
- PTB and NTB young adults only: Having a diagnosed bronchopulmonary hyperplasia, cardiovascular (cardiac or peripheral arterial disease), metabolic (Diabetes Mellitus Type 1 or 2), or renal or liver disease, and signs or symptoms of these conditions, including pain: discomfort in the chest, neck, jaw, arms, or other areas that may result from ischemia; shortness of breath at rest or with mild exertion; dizziness or syncope; orthopnea or paroxysmal nocturnal dyspnea; ankle edema; palpitations or tachycardia; intermittent claudication; known heart murmur; unusual fatigue or shortness of breath with usual activity.
Eligibility is decided by the study team after screening; this overview does not establish that a patient qualifies. Full inclusion and exclusion criteria.
Interventions
| Intervention | Type | Arms |
|---|---|---|
| ExerciseParticipants will be asked to follow a moderate-intensity aerobic exercise training program for 4-5 days per week for 40-60 minutes each session. | Behavioural | Aerobic Exercise Training |
Primary outcome
Mitochondrial DNA heteroplasmy
Time frame: Immediately after aerobic exercise training intervention; change in pre- to post-frequency
The full-length mitochondrial DNA sequence will be analyzed and assessed for heteroplasmic sites in the mitochondrial genome. Briefly, mitochondrial DNA exists in many copies, and heteroplasmy is noted when the amino acid sequence changes from the major read 2% or more across the DNA copies. The change in the mean heteroplasmy frequency and the mean number of sites with heteroplasmy with aerobic exercise training by comparing these changes in young adults born preterm to those born at term.
Mitochondrial DNA sequence variants
Time frame: Immediately after visit 1
The full-length mitochondrial DNA sequence will be determined in participants who report being born prematurely, which will be compared to their biological birth mother. In this comparison, we will assess for variants. We deem a site as an 'informative' mitochondrial DNA variant in young adults born prematurely as a change in amino acid sequence from the biological birth mother.
Change in maximal aerobic capacity
Time frame: Immediately after aerobic exercise training intervention; change in pre- to post-frequency
The change in maximal aerobic capacity will be assessed via the modified Balke-graded exercise test before and after the aerobic exercise training program.
Change in mitochondrial oxidative capacity in peripheral blood mononuclear cells
Time frame: Immediately after aerobic exercise training intervention; change in pre- to post-frequency
Mitochondrial maximal respiration (i.e., oxidative capacity) will be measured in isolated peripheral blood mononuclear cells.
1 secondary outcome
Daily sleep habits
Time frame: Daily for 16 weeks.
Results and safety
This study is still under way. Results are not available in the source record yet.
Research links
- Official record on ClinicalTrials.govLast updated by the sponsor 18 Dec 2025.
- Individual participant dataSharing planned: No
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Referral and contact
AzTrials does not enrol participants or take referrals. Contact the study team or a site listed below; they decide who can take part.
1 site in 1 country: see every site and its status.
Questions about this trial
What is this clinical trial studying?
A study testing Exercise in people with Preterm Birth, run by Texas Tech University at 1 site in United States.
The full registered description is in the About this study section and the official record.
Who may be eligible to take part?
The sponsor lists 4 inclusion and 1 exclusion criteria. Eligibility is decided by the study team after screening, so read the full criteria and contact a listed site.
Is this clinical trial currently recruiting?
The record says: looking for participants now, as of the sponsor's last update on 18 Dec 2025. Status can change between updates, so confirm with the study contact before making plans.
Where is the study taking place?
The record lists 1 site in United States. Whether a site is taking part right now should be confirmed with that site. See every site.
What are the possible benefits and risks?
They depend on the study and the treatment, and no study can promise a benefit. The study team explains the known risks during informed consent, before anyone joins; the record itself does not list them.
Are results available for this study?
This study is still under way. Results are not available in the source record yet.
How can a doctor refer a patient or contact the research team?
Contact Heather L Vellers, Ph.D. (8068348554, heather.l.vellers@ttu.edu), or a site near the patient. AzTrials does not enrol participants or take referrals.
What does the primary outcome measure?
Mitochondrial DNA heteroplasmy (time frame: Immediately after aerobic exercise training intervention; change in pre- to post-frequency). The study lists 4 primary outcomes in all. It is what the study was designed to measure, not a finding.
Where can I read the original study information?
Does a listing mean the treatment is approved or proven to work?
No. A listing means the study is registered. It does not show that the treatment is safe, works, or is approved by a regulator.
How often is this information updated?
AzTrials copies changed records from ClinicalTrials.gov every night and reloads the whole registry every week. The sponsor last updated this record on 18 Dec 2025.