Mitochondrial DNA Signatures of Poor Aerobic Exercise Trainability in Young Adults Born Preterm

Part of paid clinical trials in Lubbock, Texas.

Sponsor
Texas Tech University
Study ID
NCT06334107
Status
Recruiting
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Conditions

  • Preterm Birth

Eligibility Criteria

Sex
ALL
Age
18 Years - 35 Years
Healthy Volunteers
Accepted

Interventions

  • Exercise — BEHAVIORAL
    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 Details

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: 1. Are there mitochondrial DNA markers linked to mitochondrial dysfunction and poor exercise trainability in young adults very born preterm? 2. 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.

Key Dates

Start date
May 1, 2024
Status verified
Dec 2025
Primary completion
Dec 1, 2026
Completion
Dec 31, 2026

Study Design

Enrollment
60 participants (estimated)
Allocation
NON_RANDOMIZED
Intervention model
PARALLEL
Primary purpose
BASIC_SCIENCE

Arms

  • Experimental: Aerobic Exercise Training
    Participants will be asked to complete a 16-week aerobic exercise training program.
  • No Intervention: Mitochondrial DNA Sequencing
    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.

Primary Outcome Measure

Mitochondrial DNA heteroplasmy [ Time Frame: Immediately after aerobic exercise training intervention; change in pre- to post-frequency ]

Central Contacts

Locations (1)

FacilityCityStateZIPSite coordinators
Texas Tech University | Kinesiology and Sport Management BuildingLubbockTexas79409
Heather L Vellers, Ph.D.
[email protected]
806-834-8554
Heather L Vellers, Ph.D.
[email protected]
9792194343

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Texas Tech University | Kinesiology and Sport Management Building· Lubbock, TX

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