Summary: The impact of adverse childhood experiences on muscle function in older adults was explored in a University of Michigan study. The research revealed a connection between reported childhood adversities and decreased mitochondrial activity, leading to reduced ATP production essential for cellular energy. This underscores the enduring influence of early trauma on physical health and emphasizes the importance of addressing childhood traumas to mitigate long-term health effects.
Key Findings:
- The study linked adverse childhood events to impaired mitochondrial function in muscle tissue, resulting in decreased ATP production in older individuals.
- Approximately 45% of participants disclosed experiencing one or more adverse childhood events, significantly affecting their muscle’s bioenergetic capacity.
- Advanced techniques like high-resolution mitochondrial respirometry and 31 PMR spectroscopy were employed to evaluate ATP production and overall mitochondrial function in the muscle accurately.
Source: University of Michigan
A recent University of Michigan investigation demonstrated that childhood traumatic experiences can have lasting repercussions on muscle function in later life by compromising skeletal muscle metabolism. The study assessed the muscle function of older adults alongside surveys detailing adverse childhood events they encountered. It revealed that individuals who reported higher childhood adversity, including one or more adverse events, exhibited poorer muscle metabolism in their later years. Led by Kate Duchowny, a scientist at the University of Michigan Institute for Social Research, the research was published in Science Advances.
Duchowny’s analysis indicated that 45% of the participants reported experiencing adverse childhood events, with both male and female respondents showing reduced ATP max production if they had encountered adverse events during childhood. The study utilized muscle tissue samples from individuals participating in the Study of Muscle, Mobility, and Aging (SOMMA), comprising 879 participants aged over 70 who provided various biospecimens. In addition to physical and cognitive assessments, the participants completed questionnaires addressing their childhood experiences.
The researchers examined muscle biopsies to assess ATP production and oxidative phosphorylation, crucial processes for generating cellular energy. Mitochondria, the cell organelles, produce adenosine triphosphate (ATP), the energy source for cellular functions. Questionnaire responses revealed a significant association between adverse childhood events and reduced ATP production, indicating a potential link between early life stress and mitochondrial function in skeletal muscle.
Anthony Molina, a study co-author and professor of medicine at the University of California San Diego, contributed expertise in muscle bioenergetics. Utilizing 31 PMR spectroscopy, the researchers evaluated ATP synthesis rates by analyzing muscle responses during and after exercise. High-resolution mitochondrial respirometry was employed to assess oxygen consumption rates in muscle fiber bundles, providing insights into muscle mitochondrial function.
The study’s findings suggest that childhood adverse events can impact mitochondrial function, which plays a crucial role in various aging-related outcomes. Duchowny emphasized the importance of mitochondrial function for overall health, highlighting its implications for chronic conditions, physical function, and disability limitations. The research team accounted for various factors that could influence muscle function, confirming the enduring effects of childhood adversities on mitochondrial function in older adults.
In conclusion, the study sheds light on how early life stressors can influence health outcomes in later years through their impact on mitochondrial function in skeletal muscle.