Childhood adverse life events and skeletal muscle mitochondrial function

Marcinek et. al conducted a study to discover if a higher number of childhood adverse life events negatively impacts the power and endurance of muscles in older age in terms of the mitochondrial function in muscle cells. Mitochondria provide energy to a cell. They can sense social stress and react to it on a cellular level, such as changing the rate of mitochondrial cellular respiration, the process of using oxygen to produce energy (ATP).

The goal of this study was to fill in two gaps in understanding surrounding changes to mitochondrial function due to stress: the specific tissues that may be affected and if this finding is consistent when using a larger sample size. In order to test their hypothesis, the researchers used both skeletal muscle data from the Study of Muscle, Mobility, and Aging (SOMMA) of individuals having experienced stressful childhood events and used in vivo and in vitro studies on skeletal muscle biopsies on their sample of older adults.

This study considered age, gender, study site (2), education, parent education, BMI, depressive symptoms, smoking status, physical activity, and chronic conditions. The SOMMA studied 879 adults who were 70 years or older, BMI less than or equal to 40 kg/m², no diagnosis of dementia, ability to undergo a muscle tissue biopsy and magnetic resonance spectroscopy imaging, and the ability to walk 400 m. People that could not complete the 400 m walk did a 4 m walk instead. People with an illness or other factor that made them unable to walk ¼ mile or climb a flight of stairs were not included in the study. Information about childhood adverse life events was collected from 754 of the participants, 698 participants completed a maximum ATP test (the amount of oxygen taken in during exercise, which is made into ATP for energy) and 633 did a maximum oxidative phosphorylation test (measures ATP levels). The participants also took a survey, which inquired about six types of experiences of physical or emotional stress while growing up. Finally, participants underwent a small skeletal muscle biopsy.

The researchers discovered that of the 754 participants with complete data, 53% reported 1 or more childhood adverse life events. Of those who experienced 3 or more events, 55 experienced three, 29 experienced four, 25 reported five, and 8 reported all six types of stressful experiences. Those who did experience childhood stress were more likely to also experience depressive symptoms. The overall sample demonstrated a lower maximum ATP measurement for every adverse childhood event experienced. Men experienced greater changes to maximum ATP than women did when adjusted for participant education, smoking, physical activity, medication, BMI, and depressive symptoms. This supported the hypothesis that adverse childhood events cause later harm to energy production.

Potential limitations of this study were the many factors that were considered, which makes it highly specific and difficult to use to broadly assess the findings. This study also lacks measurements of physical activity after implementing it throughout the study. The length of time between the adverse events was not considered in this study, each event was also treated with the same severity, making it difficult to assess how the magnitude of the event effects future physical aging. The sample was predominantly white, which most likely skewed the results. There is no data on the time between the event and old age to assess influences on mitochondrial function during that time. Finally, the data may have been overadjusted since many of the factors addressed could also be intermediaries.

In the future, similar research should be done on other biological pathways and on the extent to which other intermediaries may shape energy production.