# Physical Activity, Metabolic Risk and the Primary Allostatic Load Mediators: An Explorative Study

**Authors:** Francis Osei, Pia-Maria Wippert, Andrea Block

PMC · DOI: 10.3390/sports14030107 · Sports · 2026-03-09

## TL;DR

This study explores how physical activity affects stress-related biological markers and metabolic risk in healthy adults, finding some differences in cortisol levels.

## Contribution

The study provides exploratory evidence linking regular physical activity to altered stress-regulatory activity in healthy adults.

## Key findings

- Regular physical activity was associated with higher cortisol levels compared to non-regular activity.
- No significant differences were found in other stress mediators or metabolic risk markers.
- Descriptive patterns suggest potential benefits of higher physical activity on lipid profiles.

## Abstract

Background: Chronic stress is associated with dysregulation of the body’s allostatic systems, contributing to increased allostatic load (AL) and adverse metabolic outcomes. Regular physical activity (PA) is considered a key protective factor that may attenuate AL by enhancing adaptive stress responses and supporting metabolic health. This study examined the differences between PA, primary mediators of AL, and metabolic risk markers in apparently healthy adults in Germany. Methods: Forty-six adults (18–45 years) were categorized into a moderate intensity (regular PA: ≥150 min a week vs. non-regular PA: ≤150 min a week) group according to current PA recommendations. Primary AL mediators were quantified by cortisol (μg/12 h), epinephrine (μg/12 h), norepinephrine (μg/12 h), and dehydroepiandrosterone sulfate (DHEA-S: μg/mL). Group differences in primary AL mediators and metabolic risk markers were examined using the Mann–Whitney U test. Results: A significant group difference was observed for cortisol levels, with higher values in the regular PA group (p = 0.01), with a moderate negative effect size of r = −0.38. No statistically significant differences (p > 0.05) were found between groups for epinephrine, norepinephrine, DHEA-S, or metabolic risk markers, including triglycerides, blood pressure, body mass index (BMI), and high-density lipoprotein cholesterol (HDL-C). Conclusions: The findings suggest that regular PA may be associated with altered stress-regulatory activity, as reflected by differences in cortisol. While no statistically significant group differences were observed for metabolic risk markers, descriptive patterns indicate more favorable lipid profiles and potential variation in primary AL mediators at higher PA levels. Given the exploratory nature of the analyses and the small and unequal group sizes, these findings should be interpreted with caution and warrant confirmation in future studies with larger and more balanced samples.

## Full-text entities

- **Genes:** POMC (proopiomelanocortin) [NCBI Gene 5443] {aka ACTH, CLIP, LPH, MSH, NPP, OBAIRH}, CRH (corticotropin releasing hormone) [NCBI Gene 1392] {aka CRF, CRH1}, INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, HK1 (hexokinase 1) [NCBI Gene 3098] {aka CNSHA5, HK, HK1-ta, HK1-tb, HK1-tc, HKD}, COMT (catechol-O-methyltransferase) [NCBI Gene 1312] {aka HEL-S-98n}
- **Diseases:** metabolic abnormalities (MESH:D008659), PA (MESH:D059445), LBP (MESH:D017116), MetS (MESH:D024821), hyperglycemia (MESH:D006943), hypertension (MESH:D006973), hemophilia (MESH:D006467), HPA axis hyperactivity (MESH:D007029), central adiposity (MESH:D018205), visceral adiposity (MESH:D007418), AL (MESH:C536761), injury to (MESH:D014947), insulin resistance (MESH:D007333), infections (MESH:D007239), metabolic dysregulation (MESH:D021081), depression (MESH:D003866), psychological disorders (MESH:D000067073), lipid metabolism abnormalities (MESH:D052439), abdominal obesity (MESH:D056128), impaired glucose tolerance (MESH:D018149), cardiovascular or metabolic diseases (MESH:D002318), cardiovascular, metabolic, thyroid, vascular, malignant, lung, or autoimmune diseases (MESH:D008171)
- **Chemicals:** blood glucose (MESH:D001786), Glucose (MESH:D005947), DHEA-S (MESH:D019314), LDL-C (-), Cortisol (MESH:D006854), catecholamine (MESH:D002395), DHEA-S (MESH:D003687), Lipid (MESH:D008055), norepinephrine (MESH:D009638), Epinephrine (MESH:D004837), triglyceride (MESH:D014280)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

70 references — full list in the complete paper: https://tomesphere.com/paper/PMC13030496/full.md

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Source: https://tomesphere.com/paper/PMC13030496