# Exercise interventions for sleep and cognitive dysfunction in shift workers: a systematic review of randomized trials

**Authors:** Fahad Hamoud Algharbi, Shibili Nuhmani, Mohammed Alsubaiei, Alsayed Shanb, Maher Alquaimi

PMC · DOI: 10.3389/fpubh.2026.1762359 · Frontiers in Public Health · 2026-02-06

## TL;DR

This review examines whether exercise can improve sleep and cognitive function in shift workers, finding some benefits but highlighting the need for better-designed studies.

## Contribution

A systematic review of RCTs on exercise interventions for sleep and cognition in shift workers, identifying key findings and barriers to implementation.

## Key findings

- Exercise improved sleep quality and efficiency in 8 out of 10 RCTs, though effects varied in size and clinical relevance.
- Supervised workplace-based exercise post-shift enhanced alertness and memory in three RCTs.
- Mechanistic evidence suggests exercise may shift circadian rhythms and reduce inflammation.

## Abstract

Shift work disrupts circadian rhythms and contributes to poor sleep, cardiometabolic risk, and cognitive impairment, which is especially concerning in safety-critical professions. While exercise improves sleep and cognition in the general population, its effects in shift-working adults remain unclear. This review synthesizes randomized controlled trials (RCT) evidence on structured exercise training to determine its impact on sleep and cognitive outcomes in shift workers, and examines intervention characteristics, mechanistic pathways, and barriers to clinical translation.

Following PRISMA and Cochrane recommendations, six databases were searched from inception to January 2025 for RCTs involving adult shift workers and structured exercise (aerobic, resistance, combined, HIIT, or in-shift activity breaks). Primary outcomes were sleep quality, quantity, and continuity assessed using the Pittsburgh Sleep Quality Index (PSQI), actigraphy or polysomnography, and the Karolinska Sleepiness Scale (KSS), as well as cognitive performance and alertness measured by the Psychomotor Vigilance Task (PVT). Risk of bias (RoB 2.0) and methodological quality (PEDro) were assessed. Due to heterogeneity in interventions and outcome measures, results were narratively synthesized.

Ten RCTs (n = 420; 60% healthcare settings) predominantly evaluated aerobic or mixed modalities. Eight studies reported significant improvements in PSQI, total sleep time, sleep efficiency, or wake after sleep onset, although effect sizes and clinical relevance were inconsistent. Three RCTs demonstrated improvements in alertness, reaction time, and short-term memory, particularly when interventions were timed post-shift or delivered as supervised workplace sessions. Mechanistic evidence from six studies indicated circadian phase shifting, improved autonomic balance assessed by heart rate variability (HRV), and reduced inflammatory markers. However, 80% had “some concerns” or “high” risk of bias, and adherence barriers such as fatigue and irregular schedules were common.

Structured exercise programs, tailored to shift pattern and individual chronotype, show promise for enhancing sleep and cognitive function in shift workers. Workplace-based, supervised interventions maximize adherence and real-world applicability. Future adequately powered RCTs with standardized outcomes, mechanistic markers, and sector-diverse samples are needed before guideline-level recommendations can be established.

Identifier, PROSPERO CRD420250650538. https://www.crd.york.ac.uk/PROSPERO/view/CRD420250650538.

## Full-text entities

- **Genes:** TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, IGF1 (insulin like growth factor 1) [NCBI Gene 3479] {aka IGF, IGF-I, IGFI, MGF}, BDNF (brain derived neurotrophic factor) [NCBI Gene 627] {aka ANON2, BULN2}, CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, IL1RN (interleukin 1 receptor antagonist) [NCBI Gene 3557] {aka CRMO2, DIRA, ICIL-1RA, IL-1RN, IL-1ra, IL-1ra3}, GH1 (growth hormone 1) [NCBI Gene 2688] {aka GH, GH-N, GHB5, GHN, IGHD1A, IGHD1B}
- **Diseases:** cardiovascular and metabolic disorders (MESH:D024821), inflammatory (MESH:D007249), KSS (MESH:C538175), WASO (MESH:D012893), insomnia (MESH:D007319), neurocognitive decline (MESH:D060825), anxiety (MESH:D001007), neuroinflammation (MESH:D000090862), Sleep disruption (MESH:D019958), obesity (MESH:D009765), circadian misalignment (MESH:D017760), accidents (MESH:D000081084), fatigue (MESH:D005221), Sleepiness (MESH:D000077260), HIIT (MESH:D000095027), excessive daytime sleepiness (MESH:D006970), impaired immune regulation (MESH:C565631), PVT (MESH:D000405), hypertension (MESH:D006973), fragmented sleep (MESH:D012892), sleep restriction (MESH:D002313), cognitive dysfunction (MESH:D003072)
- **Chemicals:** melatonin (MESH:D008550), DLMO (-)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## References

45 references — full list in the complete paper: https://tomesphere.com/paper/PMC12920463/full.md

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Source: https://tomesphere.com/paper/PMC12920463