Key result
Irregular sleep timing strengthens the negative association between prior-day training load and morning HRV.
Why the study?
The study examined whether nightly deviation from habitual sleep midpoint moderates the association between prior-day internal training load and next-morning cardiac vagal modulation in university sport participants.
Observational (n=54)
No
Effect estimate: b = -0.0101 (95% CI -0.0153 to -0.0048)
p-value: p=<0.001
In university sport participants, greater night-to-night deviation in sleep timing strengthens the negative association between prior-day training load and next-morning cardiac vagal modulation.
Irregular sleep timing may amplify training load effects on next-day autonomic recovery in athletes; extends observational HRV data but should not yet change practice.
Background: Heart rate variability (HRV) describes beat-to-beat variation in cardiac intervals; the root mean square of successive differences (RMSSD) is a time-domain index of short-term cardiac vagal modulation. We examined whether nightly deviation from habitual sleep midpoint moderated the association between prior-day internal training load and next-morning natural-log-transformed RMSSD (lnRMSSD), and whether analogous interactions were present for resting heart rate, wellness strain, and countermovement-jump (CMJ) height. Methods: University students engaged in regular sport training completed 28 days of habitual monitoring. Internal load was session duration multiplied by session rating of perceived exertion. Wrist actigraphy and sleep diaries estimated sleep midpoint, and 5-min morning RR recordings yielded lnRMSSD. Mixed models separated within- and between-participant components and tested within-participant load (per 100 arbitrary units [AU]) × absolute midpoint deviation (per 30 min). Results: The analysis included 1,232 mornings from 54 participants (57.4% female; age 21.0 ± 1.7 years). At each participant's mean midpoint deviation, greater-than-usual load was associated with lower next-morning lnRMSSD (β = -0.0089, 95% CI -0.0127 to -0.0051; p < 0.001). At mean load, greater-than-usual midpoint deviation was also associated with lower lnRMSSD (β = -0.0156, 95% CI -0.0268 to -0.0045; p = 0.006). The interaction was negative (β = -0.0101, 95% CI -0.0153 to -0.0048; p < 0.001). Thus, the inverse within-participant association between load and lnRMSSD strengthened as sleep-timing irregularity increased. No load-by-midpoint interaction was detected for resting heart rate, wellness strain, or CMJ height after false discovery rate adjustment. The primary interaction persisted after adjustment for prior-morning lnRMSSD (β = -0.0096, 95% CI -0.0147 to -0.0046; p < 0.001). Conclusion: The within-participant association between training load and next-morning cardiac vagal modulation was moderated by sleep-timing irregularity. These field-based associations do not establish a sleep mechanism, causal recovery effect, or decision threshold.
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A 2026 study conducted an observational in University students engaged in regular sport training (n=54). Sleep-timing irregularity (absolute sleep-midpoint deviation) vs. Habitual sleep midpoint (usual sleep timing) was evaluated on Moderation of the within-participant association between prior-day internal training load and next-morning natural-log-transformed RMSSD (lnRMSSD) (b = -0.0101, 95% CI -0.0153 to -0.0048, p=<0.001). Sleep-timing irregularity significantly moderated the within-participant association between prior-day training load and next-morning heart rate variability, strengthening the inverse relationship.
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