Impact of reduced sleep on muscle recovery and pain after intense exercise

Effect of partial sleep deprivation on acute skeletal muscle recovery, perceived muscle soreness and pro-inflammatory cytokines following an exercise-induced muscle damage protocol using Eccentric Exercise

Status

Active, not recruiting

Phases

Unknown

Study type

Interventional

Source

REBEC

Registry ID

RBR-4rqtgdy

Enrollment

Registered

2026-07-05

Start date

2024-10-20

Completion date

Unknown

Last updated

2026-08-03

For informational purposes only — not medical advice. Sourced from public registries and may not reflect the latest updates. Terms

Conditions

Muscle Skeletal Athletic Injuries

Interventions

This is a randomized, crossover, and open-label (non-blinded) clinical trial consisting of two arms with a one-week washout interval between conditions. Based on an a priori sample size calculation pe

s d effect size of 0.8 for muscle damage analysis, assuming a significance level of 5% and a statistical power of 95%. In the partial sleep deprivation condition (experimental arm), participants under

Eligibility

Sex/Gender

Male

Age

18 Years to 35 Years

Inclusion criteria

Inclusion criteria: Healthy adult men aged between eighteen and thirty-five years; with no engagement or prior experience with resistance training in the last six months; and without muscular or osteoarticular injuries that prevented evaluations

Exclusion criteria

Exclusion criteria: Use of sleep inducers stimulants psychotropics or anti-inflammatory drugs; body mass index above twenty-four point nine body; fat percentage above twenty-five percent; or non-compliance with the established sleep protocol

Design outcomes

Primary

Measure	Time frame
Expected outcome 1: To evaluate the effect of partial sleep restriction on exercise-induced muscle damage, verified through serum IL-6, TNF-a and IL-1ß concentrations measured by enzyme-linked immunosorbent assay (ELISA), observing whether a 50% reduction in habitual sleep time for two consecutive nights would prolong the acute inflammatory response compared with the habitual sleep condition.;Outcome found 1: Total sleep time was significantly reduced after the intervention (p = 0.001). The eccentric exercise protocol successfully induced muscle damage, as demonstrated by significant time effects in biochemical, morphological, perceptual and functional markers. However, no statistically significant differences were observed between the sleep restriction and habitual sleep conditions for any muscle damage marker, indicating that two consecutive nights of 50% sleep restriction did not exacerbate muscle damage or impair early muscle recovery.	—

Measure

Time frame

Expected outcome 1: To evaluate the effect of partial sleep restriction on exercise-induced muscle damage, verified through serum IL-6, TNF-a and IL-1ß concentrations measured by enzyme-linked immunosorbent assay (ELISA), observing whether a 50% reduction in habitual sleep time for two consecutive nights would prolong the acute inflammatory response compared with the habitual sleep condition.;Outcome found 1: Total sleep time was significantly reduced after the intervention (p = 0.001). The eccentric exercise protocol successfully induced muscle damage, as demonstrated by significant time effects in biochemical, morphological, perceptual and functional markers. However, no statistically significant differences were observed between the sleep restriction and habitual sleep conditions for any muscle damage marker, indicating that two consecutive nights of 50% sleep restriction did not exacerbate muscle damage or impair early muscle recovery.

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Secondary

Measure	Time frame
Expected outcome 2: To evaluate morphological alterations following exercise-induced muscle damage, verified through musculoskeletal ultrasound and localized bioelectrical impedance analysis, observing changes in muscle thickness, arm circumference, echo intensity and phase angle before exercise, immediately after exercise, and 24 and 48 hours after exercise.;Outcome found 2: Significant increases were observed in arm circumference (p = 0.001) and muscle thickness (p = 0.001), together with changes in echo intensity (p = 0.001) and phase angle (p = 0.04), verified through musculoskeletal ultrasound and localized bioelectrical impedance analysis. No significant condition × time interactions were observed for any morphological variable (arm circumference: p = 0.55; muscle thickness: p = 0.54; echo intensity: p = 0.09; phase angle: p = 0.16).;Expected outcome 3: To evaluate perceptual responses to exercise-induced muscle damage, verified through pressure algometry, observing pain threshold and pain tolerance before exercise, immediately after exercise, and 24 and 48 hours after the experimental protocol.;Outcome found 3: Significant reductions in pain threshold (p = 0.001) and pain tolerance (p = 0.001) were observed at 24 and 48 hours after exercise, verified through pressure algometry. No differences were observed between sleep conditions for pain threshold (p = 0.44) or pain tolerance (p = 0.17).;Expected outcome 4: To evaluate biochemical markers of exercise-induced muscle damage, verified through serum creatine kinase (CK) and lactate dehydrogenase (LDH) measurements, observing their concentrations before exercise and 2, 24 and 48 hours after exercise.;Outcome found 4: Creatine kinase increased significantly at 24 and 48 hours (p = 0.001), whereas lactate dehydrogenase increased immediately after exercise and returned to baseline values during subsequent assessments (p = 0.001), verified through serum enzyme measurements. No significant differences were observed b	—

Measure

Time frame

Expected outcome 2: To evaluate morphological alterations following exercise-induced muscle damage, verified through musculoskeletal ultrasound and localized bioelectrical impedance analysis, observing changes in muscle thickness, arm circumference, echo intensity and phase angle before exercise, immediately after exercise, and 24 and 48 hours after exercise.;Outcome found 2: Significant increases were observed in arm circumference (p = 0.001) and muscle thickness (p = 0.001), together with changes in echo intensity (p = 0.001) and phase angle (p = 0.04), verified through musculoskeletal ultrasound and localized bioelectrical impedance analysis. No significant condition × time interactions were observed for any morphological variable (arm circumference: p = 0.55; muscle thickness: p = 0.54; echo intensity: p = 0.09; phase angle: p = 0.16).;Expected outcome 3: To evaluate perceptual responses to exercise-induced muscle damage, verified through pressure algometry, observing pain threshold and pain tolerance before exercise, immediately after exercise, and 24 and 48 hours after the experimental protocol.;Outcome found 3: Significant reductions in pain threshold (p = 0.001) and pain tolerance (p = 0.001) were observed at 24 and 48 hours after exercise, verified through pressure algometry. No differences were observed between sleep conditions for pain threshold (p = 0.44) or pain tolerance (p = 0.17).;Expected outcome 4: To evaluate biochemical markers of exercise-induced muscle damage, verified through serum creatine kinase (CK) and lactate dehydrogenase (LDH) measurements, observing their concentrations before exercise and 2, 24 and 48 hours after exercise.;Outcome found 4: Creatine kinase increased significantly at 24 and 48 hours (p = 0.001), whereas lactate dehydrogenase increased immediately after exercise and returned to baseline values during subsequent assessments (p = 0.001), verified through serum enzyme measurements. No significant differences were observed b

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Countries

Contacts

Public ContactBruno Ribeiro

Universidade Federal do Rio Grande do Norte

contatobrunoribeiro@outlook.com.br+5584999928895

Outcome results

None listed

Source: REBEC (via WHO ICTRP) · Data processed: Aug 10, 2026