Acute effects of blood flow restriction on phase-resolved electromyographic amplitude and whole-cycle agonist-antagonist co-contraction during incremental cycling

Abstract Blood flow restriction (BFR) can modify surface electromyographic (sEMG) amplitude during exercise, but it remains unclear whether these changes differ between the power and recovery phases of cycling and whether whole-cycle temporal and co-contraction descriptors also change. Because sEMG does not directly measure central drive or motor-unit behavior, the present study evaluated functional myoelectric outcomes rather than neural mechanisms. Forty recreationally active men completed incremental cycling sessions with BFR and under control conditions (CON) in a randomized crossover design. Surface EMG was recorded from the rectus femoris (RF), vastus medialis (VM), vastus lateralis (VL), biceps femoris (BF), medial gastrocnemius (MG), and tibialis anterior (TA). Session-peak-normalized root mean square (RMS) amplitude was analyzed separately during the power (0°–180°) and recovery (180°–360°) phases. Median frequency (MF), threshold-defined activation duration, time-to-peak activation, and agonist-antagonist co-contraction indices were calculated over the complete pedal cycle. Repeated-measures analyses examined condition, exercise stage, and phase where appropriate. BFR was associated with greater session-peak-normalized RMS amplitude in all muscles during both phases (all p < 0.001), lower whole-cycle MF (all p ≤ 0.001), and longer threshold-defined activation duration (all p < 0.001). No condition effect was found for time-to-peak activation. Whole-cycle RF-BF co-contraction showed a small condition effect ( p = 0.035, partial eta squared = 0.109), whereas VL-BF and TA-MG did not. The workload at the final sampled stage was lower during BFR than CON (208.7 ± 11.0 vs. 225.0 ± 12.3 W; p < 0.001). Acute BFR changed several sEMG descriptors during incremental cycling, including phase-resolved RMS amplitude and whole-cycle MF and activation duration. These findings describe task-specific myoelectric responses; they do not identify central neural mechanisms, motor-unit recruitment strategies, independent changes in coordination, or joint stabilization. The lower final-stage workload under BFR further indicates that the EMG findings should be interpreted in the context of different task tolerance.

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Publication Details

Journal
Scientific Reports
Published
2026-09-28
DOI
https://doi.org/10.1038/s41598-026-73877-x
Primary Topic
Cardiovascular and exercise physiology
Type
article
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article

Acute effects of blood flow restriction on phase-resolved electromyographic amplitude and whole-cycle agonist-antagonist co-contraction during incremental cycling

Shahram Abbasi, Mehdi Khaleghi Tazji, Ali Abbasi
Scientific Reports
Cardiovascular and exercise physiology
article

Acute effects of blood flow restriction on phase-resolved electromyographic amplitude and whole-cycle agonist-antagonist co-contraction during incremental cycling

Shahram Abbasi, Mehdi Khaleghi Tazji, Ali Abbasi
article en

Abstract

Abstract Blood flow restriction (BFR) can modify surface electromyographic (sEMG) amplitude during exercise, but it remains unclear whether these changes differ between the power and recovery phases of cycling and whether whole-cycle temporal and co-contraction descriptors also change. Because sEMG does not directly measure central drive or motor-unit behavior, the present study evaluated functional myoelectric outcomes rather than neural mechanisms. Forty recreationally active men completed incremental cycling sessions with BFR and under control conditions (CON) in a randomized crossover design. Surface EMG was recorded from the rectus femoris (RF), vastus medialis (VM), vastus lateralis (VL), biceps femoris (BF), medial gastrocnemius (MG), and tibialis anterior (TA). Session-peak-normalized root mean square (RMS) amplitude was analyzed separately during the power (0°–180°) and recovery (180°–360°) phases. Median frequency (MF), threshold-defined activation duration, time-to-peak activation, and agonist-antagonist co-contraction indices were calculated over the complete pedal cycle. Repeated-measures analyses examined condition, exercise stage, and phase where appropriate. BFR was associated with greater session-peak-normalized RMS amplitude in all muscles during both phases (all p < 0.001), lower whole-cycle MF (all p ≤ 0.001), and longer threshold-defined activation duration (all p < 0.001). No condition effect was found for time-to-peak activation. Whole-cycle RF-BF co-contraction showed a small condition effect ( p = 0.035, partial eta squared = 0.109), whereas VL-BF and TA-MG did not. The workload at the final sampled stage was lower during BFR than CON (208.7 ± 11.0 vs. 225.0 ± 12.3 W; p < 0.001). Acute BFR changed several sEMG descriptors during incremental cycling, including phase-resolved RMS amplitude and whole-cycle MF and activation duration. These findings describe task-specific myoelectric responses; they do not identify central neural mechanisms, motor-unit recruitment strategies, independent changes in coordination, or joint stabilization. The lower final-stage workload under BFR further indicates that the EMG findings should be interpreted in the context of different task tolerance.

Scientific Reports
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Cardiovascular and exercise physiology
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