<p>This study aimed to investigate the corticospinal drive modulation to Agonist and Antagonist arm muscles following Strength training and detraining, as neural adaptations are critical for early strength gains. Seventeen healthy, untrained young adults underwent four weeks of unilateral dumbbell curl training (60–80% of one-repetition maximum) followed by four weeks of detraining. Transcranial magnetic stimulation (TMS) assessed corticospinal excitability and inhibition across multiple intensities (100–200% rMT). Strength training induced progressive 1-RM improvements in both agonist (BB: +37%, d = 4.18) and antagonist (TB: +15%, d = 0.32) muscles, with partial retention during detraining. The MEP increased selectively in the agonist (BB: +44%, d = 2.80) but not the antagonist muscle, while cSP decreased markedly in the agonist (BB: -42%, d = 2.0). No significant correlations emerged between strength changes and neural adaptations. Secondary outcomes showed transient increases in co-activation and arm circumference during training (<i>p</i> &lt; 0.001). Strength training and detraining modulate corticospinal responses in agonist and antagonist muscles, highlighting their role in early strength acquisition and loss. These neural adaptations provide insight into the mechanisms underlying strength changes during training and detraining.</p>

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Corticospinal drive modulation to agonist and antagonist arm muscles following strength training and detraining

  • Aref Basereh,
  • Hamid Rajabi,
  • Shahriar Gharibzadeh,
  • Joel Mason,
  • Shapour Jaberzadeh

摘要

This study aimed to investigate the corticospinal drive modulation to Agonist and Antagonist arm muscles following Strength training and detraining, as neural adaptations are critical for early strength gains. Seventeen healthy, untrained young adults underwent four weeks of unilateral dumbbell curl training (60–80% of one-repetition maximum) followed by four weeks of detraining. Transcranial magnetic stimulation (TMS) assessed corticospinal excitability and inhibition across multiple intensities (100–200% rMT). Strength training induced progressive 1-RM improvements in both agonist (BB: +37%, d = 4.18) and antagonist (TB: +15%, d = 0.32) muscles, with partial retention during detraining. The MEP increased selectively in the agonist (BB: +44%, d = 2.80) but not the antagonist muscle, while cSP decreased markedly in the agonist (BB: -42%, d = 2.0). No significant correlations emerged between strength changes and neural adaptations. Secondary outcomes showed transient increases in co-activation and arm circumference during training (p < 0.001). Strength training and detraining modulate corticospinal responses in agonist and antagonist muscles, highlighting their role in early strength acquisition and loss. These neural adaptations provide insight into the mechanisms underlying strength changes during training and detraining.