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ABSTRACT Background The mechanisms underlying sarcopenia‐related physical decline remain poorly understood, particularly with respect to neural contributions. Muscle atrophy has traditionally been viewed as the primary driver, but growing evidence suggests that neuromuscular impairments—especially reduced intrinsic motoneuron excitability—may play a central role. This intrinsic excitability, which is critical for modulating motoneuron discharge rates, likely contributes to age‐related weakness and mobility loss. We investigated whether intrinsic motoneuron excitability differs across older adults with sarcopenia, nonsarcopenic controls and masters athletes and whether these differences relate to physical function. Methods Fifty‐six older adults (74.3 ± 7.2 years, 50% female), including 12 sarcopenic, 23 nonsarcopenic controls and 21 masters athletes, were recruited. The Sarcopenia Definitions and Outcomes Consortium (SDOC) thresholds were used for sarcopenia screening. High‐density electromyography (HD‐EMG) was recorded from the tibialis anterior during ramped isometric contractions at intensities of 20%, 40% and 60% of maximum torque (i20%, i40%, i60%). A total of 4998 decomposed motor units were categorized by recruitment thresholds (rt0%–20%, rt20%–40% and rt40%–60%). Paired motor unit analysis was used to calculate delta frequency (Δ F ), an established index of intrinsic motoneuron excitability primarily reflecting persistent inward currents (PICs) contribution to discharge behaviour. Muscle strength, power and physical function were assessed using established performance‐based tests. Results Sarcopenic older adults had significantly lower dorsiflexion peak torque (−56%), sit‐to‐stand power (−37%) and functional capacity tests performance (−30 to −46%) compared to controls. Master athletes demonstrated higher sit‐to‐stand power (23%) and functional performance (11% to 23%) than controls. Δ F was significantly lower in sarcopenic individuals compared to both controls and master athletes across all contraction intensities and recruitment threshold bins (−22% to −38%). Master athletes did not differ from controls in Δ F for low‐threshold units (rt0%–20%) or at i20% and i40% contraction intensities. However, Δ F was higher in athletes than controls at i60% for mid‐ and high‐threshold units (rt20%–40% and rt40%–60%) by 15% and 20%. These group differences in Δ F , particularly at higher intensities, were associated with the degree of muscle weakness and physical limitations. Conclusions Intrinsic motoneuron excitability, as estimated by Δ F , is substantially reduced in this group of sarcopenic older adults, suggesting that it may be critical to functional capacity. Long‐term exercise practice preserves excitability, particularly during high‐demand motor tasks. These findings identify intrinsic motoneuron excitability as both a mechanistic marker of neuromuscular ageing and a potential target for investigations of novel interventions aiming to restore neuromotor function in sarcopenia.
Scott et al. (Tue,) studied this question.