Neural contributions to age-related handgrip weakness revealed by multi-finger force deficit and dual-task testing.

Handgrip strength (HGS) is recognized as the primary characteristic of sarcopenia. Low HGS is strongly associated with morbidity, disability, and mortality. However, the neural mechanisms underlying age-related declines in HGS have not been fully elucidated. The multi-finger force deficit (MFFD), which reflects the central nervous system's capacity to coordinate finger activation during a power grip, provides an innovative approach to assess these neural contributions. Prior MFFD studies have inferred neural contributions to grip force, but this assumes that multi-finger dynamometry captures coordination processes relevant to conventional HGS. Because prior paradigms used non-standard hand/forearm postures and generally studied younger-old, high-functioning adults, the clinical relevance of MFFD to age-related weakness remains uncertain. Therefore, we tested younger (n = 12; 23.7 ± 1.7 years) and markedly older (n = 10; 80.3 ± 8.8 years) adults using a biomimetic setup that replicated traditional HGS assessment and examined whether HGS is altered under cognitively demanding dual-task conditions. Older adults exhibited 48.8% lower HGS, greater MFFD (25.8 ± 11.4% vs. 16.5 ± 7.1%; p < 0.05), and lower performance on HGS during continuous reading aloud than younger adults (17.7 ± 6.7 kg vs. 29.8 ± 9.2 kg; p < 0.001). Further, sarcopenic older adults exhibited a higher MFFD compared to their non-sarcopenic counterparts (33.4 ± 8.6% vs. 18.0 ± 8.3%; p = 0.021), when data are pooled across hands. These findings suggest that age-related reductions in HGS are partly attributable to neural mechanisms. The MFFD may represent a candidate behavioral marker of multi-digit reserve, but its predictive and clinical utility require validation.