ECSS Paris 2023: OP-BM13
INTRODUCTION: Although aging profoundly alters both neural and musculotendinous components, their distinct contributions to age-related declines in force control of plantar flexion movements remain poorly understood. The purpose of this study was to determine the neural and musculotendinous contributions to age-related declines in accuracy and variability of ballistic goal-directed plantar flexions. METHODS: Twenty-two young (22±2 years) and twenty-two older adults (72±6 years) were instructed to match a force target accurately (30% and 80% MVC) and as fast as possible by performing 3 sets of 10 plantar flexions. We examined neuromuscular control by quantifying peak force error (PFE), Time to Peak Force (TPF), peak force and TPF variability (CV PF, CV TPF). Muscle activity was recorded using surface EMG electrodes on Gastrocnemius Medialis and Lateralis (MG, LG), Soleus (SOL), and Tibialis Anterior (TA) muscles. Achilles tendon stiffness was also quantified to examine the peripheral contribution to force control. RESULTS: Older adults exhibited longer TPF, greater PFE, as well as greater CV PF and CV TPF than young adults. In addition, they exhibited altered activation and different coordination of the agonist and antagonist muscles. Age-related increases in TPF, CV PF and CV TPF were largely predicted by greater LG time to peak EMG and its variability, as well as by greater antagonistic (TA-MG peak delay) and synergistic (LG-MG and SOL-MG overlay) coactivation. The CV PF was also predicted by Tibialis Anterior EMG area variability. Achilles tendon stiffness did not differ between the two age groups. CONCLUSION: These findings suggest that age-related impairments in force control of ballistic, goal-directed plantar flexion are primarily driven by changes in neural mechanisms and altered motor planning, rather than by structural or functional changes in tendon properties. Consequently, interventions targeting neural coordination and motor control strategies may be more effective than those focusing exclusively on peripheral tissue properties.
Read CV Martha TrapezanidouECSS Paris 2023: OP-BM13
INTRODUCTION: The ability to rapidly generate force is essential for daily movements and balance recovery following external perturbations. Because the time available to produce force in real-world scenarios is typically less than 250 ms, insufficient for the full expression of maximal strength, the rate of force development (RFD) becomes a critical determinant of balance recovery and fall prevention and declines considerably with ageing [1]. Individuals with type 2 diabetes (T2D) exhibit an even greater impairment in RFD, indicative of early neuromuscular impairment that can occur even in the absence of clinically evident complications [2]. During ballistic contractions, motor unit recruitment rate (MU-Rr) and maximal discharge rate (DRMAX) predict maximal-RFD (RFDmax) and impulse in young adults [3]. However, the neural mechanisms underlying reduced RFD in older adults with and without T2D remain unknown. This investigation aimed to determine whether age- and T2D-related reductions in RFD were mediated by alterations in these functional neural determinants. METHODS: Ten healthy older adults (62±5 yrs, BMI 24.31 ± 4.39 kg ⋅ m-2) and ten older adults with T2D (63±4 yrs, BMI 28.07 ± 4.03 kg ⋅ m-2) were enrolled in this study and compared to ten young adults (23±3 yrs, BMI 27.33 ± 4.08 kg ⋅ m-2). Participants performed ballistic isometric contractions of the ankle dorsiflexors to quantify RFDmax and impulse, while high-density surface EMG was recorded to examine MU-Rr and DRMAX, following validated approaches [3]. RESULTS: Compared with young controls, RFDmax was significantly lower in older individuals (-1034 N⋅s-1, p=0.002), with greater reductions in T2D (-1715 N⋅s-1, p<0.001). Similarly, impulse was reduced in the old (-12.6 N⋅s, p=0.03) and T2D groups (-25.9 N⋅s, p<0.001). These functional deficits were accompanied by proportional reductions in MU-Rr (p<0.001) and DRMAX (p<0.01), with impairments more pronounced in T2D than in healthy old adults (p<0.01). Importantly, MU-Rr and DRMAX correlated with RFDmax (R2>0.55, p<0.01) and impulse (R2>0.50, p<0.01) in all groups. CONCLUSION: To our knowledge, these results provide the first direct evidence that impairment of rapid force capacity with ageing and even more with T2D is associated with a proportional slowing of MU-Rr and reduced DRMAX, reflecting an impaired descending excitatory drive from the central nervous system [2,3], and identify these neural changes as primary limitations to rapid force capacity and biomarkers to target in specific rehabilitation settings. This limitation likely compromises the ability to produce corrective torque during balance disturbances and may contribute to increased fall risk, identifying rapid force activation as an important target for rehabilitation strategies. REFERENCES: [1] https://doi.org/10.1113/JP285667 [2] https://doi.org/10.1113/JP287589 [3] https://doi.org/10.1113/JP277396
Read CV Fiorella MartireECSS Paris 2023: OP-BM13
INTRODUCTION: Persistent inward currents (PICs) play a critical role in spinal motor neuron output by amplifying and prolonging excitatory synaptic inputs. Recent findings suggest that aging and repetitive muscle contractions reduce PICs contribution to motor neuron firing (1,2). However, it remains unknown whether very old individuals exhibit additional impairments compared with old adults, and whether fatigue-induced changes in PICs differ between young, old and very old adults. METHODS: Twelve young (27 ± 5 yrs), 12 old (71 ± 5 yrs) and 12 very old (83 ± 2 yrs) participants performed a fatiguing task consisting of 10 isometric triangular-shaped dorsiflexion ramps (20 s up, 20 s down) to 60% of maximal voluntary force (MVF). MVF was assessed before and immediately after the fatiguing task. Triangular contraction ramps to 20% MVF (10 s up, 10s down) were performed before and after the fatiguing task to estimate PICs. After the fatiguing task, ramps were performed up to 20% of post-fatigue MVF (relative condition) and up to 20% of initial MVF (absolute condition). Motor unit discharge rates were extracted from high-density EMG of the tibialis anterior muscle. The prolongation effect of PICs, quantified as delta F, was estimated using the paired motor unit method (3). A geometric approach was used to estimate the amplification effect of PICs (acceleration slope), the neuromodulatory drive (brace height) and the pattern of inhibition (attenuation slope) (4). RESULTS: MVF decreased after the fatiguing task (p<0.001) independent of age. Peak discharge rate was lower in old and very old than in young adults (p<0.01) and decreased after the fatiguing task in both relative and absolute conditions (p<0.001), with an interaction effect in relative condition only (p<0.001). Delta F was reduced in old and very old compared with young adults (p<0.01), and decreased after the fatiguing task in relative condition only (p<0.01). Brace height increased after the fatiguing task and acceleration slope decreased in relative condition (both p<0.01), whereas no effect was observed in absolute condition. Attenuation slope decreased after the fatiguing task in both conditions (p<0.01) independent of age. CONCLUSION: These results suggest that the similar reduction in peak discharge rate observed in old and very old adults is mainly mediated by the decrease in intrinsic motoneuron excitability, as indicated by reduced PICs prolongation effect. In addition, regardless of age, fatigue-related reduction in discharge rate appears to be explained by decreased in prolongation and amplification effects of PICs and increased synaptic inhibition. Finally, all parameters exhibited similar fatigue-induced changes across groups indicating comparable impairments in PICs prolongation and amplification effects in young, old and very old adults. (1) Orssatto LBR et al. J Physiol (2023) (2) Mackay K et al. J Neurophysiol (2023) (3) Gorassini M et al. Neurosci Lett (1998) (4) Beauchamp JA et al. J Neural Eng (2023)
Read CV Cyril ChatainECSS Paris 2023: OP-BM13