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Successful reactive balance control requires coordinated modulation of hip, knee, and ankle torques. Stabilizing joint torques arise from neurally-mediated feedforward tonic muscle activation that modulates muscle short-range stiffness, which provides instantaneous "mechanical feedback" to the perturbation. In contrast, neural feedback pathways activate muscles in response to sensory input, generating joint torques after a delay. However, the specific contributions from feedforward and feedback pathways to the balance-correcting torque response are poorly understood. As feedforward- and feedback-mediated torque responses to balance perturbations act at different delays, we modified the sensorimotor response model (SRM), previously used to analyze the muscle activation response, to reconstruct joint torques using parallel feedback loops. Each loop is driven by the same information, center of mass (CoM) kinematics, but each loop has an independent delay. We evaluated whether a torque-SRM could decompose the reactive torques during balance-correcting responses to backward support surface translations at four magnitudes into the instantaneous "mechanical feedback" torque modulated by feedforward neural commands before the perturbation and neurally-delayed feedback components. The SRM accurately reconstructed torques at the hip, knee, and ankle, across all perturbation magnitudes (R2 > 0.84 and VAF > 0.83). Moreover, the hip and knee exhibited feedforward and feedback components, while the ankle only exhibited feedback components. The lack of a feedforward component at the ankle may occur because the compliance of the Achilles tendon attenuates muscle short-range stiffness. Our model may provide a framework for evaluating changes in the feedforward and feedback contributions to balance that occur due to aging, injury, or disease. NEW & NOTEWORTHY: Reactive balance control requires coordination of neurally-mediated feedforward and feedback pathways to generate stabilizing joint torques at the hip, knee, and ankle. Using a sensorimotor response model, we decomposed reactive joint torques into feedforward and feedback contributions based on delays relative to the center of mass kinematics. Responses across joints were driven by the same signals, but contributions from feedforward versus feedback pathways differed, likely due to differences in musculotendon properties between proximal and distal muscles. [ABSTRACT FROM AUTHOR]

The habitual use of high-heeled footwear may structurally remodel user leg muscle tendons, thereby altering their functional capabilities. High heels set users' ankles in relatively plantarflexed positions, causing calf muscle tendons to operate at relatively short lengths. Habitually operating muscle tendons at relatively short lengths induces structural remodeling that theoretically affects muscle metabolism. Because structural changes occur within the body, the user's locomotor metabolism may change in any footwear condition (e.g., conventional shoes, barefoot). Here, we studied the influence of habitual high-heel use on users' leg muscle-tendon structure and metabolism during walking in flat-soled footwear. We tested eight participants before and after 14 wk of agreeing to wear high heels as their daily shoes. Overall, participants who wore high heels >1,500 steps per day, experienced a 9% decrease in their net metabolic power during walking in flat-soled footwear (d = 1.66, P ≤ 0.049), whereas participants who took <1,000 daily steps in high heels did not (d = 0.44; P = 0.524). Across participants, for every 1,000 daily steps in high heels, net metabolic power during walking in flat-soled footwear decreased 5.3% (r = -0.73; P = 0.040). Metabolic findings were partially explained (r2=0.43; P = 0.478) by trending shorter medial gastrocnemius fascicle lengths (d = 0.500, P = 0.327) and increased Achilles tendon stiffness (d = 2.889, P = 0.088). The high-heel intervention did not alter user walking stride kinematics in flat-soled footwear (d ≤ 0.567, P = 0.387). While our limited dataset is unable to establish the mechanisms underlying the high-heel-induced walking economy improvement, it appears that prescribing specific footwear use can be implemented to alter user muscle-tendon properties and augment their function in any shoes. [ABSTRACT FROM AUTHOR]

Older adults walk slower and with a higher metabolic energy expenditure than younger adults. In this review, we explore the hypothesis that age-related declines in Achilles tendon stiffness increase the metabolic cost of walking due to less economical calf muscle contractions and increased proximal joint work. This viewpoint may motivate interventions to restore ankle muscle-tendon stiffness, improve walking mechanics, and reduce metabolic cost in older adults. [ABSTRACT FROM AUTHOR]

The correct affiliation is listed below: Department of Human Physiology, Gonzaga University, Spokane, WA, USA The original Article has been corrected. Correction to: I Scientific Reports i https://doi.org/10.1038/s41598-023-34346-x, published online 11 May 2023 The original version of this Article contained an error in Affiliation 2, which was incorrectly given as "Department of Human Physiology, Gonzaga University, Spokane, USA". [Extracted from the article]

Herein, we investigate the effects of ligand design on the nuclearity and reactivity of metal-ligand multiply bonded (MLMB) complexes to access an exclusively bimetallic reaction pathway for C-H bond functionalization. To this end, the diiron alkoxide [Fe 2 ( Ph Dbf) 2 ] ( 1 ) was treated with 3,5-bis(trifluoromethyl)phenyl azide to access the diiron imido complex [Fe 2 ( Ph Dbf) 2 (μ-NC 8 H 3 F 6 )] ( 2a ) that promotes hydrogen atom abstraction (HAA) from a variety of C-H and O-H bond containing substrates. A diiron bis(amide) complex [Fe 2 ( Ph Dbf) 2 (μ-NHC 8 H 3 F 6 )(NHC 8 H 3 F 6 )] ( 3 ) was generated, prompting the isolation of the analogous bridging amide terminal alkoxide [Fe 2 ( Ph Dbf) 2 (μ-NHC 8 H 3 F 6 )(OC 19 H 15 )] ( 4 ) and the asymmetric pyridine-bound diiron imido [Fe 2 ( Ph Dbf) 2 (μ-NC 8 H 3 F 6 )(NC 5 H 5 )] ( 6a ). We found that 6a is competent for toluene amination, indicating the effect of Lewis base-enhanced C-H bond functionalization. Mechanistic investigations suggest that the bimetallic bridging imido complex is the reactive intermediate as no monometallic species is detected during the time course of the reaction.

Successful reactive balance control requires coordinated modulation of hip, knee, and ankle torques. Stabilizing joint torques arise from feedforward neural signals that modulate the musculoskeletal system's intrinsic mechanical properties, namely muscle short-range stiffness, and neural feedback pathways that activate muscles in response to sensory input. Although feedforward and feedback pathways are known to modulate the torque at each joint, the role of each pathway to the balance-correcting response across joints is poorly understood. Since the feedforward and feedback torque responses act at different delays following perturbations to balance, we modified the sensorimotor response model (SRM), previously used to analyze the muscle activation response to perturbations, to consist of parallel feedback loops with different delays. Each loop within the model is driven by the same information, center of mass (CoM) kinematics, but each loop has an independent delay. We evaluated if a parallel loop SRM could decompose the reactive torques into the feedforward and feedback contributions during balance-correcting responses to backward support surface translations at four magnitudes. The SRM accurately reconstructed reactive joint torques at the hip, knee, and ankle, across all perturbation magnitudes (R 2 >0.84 & VAF>0.83). Moreover, the hip and knee exhibited feedforward and feedback components, while the ankle only exhibited feedback components. The lack of a feedforward component at the ankle may occur because the compliance of the Achilles tendon attenuates muscle short-range stiffness. Our model may provide a framework for evaluating changes in the feedforward and feedback contributions to balance that occur due to aging, injury, or disease., News and Noteworthy: Reactive balance control requires coordination of neurally-mediated feedforward and feedback pathways to generate stabilizing joint torques at the hip, knee, and ankle. Using a sensorimotor response model, we decomposed reactive joint torques into feedforward and feedback contributions based on delays relative to center of mass kinematics. Responses across joints were driven by the same signals, but contributions from feedforward versus feedback pathways differed, likely due to differences in musculotendon properties between proximal and distal muscles.