Muscle atrophy and decline in muscle strength appear very rapidly with prolonged disuse or mechanical unloading after acute hospitalization or experimental bed rest. The current study analyzed data from short-, medium-, and long-term bed rest (5–120 days) in a pooled sample of 318 healthy adults and modeled the mathematical relationship between muscle strength decline and atrophy. The results show a logarithmic disuse-induced loss of strength and muscle atrophy of the weight-bearing knee extensor muscles. The greatest rate of muscle strength decline and atrophy occurred in the earliest stages of bed rest, plateauing later, and likely contributed to the rapid neuromuscular loss of function in the early period. In addition, during the first 2 wk of bed rest, muscle strength decline is much faster than muscle atrophy: on day 5, the ratio of muscle atrophy to strength decline as a function of bed rest duration is 4.2, falls to 2.4 on day 14, and stabilizes to a value of 1.9 after ∼35 days of bed rest. Positive regression revealed that ∼79% of the muscle strength loss may be explained by muscle atrophy, while the remaining is most likely due to alterations in single fiber mechanical properties, excitation-contraction coupling, fiber architecture, tendon stiffness, muscle denervation, neuromuscular junction damage, and supraspinal changes. Future studies should focus on neural factors as well as muscular factors independent of atrophy (single fiber excitability and mechanical properties, architectural factors) and on the role of extracellular matrix changes. Bed rest results in nonuniform loss of isometric muscle strength and atrophy over time, where the magnitude of change was greater for muscle strength than for atrophy. Future research should focus on the loss of muscle function and the underlying mechanisms, which will aid in the development of countermeasures to mitigate or prevent the decline in neuromuscular efficiency. NEW & NOTEWORTHY Our study contributes to the characterization of muscle loss and weakness processes reflected by a logarithmic decline in muscle strength induced by chronic bed rest. Acute short-term hospitalization (≤5 days) associated with periods of disuse/immobilization/prolonged time in the supine position in the hospital bed is sufficient to significantly decrease muscle mass and size and induce functional changes related to weakness in maximal muscle strength. By bringing together integrated evaluation of muscle structure and function, this work identifies that 79% of the loss in muscle strength can be explained by muscle atrophy, leaving 21% of the functional loss unexplained. The outcomes of this study should be considered in the development of daily countermeasures for preserving neuromuscular integrity as well as preconditioning interventions to be implemented before clinical bed rest or chronic gravitational unloading (e.g., spaceflights).

This investigation aimed to compare the response of young and older adult men to bed rest (BR) and subsequent rehabilitation (R). Sixteen older (OM, age 55-65 yr) and seven young (YM, age 18–30 yr) men were exposed to a 14-day period of BR followed by 14 days of R. Quadriceps muscle volume (QVOL), force (QF), and explosive power (QP) of leg extensors; single-fiber isometric force (Fo); peak aerobic power (V̇o_2peak); gait stride length; and three metabolic parameters, Matsuda index of insulin sensitivity, postprandial lipid curve, and homocysteine plasma level, were measured before and after BR and after R. Following BR, QVOL was smaller in OM (−8.3%) than in YM (−5.7%, P = 0.031); QF (−13.2%, P = 0.001), QP (−12.3%, P = 0.001), and gait stride length (−9.9%, P = 0.002) were smaller only in OM. Fo was significantly smaller in both YM (−32.0%) and OM (−16.4%) without significant differences between groups. V̇o_2peak decreased more in OM (−15.3%) than in YM (−7.6%, P < 0.001). Instead, the Matsuda index fell to a greater extent in YM than in OM (−46.0% vs. −19.8%, respectively, P = 0.003), whereas increases in postprandial lipid curve (+47.2%, P = 0.013) and homocysteine concentration (+26.3%, P = 0.027) were observed only in YM. Importantly, after R, the recovery of several parameters, among them QVOL, QP, and V̇o_2peak, was not complete in OM, whereas Fo did not recover in either age group. The results show that the effect of inactivity on muscle mass and function is greater in OM, whereas metabolic alterations are greater in YM. Furthermore, these findings show that the recovery of preinactivity conditions is slower in OM.

This study aimed at determining whether the combination of action observation and motor imagery (AO + MI) of locomotor tasks could positively affect rehabilitation outcome after hip replacement surgery. Of initially 405 screened participants, 21 were randomly split into intervention group (N=10; mean age = 64 y; AO + MI of locomotor tasks: 30 min/day in the hospital, then 3×/week in their homes for two months) and control group (N=11, mean age = 63 y, active controls). The functional outcomes (Timed Up and Go, TUG; Four Step Square Test, FSST; and single- and dual-task gait and postural control) were measured before (PRE) and 2 months after surgery (POST). Significant interactions indicated better rehabilitation outcome for the intervention group as compared to the control group: at POST, the intervention group revealed faster TUG (p=0.042), FSST (p=0.004), and dual-task fast-paced gait speed (p=0.022), reduced swing-time variability (p=0.005), and enhanced cognitive performance during dual tasks while walking or balancing (p<0.05). In contrast, no changes were observed for body sway parameters (p≥0.229). These results demonstrate that AO + MI is efficient to improve motor-cognitive performance after hip surgery. Moreover, only parameters associated with locomotor activities improved whereas balance skills that were not part of the AO + MI intervention were not affected, demonstrating the specificity of training intervention. Overall, utilizing AO + MI during rehabilitation is advised, especially when physical practice is limited.

Electroencephalographic neurofeedback (EEG-NFB) represents a broadly used method that involves a real-time EEG signal measurement, immediate data processing with the extraction of the parameter(s) of interest, and feedback to the individual in a real-time. Using such a feedback loop, the individual may gain better control over the neurophysiological parameters, by inducing changes in brain functioning and, consequently, behavior. It is used as a complementary treatment for a variety of neuropsychological disorders and improvement of cognitive capabilities, creativity or relaxation in healthy subjects. In this review, various types of EEG-NFB training are described, including training of slow cortical potentials (SCPs) and frequency and coherence training, with their main results and potential limitations. Furthermore, some general concerns about EEG-NFB methodology are presented, which still need to be addressed by the NFB community. Due to the heterogeneity of research designs in EEG-NFB protocols, clear conclusions on the effectiveness of this method are difficult to draw. Despite that, there seems to be a well-defined path for the EEG-NFB research in the future, opening up possibilities for improvement.