Traditionally, balance training has been used to rehabilitate ankle injuries and postural deficits. Prospective studies have shown preventive effects with respect to ankle and knee joint injuries. Presently, balance training is not only applied for rehabilitation and prevention but also for improving motor performance, especially muscle power. The recent application of noninvasive electrophysiological and brain imaging techniques revealed insights into the central control of posture and the adaptations induced by balance training. This information is important for our understanding of the basic control and adaptation mechanisms and to conceptualize appropriate training programmes for athletes, elderly people and patients. The present review presents neurophysiological adaptations induced by balance training and their influence on motor behaviour. It emphasizes the plasticity of the sensorimotor system, particularly the spinal and supraspinal structures. The relevance of balance training is highlighted with respect to athletic performance, postural control within elderly people as well as injury prevention and rehabilitation.
The antigravity soleus muscle (Sol) is crucial for compensation of stance perturbation. A corticospinal contribution to the compensatory response of the Sol is under debate. The present study assessed spinal, corticospinal, and cortical excitability at the peaks of short- (SLR), medium- (MLR), and long-latency responses (LLR) after posterior translation of the feet. Transcranial magnetic stimulation (TMS) and peripheral nerve stimulation were individually adjusted so that the peaks of either motor evoked potential (MEP) or H reflex coincided with peaks of SLR, MLR, and LLR, respectively. The influence of specific, presumably direct, corticospinal pathways was investigated by H-reflex conditioning. When TMS was triggered so that the MEP arrived in the Sol at the same time as the peaks of SLR and MLR, EMG remained unaffected. Enhanced EMG was observed when the MEP coincided with the LLR peak (P < 0.001). Similarly, conditioning of the H reflex by subthreshold TMS facilitated H reflexes only at LLR (P < 0.001). The earliest facilitation after perturbation occurred after 86 ms. The TMS-induced H-reflex facilitation at LLR suggests that increased cortical excitability contributes to the augmentation of the LLR peaks. This provides evidence that the LLR in the Sol muscle is at least partly transcortical, involving direct corticospinal pathways. Additionally, these results demonstrate that approximately 86 ms after perturbation, postural compensatory responses are cortically mediated.
After immobilization, patients show impaired postural control and increased risk of falling. Therefore, loss of balance control should already be counteracted during immobilization. Previously, studies have demonstrated that both motor imagery (MI) and action observation (AO) can improve motor performance. The current study elaborated how the brain is activated during imagination and observation of different postural tasks to provide recommendations about the conception of non-physical balance training. For this purpose, participants were tested in a within-subject design in an fMRI-scanner in three different conditions: (a) AO + MI, (b) AO, and (c) MI. In (a) participants were instructed to imagine themselves as the person pictured in the video whereas in (b) they were instructed simply to watch the video. In (c) subjects closed their eyes and kinesthetically imagined the task displayed in the video. Two tasks were evaluated in each condition: (i) static standing balance and (ii) dynamic standing balance (medio-lateral perturbation). In all conditions the start of a new trial was indicated every 2 sec by a sound. During AO + MI of the dynamic task, participants activated motor centers including the putamen, cerebellum, supplementary motor area, premotor cortices (PMv/d) and primary motor cortex (M1). MI showed a similar pattern but no activity in M1 and PMv/d. In the SMA and cerebellum, activity was generally higher in the dynamic than in the static condition. AO did not significantly activate any of these brain areas. Our results showed that (I) mainly AO + MI, but also MI, activate brain regions important for balance control; (II) participants display higher levels of brain activation in the more demanding balance task; (III) there is a significant difference between AO + MI and AO. Consequently, best training effects should be expected when participants apply MI during AO (AO + MI) of challenging postural tasks.
The validity of electromyographic (EMG) data recorded during whole body vibration (WBV) is controversial. Some authors ascribed a major part of the EMG signal to vibration-induced motion artifacts while others have interpreted the EMG signals as muscular activity caused at least partly by stretch reflexes. The aim of this study was to explore the origin of the EMG signal during WBV using several independent approaches. In ten participants, the latencies and spectrograms of stretch reflex responses evoked by passive dorsiflexions in an ankle ergometer were compared to those of the EMG activity of four leg muscles during WBV. Pressure application to the muscles was used to selectively reduce the stretch reflex, thus permitting to distinguish stretch reflexes from other signals. To monitor motion artifacts, dummy electrodes were placed close to the normal electrodes. Strong evidence for stretch reflexes was found: the latencies of the stretch reflex responses evoked by dorsiflexions were almost identical to the supposed stretch reflex responses during vibration (differences of less than 1 ms). Pressure application significantly reduced the amplitude of both the supposed stretch reflexes during vibration (by 61 +/- 17%, p < 0.001) and the stretch reflexes in the ankle ergometer (by 56 +/- 13%, p < 0.01). The dummy electrodes showed almost no activity during WBV (7 +/- 4% of the corresponding muscle's iEMG signal). The frequency analyses revealed no evidence of motion artifacts. The present results support the hypothesis of WBV-induced stretch reflexes. Contribution of motion artifacts to the overall EMG activity seems to be insignificant.
Classical studies in animal preparations suggest a strong role for spinal control of posture. In humans it is now established that the cerebral cortex contributes to postural control of unperturbed and perturbed standing. The age-related degeneration and accompanying functional changes in the brain, reported so far mainly in conjunction with simple manual motor tasks, may also affect the mechanisms that control complex motor tasks involving posture. This review outlines the age-related structural and functional changes at spinal and cortical levels and provides a mechanistic analysis of how such changes may be linked to the behaviorally manifest postural deficits in old adults. The emerging picture is that the age-related reorganization in motor control during voluntary tasks, characterized by differential modulation of spinal reflexes, greater cortical activation and cortical disinhibition, is also present during postural tasks. We discuss the possibility that this reorganization underlies the increased coactivation and dual task interference reported in elderly. Finally, we propose a model for future studies to unravel the structure-function-behavior relations in postural control and aging.
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