Publications

In this and the subsequent companion paper, results are presented that collectively seek to delineate the contribution that supraspinal circuits have in determining the time to task failure (TTF) of sustained submaximal contractions. The purpose of this study was to compare adjustments in supraspinal and spinal excitability taken concurrently throughout the performance of two different fatigue tasks with identical mechanical demands but different TTF (i.e., force-matching and position-matching tasks). On separate visits, ten healthy volunteers performed the force-matching or position-matching task at 15% of maximum strength with the elbow flexors to task failure. Single-pulse transcranial magnetic stimulation (TMS), paired-pulse TMS, paired cortico-cervicomedullary stimulation, and brachial plexus electrical stimulation were delivered in a 6-stimuli sequence at baseline and every 2-3 minutes throughout fatigue-task performance. Contrary to expectations, the force-matching task TTF was 42% shorter (17.5 +/- 7.9 min) than the position-matching task (26.9 +/- 15.11 min; p0.01); however, both tasks caused the same amount of muscle fatigue (p = 0.59). There were no task-specific differences for the total amount or rate of change in the neurophysiologic outcome variables over time (p>0.05). Therefore, failure occurred after a similar mean decline in motorneuron excitability developed (p0.02, ES = 0.35-0.52) coupled with a similar mean increase in measures of corticospinal excitability (p0.03, ES = 0.30-0.41). Additionally, the amount of intracortical inhibition decreased (p0.03, ES = 0.32) and the amount of intracortical facilitation (p>0.10) and an index of upstream excitation of the motor cortex remained constant (p>0.40). Together, these results suggest that as fatigue develops prior to task failure, the increase in corticospinal excitability observed in relationship to the decrease in spinal excitability results from a combination of decreasing intracortical inhibition with constant levels of intracortical facilitation and upstream excitability that together eventually fail to provide the input to the motor cortex necessary for descending drive to overcome the spinal cord resistance, thereby contributing to task failure.

INTRODUCTION: The purpose of this study was to examine the relative and absolute between-day reliability of the motor unit number index (MUNIX). METHODS: Young, healthy adults (n=19) attended two testing sessions separated by 4-weeks where their maximal pinch-grip strength, MUNIX, and motor unit size index (MUSIX) were assessed in the abductor pollicis brevis muscle. Reliability was assessed by intraclass correlation coefficients (ICC), coefficient of variation (CV) and limits of agreement (LOA). RESULTS: No mean differences were observed for MUNIX or MUSIX. The CV for the MUNIX and MUSIX measures were between 13.5% and 17.5%. The ICC for both measures were moderate to moderately-high (0.73-0.76), The LOA for both indicated a homoscedastic relationship. DISCUSSION: Our findings indicate moderate to moderately-high reliability for both MUNIX and MUSIX. Future work is needed to ensure both measures are reliable in other muscles and cohorts, and further investigations are required to examine the validity of MUNIX.

We tested the hypothesis that the nervous system, and the cortex in particular, is a critical determinant of muscle strength/weakness and that a high level of corticospinal inhibition is an important neurophysiological factor regulating force generation. A group of healthy individuals underwent 4 wk of wrist-hand immobilization to induce weakness. Another group also underwent 4 wk of immobilization, but they also performed mental imagery of strong muscle contractions 5 days/wk. Mental imagery has been shown to activate several cortical areas that are involved with actual motor behaviors, including premotor and M1 regions. A control group, who underwent no interventions, also participated in this study. Before, immediately after, and 1 wk following immobilization, we measured wrist flexor strength, voluntary activation (VA), and the cortical silent period (SP; a measure that reflect corticospinal inhibition quantified via transcranial magnetic stimulation). Immobilization decreased strength 45.1 +/- 5.0%, impaired VA 23.2 +/- 5.8%, and prolonged the SP 13.5 +/- 2.6%. Mental imagery training, however, attenuated the loss of strength and VA by approximately 50% (23.8 +/- 5.6% and 12.9 +/- 3.2% reductions, respectively) and eliminated prolongation of the SP (4.8 +/- 2.8% reduction). Significant associations were observed between the changes in muscle strength and VA (r = 0.56) and SP (r = -0.39). These findings suggest neurological mechanisms, most likely at the cortical level, contribute significantly to disuse-induced weakness, and that regular activation of the cortical regions via imagery attenuates weakness and VA by maintaining normal levels of inhibition.

BACKGROUND: Recent studies suggest that wearing high-heel shoes increases the risk of developing certain musculoskeletal pain conditions. In this study we sought to examine whether heel height alters lumbar and hip extensor muscle timing characteristics during a standardized trunk flexion task. METHODS: Thirty-one young, healthy women (22-27 years; 168.6 +/- 5.1 cm; 57.1 +/- 11.8 kg) participated in this study. Lumbar erector spinae (ES), gluteus maximus (GM), and biceps femoris (BF) electromyographic (EMG) signals were recorded during a trunk flexion task where subjects were instructed to flex their trunk in the sagittal plane and then return to a neutral posture. The task was repeated under three footwear conditions: while wearing no footwear, while wearing shoes with 4-cm heels, and while wearing shoes with 10-cm heels. EMG onset and offset times, as well as EMG duration, were calculated for each muscle and compared across conditions. RESULTS: We observed a significantly earlier onset of the ES EMG activity (1.36 +/- 0.61 vs. 1.56 +/- 0.67 s), and significantly delayed onset of the GM EMG activity (1.72 +/- 0.66 vs. 1.28 +/- 0.58 s) during the flexion phase of movement in the 10-cm heeled compared to the no footwear condition. The GM muscle also exhibited an earlier offset time in the 10-cm heel condition compared to the no footwear condition during the flexion movement (2.57 +/- 0.67 vs. 3.30 +/- 0.61 s) as well as during the return from flexion movement phase (10.87 +/- 0.58 vs. 11.69 +/- 0.65 s). These alterations in timing characteristic resulted in an overall decrease in the EMG duration for the GM muscle during the flexion movement. CONCLUSION: The results of this study suggest that high-heels alter trunk and hip extensor muscle coordination patterns. These findings, when considered in combination with other recent findings on the biomechanical effects of wearing high-heels, raise concern about whether wearing high heels results in abnormal spine loading patterns and increases the risk for developing musculoskeletal injuries.

PURPOSE OF REVIEW: Age-related muscle weakness causes a staggering economic, public, and personal burden. Most research has focused on internal muscular mechanisms as the root cause to strength loss. Here, we briefly discuss age-related impairments in the brain and peripheral nerve structures that may theoretically lead to muscle weakness in old age. RECENT FINDINGS: Neuronal atrophy in the brain is accompanied by electrical noise tied to declines in dopaminergic neurotransmission that degrades communication between neurons. Additionally, sensorimotor feedback loops that help regulate corticospinal excitability are impaired. In the periphery, there is evidence for motor unit loss, axonal atrophy, demyelination caused by oxidative damage to proteins and lipids, and modified transmission of the electrical signal through the neuromuscular junction. SUMMARY: Recent evidence clearly indicates that muscle weakness associated with aging is not entirely explained by classically postulated atrophy of muscle. In this issue, which focuses on 'Ageing: Biology and Nutrition' we will highlight new findings on how nervous system changes contribute to the aging muscle phenotype. These findings indicate that the ability to communicate neural activity to skeletal muscle is impaired with advancing age, which raises the question of whether many of these age-related neurological changes are mechanistically linked to impaired performance of human skeletal muscle. Collectively, this work suggests that future research should explore the direct link of these 'upstream' neurological adaptions and onset of muscle weakness in elders. In the long term, this new focus might lead to novel strategies to attenuate the age-related loss of muscle strength.

The purpose of this study was to determine whether anodal transcranial direct current stimulation (tDCS) delivered while performing a sustained submaximal contraction would increase time to task failure (TTF) compared to sham stimulation. Healthy volunteers (n = 18) performed two fatiguing contractions at 20% of maximum strength with the elbow flexors on separate occasions. During fatigue task performance, either anodal or sham stimulation was delivered to the motor cortex for up to 20 minutes. Transcranial magnetic stimulation (TMS) was used to assess changes in cortical excitability during stimulation. There was no systematic effect of the anodal tDCS stimulation on TTF for the entire subject set (n = 18; p = 0.64). Accordingly, a posteriori subjects were divided into two tDCS-time groups: Full-Time (n = 8), where TTF occurred prior to the termination of tDCS, and Part-Time (n = 10), where TTF extended after tDCS terminated. The TTF for the Full-Time group was 31% longer with anodal tDCS compared to sham (p = 0.04), whereas TTF for the Part-Time group did not differ (p = 0.81). Therefore, the remainder of our analysis addressed the Full-Time group. With anodal tDCS, the amount of muscle fatigue was 6% greater at task failure (p = 0.05) and the amount of time the Full-Time group performed the task at an RPE between 8-10 ("very hard") increased by 38% (p = 0.04) compared to sham. There was no difference in measures of cortical excitability between stimulation conditions (p = 0.90). That the targeted delivery of anodal tDCS during task performance both increased TTF and the amount of muscle fatigue in a subset of subjects suggests that augmenting cortical excitability with tDCS enhanced descending drive to the spinal motorpool to recruit more motor units. The results also suggest that the application of tDCS during performance of fatiguing activity has the potential to bolster the capacity to exercise under conditions required to derive benefits due to overload.

Enhancement of cardiovascular and muscular fitness through exercise and lifestyle interventions is critical to in alleviating mobility impairment in older adults. In this review article, we discuss the current knowledge-base surrounding mobility improvements in seniors following behavioral interventions that use lifestyle modifications involving physical activity and dietary interventions.