The evaluation of rate of force development during rapid contractions has recently become quite popular for characterising explosive strength of athletes, elderly individuals and patients. The main aims of this narrative review are to describe the neuromuscular determinants of rate of force development and to discuss various methodological considerations inherent to its evaluation for research and clinical purposes. Rate of force development (1) seems to be mainly determined by the capacity to produce maximal voluntary activation in the early phase of an explosive contraction (first 50–75 ms), particularly as a result of increased motor unit discharge rate; (2) can be improved by both explosive-type and heavy-resistance strength training in different subject populations, mainly through an improvement in rapid muscle activation; (3) is quite difficult to evaluate in a valid and reliable way. Therefore, we provide evidence-based practical recommendations for rational quantification of rate of force development in both laboratory and clinical settings.

Much is known about the physiological impairments that can cause muscle fatigue. It is known that fatigue can be caused by many different mechanisms, ranging from the accumulation of metabolites within muscle fibres to the generation of an inadequate motor command in the motor cortex, and that there is no global mechanism responsible for muscle fatigue. Rather, the mechanisms that cause fatigue are specific to the task being performed. The development of muscle fatigue is typically quantified as a decline in the maximal force or power capacity of muscle, which means that submaximal contractions can be sustained after the onset of muscle fatigue. There is even evidence that the duration of some sustained tasks is not limited by fatigue of the principal muscles. Here we review experimental approaches that focus on identifying the mechanisms that limit task failure rather than those that cause muscle fatigue. Selected comparisons of tasks, groups of individuals and interventions with the task-failure approach can provide insight into the rate-limiting adjustments that constrain muscle function during fatiguing contractions.

The adaptations of the ankle dorsiflexor muscles and the behaviour of single motor units in the tibialis anterior in response to 12 weeks of dynamic training were studied in five human subjects. In each training session ten series of ten fast dorsiflexions were performed 5 days a week, against a load of 30–40 % of the maximal muscle strength. Training led to an enhancement of maximal voluntary muscle contraction (MVC) and the speed of voluntary ballistic contraction. This last enhancement was mainly related to neural adaptations since the time course of the muscle twitch induced by electrical stimulation remained unaffected. The motor unit torque, recorded by the spike‐triggered averaging method, increased without any change in its time to peak. The orderly motor unit recruitment (size principle) was preserved during slow ramp contraction after training but the units were activated earlier and had a greater maximal firing frequency during voluntary ballistic contractions. In addition, the high frequency firing rate observed at the onset of the contractions was maintained during the subsequent spikes after training. Dynamic training induced brief (2–5 ms) motor unit interspike intervals, or ‘doublets’. These doublets appeared to be different from the closely spaced (±10 ms) discharges usually observed at the onset of the ballistic contractions. Motor units with different recruitment thresholds showed doublet discharges and the percentage of the sample of units firing doublets was increased by training from 5.2 to 32.7 %. The presence of these discharges was observed not only at the onset of the series of spikes but also later in the electromyographic (EMG) burst. It is likely that earlier motor unit activation, extra doublets and enhanced maximal firing rate contribute to the increase in the speed of voluntary muscle contraction after dynamic training.

Despite flourishing interest in the topic of fatigue—as indicated by the many presentations on fatigue at the 2015 annual meeting of the American College of Sports Medicine—surprisingly little is known about its impact on human performance. There are two main reasons for this dilemma: (1) the inability of current terminology to accommodate the scope of the conditions ascribed to fatigue, and (2) a paucity of validated experimental models. In contrast to current practice, a case is made for a unified definition of fatigue to facilitate its management in health and disease. Based on the classic two-domain concept of Mosso, fatigue is defined as a disabling symptom in which physical and cognitive function is limited by interactions between performance fatigability and perceived fatigability. As a symptom, fatigue can only be measured by self-report, quantified as either a trait characteristic or a state variable. One consequence of such a definition is that the word fatigue should not be preceded by an adjective (e.g., central, mental, muscle, peripheral, and supraspinal) to suggest the locus of the changes responsible for an observed level of fatigue. Rather, mechanistic studies should be performed with validated experimental models to identify the changes responsible for the reported fatigue. As indicated by three examples (walking endurance in old adults, time trials by endurance athletes, and fatigue in persons with multiple sclerosis) discussed in the review, however, it has proven challenging to develop valid experimental models of fatigue. The proposed framework provides a foundation to address the many gaps in knowledge of how laboratory measures of fatigue and fatigability impact real-world performance.

3. Although the central drive intensified during the fatigue test, as indicated by an increase in surface electromyogram (EMG), the discharge rate of the motor units during the hold phase of each contraction decreased progressively over the course of the task for motor units that were recruited at the beginning of the test, especially the low-threshold units. In contrast, the discharge rates of newly activated units first increased and then decreased.4. Such divergent behaviour of low-and high-threshold motor units could not be individually controlled by the central drive to the motoneurone pool. Rather, the different behaviours must be the consequence of variable contributions from motoneurone adaptation and afferent feedback from the muscle during the fatiguing contraction.

The aim of this study was to investigate the association between the rate of torque development and maximal motor unit discharge frequency in young and elderly adults as they performed rapid submaximal contractions with the ankle dorsiflexors. Recordings were obtained of the torque exerted by the dorsiflexors during the isometric contractions and the surface and intramuscular electromyograms (EMGs) from the tibialis anterior. The maximal rate of torque development and integrated EMG (percentage of total EMG burst) at peak rate of torque development during fast contractions were lower in elderly than young adults by 48% (P < 0.05) and 16.5% (P < 0.05), respectively. The young adults, but not the elderly adults, exhibited a positive association (r2 = 0.33; P < 0.01) between the integrated EMG computed up to the peak rate of torque development and the maximal rate of torque development achieved during the fast contractions. These age-related changes during fast voluntary contractions were accompanied by a decline (P < 0.001) in motor unit discharge frequency (19, 28, and 34% for first 3 interspike intervals, respectively) and in the percentage of units (45%; P < 0.05) that exhibited double discharges (doublets) at brief intervals (<5 ms). Because aging decreased the maximal rate of torque development of fast voluntary contractions to a greater extent ( approximately 10%) than that of an electrically evoked twitch, collectively the results indicate that the age-related decline in maximal motor unit discharge frequency likely limit, in addition to the slowing of muscle contractile properties, the performance of fast voluntary contractions.

Non-technical summary The neural control of muscle activity differs during voluntary shortening and lengthening contractions. In this paper, we show that the relative contribution of both cortical and spinal mechanisms to the modulation of neural activation is specific during lengthening contraction and differs between synergist muscles. Knowledge of spinal and corticospinal excitabilities modulations during shortening and lengthening muscle contraction improves our understanding of the processes that underlies the neural control of muscles during dynamic contractions.Abstract This study was designed to investigate the cortical and spinal mechanisms involved in the modulations of neural activation during lengthening compared with isometric and shortening maximal voluntary contractions (MVCs). Two muscles susceptible to different neural adjustments at the spinal level, the soleus (SOL) and medial gastrocnemius (MG), were compared. Twelve healthy males participated in at least two experimental sessions designed to assess corticospinal and spinal excitabilities. We compared the modulation of motor evoked potentials (MEPs) in response to transcranial magnetic stimulation and Hoffmann reflexes (H-reflexes) during isometric and anisometric MVCs. The H-reflex and MEP responses, recorded during lengthening and shortening MVCs, were compared with those obtained during isometric MVCs. The results indicate that the maximal amplitude of both MEP and H-reflex in the SOL were smaller (P < 0.01) during lengthening MVCs compared with isometric and shortening MVCs but similar (P > 0.05) in MG for all three muscle contraction types. The silent period that follows maximal MEPs was reduced (P < 0.01) during lengthening MVCs in the SOL but not the MG. Similar observations were obtained regardless of the initial length of the MG muscle. Collectively, the current results indicate that the relative contribution of both cortical and spinal mechanisms to the modulation of neural activation differs during lengthening MVCs and between two synergist muscles. The comparison of SOL and MG responses further suggests that the specific modulation of the corticospinal excitability during lengthening MVCs depends mainly on pre-and postsynaptic inhibitory mechanisms acting at the spinal level.

The purpose of this brief review is to examine the neural adaptations associated with training, by focusing on the behavior of single motor units. The review synthesizes current understanding on motor unit recruitment and rate coding during voluntary contractions, briefly describes the techniques used to record motor unit activity, and then evaluates the adaptations that have been observed in motor unit activity during maximal and submaximal contractions. Relatively few studies have directly compared motor unit behavior before and after training. Although some studies suggest that the voluntary activation of muscle can increase slightly with strength training, it is not known how the discharge of motor units changes to produce this increase in activation. The evidence indicates that the increase is not attributable to changes in motor unit synchronization. It has been demonstrated, however, that training can increase both the rate of torque development and the discharge rate of motor units. Furthermore, both strength training and practice of a force-matching task can evoke adaptations in the discharge characteristics of motor units. Because the variability in discharge rate has a significant influence on the fluctuations in force during submaximal contractions, the changes produced with training can influence motor performance during activities of daily living. Little is known, however, about the relative contributions of the descending drive, afferent feedback, spinal circuitry, and motor neuron properties to the observed adaptations in motor unit activity.