Muscle fatigue is an exercise-induced reduction in maximal voluntary muscle force. It may arise not only because of peripheral changes at the level of the muscle, but also because the central nervous system fails to drive the motoneurons adequately. Evidence for “central” fatigue and the neural mechanisms underlying it are reviewed, together with its terminology and the methods used to reveal it. Much data suggest that voluntary activation of human motoneurons and muscle fibers is suboptimal and thus maximal voluntary force is commonly less than true maximal force. Hence, maximal voluntary strength can often be below true maximal muscle force. The technique of twitch interpolation has helped to reveal the changes in drive to motoneurons during fatigue. Voluntary activation usually diminishes during maximal voluntary isometric tasks, that is central fatigue develops, and motor unit firing rates decline. Transcranial magnetic stimulation over the motor cortex during fatiguing exercise has revealed focal cha...

Spinal and Supraspinal Factors in Human Muscle Fatigue

1. Using two magnetic stimulators, we investigated the effect of a conditioning magnetic stimulus over the motor cortex of one hemisphere on the size of EMG responses evoked in the first dorsal interosseous (FDI) muscle by a magnetic test stimulus given over the opposite hemisphere. 2. A single conditioning shock to one hemisphere produced inhibition of the test response evoked from the opposite hemisphere when the conditioning-test interval was 5-6 ms or longer. We shall refer to this as interhemispheric inhibition. However, the minimum latency of inhibition observed using surface EMG responses may have underestimated the true interhemispheric conduction time. Single motor unit studies suggested values 4-7 ms longer than the minimum interval observed with surface EMG. 3. Interhemispheric inhibition was seen when the test muscle was active or relaxed. Increasing the intensity of the conditioning stimulus increased the duration of inhibition: increasing the intensity of the test stimulus reduced the depth of inhibition. 4. The conditioning coil had to be placed on the appropriate area of scalp for inhibition to occur. The effect of the conditioning stimulus was maximal when it was applied over the hand area of motor cortex, and decreased when the stimulus was moved medial or lateral to that point. 5. The inhibitory effect on the test stimulus probably occurred at the level of the cerebral cortex. In contrast to the inhibition of test responses evoked by magnetic test stimuli, test responses evoked in active FDI by a small anodal electric shock were not significantly inhibited by a contralateral magnetic conditioning stimulus. Similarly, H reflexes in relaxed forearm flexor muscles were unaffected by conditioning stimuli to the ipsilateral hemisphere. However, inhibition was observed if the experiment was repeated with the muscles active.

https://physoc.onlinelibrary.wiley.com/doi/pdf/10.1113/jphysiol.1992.sp019243

Interhemispheric inhibition of the human motor cortex.

Driven by recent empirical studies, we offer a new understanding of the degrees of freedom problem, and propose a refined concept of synergy as a neural organization that ensures a one-to-many mapping of variables providing for both stability of important performance variables and flexibility of motor patterns to deal with possible perturbations and/or secondary tasks. Empirical evidence is reviewed, including a discussion of the operationalization of stability/flexibility through the method of the uncontrolled manifold. We show how this concept establishes links between the various accounts for how movement is organized in redundant effector systems.

Toward a New Theory of Motor Synergies

There continues to be great interest in evaluating the adaptive plasticity of the human nervous system in response to exercise training or other interventions. For various reasons, researchers have been interested in estimates of spinal reflex processing in intact human subjects before and after training. A reflex pathway that has been employed in this regard is the Hoffmann (H) reflex. This brief review describes the basic procedure for evoking the H reflex in different muscles. Other sections address methodological issues that affect interpretation of the H reflex. In particular, the role that presynaptic inhibition serves in the modification of the H reflex and how this precludes its use as an unambiguous measure of alpha-motoneuron excitability will be discussed. Applications of the H reflex to study adaptive plasticity in humans is also reviewed, and methodological requirements that should be maintained for accurate interpretation of H reflexes in exercise studies are presented.

Considerations for use of the Hoffmann reflex in exercise studies.

https://www.cs.cmu.edu/~hgeyer/Teaching/R16-899B/Papers/Knikou08JNeurosciMethods.pdf

The H-reflex as a probe: pathways and pitfalls.

1. Reciprocal inhibition between elbow flexor and extensor muscles (biceps and triceps brachii) has been investigated in nine healthy subjects. Two techniques were used to assess changes in motoneurone excitability after stimulation of antagonist muscle afferents: (1) monosynaptic reflexes elicited by a mechanical stimulation of the distal muscle tendon (tendon tap); (2) post-stimulus time histograms (PSTH) of voluntarily activated motor units. 2. Electrical stimulation of the antagonist muscle nerve produced a short-latency and short-lasting inhibition of the flexor and extensor motoneurones. The amount of this inhibition was found to be similar in both motor nuclei. 3. The inhibition could be evoked with conditioning electrical stimuli as low as 0.7 x motor threshold (MT) or by very weak tendon taps applied to the antagonist tendon. In the former case the threshold of this inhibition was found to be consistently increased after raising the threshold of Ia afferent fibres by a long-lasting muscle vibration. Since a contribution from cutaneous afferent fibres was ruled out, it is concluded that this inhibition was Ia in origin. 4. Post-stimulus time histograms of voluntarily activated triceps and biceps motor units were made following electrical stimulation of homonymous and antagonist muscle afferents. This enabled an estimate of the central synaptic delay of the inhibitory process. An average central delay of 0.94 ms in excess of that of monosynaptic facilitation was found, thus suggesting that the inhibitory process could be mediated by only one interneurone. 5. A conditioning reflex discharge elicited in the antagonist muscle by a tendon tap depressed or suppressed this inhibition. This depression was maximal when the reflex discharge was elicited 10-20 ms before the conditioning stimulus for the inhibition and never lasted more than 30 ms. It is argued that the only mechanism compatible with such a depression is the inhibitory activity of Renshaw cells acting on the pathway mediating reciprocal inhibition. 6. We conclude that group Ia afferent fibres from elbow extensor and flexor muscles project monosynaptically onto Ia inhibitory interneurones to mediate disynaptic reciprocal inhibition of antagonist motoneurones.

https://physoc.onlinelibrary.wiley.com/doi/pdf/10.1113/jphysiol.1991.sp018595

Reciprocal Ia inhibition between elbow flexors and extensors in the human

The distribution of homonymous and heteronymous recurrent inhibition among the motor nuclei innervating the main muscles of the human upper limb has been investigated in 25 healthy subjects. Homonymous recurrent inhibition was studied with a specially designed electrophysiological method with paired H-reflexes, previously described by Bussel & Pierrot-Deseilligny (1977), combined with a pharmacological study using a cholinergic agonist, the L-acetylcarnitine (Rossi & Mazzocchio 1991). These methods were used to investigate the Flexor Carpi Radialis (FCR), Extensor Carpi Radialis (ECR), Opponens Pollicis (OP) and Abductor Digiti Minimi (ADM) motor nuclei

Distribution of recurrent inhibition in the human upper limb.

1. Effects of conditioning motor volleys of increasing amplitude on antagonistic motor nuclei were tested at the wrist and elbow level in man. 2. The modifications of biceps, triceps, flexor carpi radialis (FCR) and extensor carpi radialis (ECR) motoneurone excitability were tested both in post-stimulus time histogram (PSTH) and rectified averaged EMG experiments. 3. Conditioning motor volleys were evoked in biceps, triceps, FCR and ECR muscles by electrical stimuli applied to the corresponding nerves. The intensity of the conditioning stimuli was systematically varied from an intensity just below motor threshold to one giving rise to a motor response equal to half of the maximal direct motor response (Mmax). 4. The effect of the injection of a cholinergist agonist, L-acetylcarnitine (L-Ac), on antagonistic conditioning motor volleys was tested for each motor nucleus. 5. Results obtained at the wrist and elbow level were strikingly different. Antagonistic motor volleys resulted in an early and long-lasting inhibition enhanced by L-Ac injection in wrist motor nuclei, while no modification was observed in elbow motor nuclei. 6. The characteristics of the early and long-lasting inhibition evoked in wrist motor nuclei by antagonistic motor volleys suggest that they are due to the activation of Renshaw cells by the conditioning motor volleys. 7. It is therefore concluded that these experiments provide further evidence that the interconnections between motoneurones, interneurones mediating reciprocal inhibition and Renshaw cells at the wrist level are different from those described elsewhere. Indeed, it has already been shown that the interneurones mediating reciprocal inhibition between FCR and ECR are not inhibited by Renshaw cells, and the results presented here suggest that FCR-coupled Renshaw cells inhibit ECR motoneurones and vice versa.

https://physoc.onlinelibrary.wiley.com/doi/pdf/10.1113/jphysiol.1997.sp021925

R Katz

Papers

Reciprocal Ia inhibition between elbow flexors and extensors in the human

Distribution of recurrent inhibition in the human upper limb.

Recurrent inhibition between motor nuclei innervating opposing wrist muscles in the human upper limb.