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

This paper concerns how motor actions are neurally represented and coded. Action planning and motor preparation can be studied using a specific type of representational activity, motor imagery. A close functional equivalence between motor imagery and motor preparation is suggested by the positive effects of imagining movements on motor learning, the similarity between the neural structures involved, and the similar physiological correlates observed in both imaging and preparing. The content of motor representations can be inferred from motor images at a macroscopic level, based on global aspects of the action (the duration and amount of effort involved) and the motor rules and constraints which predict the spatial path and kinematics of movements. A more microscopic neural account calls for a representation of object-oriented action. Object attributes are processed in different neural pathways depending on the kind of task the subject is performing. During object-oriented action, a pragmatic representation is activated in which object affordances are transformed into specific motor schemas (independently of other tasks such as object recognition). Animal as well as human clinical data implicate the posterior parietal and premotor cortical areas in schema instantiation. A mechanism is proposed that is able to encode the desired goal of the action and is applicable to different levels of representational organization.

https://www.cambridge.org/core/services/aop-cambridge-core/content/view/S0140525X00034026

The representing brain: Neural correlates of motor intention and imagery

Functional anatomy of the basal ganglia. II. The place of subthalamic nucleus and external pallidum in basal ganglia circuitry.

Vagally mediated heart rate recovery after exercise is accelerated in athletes but blunted in patients with chronic heart failure

▪ Abstract Breathing is a vital behavior that is particularly amenable to experimental investigation. We review recent progress on three problems of broad interest. (i) Where and how is respiratory rhythm generated? The preBotzinger Complex is a critical site, whereas pacemaker neurons may not be essential. The possibility that coupled oscillators are involved is considered. (ii) What are the mechanisms that underlie the plasticity necessary for adaptive changes in breathing? Serotonin-dependent long-term facilitation following intermittent hypoxia is an important example of such plasticity, and a model that can account for this adaptive behavior is discussed. (iii) Where and how are the regulated variables CO2 and pH sensed? These sensors are essential if breathing is to be appropriate for metabolism. Neurons with appropriate chemosensitivity are spread throughout the brainstem; their individual properties and collective role are just beginning to be understood.

Breathing: Rhythmicity, plasticity, chemosensitivity

Stimulation by central command of locomotion, respiration and circulation during exercise.

Unanesthetized decorticate cats walked or ran normally on a treadmill either spontaneously or during electrical stimulation of the subthalamic "locomotor" region. The respiratory response usually preceded the locomotor response and increased in proportion to locomotor activity despite control or ablation of respiratory feedback mechanisms. Respiration increased similarly in paralyzed animals during fictive locomotion despite the absence of muscular contraction or movement. Hypothalamic command signals are thus primarily responsible for the proportional driving of locomotion and respiration during exercise.

https://science.sciencemag.org/content/sci/211/4484/844.full.pdf

Exercise hyperpnea and locomotion: parallel activation from the hypothalamus

Static contraction of the hindlimb muscles of cats reflexly increases cardiovascular function, an effect that is potentiated by occlusion of the arterial supply to the working muscles. Although group III and IV afferents are known to be stimulated by and to cause the reflex cardiovascular responses to static muscular contraction, little is known about the responses of these afferents to static contraction when the arterial supply to a working muscle is occluded. We therefore recorded the impulse activity of 24 group III afferents and 30 group IV afferents with endings in the triceps surae while we statically contracted this muscle group, both when the abdominal aorta was occluded and when it was patent. A chi 2 analysis revealed that ischemia increased the responses to static contractions of a significantly higher percentage of group IV afferents than group III afferents (46.7% vs. 12.5%, respectively; P less than 0.02). In addition, two patterns of responses to ischemic contraction were observed. The first pattern was displayed by afferents (n = 10) that were stimulated by nonischemic contraction but were stimulated more by ischemic contraction. The second pattern was displayed by afferents (n = 7) that were not stimulated by nonischemic contraction but were stimulated by ischemic contraction. We conclude that afferents displaying both patterns are likely to contribute to the reflex cardiovascular responses to ischemic contraction.

Effect of ischemia on responses of group III and IV afferents to contraction

Prolonged stimulation of respiration by a new central neural mechanism

The sections in this article are:


1
Respiration

2
Circulation

3
Central Command Mechanisms
31
Central Drive of Locomotion

32
Locomotor Pattern Generator

33
Supraspinal Locomotor Sites




4
Central Command Control of Respiration and Circulation in Animals
41
Cerebral Cortex

42
Hypothalamic Locomotor Region

43
Mesencephalic Locomotor Region

44
Amygdala

45
Awake, Exercising Animal Studies




5
Short-Term Potentiation
51
Respiration




6
Central Command Control of Respiration and Circulation in Humans
61
Respiration

62
Circulation




7
Interactions Between Central Command and Peripheral Feedback

8
Interaction of Central Command with Cardiorespiratory Reflexes
81
Baroreceptor Reflex

82
Hering-Breuer Reflex

83
Chemoreceptor Reflexes




9
Conclusions

Tony G. Waldrop

Papers

Stimulation by central command of locomotion, respiration and circulation during exercise.

Exercise hyperpnea and locomotion: parallel activation from the hypothalamus

Effect of ischemia on responses of group III and IV afferents to contraction

Prolonged stimulation of respiration by a new central neural mechanism

Central Neural Control of Respiration and Circulation During Exercise