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"Central Nervous System - physiology"
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Sex differences in measures of central sensitization and pain sensitivity to experimental sleep disruption: implications for sex differences in chronic pain
Females demonstrate heightened central sensitization (CS), a risk factor for chronic pain characterized by enhanced responsivity of central nervous system nociceptors to normal or subthreshold input. Sleep disruption increases pain sensitivity, but sex has rarely been evaluated as a moderator and few experiments have measured CS. We evaluated whether two nights of sleep disruption alter CS measures of secondary hyperalgesia and mechanical temporal summation in a sex-dependent manner. We also evaluated differences in measures of pain sensitivity.
Seventy-nine healthy adults (female n = 46) participated in a randomized crossover experiment comparing two consecutive nights of eight pseudorandomly distributed forced awakenings (FA [-200 min sleep time]) against two nights of undisturbed sleep (US). We conducted sensory testing the mornings following Night 2; the heat-capsaicin pain model was used to induce secondary hyperalgesia.
FA reduced total sleep time (REM and NREM Stage 3) more profoundly in males. We observed divergent, sex-dependent effects of FA on secondary hyperalgesia and temporal summation. FA significantly increased secondary hyperalgesia in males and significantly increased temporal summation in females. Sex differences were not attributable to differential sleep loss in males. FA also significantly reduced heat-pain threshold and cold pressor pain tolerance, independently of sex.
Sleep disruption enhances different pain facilitatory measures of CS in males and females suggesting that sleep disturbance may increase risk for chronic pain in males and females via distinct pathways. Findings have implications for understanding sex differences in chronic pain and investigating sleep in chronic pain prevention efforts.
Journal Article
Neurocomic
Nonfiction graphic novel explaining the physiology of the brain and describing theoretical and experimental developments that led to our present understanding.
Book
Interaction of Central and Peripheral Factors during Repeated Sprints at Different Levels of Arterial O2 Saturation
To investigate the interaction between the development of peripheral locomotor muscle fatigue, muscle recruitment and performance during repeated-sprint exercise (RSE).
In a single-blind, randomised and cross-over design, ten male team-sport athletes performed two RSE (fifteen 5-s cycling sprints interspersed with 25 s of rest; power self-selected) in normoxia and in acute moderate hypoxia (FIO2 0.138). Mechanical work, total electromyographic intensity (summed quadriceps electromyograms, RMSsum) and muscle (vastus lateralis) and pre-fontal cortex near-infrared spectroscopy (NIRS) parameters were calculated for every sprint. Blood lactate concentration ([Lac(-)]) was measured throughout the protocol. Peripheral quadriceps fatigue was assessed via changes in potentiated quadriceps twitch force (ΔQtw,pot) pre- versus post-exercise in response to supra-maximal magnetic femoral nerve stimulation. The central activation ratio (QCAR) was used to quantify completeness of quadriceps activation.
Compared with normoxia, hypoxia reduced arterial oxygen saturation (-13.7%, P=0.001), quadriceps RMSsum (-13.7%, P=0.022), QCAR (-3.3%, P=0.041) and total mechanical work (-8.3%, P=0.019). However, the magnitude of quadriceps fatigue induced by RSE was similar in the two conditions (ΔQtw,pot: -53.5% and -55.1%, P=0.71). The lower cycling performance in hypoxia occurred despite similar metabolic (muscle NIRS parameters and blood [Lac(-)]) and functional (twitch and M-wave) muscle states.
Results suggest that the central nervous system regulates quadriceps muscle recruitment and, thereby, performance to limit the development of muscle fatigue during intermittent, short sprints. This finding highlights the complex interaction between muscular perturbations and neural adjustments during sprint exercise, and further supports the presence of pacing during intermittent sprint exercise.
Journal Article
Exercising with reserve: evidence that the central nervous system regulates prolonged exercise performance
Objective: The purpose of this study was to measure the effects of an amphetamine (methylphenidate) on exercise performance at a fixed rating of perceived exertion of 16. Methods: Eight elite cyclists ingested 10 mg methylphenidate in a randomised, placebo-controlled crossover trial. Results: Compared with placebo, subjects receiving methylphenidate cycled for approximately 32% longer before power output fell to 70% of the starting value. At the equivalent time at which the placebo trial terminated, subjects receiving methylphenidate had significantly higher power outputs, oxygen consumptions, heart rates, ventilatory volumes and blood lactate concentrations although electromyographic activity remained unchanged. The ingestion of a centrally acting stimulant thus allowed subjects to exercise for longer at higher cardiorespiratory and metabolic stress indicating the presence of a muscular reserve in the natural state. Conclusions: This suggests that endurance performance is not only “limited” by mechanical failure of the exercising muscles (“peripheral fatigue”). Rather performance during prolonged endurance exercise under normal conditions is highly regulated by the central nervous system to ensure that whole-body homeostasis is protected and an emergency reserve is always present.
Journal Article
Cortical voluntary activation testing methodology impacts central fatigue
Purpose
Currently, cortical voluntary activation (VA
TMS
) is assessed by superimposing transcranial magnetic stimulation (TMS) on a maximal voluntary contraction (MVC), 75% MVC and 50% MVC, each contraction being interspersed with 5–10 s of relaxation. Here, we assessed whether this traditional approach (TRADI) underestimates central fatigue due to this short recovery compared to a continuous method (CONTI).
Methods
VA
TMS
, motor-evoked potential (MEP), and cortical silent period (CSP) of the
vastus lateralis
were determined in 12 young healthy adults before and after a 2-min sustained MVC of knee extensors in two randomly assigned sessions. In TRADI, evaluations comprised a 7-s rest between the three contractions (100, 75, and 50% MVC) and evaluation following the 2-min sustained MVC started after a minimal rest (3–4 s). In CONTI, evaluations were performed with no rest allowed between the three levels of contraction, and evaluation after the 2-min sustained MVC commenced without any rest.
Results
MVC was equally depressed at the end of the 2 min in both conditions. Post 2-min sustained MVC, VA
TMS
change was greater in CONTI than in TRADI (−29 (15)% [−42, −17] vs. −9 (4)% [−13, −5], respectively,
P
< 0.001). Differences were also observed between TRADI and CONTI for MEP and CSP immediately after the fatiguing exercise. All differences between the two methods disappeared after 2 min of recovery.
Conclusion
After a 2-min sustained MVC, a few seconds of recovery change the amount of measured VA
TMS
and associated parameters of central fatigue. The continuous method should be preferred to determine deficits in voluntary activation.
Journal Article
Improved tolerance of peripheral fatigue by the central nervous system after endurance training
Purpose
The purposes of this study were to evaluate the effect of endurance training on central fatigue development and recovery.
Methods
A control group was compared to a training group, which followed an 8-week endurance-training program, consisting in low-force concentric and isometric contractions. Before (PRE) and after (POST) the training period, neuromuscular function of the knee extensor (KE) muscles was evaluated before, immediately after and during 33 min after an exhausting submaximal isometric task at 15 % of the maximal voluntary contraction (MVC) force. After training, the trained group performed another test at iso-time, i.e., with the task maintained until the duration completed before training was matched (POST2). The evaluation of neuromuscular function consisted in the determination of the voluntary activation level during MVCs, from peripheral nerve electrical (VA
PNS
) and transcranial magnetic stimulations (VA
TMS
). The amplitude of the potentiated twitch (Pt), the evoked [motor evoked potentials, cortical silent period (CSP)] and voluntary EMG activities were also recorded on the KE muscles.
Results
Before training, the isometric task induced significant reductions of VA
PNS
, VA
TMS
and Pt, and an increased CSP. The training period induced a threefold increase of exercise duration, delayed central fatigue appearance, as illustrated by the absence of modification of VA
PNS
, VA
TMS
and CSP after POST2. At POST, central fatigue magnitude and recovery were not modified but Pt reduction was greater.
Conclusion
These results suggest that central fatigue partially adapts to endurance training. This adaptation principally translates into improved tolerance of peripheral fatigue by the central nervous system.
Journal Article
Abnormal endogenous pain modulation is a shared characteristic of many chronic pain conditions
The intensity of acute and chronic pain depends on interactions between peripheral impulse input and CNS pain mechanisms, including facilitation and inhibition. Whereas tonic pain inhibition is a characteristic of most pain-free individuals, pain facilitation can be detected in many chronic pain patients. The capability to inhibit pain is normally distributed along a wide continuum in the general population and can be used to predict chronic pain. Accumulating evidence suggests that endogenous pain inhibition depends on activation of the prefrontal cortex, periaqueductal gray and rostral ventral medulla. Quantitative sensory test paradigms have been designed to acquire detailed information regarding each individual's endogenous pain inhibition and facilitation. Such tests include: temporal summation of pain, which is mostly used to assess facilitatory pain modulation by measuring the change in pain perception during a series of identical nociceptive stimuli; and conditioned pain modulation, which tests pain inhibition by utilizing two simultaneously applied painful stimuli (the 'pain inhibits pain' paradigm). Considerable indirect evidence seems to indicate that not only increased pain facilitation but also ineffective pain inhibition represents a predisposition for chronic pain. This view is supported by the fact that many chronic pain syndromes (e.g., fibromyalgia, temporomandibular joint disorder, irritable bowel syndrome, headache and chronic fatigue syndrome) are associated with hypersensitivity to painful stimuli and reduced endogenous pain inhibition. However, future prospective studies will be necessary to provide definitive evidence for this relationship. Such research would not only provide important information about mechanisms relevant to chronic pain but would also permit identification of individuals at high risk for future chronic pain.
Journal Article
Pharmacological Modulation of Pain-Related Brain Activity during Normal and Central Sensitization States in Humans
Abnormal processing of somatosensory inputs in the central nervous system (central sensitization) is the mechanism accounting for the enhanced pain sensitivity in the skin surrounding tissue injury (secondary hyperalgesia). Secondary hyperalgesia shares clinical characteristics with neurogenic hyperalgesia in patients with neuropathic pain. Abnormal brain responses to somatosensory stimuli have been found in patients with hyperalgesia as well as in normal subjects during experimental central sensitization. The aim of this study was to assess the effects of gabapentin, a drug effective in neuropathic pain patients, on brain processing of nociceptive information in normal and central sensitization states. Using functional magnetic resonance imaging (fMRI) in normal volunteers, we studied the gabapentin-induced modulation of brain activity in response to nociceptive mechanical stimulation of normal skin and capsaicin-induced secondary hyperalgesia. The dose of gabapentin was 1,800 mg per os, in a single administration. We found that (i) gabapentin reduced the activations in the bilateral operculoinsular cortex, independently of the presence of central sensitization; (ii) gabapentin reduced the activation in the brainstem, only during central sensitization; (iii) gabapentin suppressed stimulus-induced deactivations, only during central sensitization; this effect was more robust than the effect on brain activation. The observed drug-induced effects were not due to changes in the baseline fMRI signal. These findings indicate that gabapentin has a measurable antinociceptive effect and a stronger antihyperalgesic effect most evident in the brain areas undergoing deactivation, thus supporting the concept that gabapentin is more effective in modulating nociceptive transmission when central sensitization is present.
Journal Article
Natriuretic Peptides
In 1981, de Bold and his colleagues made the seminal observation that infusion of extracts of atrial tissue into rats caused a copious natriuresis.
1
This then led to the isolation and cloning of atrial natriuretic peptide, the first member of a family of peptides with potent natriuretic, diuretic, and vasorelaxant activity.
2
Subsequent contributions from many investigators have expanded our understanding of the family of natriuretic peptides, their receptors, and their cellular actions that regulate physiologic functions. Studies using drugs to inhibit the function of some natriuretic peptide receptors or to prevent the degradation of natriuretic peptides have confirmed the importance . . .
Journal Article