Prophylactic stretching does not reduce cramp susceptibility

Introduction: Some clinicians advocate stretching to prevent muscle cramps. It is unknown whether static or proprioceptive neuromuscular facilitation (PNF) stretching increases cramp threshold frequency (TF_c), a quantitative measure of cramp susceptibility. Methods: Fifteen individuals completed this randomized, counterbalanced, cross‐over study. We measured passive hallux range of motion (ROM) and then performed 3 minutes of either static stretching, PNF stretching (hold–relax—with agonist contraction), or no stretching. ROM was reassessed and TF_c was measured. Results: PNF stretching increased hallux extension (pre‐PNF 81 ± 11°, post‐PNF 90 ± 10°; P < 0.05) but not hallux flexion (pre‐PNF 40 ± 7°, post‐PNF 40 ± 7°; P > 0.05). Static stretching increased hallux extension (pre‐static 80 ± 11°, post‐static 88 ± 9°; P < 0.05) but not hallux flexion (pre‐static 38 ± 9°, post‐static 39 ± 8°; P > 0.05). No ROM changes occurred with no stretching (P > 0.05). TF_c was unaffected by stretching (no stretching 18 ± 7 Hz , PNF 16 ± 4 Hz , static 16 ± 5 Hz ; P = 0.37). Discussion: Static and PNF stretching increased hallux extension, but neither increased TF_c. Acute stretching may not prevent muscle cramping. Muscle Nerve 57 : 473–477, 2018     

Effect of caffeine ingestion on torque and muscle activity during resistance exercise in men

Introduction: We examined the effect of caffeine ingestion on muscle torque production and muscle activity at different contraction speeds in trained men. Methods: 10 men (mean age ± SD = 22 ± 1.1 years) volunteered to participate. A double‐blind, randomized cross‐over design was used. Sixty minutes postingestion of caffeine (6 mg kg^?1) or placebo, participants completed 6 repetitions of isokientic knee extension at 3 angular velocities (30°s^?1, 150°s^?1, 300°s^?1) from which peak torque was determined. Electromyographic activity of the vastus medialis was also collected. Results: Repeated measures analysis of variance indicated that muscle torque production was significantly higher (P = 0.02) with caffeine compared with placebo. A significant (P = 0.02) substance by velocity interaction for muscle activity indicated significantly higher vastus medialis muscle activity in the presence of caffeine versus placebo, and this difference was amplified as angular velocity increased. Conclusions: Acute caffeine ingestion improves muscle performance and increases muscle activity during short‐duration maximal dynamic contractions. Muscle Nerve 50: 523–527, 2014     

Electrical stimulation cramp threshold frequency correlates well with the occurrence of skeletal muscle cramps

The minimum electrical stimulation frequency (HZ ) at which a muscle cramps is termed threshold frequency (TF). TF is theorized to represent one's predisposition to cramping; however, TF and cramp occurrence have never been correlated. We hypothesized that TF would be lower in individuals with a cramp history and lower on the second of two days of testing; genetics may partially explain this lower TF. Cramp TF was measured in 19 subjects with (Group 1), and 12 subjects without (Group 2), a cramp history. Group 1 had a lower TF (14.9 ± 1.3 vs. 25.5 ± 1.6 HZ ; P < 0.001) and a higher family history of cramping than Group 2 (89% vs. 27%; P < 0.001). TF was lower on day 2 (18.3 ± 0.26 HZ ) than day 1 (19.7 ± 0.25 HZ ; P = 0.03). Lower TFs are correlated with cramp history, supporting the inference that lower TFs may represent increased predisposition toward cramping. TF may be used to identify individuals at risk of cramping. Muscle Nerve 39: 364–368, 2009     

Vastus lateralis NA+‐K+‐ATpase activity,protein, and isoform distribution in chronic obstructive pulmonary disease

In this study we investigate the hypothesis that protein abundance, isoform distribution, and maximal catalytic activity of sodium–potassium–adenosine triphosphatase (Na⁺‐K⁺‐ATPase) would be altered in muscle of patients with moderate to severe chronic obstructive pulmonary disease (COPD). Tissue samples were obtained from the vastus lateralis of 10 patients with COPD (mean ± SE: age = 67 ± 2.9 years; FEV₁ = 39 ± 5.5%) and 10 healthy, matched controls (CON: age = 68 ± 2 years; FEV₁ = 114 ± 4.2%). The samples were assessed for maximal catalytic activity (V_max) of the enzyme using the K⁺‐stimulated 3‐O‐methylfluorescein‐phosphatase (3‐O‐MFPase) assay, enzyme abundance using the [³H]‐ouabain assay, and isoform content of both α (α₁, α₂, α₃) and β (β₁, β₂, β₃) using Western blot techniques. A 19.4% lower (P < 0.05) V_max was observed in COPD compared with CON (90.7 ± 6.7 vs. 73.1 ± 4.7 nmol · mg protein^?1 h^?1). No differences between groups were observed for pump concentration (259 ± 15 vs. 243 ± 17 pmol · g wet weight). For the isoforms, α₁ was decreased by 28% (P < 0.05), and α₂ was increased by 12% (P < 0.05) in COPD compared with CON. No differences between groups were observed for α₃ or for the β isoforms. We conclude that moderate COPD compromises V_max, which occurs in the absence of changes in pump abundance. The reduction in V_max could be due to a shift in isoform expression (α₁, α₂), alterations in intrinsic regulation, or to structural changes in the enzyme. The changes observed in the catalytic activity of the pump could have major effects on membrane excitability and fatigability, which are typically compromised in COPD. Muscle Nerve, 2009     

Aerobic training in patients with anoctamin 5 myopathy and hyperckemia

Introduction: Anoctamin 5 deficiency has recently been defined to cause limb‐girdle muscular dystrophy type 2L (LGMD2L) with pronounced hyperCKemia. No treatment interventions have been made so far in this condition. Methods: In 6 patients with LGMD2L, we studied the effect of home‐based, pulse‐watch monitored, moderate‐intensity exercise on a cycle ergometer for 30 minutes, 3 times weekly, for 10 weeks. Plasma creatine kinase (CK) was assessed before, during, and after the program as a marker of muscle damage. Primary outcome measures were maximum oxygen uptake (VO_2max) and time in the 5‐repetitions‐sit‐to‐stand test (FRSTST). Results: Training resulted in improvements in VO_2max (27 ± 7%; P = 0.0001) and FRSTST time (35 ± 12%; P = 0.007). Improvements in physiologic and functional muscle testing were accompanied by stable CK levels and no reports of adverse effects. Conclusions: These findings suggest that supervised aerobic exercise training is safe and effective in improving oxidative capacity and muscle function in patients with anoctamin 5 deficiency. Muscle Nerve 50 : 119–123, 2014     

Voluntary rate of torque development is impaired after a voluntary versus tetanic conditioning contraction

Introduction: Both voluntary and evoked conditioning contractions will potentiate muscle twitch contractile properties. The response of a voluntary contraction to each condition type is not well understood but it may be a more functional model than evoked twitch potentiation. Methods: Baseline measurements from tibialis anterior included: maximal isometric twitch torque and rate of torque development (RTD); maximal evoked 50‐Hz torque; and maximal voluntary ballistic RTD. Potentiation was induced by a 10‐s voluntary or tetanic contraction (∽78% MVC), followed by 2 twitches and 2 ballistic contractions. Results: Twitch properties (torque and RTD) were potentiated equally after each conditioning contraction. Ballistic RTD was greater post‐tetanus (390.2 ± 59.3 Nm/s) than post‐voluntary (356.4 ± 69.1 Nm/s), but both were reduced from baseline (422.0 ± 88.9 Nm/s). Conclusions: Twitch potentiation was similar between conditioning contraction types, but ballistic RTD was lower after post‐tetanus than post‐voluntary. The results indicate central inhibition or fatigue concurrent with peripheral potentiation. Muscle Nerve 49 : 218–224, 2014     

The effect of gastric secretion on gastric physiology and emptying in the fasted and fed state assessed by magnetic resonance imaging

Abstract Conventional measurement of gastric secretion is invasive and cannot assess the intra‐gastric distribution of gastric contents or the effects of secretion on gastric function. This study assessed the effect of gastric secretion on gastric volume responses and emptying (GE) using a validated fast T₁ mapping magnetic resonance imaging (MRI) technique. Twelve healthy participants were studied in the fasted state and after 200 kcal Gadolinium‐DOTA labelled glucose meal during intravenous infusion of pentagastrin or placebo in double‐blind, randomized order. Total gastric volume (TGV) and gastric content volume (GCV) was assessed by MRI volume scans and secretion by fast T₁ mapping. Data was described by the κ‐coefficient (volume change after meal ingestion), by GE half time (T₅₀) and maximal GE rate (GER_max) derived all from a GE model. Pentagastrin increased GCV and TGV compared to placebo [κ(GCV):1.6 ± 0.1 vs 0.6 ± 0.1; κ(TGV): 1.6 ± 0.1 vs 0.7 ± 0.1; P < 0.001]. T₁ maps revealed a secretion layer above the meal, the volume of which was associated with κ (R² = 83%, P < 0.001). TGV and GCV change were similar in both conditions (κ; P = ns). T₅₀ was higher for pentagastrin than for placebo (84 ± 7 vs 56 ± 4min, P < 0.001); however, GER_max was similar (5.9 ± 0.6 vs 4.9 ± 0.4 mL min^?1, P = ns). This study shows volume and distribution of gastric secretion can be quantified in‐vivo by non‐invasive MRI T₁ mapping. Increased GCV drove TGV accommodation without evidence of a direct effect of pentagastrin or excess acid on gastric function. Secretion increases GCV thus prolongs GE as assessed by T₅₀; however, GE rate is unchanged.     

Bioenergetics and intermuscular fat in chronic obstructive pulmonary disease‐associated quadriceps weakness

Introduction: Chronic obstructive pulmonary disease (COPD) is associated with metabolic abnormalities in muscles of the lower limbs, but it is not known whether these abnormalities are generalized or limited to specific muscle groups, nor is there an easy way of predicting their presence. Methods: Metabolism in the quadriceps and biceps of 14 COPD patients and controls was assessed during sustained contraction using 31‐phosphorus magnetic resonance spectroscopy (³¹P MRS). T1 MRI was used to measure quadriceps intermuscular adipose tissue (IMAT). Results: COPD patients had prolonged quadriceps phosphocreatine time (patients: 38.8 ± 12.7 s; controls: 25.2 ± 10.6 s; P = 0.006) and a lower pH (patents: 6.88 ± 0.1; controls: 6.99 ± 0.06; P = 0.002). Biceps measures were not significantly different. IMAT was associated with a nadir pH <7.0 (area under the curve = 0.84). Conclusions: Anaerobic metabolism during contraction was characteristic of quadriceps, but not biceps, muscles of patients with COPD and was associated with increased IMAT. Because IMAT can be assessed quickly by conventional MRI, it may be a useful approach for identifying patients with abnormal muscle bioenergetics. Muscle Nerve 51 : 214–221, 2015     

A narrative review of exercise‐associated muscle cramps: Factors that contribute to neuromuscular fatigue and management implications

Although exercise‐associated muscle cramps (EAMC) are highly prevalent among athletic populations, the etiology and most effective management strategies are still unclear. The aims of this narrative review are 3‐fold: (1) briefly summarize the evidence regarding EAMC etiology; (2) describe the risk factors and possible physiological mechanisms associated with neuromuscular fatigue and EAMC; and (3) report the current evidence regarding prevention of, and treatment for, EAMC. Based on the findings of several large prospective and experimental investigations, the available evidence indicates that EAMC is multifactorial in nature and stems from an imbalance between excitatory drive from muscle spindles and inhibitory drive from Golgi tendon organs to the alpha motor neurons rather than dehydration or electrolyte deficits. This imbalance is believed to stem from neuromuscular overload and fatigue. In concert with these findings, the most successful treatment for an acute bout of EAMC is stretching, whereas auspicious methods of prevention include efforts that delay exercise‐induced fatigue. Muscle Nerve 54 : 177–185, 2016     

Phrenic nerve involvement and respiratory muscle weakness in patients with Charcot‐Marie‐Tooth disease 1A

Diaphragm weakness in Charcot‐Marie‐Tooth disease 1A (CMT1A) is usually associated with severe disease manifestation. This study comprehensively investigated phrenic nerve conductivity, inspiratory and expiratory muscle function in ambulatory CMT1A patients. Nineteen adults with CMT1A (13 females, 47 ± 12 years) underwent spiromanometry, diaphragm ultrasound, and magnetic stimulation of the phrenic nerves and the lower thoracic nerve roots, with recording of diaphragm compound muscle action potentials (dCMAP, n = 15), transdiaphragmatic and gastric pressures (twPdi and twPgas, n = 12). Diaphragm motor evoked potentials (dMEP, n = 15) were recorded following cortical magnetic stimulation. Patients had not been selected for respiratory complaints. Disease severity was assessed using the CMT Neuropathy Scale version 2 (CMT‐NSv2). Healthy control subjects were matched for age, sex, and body mass index. The following parameters were significantly lower in CMT1A patients than in controls (all P < .05): forced vital capacity (91 ± 16 vs 110 ± 15% predicted), maximum inspiratory pressure (68 ± 22 vs 88 ± 29 cmH₂O), maximum expiratory pressure (91 ± 23 vs 123 ± 24 cmH₂O), and peak cough flow (377 ± 135 vs 492 ± 130 L/min). In CMT1A patients, dMEP and dCMAP were delayed. Patients vs controls showed lower diaphragm excursion (5 ± 2 vs 8 ± 2 cm), diaphragm thickening ratio (DTR, 1.9 [1.6‐2.2] vs 2.5 [2.1‐3.1]), and twPdi (8 ± 6 vs 19 ± 7 cmH₂O; all P < .05). DTR inversely correlated with the CMT‐NSv2 score (r = ?.59, P = .02). There was no group difference in twPgas following abdominal muscle stimulation. Ambulatory CMT1A patients may show phrenic nerve involvement and reduced respiratory muscle strength. Respiratory muscle weakness can be attributed to diaphragm dysfunction alone. It relates to neurological impairment and likely reflects a disease continuum.     

Anconeus motor unit number estimates using decomposition‐based quantitative electromyography

Introduction: Motor unit number estimates (MUNEs) provide important information in health, aging, and disease, and can be determined using decomposition‐enhanced spike‐triggered averaging (DE‐STA). Discrimination of surface‐detected motor unit potentials (S‐MUPs) has been limited to contractile forces of ∽30% maximum voluntary contraction (MVC), which is insufficient to recruit a representative sample of the entire MU pool in most muscles. Unique features of the anconeus may permit MUNEs at high muscle activation levels. Methods: In 10 men (25 ± 3 years), anconeus MUNEs were performed using DE‐STA at 10%, 30%, and 50% root‐mean‐square of MVC (RMS_MVC). Results: The mean compound muscle action potential of the anconeus was ∽6 mV, and average S‐MUP amplitudes were ∽100 μV, 145 μV, and 235 μV at 10%, 30%, and 50% RMS_MVC, resulting in low average MUNEs of 58, 38, and 25, respectively. Conclusions: Elbow extensor force–EMG relationships suggest full recruitment of the anconeus MU pool at 50% RMS_MVC, thus providing a representative sample for MUNE. Muscle Nerve 50 : 52–59, 2014     

Concentric needle jitter on voluntary activated frontalis in 20 healthy subjects

Introduction: Normative data for jitter parameters using a disposable concentric needle have been described in a few studies. Methods: Jitter, expressed as the mean consecutive difference (MCD), was measured in the frontalis muscle in 20 subjects by voluntary contraction. Results: Mean MCD for individual studies (20, Gaussian), all potentials (400, non‐Gaussian), and 18th highest value (20, Gaussian) were 19.9 ± 2.9 μs, 19.9 ± 6.6 μs, and 26.9 ± 4.4 μs, respectively. Conclusion: The suggested upper normal limit for mean MCD is 26 μs and for outliers is 36 μs. Muscle Nerve 47:440‐442, 2013     

Wavelet analysis of quadriceps power spectra and amplitude under varying levels of contraction intensity and velocity

Introduction: We investigated the effect of contraction intensity [100%, 75%, 50%, and 25% maximum voluntary contraction (MVC)] and movement velocity (50°, 100°, 200°, and 400°/s) on surface electromyography root mean square amplitude (SEMG_RMS) and median frequency (SEMG_MDF) of rectus femoris (RF), vastus lateralis (VL), and vastus medialis (VM). Methods: SEMGs during knee extension were resolved into their respective frequencies using wavelet transformations. Results: RF, VL, and VM muscles displayed increased SEMG_MDF as contraction intensity increased from 25% to 50% MVC and from 75% to 100% MVC, and each muscle displayed its own unique frequency shifting patterns. The SEMG_MDF was not influenced by movement velocity. SEMG_RMS increased in all 3 muscles as contraction intensity increased and was influenced by movement velocity, with the highest values observed at 400° and 200°/s. Conclusions: We infer that increasing contraction intensity facilitates greater recruitment of fast‐twitch muscle fibers, but there are differing responses in RF, VL, and VM muscles. Muscle Nerve 50 : 844–853, 2014     

Decomposition-enhanced spike-triggered averaging: Contraction level effects

Decomposition-enhanced spike-triggered averaging (DE-STA) was applied to the vastus medialis muscle to examine size distributions of surface-detected motor unit action potentials (S-MUAPs) at various force levels. Using DE-STA, 15–20 S-MUAPs were identified during 5%, 10%, 20%, and 30% of maximum voluntary contraction. Average S-MUAPs showed increase in peak to peak (and negative peak) amplitude with force (in μV): 5% = 37.9 ± 6.1 (16.6 ± 2.5), 10% = 44.0 ± 4.0 (20.4 ± 1.8), 20% = 80.7 ± 9.3 (41.3 ± 4.5), and 30% = 102.5 ± 10.3 (53.6 ± 5.0). Test-retest variability of peak to peak (and negative peak amplitude) between repeated trials was 0.10 (0.14), 0.14 (0.14), 0.17 (0.15), and 0.21 (0.20) at 5%, 10%, 20%, and 30% respectively. A relationship was found between the S-MUAP amplitude and force (r² = 0.78, df = 90, F = 160, P < 0.001). Increase in average S-MUAP amplitude with force suggests that STA performed only at low levels of contraction may result in a biased sampling and small average S-MUAP amplitudes. © 1997 John Wiley & Sons, Inc. Muscle Nerve 20: 976–982, 1997     

Effect of GABA‐ergic mechanisms on synaptosomal NO synthesis and the nitrergic component of NANC relaxation in rat ileum

Background  γ‐Aminobutyric acid (GABA) acts on specific neural receptors [A, B and C(Aρ)] to modulate gastrointestinal function. The precise role of GABA receptor activation in the regulation of presynaptic nitric oxide (NO) synthesis in nerve terminals is unknown. Methods  Rat ileal nerve terminals were isolated by differential centrifugation. Nitric oxide synthesis was analysed using a L‐[³H]arginine assay. In vitro studies were performed under non‐adrenergic non‐cholinergic (NANC) conditions on isolated ileal segments. Key Results  γ‐Aminobutyric acid inhibited NO synthesis significantly (n = 6, P < 0.05) [(fmol mg⁻¹ min⁻¹) control: 27.7 ± 1.5, 10⁻⁶ mol L⁻¹: 19.7 ± 1.3; 10⁻⁵ mol L⁻¹: 17.5 ± 3.0]. This effect was antagonized by the GABA A receptor antagonist bicuculline and the GABA C receptor antagonist (1,2,5,6‐tetrahydropyridin‐4‐yl)methylphosphinic acid (TPMPA), but not by the GABA B receptor antagonist SCH 50911. The GABA A receptor agonist muscimol [(fmol mg⁻¹ min⁻¹) control: 27.6 ± 1.0, 10⁻⁶ mol L⁻¹: 19.1 ± 1.7, n = 5, P < 0.05] and the GABA C receptor agonist cis‐4‐aminocrotonic acid (CACA) [(fmol mg⁻¹ min⁻¹) control: 29.5 ± 3.2, 10⁻³ mol L⁻¹: 20.3 ± 2.5, n = 6, P < 0.05], mimicked the GABA‐effect, whereas the GABA B agonist baclofen was ineffective. Bicuculline reversed the inhibitory effect of muscimol, TPMPA antagonized the effect of CACA. In functional experiments the GABA A and C receptor agonists reduced the NANC relaxation induced by electrical field stimulation in rat ileum by about 40%. After NOS‐inhibition by Nε‐nitro‐l ‐arginine methyl ester (l ‐NAME) the GABA A receptor agonist had no effect, whereas the GABA C receptor agonist still showed a residual response. Conclusions & Inferences  γ‐Aminobutyric acid inhibits neural NO synthesis in rat ileum by GABA A and GABA C(Aρ) receptor‐mediated mechanisms.     

Redetermination of the optimal stimulation intensity modifies resting H‐reflex recovery after a sustained moderate‐intensity muscle contraction

This study aimed to determine whether the time‐course of maximal resting H‐reflex amplitude (H_max) recovery after a prolonged moderate‐intensity muscle contraction differs according to the optimal stimulation intensity used (predetermined vs. readjusted). Thirteen males performed a sustained isometric plantar flexion at 40% of their maximal voluntary contraction torque output until exhaustion. H_max of the soleus muscle was recorded before and 2, 6, 10, and 14 min after the end of the contraction, then normalized by the respective maximal M‐wave to form the H_max/M_max ratio. During recovery, pre‐ and redetermined optimal stimulation intensities (mini‐recruitment curve drawn before each recovery measurement) were applied randomly to measure H_max. When using redetermined stimulation intensities, normalized H‐reflex values were systematically greater (+11, +16, +15, and +15% after 2‐, 6‐, 10‐, and 14‐min recovery periods, respectively) than those obtained with the predetermined intensity. Keeping the stimulation intensity constant to evoke H_max after a sustained muscle contraction can underestimate the H‐reflex facilitation occurring after exhaustive exercise. It is therefore more appropriate to redefine the optimal stimulation intensity to evoke H_max (using mini‐recruitment curves) when the purpose is to analyze spinal modulation during the recovery phase. Muscle Nerve, 2010     

Abnormal postexcitatory and interhemispheric motor cortex inhibition in writer's cramp

Focal transcranial magnetic stimulation (TMS) of the motor cortex was used to study excitatory and inhibitory stimulation effects in 25 patients with writer's cramp and 25 healthy volunteers. We investigated excitatory and inhibitory corticospinally mediated motor effects in muscles contralateral to the stimulation side as well as interhemispheric inhibition of tonic motor activity in muscles ipsilateral to stimulation. Motor evoked potentials (MEPs) were recorded from both first dorsal interosseus muscles. Motor thresholds at rest and amplitudes and latencies of MEPs obtained during maximal contraction were always bilaterally normal. The duration of postexcitatory inhibition was significantly shortened (168±55 vs. 198±39 ms in normal subjects, P=0.001) and the duration of interhemispheric inhibition prolonged (30.3±6.6 vs. 26±3.9 ms in normal subjects, P < 0.001). Both observations would be compatible with a decreased inhibition of corticospinal and transcallosal outputs of the motor cortex. The results were not influenced by fatigue effects. Abnormal motor cortex inhibition seems to be a generalized phenomenon in writer's cramp since it was detected in both hemispheres and during a simple isometric motor task which did not evoke dystonic symptoms. Received: 28 February 2000 / Received in revised form: 29 June 2000 / Accepted: 1 August 2000     

Cognitive impairment in rapid‐onset dystonia‐parkinsonism

Rapid‐onset dystonia‐parkinsonism (RDP) is caused by mutations in the ATP1A3 gene. This observational study sought to determine if cognitive performance is decreased in patients with RDP compared with mutation‐negative controls. We studied 22 familial RDP patients, 3 non‐motor‐manifesting mutation‐positive family members, 29 mutation‐negative family member controls in 9 families, and 4 unrelated RDP patients, totaling 58 individuals. We administered a movement disorder assessment, including the Burke‐Fahn‐Marsden Dystonia Rating Scale (BFMDRS) and the Unified Parkinson's Disease Rating Scale (UPDRS) and a cognitive battery of memory and learning, psychomotor speed, attention, and executive function. The cognitive battery was designed to evaluate a wide range of functions; recognition memory instruments were selected to be relatively pure measures of delayed memory, devoid of significant motor or vocal production limitations. Comparisons of standardized cognitive scores were assessed both with and without controlling for psychomotor speed and similarly for severity of depressive symptoms. A majority of RDP patients had onset of motor symptoms by age 25 and had initial symptom presentation in the upper body (face, mouth, or arm). Among patients, the BFMDRS (mean ± SD, 52.1 ± 29.5) and UPDRS motor subscore (29.8 ± 12.7) confirmed dystonia‐parkinsonism. The affected RDP patients performed more poorly, on average, than mutation‐negative controls for all memory and learning, psychomotor speed, attention, and executive function scores (all P ≤ 0.01). These differences persisted after controlling for psychomotor speed and severity of depressive symptoms. Impaired cognitive function may be a manifestation of ATP1A3 mutation and RDP. © 2014 International Parkinson and Movement Disorder Society     

Origin and modulation of circular smooth muscle layer contractions in the porcine esophagus

Background The origin and modulation mechanisms controlling timing and amplitude of esophageal body peristalsis are not fully understood. We aimed to characterize the neurotransmitters involved in the origin and modulation of circular smooth muscle esophageal body (EB) contractions. Methods Responses of porcine EB strips to electrical stimulation of motor neurons (MNs) were assessed in organ baths and with microelectrodes. The effect of antagonists of inhibitory (L‐NAME 1 mmol L^?1, MRS2179 10 μmol L^?1) and excitatory neurotransmitters (atropine 1 μmol L^?1; SR140333 1 μmol L^?1‐NK₁ra‐, GR94800 1 μmol L^?1‐NK₂ra‐) and of ganglionic neurotransmitters (hexamethonium 100 μmol L^?1, ondansetron 1 μmol L^?1, NF279 10 μmol L^?1) were characterized. Key Results Electrical field stimulation (EFS) induced a frequency‐dependent off‐contraction (16.8 ± 0.8 g) following a latency period. Latency was significantly reduced by L‐NAME (?66.1 ± 4.1%) and MRS2179 (?25.9 ± 5.6%), and strongly increased by atropine (+36.8 ± 5.8%). Amplitude was reduced by L‐NAME (?69.9 ± 10.4%), MRS2179 (?34.1 ± 6.0%), atropine (?42.3 ± 4.7%), hexamethonium (?18.9 ± 3.3%), NF279 (?20.7 ± 3.5%), ondansetron (?16.3 ± 3.2%), GR94800 (?28.0 ± 4.8%) SR140333 (?20.9 ± 7.1%), and α‐chymotrypsin (?31.3 ± 7.0%). The EFS induced a monophasic nitrergic inhibitory junction potential. Conclusions & Inferences Our results suggest that timing (latency) and amplitude of esophageal contractions are determined by a balance of complex interactions between excitatory and inhibitory MNs. Latency depends on the activation of inhibitory MNs releasing NO and a minor purinergic contribution through P2Y₁ receptors, and excitatory MNs releasing ACh. Amplitude depends on a major contribution of excitatory MNs releasing ACh and tachykinins, and also on inhibitory MNs releasing NO, ATP or related purines, and peptidergic neurotransmitters acting as strong modulators of the excitatory neuroeffector transmission.     

Abdominal accommodation induced by meal ingestion: differential responses to gastric and colonic volume loads

Background Using an experimental model of colonic gas infusion, we previously showed that the abdominal walls adapt to its content by an active phenomenon of abdominal accommodation. We now hypothesized that abdominal accommodation is a physiological phenomenon, and aimed to confirm that it can be induced by ingestion of a meal; a secondary aim was to determine whether the response to gut filling is region‐specific. Methods In healthy subjects (n = 24) a nutrient test meal was administered until tolerated at a rate of 50 mL min^?1. Electromyographic (EMG) activity of the anterior wall (upper and lower rectus, external and internal oblique) was measured via four pairs of surface electrodes, and EMG activity of the diaphragm via intraluminal electrodes on an esophageal tube. To address the secondary aim, the response to gastric filling was compared with that induced by colonic filling (1440 mL 30 min^?1 anal gas infusion; n = 8). Key Results Participants tolerated 927 ± 66 mL of meal (450–1500 mL). Meal ingestion induced progressive diaphragmatic relaxation (EMG reduction by 16 ± 2%; P < 0.01) and selective contraction of the upper abdominal wall (24 ± 2% increase in activity of the upper rectus and external oblique; P < 0.01 for both), with no significant changes in the lower rectus (4 ± 2%) or internal oblique (5 ± 3%). Colonic gas infusion induced a similar response, but with an overall contraction of the anterior wall. Conclusions & Inferences Meal ingestion induces a metered and region‐specific response of the abdominal walls to accommodate the volume load. Abnormal abdominal accommodation could be involved in postprandial bloating.