Cardiac parasympathetic reactivation following exercise : implications for training prescription

The objective of exercise training is to initiate desirable physiological adaptations that ultimately enhance physical work capacity. Optimal training prescription requires an individualized approach, with an appropriate balance of training stimulus and recovery and optimal periodization. Recovery from exercise involves integrated physiological responses. The cardiovascular system plays a fundamental role in facilitating many of these responses, including thermoregulation and delivery/removal of nutrients and waste products. As a marker of cardiovascular recovery, cardiac parasympathetic reactivation following a training session is highly individualized. It appears to parallel the acute/intermediate recovery of the thermoregulatory and vascular systems, as described by the supercompensation theory. The physiological mechanisms underlying cardiac parasympathetic reactivation are not completely understood. However, changes in cardiac autonomic activity may provide a proxy measure of the changes in autonomic input into organs and (by default) the blood flow requirements to restore homeostasis. Metaboreflex stimulation (e.g. muscle and blood acidosis) is likely a key determinant of parasympathetic reactivation in the short term (0–90 min post-exercise), whereas baroreflex stimulation (e.g. exercise-induced changes in plasma volume) probably mediates parasympathetic reactivation in the intermediate term (1–48 h post-exercise). Cardiac parasympathetic reactivation does not appear to coincide with the recovery of all physiological systems (e.g. energy stores or the neuromuscular system). However, this may reflect the limited data currently available on parasympathetic reactivation following strength/resistance-based exercise of variable intensity. In this review, we quantitatively analyse post-exercise cardiac parasympathetic reactivation in athletes and healthy individuals following aerobic exercise, with respect to exercise intensity and duration, and fitness/training status. Our results demonstrate that the time required for complete cardiac autonomic recovery after a single aerobic-based training session is up to 24 h following low-intensity exercise, 24–48 h following threshold-intensity exercise and at least 48 h following high-intensity exercise. Based on limited data, exercise duration is unlikely to be the greatest determinant of cardiac parasympathetic reactivation. Cardiac autonomic recovery occurs more rapidly in individuals with greater aerobic fitness. Our data lend support to the concept that in conjunction with daily training logs, data on cardiac parasympathetic activity are useful for individualizing training programmes. In the final sections of this review, we provide recommendations for structuring training microcycles with reference to cardiac parasympathetic recovery kinetics. Ultimately, coaches should structure training programmes tailored to the unique recovery kinetics of each individual.

Integrating 40Ar-39Ar, 87Rb-87Sr and 147Sm-143Nd geochronology of authigenic illite to evaluate tectonic reactivation in an intraplate setting, central Australia

The Warburton-Cooper basins, central Australia, include a multitude of reactivated fracture-fault networks related to a complex, and poorly understood, tectonic evolution. We investigated authigenic illites from a granitic intrusion and sedimentary rocks associated with prominent structural features (Gidgealpa-Merrimelia-Innamincka Ridge and the Nappamerri Trough). These were analysed by 40Ar-39Ar, 87Rb-87Sr and 147Sm-143Nd geochronology to explore the thermal and tectonic histories of central Australian basins. The combined age data provide evidence for three major periods of fault reactivation throughout the Phanerozoic. While Carboniferous (323.3 ± 9.4 Ma) and Late Triassic ages (201.7 ± 9.3 Ma) derive from basin-wide hydrothermal circulation, Cretaceous ages (~128 to ~86 Ma) reflect episodic fluid flow events restricted to the synclinal Nappamerri Trough. Such events result from regional extensional tectonism derived from the transferral of far-field stresses to mechanically and thermally weakened regions of the Australian continent. Specifically, Cretaceous ages reflect continent-wide transmission of tensional stress from a > 2500 km long rifting event on the Eastern (and southern) Australian margin associated with break-up of Gondwana and opening of the Tasman Sea. By integrating 40Ar-39Ar, 87Rb-87Sr and 147Sm-143Nd dating, this study highlights the use of authigenic illite in temporally constraining the tectonic evolution of intracontinental basins that would otherwise remain unknown. Furthermore, combining Sr- and Ar-isotopic systems enables more accurate dating of authigenesis whilst significantly reducing geochemical pitfalls commonly associated with these radioisotopic dating methods.

Late reactivation of herpes zoster keratitis results in band keratopathy

Purpose To report an unusual case of a late-stage reactivation of immune stromal keratitis associated with herpes zoster ophthalmicus (HZO), occurring without any apparent predisposing factors, more than 4 years after an acute zoster dermatomal rash. Significant corneal hypoesthesia and a central band keratopathy developed within 6 months of the late-stage reactivation. The clinical case management, issues associated with management, and management options are discussed, including the use of standardized, regulatory approved, antibacterial medical honey. Case Report An 83-year-old woman presented for routine review with a reactivation of right anterior stromal keratitis and mild anterior uveitis, occurring more than 4 years after an acute HZO dermatomal rash and an associated initial episode of anterior stromal keratitis. Corneal sensation became markedly impaired, and over the subsequent 6 months, a right central band keratopathy developed despite oral antiviral and topical steroid therapy. Visual acuity with pinhole was reduced to 20/100 in the affected eye and moderate irritation and epiphora were experienced. The patient declined the surgical intervention options of chelation, lamellar keratectomy, and phototherapeutic keratectomy to treat the band keratopathy. Longer-term management has involved preservative-free artificial tears, eyelid hygiene, standardized antibacterial medical honey, topical nonpreserved steroid, and UV-protective wraparound sunglasses. The clinical condition has improved over 14 months with this ocular surface management regimen, and visual acuity of 20/30 is currently achieved in a comfortable eye. Conclusions The chronic and recurrent nature of HZO can be associated with significant corneal morbidity, even many years after the initial zoster episode. Long-term review and management of patients with a history of herpes zoster stromal keratitis are indicated following the initial corneal involvement. Standardized antibacterial medical honey can be considered in the management of the chronic ocular surface disease associated with HZO and warrants further evaluation in clinical trials.

Fear memory reactivation after extinction activates plasticity in the lateral amygdala

Little is known about the neuronal changes that occur within the lateral amygdala (LA) following fear extinction. In fear extinction, the repeated presentation of a conditioned stimulus (CS), in the absence of a previously paired aversive unconditioned stimulus (US), reduces fear elicited by the CS. Fear extinction is an active learning process that leads to the formation of a consolidated extinction memory, however it is fragile and prone to spontaneous recovery and renewal under environmental changes such as context. Understanding the neural mechanisms underlying fear extinction is of great clinical relevance, as psychological treatments of several anxiety disorders rely largely on extinction-based procedures and relapse is major clinical problem. This study investigated plasticity in the LA following fear memory reactivation in rats with and without extinction training. Phosphorylated MAPK (p44/42 ERK/MAPK), a protein kinase required in the amygdala for fear learning and its extinction, was used as a marker for neuronal plasticity. Rats (N = 11) underwent a Pavlovian auditory fear conditioning and extinction paradigm, and later received a single conditioned stimulus presentation to reactivate the fear memory. Results showed more pMAPK+ expressing neurons in the LA following extinction-reactivation compared to control rats, with the largest number of pMAPK+ neurons counted in the ventral LA, especially including the ventro-lateral subdivision (LAvl). These findings indicate that LA subdivision specific plasticity occurs to the conditioned fear memory in the LAvl following extinction-reactivation. These findings provide important insight into the organisation of fear memories in the LA, and pave the way for future research in the memory mechanisms of fear extinction and its pathophysiology.

Reactivation kinetics of acceptors in hydrogenated InP during unbiased annealing

The reactivation kinetics of passivated Mg acceptors in hydrogenated InP during unbiased annealing of a Schottky diode is reported. The reactivation is found to slow down gradually with annealing time and this phenomenon is attributed to substantial retrapping of H at the acceptor sites. It is found from the concentration profiles and the kinetics data that the reactivation is most likely limited by H2 molecule formation processes for longer annealing times; for shorter annealing times, contributions from in-diffusion of H also become significant. The diffusion of H during the initial period follows an Arrhenius relation with an activation energy for the effective diffusion coefficient of 1.13±0.10 eV. In the H2 formation regime, the reactivation is thermally activated with an activation energy for the annealing parameter of 1.71±0.10 eV. The H2 formation-limited regime of reactivation occurs sooner as the annealing temperature is increased.

Reactivation kinetics of boron acceptors in hydrogenated silicon during zero bias anneal

The reactivation kinetics of passivated boron accepters in hydrogenated silicon during zero bias annealing in the temperature range of 65-130 degrees C are reported, For large annealing times and high annealing temperatures, the reactivation process follows second-order kinetics and is rate limited by a thermally activated <(H)over tilde (2)> complex formation process, For short annealing times and low annealing temperatures, the reactivation rate is found to be larger than that due to <(H)over tilde (2)> complex formation alone. We conclude that the faster reactivation is caused by the diffusion of the liberated hydrogen atoms into the bulk as well as <(H)over tilde (2)> complex formation. The effective diffusion coefficient of hydrogen is measured and found to obey the Arrhenius relation with an activation energy (1.41 +/- 0.1) eV. (C) 1997 American Institute of Physics.

The June 2010 Nicobar Earthquake: Fault Reactivation on the Subducting Oceanic Plate

The similar to 1300-km-long rupture zone of the 2004 Andaman-Sumatra megathrust earthquake continues to generate a mix of thrust, normal, and strike-slip faulting events. The 12 June 2010 M(w) 7.5 event on the subducting plate is the most recent large earthquake on the Nicobar segment. The left-lateral faulting mechanism of this event is unusual for the outer-rise region, considering the stress transfer processes that follow great underthrusting earthquakes. Another earthquake (M(w) 7.2) with a similar mechanism occurred very close to this event on 24 July 2005. These earthquakes and most of their aftershocks on the subducting plate were generated by left-lateral strike-slip faulting on north-northeast-south-southwest oriented near-vertical faults, in response to north-northwest-south-southeast directed compression. Pre-2004 earthquake faulting mechanisms on the subducting oceanic plate are consistent with this pattern. Post-2004, left-lateral faulting on the subducting oceanic plate clusters between 5 degrees N and 9 degrees N, where the 90 degrees E ridge impinges the trench axis. Our study observes that the subducting plate off the Sumatra and Nicobar segments behaves similarly to a chip of the India-Australia plate, deforming in response to a generally northwest-southeast oriented compression, an aspect that must be factored into the plate deformation models.

Studies on reactivation of regressing bonnet monkey corpus luteum on day 1 of menses: A pilot study

Studies on functional characteristics of the regressing primate corpus luteum (CL) to luteotrophic stimulus on day 1 of the non-fertile menstrual cycle are scarce. Recombinant human luteinizing hormone (rhLH) (20 IU/Kg BW; n = 10) or human chorionic gonadotropin (hCG) (180 IU; n = 6) were administered intravenously to female bonnet monkeys on day 1 of menses. Exogenous treatment of rhLH or hCG caused a significant increase in circulating progesterone (P4) levels 2-4 hours post treatment (P < 0.05). Lutectomy prior to onset of menses confirmed that CL is the site of the increased P4 concentrations. Increased levels of phosphorylated P44/42 MAPK, MKK3/6 activation and concomitant histological changes were observed within 4 hours in CL of monkeys receiving hCG treatment. The results from this study demonstrate the acute progesterone synthesizing capacity of regressing monkey CL after LH or hCG challenge. This has potential implications for interpreting the steroidogenic response after gonadotropin stimulation tests in the early follicular phase of the normal ovulatory and anovulatory women undergoing controlled ovarian stimulation protocols as part of assisted reproductive technology (ART) and in women with polycystic ovarian syndrome.

Dynamics of HIV latency and reactivation in a primary CD4+ T cell model.

HIV latency is a major obstacle to curing infection. Current strategies to eradicate HIV aim at increasing transcription of the latent provirus. In the present study we observed that latently infected CD4+ T cells from HIV-infected individuals failed to produce viral particles upon ex vivo exposure to SAHA (vorinostat), despite effective inhibition of histone deacetylases. To identify steps that were not susceptible to the action of SAHA or other latency reverting agents, we used a primary CD4+ T cell model, joint host and viral RNA sequencing, and a viral-encoded reporter. This model served to investigate the characteristics of latently infected cells, the dynamics of HIV latency, and the process of reactivation induced by various stimuli. During latency, we observed persistence of viral transcripts but only limited viral translation. Similarly, the reactivating agents SAHA and disulfiram successfully increased viral transcription, but failed to effectively enhance viral translation, mirroring the ex vivo data. This study highlights the importance of post-transcriptional blocks as one mechanism leading to HIV latency that needs to be relieved in order to purge the viral reservoir.

Treatment-dependent loss of polyfunctional CD8+ T-cell responses in HIV-infected kidney transplant recipients is associated with herpesvirus reactivation.

Antiretroviral-therapy has dramatically changed the course of HIV infection and HIV-infected (HIV(+)) individuals are becoming more frequently eligible for solid-organ transplantation. However, only scarce data are available on how immunosuppressive (IS) strategies relate to transplantation outcome and immune function. We determined the impact of transplantation and immune-depleting treatment on CD4+ T-cell counts, HIV-, EBV-, and Cytomegalovirus (CMV)-viral loads and virus-specific T-cell immunity in a 1-year prospective cohort of 27 HIV(+) kidney transplant recipients. While the results show an increasing breadth and magnitude of the herpesvirus-specific cytotoxic T-cell (CTL) response over-time, they also revealed a significant depletion of polyfunctional virus-specific CTL in individuals receiving thymoglobulin as a lymphocyte-depleting treatment. The disappearance of polyfunctional CTL was accompanied by virologic EBV-reactivation events, directly linking the absence of specific polyfunctional CTL to viral reactivation. The data provide first insights into the immune-reserve in HIV+ infected transplant recipients and highlight new immunological effects of thymoglobulin treatment. Long-term studies will be needed to assess the clinical risk associated with thymoglobulin treatment, in particular with regards to EBV-associated lymphoproliferative diseases.

Intraplate earthquake swarm in Belo Jardim, NE Brazil: reactivation of a major Neoproterozoic shear zone (Pernambuco Lineament)

Intraplate earthquakes in stable continental areas have been explained basically by reactivation of pre-existing zones of weakness, stress concentration, or both. Zones of weakness are usually identified as sites of the last major orogeny, provinces of recent alkaline intrusions, or stretched crust in ancient rifts. However, it is difficult to identify specific zones of weakness and intraplate fault zones are not always easily correlated with known geological features. Although Northeastern Brazil is one of the most seismically active areas in the country (magnitudes 5 roughly every 5 yr), with hypocentral depths shallower than similar to 10 km and seismic zones as long as 30-40 km, no clear relationship with the known surface geology can be usually established with confidence, and a clear identification of zones of weakness has not yet been possible. Here we present the first clear case of seismic activity occurring as reactivation of an old structure in Brazil: the Pernambuco Lineament, a major Neoproterozoic shear zone. The 2004 earthquake swarm of Belo Jardim (magnitudes up to 3.1) and the recurrent activities in the nearby towns of Sao Caetano and Caruaru (magnitudes up to 4.0 and 3.8), show that the Pernambuco Lineament is a weak zone. A local seismic network showed that the Belo Jardim swarm of 2004 November occurred by normal faulting on a North dipping, E-W oriented fault plane in close agreement with the E-W trending structures within the Pernambuco Lineament. The Belo Jardim activity was concentrated in a 1.5 km (E-W) by 2 km (downdip) fault area, and average depth of 4.5 km. The nearby Caruaru activity occurs as both strike-slip and normal faulting, also consistent with local structures of the Pernambuco Lineament. The focal mechanisms of Belo Jardim, Caruaru and S. Caetano, indicate E-W compressional and N-S extensional principal stresses. The NS extension of this stress field is larger than that predicted by numerical models such as those of Coblentz & Richardson and we propose that additional factors such as flexural stresses from the nearby Sergipe-Alagoas marginal basin could also affect the current stress field in the Pernambuco Lineament.