Upper Limb Anaerobic Metabolism Capacity is Reduced in Mild and Moderate COPD Patients.

Limited information is available regarding the role of anaerobic metabolism capacity on GOLD 1 and 2 COPD patients during upper limb exercise. We aimed to compare the upper limb anaerobic power capacity, blood lactate concentration, cardiovascular and respiratory responses, in male COPD patients versus healthy subjects during the 30-s Wingate anaerobic test (WAnT). The rate of fatigue and time constant of the power output decay (τ, tau) were also calculated and a regression analysis model was built to assess the predictors of τ in these patients. Twenty-four male COPD patients (post-bronchodilator FEV1 73.2 ± 15.3% of predicted) and 17 healthy subjects (FEV1 103.5 ± 10.1% of predicted) underwent the WAnT. Measurements were performed at rest, at the end of the WAnT, and during 3' and 5' of recovery time. Peak power (p = 0.04), low power (p = 0.002), and mean power output (p = 0.008) were significantly lower in COPD patients than in healthy subjects. Power output decreased exponentially in both groups, but at a significantly faster rate (p = 0.007) in COPD patients. The time constant of power decay was associated with resistance (in ohms) and fat-free mass (r2 = 0.604, adjusted r2 = 0.555, and p = 0.002). Blood lactate concentration was significantly higher in healthy subjects at the end of the test, as well as during 3' and 5' of recovery time (p < 0.01). Compared with healthy subjects, COPD patients with GOLD 1 and 2 presented lower upper limb anaerobic capacity and a faster rate of power output decrease during a maximal intensity exercise. Also, the WAnT proved to be a valid tool to measure the upper limb anaerobic capacity in these patients.

Baroreflex responses to activity at different temperatures in the South American rattlesnake, Crotalus durissus.

In humans, physical exercise imposes narrower limits for the heart rate (fH) response of the baroreflex, and vascular modulation becomes largely responsible for arterial pressure regulation. In undisturbed reptiles, the baroreflex-related fH alterations at the operating point (Gop) decreases at elevated body temperatures (Tb) and the vascular regulation changes accordingly. We investigated how the baroreflex of rattlesnakes, Crotalus durissus, is regulated during an activity at different Tb, expecting that activity would reduce the capacity of the cardiac baroreflex neural pathway to buffer arterial pressure fluctuations while being compensated by the vascular neural pathway regulation. Snakes were catheterized for blood pressure assessment at three different Tb: 15, 20 and 30 °C. Data were collected before and after activity at each Tb. Baroreflex gain (Gop) was assessed with the sequence method; the vascular limb, with the time constant of pressure decay (τ), using the two-element Windkessel equation. Both Gop and τ reduced when Tb increased. Activity also reduced Gop and τ in all Tb. The relationship between τ and pulse interval (τ/PI) was unaffected by the temperature at resting snakes, albeit it reduced after activity at 20 °C and 30 °C. The unchanged τ/PI and normalized Gop at different Tb indicated those variables are actively adjusted to work at different fH and pressure conditions at rest. Our data suggest that during activity, the baroreflex-related fH response is attenuated and hypertension is buffered by a disproportional increase in the rate which pressure decays during diastole. This compensation seems especially important at higher Tb where Gop is already low.

Bilateral enucleation at birth modifies calcium spike amplitude, but not frequency, in neurons of the somatosensory thalamus and cortex: Implications for developmental cross-modal plasticity.

Bilateral eye enucleation at birth (BE) leads to an expansion of the primary somatosensory cortex (S1) in rat pups. Although increased growth of the somatosensory thalamo-cortical afferents (STCAs) in part explains S1 expansion, timing mechanisms governing S1 formation are also involved. In this work, we begin the search of a developmental clock by intending to document the existence of putative clock neurons in the somatosensory thalamus (VPM) and S1 based upon changes of spontaneous spike amplitude; a biophysical property sensitive to circadian regulation; the latter known to be shifted by enucleation. In addition, we also evaluated whether STCAs growth rate and segregation timing were modified, as parameters the clock might time. We found that spontaneous spike amplitude transiently, but significantly, increased or decreased in VPM and S1 neurons of BE rat pups, respectively, as compared to their control counterparts. The growth rate and segregation timing of STCAs was, however, unaffected by BE. These results support the existence of a developmental clock that ticks differently in the VPM and S1 after BE. This observation, together with the fact that STCAs growth rate and segregation timing is unchanged, suggests that S1 expansion in BE rats may in part be controlled at the cortical level.

Non-Decaying postsynaptics potentials and delayed spikes in hippocampal pyramidal neurons generated by a zero slope conductance created by the persistent Na+ current.

The negative slope conductance created by the persistent sodium current (INaP) prolongs the decay phase of excitatory postsynaptic potentials (EPSPs). In a recent study, we demonstrated that this effect was due to an increase of the membrane time constant. When the negative slope conductance opposes completely the positive slope conductances of the other currents it creates a zero slope conductance region. In this region the membrane time constant is infinite and the decay phase of the EPSPs is virtually absent. Here we show that non-decaying EPSPs are present in CA1 hippocampal pyramidal cells in the zero slope conductance region, in the suprathreshold range of membrane potential. Na+ channel block with tetrodotoxin abolishes the non-decaying EPSPs. Interestingly, the non-decaying EPSPs are observed only in response to artificial excitatory postsynaptic currents (aEPSCs) of small amplitude, and not in response to aEPSCs of big amplitude. We also observed concomitantly delayed spikes with long latencies and high variability only in response to small amplitude aEPSCs. Our results showed that in CA1 pyramidal neurons INaP creates non-decaying EPSPs and delayed spikes in the subthreshold range of membrane potentials, which could potentiate synaptic integration of synaptic potentials coming from distal regions of the dendritic tree.

Cerebral Critical Closing Pressure: Is the Multiparameter Model Better Suited to Estimate Physiology of Cerebral Hemodynamics?

BACKGROUND: Cerebral critical closing pressure (CrCP) is the level of arterial blood pressure (ABP) at which small brain vessels close and blood flow stops. This value is always greater than intracranial pressure (ICP). The difference between CrCP and ICP is explained by the tone of the small cerebral vessels (wall tension). CrCP value is used in several dynamic cerebral autoregulation models. However, the different methods for calculation of CrCP show frequent negative values. These findings are viewed as a methodological limitation. We intended to evaluate CrCP in patients with severe traumatic brain injury (TBI) with a new multiparameter impedance-based model and compare it with results found earlier using a transcranial Doppler (TCD)-ABP pulse waveform-based method. METHODS: Twelve severe TBI patients hospitalized during September 2005-May 2007. Ten men, mean age 32 years (16-61). Four had decompressive craniectomies (DC); three presented anisocoria. Patients were monitored with TCD cerebral blood flow velocity (FV), invasive ABP, and ICP. Data were acquired at 50 Hz with an in-house developed data acquisition system. We compared the earlier studied "first harmonic" method (M1) results with results from a new recently developed (M2) "multiparameter method." RESULTS: M1: In seven patients CrCP values were negative, reaching -150 mmHg. M2: All positive values; only one lower than ICP (ICP 60 mmHg/ CrCP 57 mmHg). There was a significant difference between M1 and M2 values (M1 < M2) and between ICP and M2 (M2 > ICP). CONCLUSION: M2 results in positive values of CrCP, higher than ICP, and are physiologically interpretable.

Variação diurna e resposta da cinética do VO2 de ciclistas durante exercício muito intenso / Diurnal variation and Vo2 kinetic response of cyclists during heavy exercise

O objetivo do presente estudo foi avaliar a influência da hora do dia nos parâmetros da cinética do consumo de oxigênio de ciclistas durante exercício muito intenso. Nove voluntários do sexo masculino realizaram exercícios de carga constante às 08:00, 13:00 e 18:00 h, em dias diferentes. Estes exercícios foram realizados duas vezes em cada visita, com um intervalo de 1 h entre eles. A intensidade usada foi de 75 por centoΔ (75 por cento da diferença entre o VO2 no limiar de lactato e o VO2max. A amplitude do componente primário do VO2 (2597 ± 273 ml.min-1, 2513 ± 268 ml.min-1 e 2609 ± 370 ml.min-1), a constante de tempo do componente primário do VO2 (19.3 ± 2.5 s, 18.4 ± 3.0 s e 19.7 ± 3.9 s), o componente lento do VO2 (735 ± 81 ml.min-1, 764 ± 99 ml.min-1 e 680 ± 121 ml.min-1) e o tempo de resposta média (51.8 ± 4.2 s, 51.2 ± 4.2 s e 51.4 ± 3.4 s) não apresentaram diferenças significativas entre os diferentes horários do dia (08:00, 13:00 e 18:00 h), assim como os demais parâmetros da cinética do VO2. Estes resultados sugerem que a resposta da cinética do VO2 de ciclistas durante exercício muito intenso (75 por centoΔ) não é influenciada pela hora do dia.

The objective of the present study was to evaluate the influence of the time of day on the parameters of oxygen uptake kinetics of trained cyclists during high intensity exercise. Nine male volunteers repeated bouts at constant loads at 08:00, 13:00 and 18:00 h on different days. These exercise bouts were performed twice on each occasion, with an interval of 1 h between them. The load intensity used was 75 percentΔ (75 percent of the difference between the VO2 at the lactate threshold and the VO2max). The primary VO2 amplitude (2597 ± 273 ml.min-1, 2513 ± 268 ml.min-1 and 2609 ± 370 ml.min-1), the primary VO2 time constant (19.3 ± 2.5 s, 18.4 ± 3.0 s and 19.7 ± 3.9 s), the VO2 slow component (735 ± 81 ml.min-1, 764 ± 99 ml.min-1 and 680 ± 121 ml.min-1) and the mean response time (51.8 ± 4.2 s, 51.2 ± 4.2 s and 51.4 ± 3.4 s) did not present significant differences at the different times (08:00, 13:00 and 18:00 h), neither did the other parameters of the VO2 kinetics. These results suggest that the response of the VO2 kinetics of cyclists exercising at high intensity (75 percentΔ) is not influenced by the time of day.