Have immigrant children been left behind in COVID-19 testing rates? - A quantitative study in the Lisbon metropolitan area between march 2020 and may 2023.

Immigrant children often encounter additional barriers in accessing health care than their peers. However, there is a lack of evidence globally regarding how migrant status may have affected access to COVID-19 testing during the pandemic. This study aimed to analyze migrant status as a determinant of COVID-19 testing rates among children in the Lisbon metropolitan area, Portugal. This cross-sequential study included 722 children aged 2-8 years (47% non-immigrants; 53% immigrants). We collected data from a national surveillance system on laboratory-confirmed COVID-19 tests conducted between March 2020 and May 2023 and assessed whether children were ever tested for COVID-19 and testing frequency. We employed robust and standard Poisson regression models to estimate Adjusted Prevalence Ratios and Relative Risks with 95% confidence intervals. A total of 637 tests were performed. Immigrant children had lower testing rates (53% vs. 48%) and fewer tests per child (median: 2 vs. 3). Moreover, they were 17% less likely to be ever tested (PR = 0.83, 95% CI: 0.76-0.89) and performed 26% fewer tests (RR = 0.74, 95% CI: 0.67-0.82) compared to non-immigrant children. Caregiver's age, education, employment status, child's birth weight, and perceived health status were associated factors. Our findings suggest that the COVID-19 pandemic has left immigrant children somewhat behind. We conclude that specific interventions targeting vulnerable populations, such as immigrant children, are needed in future health crises.

Adenosine A2A Receptor Up-Regulation Pre-Dates Deficits of Synaptic Plasticity and of Memory in Mice Exposed to Aß1-42 to Model Early Alzheimer's Disease.

The intracerebroventricular (icv) injection of amyloid peptides (Aß) models Alzheimer's disease (AD) in mice, as typified by the onset within 15 days of deficits of memory and of hippocampal long-term potentiation (LTP) that are prevented by the blockade of adenosine A2A receptors (A2AR). Since A2AR overfunction is sufficient to trigger memory deficits, we tested if A2AR were upregulated in hippocampal synapses before the onset of memory deficits to support the hypothesis that A2AR overfunction could be a trigger of AD. Six to eight days after Aß-icv injection, mice displayed no alterations of hippocampal dependent memory; however, they presented an increased excitability of hippocampal synapses, a slight increase in LTP magnitude in Schaffer fiber-CA1 pyramid synapses and an increased density of A2AR in hippocampal synapses. A2AR blockade with SCH58261 (50 nM) normalized excitability and LTP in hippocampal slices from mice sacrificed 7-8 days after Aß-icv injection. Fifteen days after Aß-icv injection, mice displayed evident deficits of hippocampal-dependent memory deterioration, with reduced hippocampal CA1 LTP but no hyperexcitability and a sustained increase in synaptic A2AR, which blockade restored LTP magnitude. This shows that the upregulation of synaptic A2AR precedes the onset of deterioration of memory and of hippocampal synaptic plasticity, supporting the hypothesis that the overfunction of synaptic A2AR could be a trigger of memory deterioration in AD.

Obtaining the spectroscopic quality factor through the luminescent thermometry in 50Li2O · 45B2O3 · 5Al2O3 glasses doped with Nd3+ and fluorides.

Lithium-boron-aluminum (LBA) glasses doped with N d 3+ and fluorides were produced. From the absorption spectra, their Judd-Ofelt intensity parameters, Ω 2,4,6, and spectroscopic quality factors were calculated. Exploiting their near infrared temperature dependent luminescence, we investigated their potential for optical thermometry based on the luminescence intensity ratio (LIR) methodology. Three LIR schemes were proposed, and relative sensitivity values up to 3.57±0.06% K -1 were obtained. From the temperature dependent luminescence, we alternatively calculated their corresponding spectroscopic quality factors. The results indicated that N d 3+-doped LBA glasses are promising systems for optical thermometry and as gain mediums for solid-state lasers.

Effect of glyphosate in Johnsongrass submitted to different soil water potentials.

This work aimed to study the efficiency of herbicide glyphosate to control Johnsongrass plants (Sorghum halepense) in different phenological stages of development and when submitted to different types of soil water potentials. The study was conducted in a completely randomized design, with four repetitions. The treatments were arranged in a triple factor scheme 3 × 3 × 2, being: three soil water conditions [no water deficit (-0.03 MPa), intermediate water deficit (-0.07 MPa), and high water deficit (-1.5 MPa)], associated with three doses of glyphosate (0.0, 270.0, and 540.0 g a.e. ha-1) applied in two phenological stages (4-6 leaves and 1-3 tillers). Visual control evaluations were conducted at 7, 14, 21, and 35 days after the herbicide application. Biometric and morphophysiological parameters were also analyzed. With the increase of water restriction, there was a decrease in Johnsongrass morphophysiological components, such as specific leaf area, stomatal conductance, and the difference between environment and leaf temperature, as well as the accumulation of aerial part and roots dry matter, independently of the phenological stage evaluated. The development stage of Johnsongrass influenced the control provided by glyphosate, independently of the dose used. The different water deficits studied reduced the control of glyphosate in the two Johnsongrass development stages evaluated. Severe water deficits reduced the control of glyphosate in Johnsongrass using the recommended dose. In conditions of moderate water deficit, the control was not affected. Thus, the control with lower doses can be the most affected by water deficit.

Increased ATP Release and Higher Impact of Adenosine A2A Receptors on Corticostriatal Plasticity in a Rat Model of Presymptomatic Parkinson's Disease.

Extracellular ATP can be a danger signal, but its role in striatal circuits afflicted in Parkinson's disease (PD) is unclear and was now investigated. ATP was particularly released at high stimulation intensities from purified striatal nerve terminals of mice, which were endowed with different ATP-P2 receptors (P2R), although P2R antagonists did not alter corticostriatal transmission or plasticity. Instead, ATP was extracellularly catabolized into adenosine through CD73 to activate adenosine A2A receptors (A2AR) modulating corticostriatal long-term potentiation (LTP) in mice. In the presymptomatic phase of a 6-hydroxydopamine rat model of PD, ATP release from striatal nerve terminals was increased and was responsible for a greater impact of CD73 and A2AR on corticostriatal LTP. These observations identify increased ATP release and ATP-derived formation of extracellular adenosine bolstering A2AR activation as a key pathway responsible for abnormal synaptic plasticity in circuits involved in the onset of PD motor symptoms. The translation of these findings to humans prompts extending the use of A2AR antagonists from only co-adjuvants of motor control in Parkinsonian patients to neuroprotective drugs delaying the onset of motor symptoms.

Are immigrants more vulnerable to the socioeconomic impact of COVID-19? A cross-sectional study in Amadora Municipality, Lisbon metropolitan area.

Introduction: Immigrants carry an extra burden of morbidities and mortalities since the beginning of the coronavirus disease 2019 (COVID-19) pandemic. Pre-existing inequalities among immigrants may threaten their economic wellbeing during the pandemic. This study analyzed the socioeconomic impact of COVID-19 on immigrants and natives living in Amadora, Metropolitan Region of Lisbon and the extent to which preexisting inequalities had been exacerbated during the pandemic. Materials and methods: This cross-sectional study was conducted in Amadora Municipality, Lisbon Region, through phone interviews and using a structured questionnaire. Data collected in July 2020, included information on a cohort of 420 households, of which 51% were immigrants. To evaluate the socioeconomic position and economic wellbeing changes occurring during the pandemic we estimate crude and adjusted odds ratio (OR) and 95% CI, using Portuguese natives as the reference group. Results: Overall, 287 (70%) participants responded to the questionnaire, of which 47% are immigrants. Preexisting socioeconomic inequalities were exacerbated during the pandemic. Compared with natives, immigrants were more likely to experience job loss, temporary lay-off, and income loss during the COVID-19 pandemic. Immigrants were also more likely to face several kinds of financial hardship during the pandemic, such as difficulties in buying food, hygiene products, and paying bills. Conclusion: To the best of our knowledge, this study is the first to capture the direct socioeconomic impact of COVID-19 among immigrants and natives in Portugal. It highlights the bidirectional relation between inequalities deeply rooted among immigrants and COVID-19. Socioeconomic inequalities affect local patterns of COVID-19 burden, as confirmed in previous studies, but COVID-19 also has an impact on the economic wellbeing of Amadora immigrants during the pandemic. Urgent policies must be implemented to mitigate the economic burden of COVID-19 among immigrants, namely in Amadora, Lisbon Region.

Chronic total occlusion percutaneous coronary intervention in Latin America.

OBJECTIVES: To report clinical, angiographic characteristics, outcomes, and predictors of unsuccessful procedures in patients who underwent chronic total occlusion (CTO) percutaneous coronary interventions (PCI) in Latin America. BACKGROUND: CTO PCI has been increasingly performed worldwide, but there is a lack of information in this region. METHODS: An international multicenter registry was developed to collect data on CTO PCI performed in centers in Latin America. Patient, angiographic, procedural and outcome data were evaluated. Predictors of unsuccessful procedures were assessed by multivariable analysis. RESULTS: We have included data related to 1,040 CTO PCIs performed in seven countries in Latin America (Argentina, Brazil, Chile, Colombia, Ecuador, Mexico, and Puerto Rico). The mean age was 64 ± 10 years, and CTO PCI was performed mainly for angina control (81%) or treatment of a large ischemic area (30%). Overall technical success rate was 82.5%, and it was achieved with antegrade wire escalation in 81%, antegrade dissection/re-entry in 8% and with retrograde techniques in 11% of the successful procedures. Multivariable analysis identified moderate/severe calcification, a blunt proximal cap and a previous attempt as independent predictors of unsuccessful procedures. In-hospital major adverse cardiovascular events (MACE) occurred in 3.1% of the cases, death in 1% and cardiac tamponade in 0.9% CONCLUSIONS: CTO PCI in Latin America has been performed mainly for ischemia relief. Procedures were associated with a success rate above 80% and low incidence of MACE. Predictors of unsuccessful procedures were similar to those previously reported in the literature.

Synaptic and memory dysfunction in a ß-amyloid model of early Alzheimer's disease depends on increased formation of ATP-derived extracellular adenosine.

Adenosine A2A receptors (A2AR) overfunction causes synaptic and memory dysfunction in early Alzheimer's disease (AD). In a ß-amyloid (Aß1-42)-based model of early AD, we now unraveled that this involves an increased synaptic release of ATP coupled to an increased density and activity of ecto-5'-nucleotidase (CD73)-mediated formation of adenosine selectively activating A2AR. Thus, CD73 inhibition with α,ß-methylene-ADP impaired long-term potentiation (LTP) in mouse hippocampal slices, which is occluded upon previous superfusion with the A2AR antagonist SCH58261. Furthermore, α,ß-methylene-ADP did not alter LTP amplitude in global A2AR knockout (KO) and in forebrain neuron-selective A2AR-KO mice, but inhibited LTP amplitude in astrocyte-selective A2AR-KO mice; this shows that CD73-derived adenosine solely acts on neuronal A2AR. In agreement with the concept that ATP is a danger signal in the brain, ATP release from nerve terminals is increased after intracerebroventricular Aß1-42 administration, together with CD73 and A2AR upregulation in hippocampal synapses. Importantly, this increased CD73 activity is critically required for Aß1-42 to impair synaptic plasticity and memory since Aß1-42-induced synaptic and memory deficits were eliminated in CD73-KO mice. These observations establish a key regulatory role of CD73 activity over neuronal A2AR and imply CD73 as a novel target for modulation of early AD.

Ischemic preconditioning boosts post-exercise but not resting cardiac vagal control in endurance runners.

PURPOSE: High cardiac vagal control in endurance athletes has been generally associated with adequate recovery from training and readiness to cope high-intensity training. A method that improves cardiac vagal control in endurance athletes could therefore be advantageous. Accordingly, we sought to test whether ischemic preconditioning (IPC) could enhance cardiac vagal control in endurance runners. METHODS: Fifteen subjects underwent IPC, sham ultrasound (SHAM) or control (CT), in random order. Subjects were informed both IPC and SHAM would be beneficial vs. CT (i.e., similar placebo induction), and IPC would be harmless despite ischemia sensations (i.e., nocebo avoidance). Resting cardiac vagal control was assessed via respiratory sinus arrhythmia (RSA) and heart rate variability (HRV) indexes. Post-exercise cardiac vagal control was assessed via heart rate recovery [HR time constant decay (T30) and absolute HR decay (HRR30s)] during 30-s breaks of a discontinuous incremental test. Capillary blood samples were collected for lactate threshold identification. RESULTS: RSA and HRV were similar among interventions at pre- and post-intervention assessments. Lactate threshold occurred at 85 ± 4% of maximal effort. T30 was similar among interventions, but IPC increased HRR30s at 70% and 75% of maximal effort vs. SHAM and CT (70%: IPC = 31 ± 2 vs. SHAM = 26 ± 3 vs. CT = 26 ± 2 bpm, mean ± SEM, P < 0.01; 75%: IPC = 29 ± 2 vs. SHAM = 25 ± 2 vs. CT = 24 ± 2 bpm, P < 0.01). CONCLUSION: IPC did not change resting cardiac vagal control, but boosted fast post-exercise cardiac vagal reactivation at exercise intensities below lactate threshold in endurance runners.

Effect of Ischemic Preconditioning on the Recovery of Cardiac Autonomic Control From Repeated Sprint Exercise.

Repeated sprint exercise (RSE) acutely impairs post-exercise heart rate (HR) recovery (HRR) and time-domain heart rate variability (i. e., RMSSD), likely in part, due to lactic acidosis-induced reduction of cardiac vagal reactivation. In contrast, ischemic preconditioning (IPC) mediates cardiac vagal activation and augments energy metabolism efficiency during prolonged ischemia followed by reperfusion. Therefore, we investigated whether IPC could improve recovery of cardiac autonomic control from RSE partially via improved energy metabolism responses to RSE. Fifteen men team-sport practitioners (mean ± SD: 25 ± 5 years) were randomly exposed to IPC in the legs (3 × 5 min at 220 mmHg) or control (CT; 3 × 5 min at 20 mmHg) 48 h, 24 h, and 35 min before performing 3 sets of 6 shuttle running sprints (15 + 15 m with 180° change of direction and 20 s of active recovery). Sets 1 and 2 were followed by 180 s and set 3 by 360 s of inactive recovery. Short-term HRR was analyzed after all sets via linear regression of HR decay within the first 30 s of recovery (T30) and delta from peak HR to 60 s of recovery (HRR60s). Long-term HRR was analyzed throughout recovery from set 3 via first-order exponential regression of HR decay. Moreover, RMSSD was calculated using 30-s data segments throughout recovery from set 3. Energy metabolism responses were inferred via peak pulmonary oxygen uptake ( V ˙ O 2 peak), peak carbon dioxide output ( V ˙ O 2 peak), peak respiratory exchange ratio (RERpeak), first-order exponential regression of V ˙ O 2 decay within 360 s of recovery and blood lactate concentration ([Lac-]). IPC did not change T30, but increased HRR60s after all sets (condition main effect: P = 0.03; partial eta square (η2 p ) = 0.27, i.e., large effect size). IPC did not change long-term HRR and RMSSD throughout recovery, nor did IPC change any energy metabolism parameter. In conclusion, IPC accelerated to some extent the short-term recovery, but did not change the long-term recovery of cardiac autonomic control from RSE, and such accelerator effect was not accompanied by any IPC effect on surrogates of energy metabolism responses to RSE.

Blockade of adenosine A2A receptors recovers early deficits of memory and plasticity in the triple transgenic mouse model of Alzheimer's disease.

Alzheimer's disease (AD) begins with a deficit of synaptic function and adenosine A2A receptors (A2AR) are mostly located in synapses controlling synaptic plasticity. The over-activation of adenosine A2A receptors (A2AR) causes memory deficits and the blockade of A2AR prevents memory damage in AD models. We now enquired if this prophylactic role of A2AR might be extended to a therapeutic potential. We used the triple transgenic model of AD (3xTg-AD) and defined that the onset of memory dysfunction occurred at 4 months of age in the absence of locomotor or emotional alterations. At the onset of memory deficits, 3xTg mice displayed a decreased density of markers of excitatory synapses (10.6 ±â€¯3.8% decrease of vGluT1) without neuronal or glial overt damage and an increase of synaptic A2AR in the hippocampus (130 ±â€¯22%). After the onset of memory deficits in 3xTg-AD mice, a three weeks treatment with the selective A2AR antagonist normalized the up-regulation of hippocampal A2AR and restored hippocampal-dependent reference memory, as well as the decrease of hippocampal synaptic plasticity (60.0 ±â€¯3.7% decrease of long-term potentiation amplitude) and the decrease of global (syntaxin-I) and glutamatergic synaptic markers (vGluT1). These findings show a therapeutic-like ability of A2AR antagonists to recover synaptic and memory dysfunction in early AD.

Adenosine A2A Receptors in the Rat Prelimbic Medial Prefrontal Cortex Control Delay-Based Cost-Benefit Decision Making.

Adenosine A2A receptors (A2ARs) were recently described to control synaptic plasticity and network activity in the prefrontal cortex (PFC). We now probed the role of these PFC A2AR by evaluating the behavioral performance (locomotor activity, anxiety-related behavior, cost-benefit decision making and working memory) of rats upon downregulation of A2AR selectively in the prelimbic medial PFC (PLmPFC) via viral small hairpin RNA targeting the A2AR (shA2AR). The most evident alteration observed in shA2AR-treated rats, when compared to sh-control (shCTRL)-treated rats, was a decrease in the choice of the large reward upon an imposed delay of 15 s assessed in a T-maze-based cost-benefit decision-making paradigm, suggestive of impulsive decision making. Spontaneous locomotion in the open field was not altered, suggesting no changes in exploratory behavior. Furthermore, rats treated with shA2AR in the PLmPFC also displayed a tendency for higher anxiety levels in the elevated plus maze (less entries in the open arms), but not in the open field test (time spent in the center was not affected). Finally, working memory performance was not significantly altered, as revealed by the spontaneous alternation in the Y-maze test and the latency to reach the platform in the repeated trial Morris water maze. These findings constitute the first direct demonstration of a role of PFC A2AR in the control of behavior in physiological conditions, showing their major contribution for the control of delay-based cost-benefit decisions.

Assessment of the antiproliferative and antigenotoxic activity and phytochemical screening of aqueous extracts of Sambucus australis Cham. & Schltdl. (ADOXACEAE).

The purpose of this study was to evaluate the antiproliferative and antigenotoxic activity of Sambucus australis Cham. & Schltdl. aqueous extracts on the cell cycle of Allium cepa L. as well as determine the phenolic compounds in such extracts. S. australis inflorescences and leaves of two accessions were used for aqueous extract preparation at concentrations: 0.003 g/ml and 0.012 g/ml. A. cepa bulbs were rooted in distilled water and, subsequently, placed in treatments for 24 hours. Rootlets were collected and fixed in modified Carnoy's solution for 24 hours and kept. The squash technique was performed for slide preparation. Root tips were smashed and stained with 2% acetic orcein, and a total of 4000 cells per treatment were analyzed. The phenolic compounds were determined using high-performance liquid chromatography and data was analyzed using the Scott-Knott test. The results show that S. australis aqueous extracts have antiproliferative potential. Besides, the extracts prepared from S. australis leaves of both accessions at a concentration of 0.012 g/ml have shown antigenotoxic activity. The phytochemical analysis allowed us to determine the presence of flavonoids and phenolic acids, of which kaempferol and chrologenic acid were the most predominant compounds in the extracts from the inflorescences and leaves, respectively.

Effect of Ischemic Preconditioning on Endurance Performance Does Not Surpass Placebo.

PURPOSE: Recent studies have reported ischemic preconditioning (IPC) can acutely improve endurance exercise performance in athletes. However, placebo and nocebo effects have not been sufficiently controlled, and the effect on aerobic metabolism parameters that determine endurance performance (e.g., oxygen cost of running, lactate threshold, and maximal oxygen uptake [V˙O2max]) has been equivocal. Thus, we circumvented limitations from previous studies to test the effect of IPC on aerobic metabolism parameters and endurance performance in well-trained runners. METHODS: Eighteen runners (14 men/4 women) were submitted to three interventions, in random order: IPC; sham intervention (SHAM); and resting control (CT). Subjects were told both IPC and SHAM would improve performance compared to CT (i.e., similar placebo induction), and IPC would be harmless despite circulatory occlusion sensations (i.e., nocebo avoidance). Next, pulmonary ventilation and gas exchange, blood lactate concentration, and perceived effort were measured during a discontinuous incremental test on a treadmill. Then, a supramaximal test was used to verify the V˙O2max and assess endurance performance (i.e., time to exhaustion). RESULTS: Ventilation, oxygen uptake, carbon dioxide output, lactate concentration, and perceived effort were similar among IPC, SHAM, and CT throughout the discontinuous incremental test (P > 0.05). Oxygen cost of running, lactate threshold, and V˙O2max were also similar among interventions (P > 0.05). Time to exhaustion was longer after IPC (mean ± SEM, 165.34 ± 12.34 s) and SHAM (164.38 ± 11.71 s) than CT (143.98 ± 12.09 s; P = 0.02 and 0.03, respectively), but similar between IPC and SHAM (P = 1.00). CONCLUSIONS: IPC did not change aerobic metabolism parameters, whereas improved endurance performance. The IPC improvement, however, did not surpass the effect of a placebo intervention.

Assessment of the antiproliferative and antigenotoxic activity and phytochemical screening of aqueous extracts of Sambucus australis Cham. & Schltdl. (ADOXACEAE)

ABSTRACT The purpose of this study was to evaluate the antiproliferative and antigenotoxic activity of Sambucus australis Cham. & Schltdl. aqueous extracts on the cell cycle of Allium cepa L. as well as determine the phenolic compounds in such extracts. S. australis inflorescences and leaves of two accessions were used for aqueous extract preparation at concentrations: 0.003 g/ml and 0.012 g/ml. A. cepa bulbs were rooted in distilled water and, subsequently, placed in treatments for 24 hours. Rootlets were collected and fixed in modified Carnoy's solution for 24 hours and kept. The squash technique was performed for slide preparation. Root tips were smashed and stained with 2% acetic orcein, and a total of 4000 cells per treatment were analyzed. The phenolic compounds were determined using high-performance liquid chromatography and data was analyzed using the Scott-Knott test. The results show that S. australis aqueous extracts have antiproliferative potential. Besides, the extracts prepared from S. australis leaves of both accessions at a concentration of 0.012 g/ml have shown antigenotoxic activity. The phytochemical analysis allowed us to determine the presence of flavonoids and phenolic acids, of which kaempferol and chrologenic acid were the most predominant compounds in the extracts from the inflorescences and leaves, respectively.

Two new species of Curuapira Martins & Galileo, 1998 (Coleoptera, Cerambycidae, Lamiinae, Desmiphorini).

Two new species of Curuapira Martins & Galileo, 1998 are described: C. hovorei sp. nov. from Ecuador and C. armandi sp. nov. from Panama. A key to species of the genus is provided.

Effect of Intermittent Hypoxic Training Followed by Intermittent Hypoxic Exposure on Aerobic Capacity of Long Distance Runners.

Effects of intermittent hypoxic training (IHT) are still controversial and detraining effects remain uninvestigated. Therefore, we investigated (a) whether IHT improves aerobic capacity; (b) whether aerobic detraining occurs post-IHT; and (c) whether intermittent hypoxic exposure (IHE) at rest reduces a possible aerobic detraining post-IHT. Twenty eight runners (21 men/7 women; 36 ± 2 years; maximal oxygen uptake [V[Combining Dot Above]O2max] 55.4 ± 1.3 ml·kg·min) participated in a single-blinded placebo-controlled trial. Twice a week, 1 group performed 6 weeks of IHT (n = 11), followed by 4 weeks of IHE (n = 11) at rest (IHT+IHE group). Another group performed 6 weeks of IHT (n = 10), followed by 4 weeks of normoxic exposure (NE, n = 9) at rest (IHT+NE group). A control group performed 6 weeks of normoxic training (NT, n = 7), followed by 4 weeks of NE (n = 6) at rest (NT+NE group). Hematological and submaximal/maximal aerobic measurements were conducted in normoxia at pretraining, posttraining, and postexposure. Hemoglobin concentration did not change, but lactate threshold and running economy improved in all groups at posttraining (p ≤ 0.05 vs. pretraining). Ventilatory threshold, respiratory compensation point, and V[Combining Dot Above]O2max increased after IHT (IHT+IHE group: 7.3, 5.4, and 9.2%, respectively; IHT+NE group: 10.7, 7.5, and 4.8%; p ≤ 0.05 vs. pretraining), but not after NT (-1.1, -1.0, and -3.8%; p > 0.05 vs. pretraining). Such IHT-induced adaptations were maintained at postexposure (p > 0.05 vs. postexposure). In conclusion, IHT induced further aerobic improvements than NT. These additional IHT adaptations were maintained for 4 weeks post-IHT, regardless of IHE.

Are heart rate deflection point and peak velocity determined in the Université of Montréal Track Test valid to approximate aerobic parameters measured in the laboratory?

BACKGROUND: The aim of this study was to compare the respiratory compensation point (RCP) and maximal aerobic velocity (vVO2max) measured in the laboratory, respectively, with the heart rate deflection point (HRDP) and the peak velocity (PV) determined in the Université of Montréal Track Test (UMTT). Beside, we investigated the relationship of these parameters with endurance performance. METHODS: Eighteen long distance runners randomly performed (in different days) two incremental exercise tests (laboratory and UMTT). RCP and vVO2max were identified in a treadmill test. The HRDP was identified using the Dmax method, while the PV was identified as the velocity of the last complete stage (PVc) and the time-corrected velocity of the last incomplete stage (PVi). Endurance performance was the reported 10-km race time from the closest race to the test visits. RESULTS: RCP heart rate (176±14 bpm) was not significantly different from HRDP (173±10 bpm). The agreement was reasonable [bias: 4 bpm (95% limit of agreement: -16 to 24 bpm)]. vVO2max (18.0±2.1 km.h-1) was not significantly different from PVi (17.6±2.1 km.h-1), but was significantly higher than PVc (17.3±2.0 km.h-1). The agreement between vVO2max and PVi was acceptable [0.4 km.h-1 (-1.6 to 2.4 km.h-1)]. Endurance performance correlations (2212±277 s) with HRDP velocity (r=-0.75) and PVi (r=-0.83) tended to be lower than with RCP velocity (r=-0.91) and vVO2max (r=-0.85). CONCLUSIONS: It is possible to estimate with reasonable accuracy the vVO2max using the UMTT. However, care must be taken to use the HRDP identified through the UMTT to prescribe training intensities.

Differences in muscle strength after ACL reconstruction do not influence cardiorespiratory responses to isometabolic exercise.

OBJECTIVES: To investigate whether the muscle strength decrease that follows anterior cruciate ligament (ACL) reconstruction would lead to different cardiorespiratory adjustments during dynamic exercise. METHOD: Eighteen active male subjects were submitted to isokinetic evaluation of knee flexor and extensor muscles four months after ACL surgery. Thigh circumference was also measured and an incremental unilateral cardiopulmonary exercise test was performed separately for both involved and uninvolved lower limbs in order to compare heart rate, oxygen consumption, minute ventilation, and ventilatory pattern (breath rate, tidal volume, inspiratory time, expiratory time, tidal volume/inspiratory time) at three different workloads (moderate, anaerobic threshold, and maximal). RESULTS: There was a significant difference between isokinetic extensor peak torque measured in the involved (116.5 ± 29.1 Nm) and uninvolved (220.8 ± 40.4 Nm) limbs, p=0.000. Isokinetic flexor peak torque was also lower in the involved limb than in the uninvolved limb (107.8 ± 15.4 and 132.5 ± 26.3 Nm, p=0.004, respectively). Lower values were also found in involved thigh circumference as compared with uninvolved limb (46.9 ± 4.3 and 48.5 ± 3.9 cm, p=0.005, respectively). No differences were found between the lower limbs in any of the variables of the incremental cardiopulmonary tests at all exercise intensities. CONCLUSIONS: Our findings indicate that, four months after ACL surgery, there is a significant deficit in isokinetic strength in the involved limb, but these differences in muscle strength requirement do not produce differences in the cardiorespiratory adjustments to exercise. Based on the hypotheses from the literature which explain the differences in the physiological responses to exercise for different muscle masses, we can deduce that, after 4 months of a rehabilitation program after an ACL reconstruction, individuals probably do not present differences in muscle oxidative and peripheral perfusion capacities that could elicit higher levels of peripheral cardiorepiratory stimulus during exercise.

Differences in muscle strength after ACL reconstruction do not influence cardiorespiratory responses to isometabolic exercise

Objectives: To investigate whether the muscle strength decrease that follows anterior cruciate ligament (ACL) reconstruction would lead to different cardiorespiratory adjustments during dynamic exercise. Method: Eighteen active male subjects were submitted to isokinetic evaluation of knee flexor and extensor muscles four months after ACL surgery. Thigh circumference was also measured and an incremental unilateral cardiopulmonary exercise test was performed separately for both involved and uninvolved lower limbs in order to compare heart rate, oxygen consumption, minute ventilation, and ventilatory pattern (breath rate, tidal volume, inspiratory time, expiratory time, tidal volume/inspiratory time) at three different workloads (moderate, anaerobic threshold, and maximal). Results: There was a significant difference between isokinetic extensor peak torque measured in the involved (116.5±29.1 Nm) and uninvolved (220.8±40.4 Nm) limbs, p=0.000. Isokinetic flexor peak torque was also lower in the involved limb than in the uninvolved limb (107.8±15.4 and 132.5±26.3 Nm, p=0.004, respectively). Lower values were also found in involved thigh circumference as compared with uninvolved limb (46.9±4.3 and 48.5±3.9 cm, p=0.005, respectively). No differences were found between the lower limbs in any of the variables of the incremental cardiopulmonary tests at all exercise intensities. Conclusions: Our findings indicate that, four months after ACL surgery, there is a significant deficit in isokinetic strength in the involved limb, but these differences in muscle strength requirement do not produce differences in the cardiorespiratory adjustments to exercise. Based on the hypotheses from the literature which explain the differences in the physiological responses to exercise for different muscle masses, we can deduce that, after 4 months of a rehabilitation program after an ACL reconstruction, individuals probably ...