The present study aimed to analyze and compare the effects of four different interval-training protocols on aerobic fitness and muscle strength. Thirty-seven subjects (23.8 ± 4 years; 171.7 ± 9.5 cm; 70 ± 11 kg) were assigned to one of four groups: low-intensity interval training with (BFR, n = 10) or without (LOW, n = 7) blood flow restriction, high-intensity interval training (HIT, n = 10), and combined HIT and BFR (BFR + HIT, n = 10, every session performed 50% as BFR and 50% as HIT). Before and after 4 weeks training (3 days a week), the maximal oxygen uptake (VO2max ), maximal power output (Pmax ), onset blood lactate accumulation (OBLA), and muscle strength were measured for all subjects. All training groups were able to improve OBLA (BFR, 16%; HIT, 25%; HIT + BFR, 22%; LOW, 6%), with no difference between groups. However, VO2max and Pmax improved only for BFR (6%, 12%), HIT (9%, 15%) and HIT + BFR (6%, 11%), with no difference between groups. Muscle strength gains were only observed after BFR training (11%). This study demonstrates the advantage of short-term low-intensity interval BFR training as the single mode of training able to simultaneously improve aerobic fitness and muscular strength.

Pharmaceuticals are environmental contaminants that have been widely detected in aquatic media. In this review, the occurrence of pharmaceuticals in the environment, its major causes, and implications along with effective procedures for their removal from contaminated water have been studied. Adsorption stands out as a promising treatment method, since it offers advantages such as lower energy consumption and simpler operation conditions in comparison to other tertiary treatments. Although commercial activated carbon is extensively studied as an adsorbent of pharmaceuticals, its large-scale application is limited by the high costs. Therefore, different nonconventional low-cost materials have been investigated and adsorbents based on clays, biochars, chitosan, agricultural and industrial wastes, and metal–organic frameworks have been addressed in many studies for pharmaceuticals uptake from water and wastewater. This article reviews key publications on this subject, discussing adsorption performance in terms of kinetics, equilibrium, thermodynamics, continuous fixed-bed process, regeneration capability, and historical, economical, and practical aspects.

The absolute configurations of fistularin-3, 11-epi-fistularin-3, and a related bis-oxazolidinone were determined by microscale hydrolysis followed by derivatization with 1-fluoro-2,4-dinitrophenyl-5-l-alaninamide. Samples of fistularin-3 from Verongid marine sponges collected in the Great Barrier Reef (Australia), Baía de Todos os Santos (Brazil), and the Key Largo, Florida (USA) varied in configuration at C11, a phenomenon that may be attributed to the involvement of stereochemically promiscuous hydroxylase enzymes. Variability in C11 configuration in fistularin-3 samples may have been overlooked in previously reported encounters due to the similarity of spectroscopic properties of fistularin-3 and 11-epi-fistularin-3 and their coelution under chromatographic conditions. Stereochemical heterogeneity at C11 in fistularin-3 samples suggests a possibility of a native biotransformation of suitable precursor in Verongid sponges by their associated microbial flora.

A screening of 500 crude extracts of marine invertebrates against the growth of Mycobacterium tuberculosis H37Rv yielded MeOH extracts of the sponges Aplysina cauliformis and Pachychalina sp. with significant activity. Further bioassay-guided fractionation of both crude extracts led to the isolation of four bromine-containing metabolites. The known (+)-fistularin-3 (1) and 11-deoxyfistularin-3 (2), and the new compound 2-(3-amino-2,4-dibromo-6-hydroxyphenyl)acetic acid (3) were isolated from the sponge A. cauliformis, while the new bromotyrosine-derived 3-(3,5-dibromo-4-methoxyphenyl)-2-methoxy- N-methylpropan-1-ammonium (4) was isolated from Pachychalina sp. Compound 4 exhibited weak antimycobacterial activity while compounds 1-3 displayed activity against Mycobacterium tuberculosis H37Rv, with MICs of 7.1, 7.3 and 49 microM, respectively. Compounds 1 and 2 also exhibited low cytotoxicity against J744 macrophages, indicating that both 1 and 2 are interesting leads for the development of new anti-tuberculosis agents.

The purpose of this study was to identify the boundary of submaximal speed zones (i.e., exercise intensity domains) between maximal aerobic speed (S-400) and lactate threshold (LT) in swimming. A 400-m all-out test, a 7 × 200 m incremental step test, and two to four 30-minute submaximal tests were performed by 12 male endurance swimmers (age = 24.5 ± 9.6 years; body mass = 71.3 ± 9.8 kg) to determine S-400, speed corresponding to LT, and maximal lactate steady state (MLSS). S-400 was 1.30 ± 0.09 m·s (400 m-5:08 minutes:seconds). The speed at LT (1.08 ± 0.02 m·s; 83.1 ± 2.2 %S-400) was lower than the speed at MLSS (1.14 ± 0.02 m·s; 87.5 ± 1.9 %S-400). Maximal lactate steady state occurred at 26 ± 10% of the difference between the speed at LT and S-400. Mean blood lactate values at the speeds corresponding to LT and MLSS were 2.45 ± 1.13 mmol·L and 4.30 ± 1.32 mmol·L, respectively. The present findings demonstrate that the range of intensity zones between LT and MLSS (i.e., heavy domain) and between MLSS and S-400 (i.e., severe domain) are very narrow in swimming with LT occurring at 83% S-400 in trained swimmers. Precision and sensitivity of the measurement of aerobic indexes (i.e., LT and MLSS) should be considered when conducting exercise training and testing in swimming.

Lactate is a highly dynamic metabolite that can be used as a fuel by several cells of the human body, particularly during physical exercise. Traditionally, it has been believed that the first step of lactate oxidation occurs in cytosol; however, this idea was recently challenged. A new hypothesis has been presented based on the fact that lactate-to-pyruvate conversion cannot occur in cytosol, because the LDH enzyme characteristics and cytosolic environment do not allow the reaction in this way. Instead, the Intracellular Lactate Shuttle hypothesis states that lactate first enters in mitochondria and only then is metabolized. In several tissues of the human body this idea is well accepted but is quite resistant in skeletal muscle. In this paper, we will present not only the studies which are protagonists in this discussion, but the potential mechanism by which this oxidation occurs and also a link between lactate and mitochondrial proliferation. This new perspective brings some implications and comes to change our understanding of the interaction between the energy systems, because the product of one serves as a substrate for the other.

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New Findings What is the central question of this study? Can interval blood‐flow‐restricted (BFR) cycling training, undertaken at a low intensity, promote a similar adaptation to oxygen uptake (V̇normalO2) kinetics to high‐intensity interval training? What is the main finding and its importance? Speeding of pulmonary V̇normalO2 on‐kinetics in healthy young subjects was not different between low‐intensity interval BFR training and traditional high‐intensity interval training. Given that very low workloads are well tolerated during BFR cycle training and speed V̇normalO2 on‐kinetics, this training method could be used when high mechanical loads are contraindicated. Abstract Low‐intensity blood‐flow‐restricted (BFR) endurance training is effective to increase aerobic capacity. Whether it speeds pulmonary oxygen uptake (V̇O2normalp), CO2 output (V̇normalCO2normalp) and ventilatory (V̇ Ep ) kinetics has not been examined. We hypothesized that low‐intensity BFR training would reduce the phase 2 time constant (τp) of V̇O2normalp, V̇normalCO2normalp and V̇ Ep by a similar magnitude to traditional high‐intensity interval training (HIT). Low‐intensity interval training with BFR served as a control. Twenty‐four participants (25 ± 6 years old; maximal V̇normalO2 46 ± 6 ml kg−1 min−1) were assigned to one of the following: low‐intensity BFR interval training (BFR; n = 8); low‐intensity interval training without BFR (LOW; n = 7); or high‐intensity interval training without BFR (HIT; n = 9). Training was 12 sessions of two sets of five to eight × 2 min cycling and 1 min resting intervals. LOW and BFR were conducted at 30% of peak incremental power (Ppeak), and HIT was at ∼103% Ppeak. For BFR, cuffs were inflated on both thighs (140–200 mmHg) during exercise and deflated during rest intervals. Six moderate‐intensity step transitions (30% Ppeak) were averaged for analysis of pulmonary on‐kinetics. Both BFR (pre‐ versus post‐training τp = 18.3 ± 3.2 versus 14.5 ± 3.4 s; effect size = 1.14) and HIT (τp = 20.3 ± 4.0 versus 13.1 ± 2.9 s; effect size = 1.75) reduced the V̇O2normalp τp (P < 0.05). As expected, there was no change in LOW (V̇O2normalp τp = 17.9 ± 6.2 versus 17.7 ± 4.3 s; P = 0.9). The kinetics of V̇normalCO2normalp and V̇ Ep were speeded only after HIT (38.5 ± 10.6%, P < 0.001 and 31.2 ± 24.7%, P = 0.004, respectively). Both HIT and low‐intensity BFR training were effective in speeding moderate‐intensity V̇O2normalp kinetics. These data support the findings of others that low‐intensity cycling training with BFR increases muscle oxidative capacity.