Critical load: a novel approach to determining a sustainable intensity during resistance exercise.

BACKGROUND: A hyperbolic function as well as a linear relationship between power output and time to exhaustion (Tlim) has been consistently observed during dynamic non-resistive exercises. However, little is known about its concept to resistance exercises (RE), which could be defined as critical load (CL). This study aimed to verify the existence of CL during dynamic RE and to verify the number of workbouts necessary to determine the optimal modeling to achieve it. METHODS: Fifteen healthy men (23±2.5 yrs) completed 1 repetition maximum test (1RM) on a leg press and 3 (60%, 75% and 90% of 1RM) or 4 (+ 30% of 1RM) workbouts protocols to obtain the CL by hyperbolic and linear regression models between Tlim and load performed. Blood lactate and leg fatigue were also measured. RESULTS: CL was obtained during RE and 3 workbouts protocol estimate it at 53% while 4 tests at 38% of 1 RM. However, based on coefficients of determination, 3 protocols provided a better fit than the 4-parameter model, respectively (R2>0.95 vs. >0.77). Moreover, all intensities increased blood lactate and leg fatigue, however, when corrected by Tlim, were significantly lower at CL. CONCLUSIONS: It was possible to determinate CL during dynamic lower limbs RE and that 3 exhaustive workbouts can be used to better estimate the CL, constituting a new concept of determining this threshold during dynamic RE and reducing the physically demanding nature of the protocol. These findings may have important applications for functional performance evaluation and prescription of RE programs.

Delta-aminolevulinate dehydratase (delta-ALA-D) activity in diabetes and hypothyroidism.

OBJECTIVES: This study analyzed the influence of type 2 diabetes mellitus and primary hypothyroidism on the activity of the delta-aminolevulinate dehydratase (delta-ALA-D) in human blood. DESIGN AND METHODS: Delta-ALA-D enzyme activity was determined in normal (healthy) people (n=29), compensated (DMC, n=11) and non-compensated diabetic patients (NDMC, n=23), and in patients with compensated (CH, n=19) and non-compensated primary hypothyroidism (NCH, n=10). The determination of lead, copper, zinc and magnesium was performed by graphite furnace atomic absorption spectrometry. RESULTS: This study shows that delta-ALA-D activity was decreased (P<0.05) in situations associated to hyperglycemia maintained for long periods (HbA1c high). Another finding of this study suggests that states of hypofunction of the thyroid gland, when non-compensated, increase the activity of delta-ALA-D (P<0.001). In addition, copper was elevated in HNC, zinc was diminished in DMC, HC and HNC, and magnesium was diminished in the HNC group. CONCLUSION: This result points out that there is a correlation among diabetes, hypothyroidism and delta-ALA-D activity.

1,1,2-Tris-organoselenide alkene derivatives, but not 1,2-bis-organoselenide alkene derivatives, inhibited delta-aminolevulinate dehydratase activity from human erythrocytic cells in vitro.

Organochalcogens are important intermediates and useful reagents in organic synthesis. Recent data from our laboratory demonstrated that bis and tris-selenide alkene derivatives are attractive synthetic targets because of their chemio-, regio- and stereo-selective reactions. Since the erythrocytic delta-aminolevulinate dehydratase (delta-ALA-D) activity could be an important indicator of toxicity, this report investigated bis and tris-selenide alkene derivatives effects on blood delta-ALA-D in vitro. To investigate the mechanisms by which these compounds inhibit human blood delta-ALA-D activity, a thiol reducing agent or zinc chloride were used. 1,2-Bis-selenide alkene derivatives 1a (R=4-MeOC(6)H(4)), 1b (R=4-ClC(6)H(4)) and 1c (R=2,4,6-Me(3)C(6)H(2)) did not inhibit human blood delta-ALA-D activity. 1,1,2-Tris-selenide alkene derivative 2a (R=C(6)H(5)) was the most potent delta-ALA-D inhibitor. Compounds 2b (R=4-MeOC(6)H(4)) and 2c (R=4-ClC(6)H(4)) displayed similar inhibitory potency towards delta-ALA-D activity. Dithiothreitol, a hydrophobic SH-reducing agent, was able to restore and to protect delta-ALA-D activity inhibited by tris-selenide alkene derivatives. Conversely, ZnCl(2) did not alter the enzyme inhibition induced by tris-selenide alkene derivatives. From these findings we suggest that 1,1,2-tris-selenide alkene derivatives inhibited delta-ALA-D activity by an interaction with essential sulfhydryl groups for the enzyme activity.

Evaluation of antioxidant activity and potential toxicity of 1-buthyltelurenyl-2-methylthioheptene.

The aim of the present study was to evaluate pharmacological and toxicological properties of 1-buthyltelurenyl-2-methylthioheptene (compound 1). In vitro, compound 1 at 1 microM was effective in reducing lipid peroxidation induced by Fe/EDTA. Compound 1 presented neither thiol peroxidase nor thiol oxidase activity and did not change delta-ALA-D (delta-aminolevulinate dehydratase) activity (10-400 microM). Calculated LD(50) of compound 1, administered by oral route, was 65.1 micromol/kg. Rats treated with compound 1 did not reveal any motor impairment in the open field. Hepatic, renal and cerebral lipid peroxidation in treated rats did not differ from those in control rats. Conversely, 0.5 micromol/kg of compound 1 decreased lipid peroxidation in spleen. Delta-ALA-D activity in liver and spleen was inhibited in rats treated with the higher dose of compound 1 but no significant differences were detected in renal delta-ALA-D activity. AST (aspartate aminotransferase) and ALT (alanine aminotransferase) activities as well as urea and creatinine levels were increased by high doses of compound 1 (50-75 micromol/kg). Compound 1 induced a significant decrease in plasma triglyceride levels but none of the doses tested changed the cholesterol level. This is a promising compound for more detailed pharmacological studies involving organotellurium compounds.

Dihydropyrimidin-(2H)-ones obtained by ultrasound irradiation: a new class of potential antioxidant agents.

An efficient and simple synthetic protocol for the Biginelli reaction has been developed for the preparation of several new dihydropyrimidinones, under ultrasound irradiation in the presence of NH(4)Cl, in good yields and short reaction time. Some of the synthesized compounds were tested in vitro for their antioxidant activity. All of the selected compounds showed some antioxidant activity. Analogues compounds 3b and 4b exhibited a strong activity against lipid peroxidation induced by Fe + EDTA, while compounds 3b and 3d were the most potent in reducing ROS levels.

Bis selenide alkene derivatives: A class of potential antioxidant and antinociceptive agents.

Bis and tris-selenide alkene derivatives, a class of organoselenium compounds, were screened for antinociceptive and antioxidant activities. In vitro, bis-selenide alkene 1c (R=2,4,6-Me(3)C(6)H(2)), 1d (R=4-ClC(6)H(4)) and 1e (R=4-MeOC(6)H(4)) protected against lipid peroxidation about 50%, whereas 1b (R=C(6)H(5)) and 1a (R=C(4)H(9)) protected only 23%. Compound 1d presented lesser IC(50) against lipid peroxidation than other bis-selenide alkene compounds (1d>1e> or =1c>1a=1b). The maximal inhibitory effect of tris-selenide alkenes on lipid peroxidation was in the following order 2c>2a=2b. Compound 1e increased the rate of GSH, but not DTT, oxidation. Tris-selenide alkene 2c (R=4-MeOC(6)H(4)) demonstrated the higher rate of thiol oxidation, while 2a (R=C(6)H(5)) did not change DTT oxidation but oxidized GSH. Conversely, compound 2b (R=4-ClC(6)H(4)) did not change the rate of GSH oxidation, but oxidized DDT. Bis-selenide alkene derivatives 1c, 1d and 1e were the most promising compounds tested in vitro. In vivo, compounds 1c and 1d (5-50mg/kg, subcutaneously) produced significant inhibition of acetic acid- and capsaicin-induced pain. Compounds 1c and 1d increased the tail-flick response latency time. The antinociception effect of 1c and 1d was not abolished by naloxone (an antagonist of opioid receptor, 1mg/kg, subcutaneously), suggesting that the antinociceptive effect is not influenced by the opioidergic mechanism.

Changes in [(3)H]-glutamate uptake into platelets from patients with bipolar I disorder.

Glutamate is the most abundant excitatory neurotransmitter in the mammalian brain, and it is increasingly being implicated in the pathophysiology of mental illness. In fact, changes in glutamate neurotransmission seem to be involved in the etiology of schizophrenia, major depression and bipolar disorders. Furthermore, the alterations in platelet sensitivity in major depression are distinct from those of bipolar disorders. The aim of the present investigation was to determine whether patients with bipolar disorders exhibited differences in [(3)H]-glutamate uptake of platelets. [(3)H]-Glutamate uptake of platelets from controls (n=14), patients with bipolar disorders under lithium treatment (600-1800 mg/day for 6 months) (n=7) and patients with bipolar disorders with psychotic features (n=8) were carried out. Analysis of blood platelets from the three groups of subjects revealed significant differences in [(3)H]-glutamate uptake between the control and psychotic patients. The specific glutamate uptake for the control and psychotic groups was 20.5+/-8.4 and 37.5+/-18.1 pmol glutamate/mg protein/10 min, respectively (mean+/-SD). These results indicate that peripheral glutamate metabolism of platelets is modified in bipolar disorders and that more detailed studies must be carried out to determine whether these peripheral modifications correlate with central modifications in humans and in animal models of the disease.