Apolipoprotein B and angiotensin-converting enzyme polymorphisms and aerobic interval training: randomized controlled trial in coronary artery disease patients.

Physical training has been strongly recommended as a non-pharmacological treatment for coronary artery disease (CAD). Genetic polymorphisms have been studied to understand the biological variability in response to exercise among individuals. This study aimed to verify the possible influence of apolipoprotein B (ApoB: rs1042031 and rs693) and angiotensin-converting enzyme (ACE-ID: rs1799752) genotypes on the lipid profile and functional aerobic capacity, respectively, after an aerobic interval training (AIT) program in patients with CAD and/or cardiovascular risk factors. Sixty-six men were randomized and assigned to trained group (n=32) or control group (n=34). Cardiopulmonary exercise test was performed to determine the ventilatory anaerobic threshold (VAT) from cardiorespiratory variables. The AIT program, at an intensity equivalent to %VAT (70-110%), was conducted three times a week for 16 weeks. ApoB gene polymorphisms (-12669C>T (rs1042031) and -7673G>A (rs693)) were identified by real-time polymerase chain reaction (PCR). I/D polymorphism in the ACE gene (rs1799752) was identified through PCR and fragment size analysis. After 16 weeks, low-density lipoprotein (LDL) levels increased in the trained and control groups with the GA+AA genotype (-7673G>A) of the ApoB gene. Trained groups with ACE-II and ACE-ID genotypes presented an increase in oxygen consumption (VO2VAT) and power output after the AIT program. The presence of the ACE I-allele was associated with increased aerobic functional capacity after the AIT program. Increased LDL levels were observed over time in patients with the -7673G>A polymorphism of the ApoB gene. Trial Registration Information: ClinicalTrials.gov: NCT02313831.

Apolipoprotein B and angiotensin-converting enzyme polymorphisms and aerobic interval training: randomized controlled trial in coronary artery disease patients

Physical training has been strongly recommended as a non-pharmacological treatment for coronary artery disease (CAD). Genetic polymorphisms have been studied to understand the biological variability in response to exercise among individuals. This study aimed to verify the possible influence of apolipoprotein B (ApoB: rs1042031 and rs693) and angiotensin-converting enzyme (ACE-ID: rs1799752) genotypes on the lipid profile and functional aerobic capacity, respectively, after an aerobic interval training (AIT) program in patients with CAD and/or cardiovascular risk factors. Sixty-six men were randomized and assigned to trained group (n=32) or control group (n=34). Cardiopulmonary exercise test was performed to determine the ventilatory anaerobic threshold (VAT) from cardiorespiratory variables. The AIT program, at an intensity equivalent to %VAT (70-110%), was conducted three times a week for 16 weeks. ApoB gene polymorphisms (−12669C>T (rs1042031) and −7673G>A (rs693)) were identified by real-time polymerase chain reaction (PCR). I/D polymorphism in the ACE gene (rs1799752) was identified through PCR and fragment size analysis. After 16 weeks, low-density lipoprotein (LDL) levels increased in the trained and control groups with the GA+AA genotype (−7673G>A) of the ApoB gene. Trained groups with ACE-II and ACE-ID genotypes presented an increase in oxygen consumption (VO2VAT) and power output after the AIT program. The presence of the ACE I-allele was associated with increased aerobic functional capacity after the AIT program. Increased LDL levels were observed over time in patients with the −7673G>A polymorphism of the ApoB gene. Trial Registration Information: ClinicalTrials.gov: NCT02313831

Greater muscle damage in athletes with ACTN3 R577X (RS1815739) gene polymorphism after an ultra-endurance race: a pilot study.

In this study, we aimed to investigate the influence of ACTN3 R577X gene polymorphism on muscle damage responses in athletes competing in an ultra-endurance race. Twenty moderate to well-trained ultra-runners who had entered in an official 37.1 km adventure race (22.1 km mountain biking, 10.9 km trekking, 4.1 km water trekking, 30 m rope course, and orienteering) volunteered for the study. Blood samples were collected for genotyping and analysis of muscle protein levels before and after the race. Percentage changes (pre- to post-race) of serum myoglobin [XX = 5,377% vs. RX/RR = 1,666%; P = 0.005, effect size (ES) = 1.73], creatine kinase (XX = 836.5% vs. RX/RR = 455%; P = 0.04, ES = 1.29), lactate dehydrogenase (XX = 82% vs. RX/RR = 65%; P = 0.002, ES = 1.61), and aspartate aminotransferase (XX = 148% vs. RX/RR = 75%; P = 0.02, ES = 1.77) were significantly greater for XX than RX/RR genotypes. ES analysis confirmed a large magnitude of muscle damage in XX genotype ultra-runners. Therefore, athletes with the ACTN3 577XX genotype experienced more muscle damage after an adventure race. This suggests that ultra-runners with alpha-actinin-3 deficiency may be more susceptible to rhabdomyolysis and associated health complications during ultra-endurance competitions.

MCT1 and MCT4 kinetic of mRNA expression in different tissues after aerobic exercise at maximal lactate steady state workload.

We evaluate the mRNA expression of monocarboxylate transporters 1 and 4 (MCT1 and MCT4) in skeletal muscle (soleus, red and white gastrocnemius), heart and liver tissues in mice submitted to a single bout of swimming exercise at the maximal lactate steady state workload (MLSSw). After 72 h of MLSS test, the animals were submitted to a swimming exercise session for 25 min at individual MLSSw. Tissues and muscle samples were obtained at rest (control, n=5), immediately (n=5), 5 h (n=5) and 10 h (n=5) after exercise for determination of the MCT1 and MCT4 mRNA expression (RT-PCR). The MCT1 mRNA expression in liver increased after 10 h in relation to the control, immediate and 5 h groups, but the MCT4 remained unchanged. The MCT1 mRNA expression in heart increased by 31 % after 10 h when compared to immediate, but no differences were observed in relation to the control group. No significant differences were observed for red gastrocnemius in MCT1 and MCT4 mRNA expression. However, white gastrocnemius increased MCT1 mRNA expression immediately when compared to rest, 5 and 10 h test groups. In soleus muscle, the MCT1 mRNA expression increased immediately, 5 and 10 h after exercise when compared to the control. In relation to MCT4 mRNA expression, the soleus increased immediately and 10 h after acute exercise when compared to the control group. The soleus, liver and heart were the main tissues that showed improved the MCT1 mRNA expression, indicating its important role in controlling MLSS concentration in mice.

Interval versus continuous training with identical workload: physiological and aerobic capacity adaptations.

The interval model training has been more recommended to promote aerobic adaptations due to recovery period that enables the execution of elevated intensity and as consequence, higher workload in relation to continuous training. However, the physiological and aerobic capacity adaptations in interval training with identical workload to continuous are still uncertain. The purpose was to characterize the effects of chronic and acute biomarkers adaptations and aerobic capacity in interval and continuous protocols with equivalent load. Fifty Wistar rats were divided in three groups: Continuous training (GTC), interval training (GTI) and control (CG). The running training lasted 8 weeks (wk) and was based at Anaerobic Threshold (AT) velocity. GTI showed glycogen super-compensation (mg/100 mg) 48 h after training session in relation to CG and GTC (GTI red gastrocnemius (RG)=1.41+/-0.16; GTI white gastrocnemius (WG)=1.78+/-0.20; GTI soleus (S)=0.26+/-0.01; GTI liver (L)=2.72+/-0.36; GTC RG=0.42+/-0.17; GTC WG=0.54+/-0.22; GTC S=0.100+/-0.01; GTC L=1.12+/-0.24; CG RG=0.32+/-0.05; CG WG=0.65+/-0.17; CG S=0.14+/-0.01; CG L=2.28+/-0.33). The volume performed by GTI was higher than GTC. The aerobic capacity reduced 11 % after experimental period in GTC when compared to GTI, but this change was insignificant (19.6+/-5.4 m/min; 17.7+/-2.5 m/min, effect size = 0.59). Free fatty acids and glucose concentration did not show statistical differences among the groups. Corticosterone concentration increased in acute condition for GTI and GTC. Testosterone concentration reduced 71 % in GTC immediately after the exercise in comparison to CG. The GTI allowed positive adaptations when compared to GTC in relation to: glycogen super-compensation, training volume performed and anabolic condition. However, the GTI not improved the aerobic performance.

Acute effects of movement velocity on blood lactate and growth hormone responses after eccentric bench press exercise in resistance-trained men.

This study aimed to compare the effects of different velocities of eccentric muscle actions on acute blood lactate and serum growth hormone (GH) concentrations following free weight bench press exercises performed by resistance-trained men. Sixteen healthy men were divided into two groups: slow eccentric velocity (SEV; n = 8) and fast eccentric velocity (FEV; n = 8). Both groups performed four sets of eight eccentric repetitions at an intensity of 70% of their one repetition maximum eccentric (1RMecc) test, with 2-minute rest intervals between sets. The eccentric velocity was controlled to 3 seconds per range of motion for SEV and 0.5 seconds for the FEV group. There was a significant difference (P < 0.001) in the kinetics of blood lactate removal (at 3, 6, 9, 15, and 20 min) and higher mean values for peak blood lactate (P = 0.001) for the SEV group (9.1 ± 0.5 mM) compared to the FEV group (6.1 ± 0.4 mM). Additionally, serum GH concentrations were significantly higher (P < 0.001) at 15 minutes after bench press exercise in the SEV group (1.7 ± 0.6 ng · mL(-1)) relative to the FEV group (0.1 ± 0.0 ng · mL(-1)). In conclusion, the velocity of eccentric muscle action influences acute responses following bench press exercises performed by resistance-trained men using a slow velocity resulting in a greater metabolic stress and hormone response.

La velocidad de contracción rápida en ejercicio de fuerza produce mayor volumen de carga total levantada y pérdida de la fuerza muscular en hombres entrenados / Fast contraction velocity in resistance exercise induces greater total volume load lifted and muscle strength loss in resistance-trained men

Objetivo. Comparar la influencia de las velocidades de contracción lenta y rápida en el volumen total de carga levantada en una sesión de entrenamiento de resistencia con ejercicios de pesos libres para miembros superiores, y analizar el tiempo de recuperación de la fuerza máxima del músculo después del ejercicio en la resistencia de hombres entrenados. Métodos. Dieciséis hombres jóvenes que tenían experiencia en el entrenamiento de la resistencia fueron divididos aleatoriamente en dos grupos: la velocidad de contracción rápida (FCV - n = 8) y la velocidad de contracción lenta (SCV - n = 8). Ambos grupos realizaron el ejercicio de press de banca y press banca inclinado (pesos libres) con 4 series de 12 repeticiones máximo; y un intervalo de 50 segundos de descanso entre cada serie y 2 minutos entre los ejercicios. La velocidad de contracción fue de 6 segundos para el grupo SCV y 1,5 segundos para el grupo de FCV. El volumen total de carga fue anotado durante la sesión de ejercicio; y una repetición máxima (1RM) fue evaluada antes (basal) y durante 96 horas después del ejercicio para medir la función neuromuscular. Resultados. Los resultados demostraron que el grupo de FCV proporcionó un mayor (p < 0,05) volumen de carga levantada durante la sesión de ejercicio, y tuvo una disminución significativa (p < 0,05) en el rendimiento neuromuscular después del ejercicio, en comparación con el grupo SCV. Conclusión. Estos datos sugieren que además de la velocidad de contracción, el volumen total de carga elevada determina la disminución de la función neuromuscular después del ejercicio en la resistencia de hombres entrenados(AU)

Objective. To compare the influence of slow and fast contraction velocities in the total volume of load lifted in a resistance training bout with free weights exercises for upper limbs, and analyze the recovery time of the maximum muscle strength post-exercise in resistance-trained men. Methods. Sixteen young men, who were experienced in resistance training were randomly divided into two groups: fast contraction velocity (FCV - n = 8) and slow contraction velocity (SCV - n = 8). Both groups performed bench press and incline bench press exercises (free weights) with 4 sets of 12 repetitions maximum. There was a 50 seconds rest interval between each set, and 2 minutes interval between the exercises. The contraction velocity was 6 seconds for the SCV group and 1.5 seconds for the FCV group. The total volume of load was recorded during the exercise bout, and the one repetition maximum (1RM) was evaluated before (baseline) and for 96 hours after exercise to measure the neuromuscular function. Results. The results demonstrated that the FCV group provide a higher (p < 0.05) volume of load lifted during the exercise bout, and had a significant decline (p < 0.05) in the neuromuscular performance post-exercise, when compared to the SCV group. Conclusion. These data suggest that besides the contraction velocity, the total volume of load lifted determines the decline of neuromuscular function post-exercise in resistance-trained men(AU)

Lymphocyte and cytokines after short periods of exercise.

The purpose of this study was to verify the effects of short periods of exercise of different intensity on lymphocyte function and cytokines. Thirty Wistar rats, 2 months old, were used. They were divided into five groups of six rats: a sedentary control group; a group exercised for 5 minutes at low intensity (5 L); a group exercised for 15 minutes at low intensity (15 L); and groups exercised at moderate intensity (additional load of 5 % of body weight) for 5 minutes (5 M) or for 15 minutes (15 M). The parameters measured were: total leukocytes, neutrophils, lymphocytes, monocytes, lymphocytes from lymph nodes, serum cytokines (IL-2, IL-6 and TNF-alpha), lymphocyte mitochondrial transmembrane potential, viability and DNA fragmentation. ANOVA two way followed by Tukey's post hoc test (p

Cholesterol induces fetal rat enterocyte death in culture.

The effect of cholesterol on fetal rat enterocytes and IEC-6 cells (line originated from normal rat small intestine) was examined. Both cells were cultured in the presence of 20 to 80 microM cholesterol for up to 72 h. Apoptosis was determined by flow cytometric analysis and fluorescence microscopy. The expression of HMG-CoA reductase and peroxisome proliferator-activated receptor gamma (PPARgamma) was measured by RT-PCR. The addition of 20 microM cholesterol reduced enterocyte proliferation as early as 6 h of culture. Reduction of enterocyte proliferation by 28 and 41% was observed after 24 h of culture in the presence and absence of 10% fetal calf serum, respectively, with the effect lasting up to 72 h. Treatment of IEC-6 cells with cholesterol for 24 h raised the proportion of cells with fragmented DNA by 9.7% at 40 microM and by 20.8% at 80 microM. When the culture period was extended to 48 h, the effect of cholesterol was still more pronounced, with the percent of cells with fragmented DNA reaching 53.5% for 40 microM and 84.3% for 80 microM. Chromatin condensation of IEC-6 cells was observed after treatment with cholesterol even at 20 microM. Cholesterol did not affect HMG-CoA reductase expression. A dose-dependent increase in PPARgamma expression in fetal rat enterocytes was observed. The expression of PPAR-gamma was raised by 7- and 40-fold, in the presence and absence of fetal calf serum, respectively, with cholesterol at 80 mM. The apoptotic effect of cholesterol on enterocytes was possibly due to an increase in PPARgamma expression.

Diabetes induces apoptosis in lymphocytes.

The occurrence of DNA fragmentation in lymphocytes obtained from alloxan-induced diabetic rats and diabetic patients was investigated. A high proportion of apoptotic lymphocytes in diabetic states may explain the impaired immune function in poorly controlled diabetic patients. Rat mesenteric lymph node lymphocytes were analysed for DNA fragmentation by using flow cytometry and agarose gel, and for chromatin condensation by Hoescht 33342 staining under different situations. Immediately after being obtained, the proportion of lymphocytes with fragmented DNA was twofold higher in alloxan-induced diabetic rats than in cells from control rats. After 48 h in culture, the occurrence of DNA fragmentation was also higher (81%) in cells from diabetic rats. Hoescht staining and fragmented DNA visualized in agarose gel were also higher in lymphocytes from alloxan-induced diabetic rats than in control cells. To investigate if this phenomenon also occurs in humans, blood lymphocytes from 14 diabetic subjects were examined. Similar results to those of rat lymphocytes were found in cells from diabetic patients immediately after being obtained and after 48 h in culture. The high occurrence of apoptosis in lymphocytes was accompanied by a reduced number of blood-circulating lymphocytes in diabetic patients. The involvement of low insulinaemia for the occurrence of apoptosis in lymphocytes was also examined. Insulin treatment markedly reduced the proportion of lymphocytes with fragmented DNA in alloxan-induced diabetic rats.

Cholesterol induces fetal rat enterocyte death in culture

The effect of cholesterol on fetal rat enterocytes and IEC-6 cells (line originated from normal rat small intestine) was examined. Both cells were cultured in the presence of 20 to 80 æM cholesterol for up to 72 h. Apoptosis was determined by flow cytometric analysis and fluorescence microscopy. The expression of HMG-CoA reductase and peroxisome proliferator-activated receptor gamma (PPARgamma) was measured by RT-PCR. The addition of 20 æM cholesterol reduced enterocyte proliferation as early as 6 h of culture. Reduction of enterocyte proliferation by 28 and 41 percent was observed after 24 h of culture in the presence and absence of 10 percent fetal calf serum, respectively, with the effect lasting up to 72 h. Treatment of IEC-6 cells with cholesterol for 24 h raised the proportion of cells with fragmented DNA by 9.7 percent at 40 æM and by 20.8 percent at 80 æM. When the culture period was extended to 48 h, the effect of cholesterol was still more pronounced, with the percent of cells with fragmented DNA reaching 53.5 percent for 40 æM and 84.3 percent for 80 æM. Chromatin condensation of IEC-6 cells was observed after treatment with cholesterol even at 20 æM. Cholesterol did not affect HMG-CoA reductase expression. A dose-dependent increase in PPARgamma expression in fetal rat enterocytes was observed. The expression of PPAR-gamma was raised by 7- and 40-fold, in the presence and absence of fetal calf serum, respectively, with cholesterol at 80 mM. The apoptotic effect of cholesterol on enterocytes was possibly due to an increase in PPARgamma expression.

Ranking the toxicity of fatty acids on Jurkat and Raji cells by flow cytometric analysis.

The fatty acids have an important role in the control of leukocyte metabolism and function. Higher concentrations of certain fatty acids, particularly polyunsaturated fatty acids (PUFAs) and volatile fatty acids, can cause cell death via apoptosis or, when concentrations are greater, necrosis. In this study, we determined the highest concentrations of various fatty acids that are non-toxic to two human leukemic cell lines, Jurkat (T-lymphocyte) and Raji (B-lymphocyte). Toxicity was evaluated by either loss of membrane integrity and/or DNA fragmentation using flow cytometric analysis. There were no remarkable differences for the toxicity of the fatty acids between B and T cell lines. The cytotoxicity of the fatty acids was related to the carbon chain length and number of double bonds: docosahexaenoic acid=eicosapentaenoic acid=arachidonic acid=gamma-linolenic acid=stearic acid=palmitic acid > linoleic acid=palmitoleic acid > vacenic acid=lauric acid > oleic acid > elaidic acid > capric acid > butyric acid > caprylic acid=caproic acid=propionic acid. The proportion of cells undergoing apoptosis or necrosis, induced by the fatty acids tested, remains to be investigated.

Detection of Ureaplasma diversum in cattle using a newly developed PCR-based detection assay.

Ureaplasma diversum has been associated with different clinical manifestations including bovine vulvitis, endometritis, salpingitis, spontaneous abortion and infertility. Because the isolation of this ureaplasma from clinical samples is difficult, there is a need for improved detection methods. We developed a PCR assay based on amplification of a region of the gene encoding 16S rRNA. The specificity of the amplification was verified by sequence analysis. Female bovine vaginal swabs (n=168) were collected and the presence of U. diversum evaluated by both culture methods and by the PCR assay. Culture was positive for 60 samples (35.7%), and PCR-specific amplification was obtained for 89 samples (52.9%). These results indicated a high prevalence of U. diversum in the selected animals and the higher sensitivity of this PCR assay as compared to culture.