Six weeks of aerobic training improves VO2max and MLSS but does not improve the time to fatigue at the MLSS

The purpose of this study was to investigate the effects of a 6-week aerobic training period on the time to fatigue (t _lim) during exercise performed at the maximal lactate steady state (MLSS). Thirteen untrained male subjects (TG; age 22.5 ± 2.4 years, body mass 72.9 ± 6.7 kg and VO_2max 44.9 ± 4.8 mL kg^?1 min^?1) performed a cycle ergometer test until fatigue at the MLSS power output before and after 6 weeks of aerobic training. A group of eight control subjects (CG; age 25.1 ± 2.4 years, body mass 70.1 ± 9.8 kg and VO_2max 45.2 ± 4.1 mL kg^?1 min^?1) also performed the two tests but did not train during the 6-week period. There were no differences between the groups with respect to the VO_2max or MLSS power output (MLSSw) before the treatment period. The VO_2max and the MLSSw of the TG increased by 11.2 ± 7.2 % (pre-treatment = 44.9 ± 4.8 vs. post-treatment = 49.8 ± 4.5 mL kg^?1 min^?1) and 14.7 ± 8.9 % (pre-treatment = 150 ± 27 vs. post-treatment = 171 ± 26 W), respectively, after 6 weeks of training. The results of the CG were unchanged. There were no differences in t _lim between the groups or within groups before and after training. Six weeks of aerobic training increases MLSSw and VO_2max, but it does not alter the t _lim at the MLSS.     

Selective,stepwise, or nonselective removal of carious tissue: which technique offers lower risk for the treatment of dental caries in permanent teeth? A systematic review and meta-analysis

This study aimed to systematically review the literature regarding the risk of selective removal—in comparison with stepwise and nonselective removal     

Amlodipine reduces blood pressure during dynamic resistance exercise in hypertensive patients

This study investigated the effect of the dihydropyridine calcium channel antagonist, amlodipine, on blood pressure (BP) during resistance exercise performed at different intensities in hypertensives. Eleven hypertensives underwent 4 weeks of placebo and amlodipine (random double‐blinded crossover design). In each phase, they performed knee extension exercise until exhaustion following three protocols: one set at 100% of 1 RM (repetition maximum), three sets at 80% of 1 RM, and three sets at 40% of 1 RM. Intraarterial BP was measured before and during exercise. Amlodipine reduced maximal systolic/diastolic BP values achieved at all intensities (100% = 225 ± 6/141 ± 3 vs. 207 ± 6/130 ± 6 mmHg; 80% = 289 ± 8/178 ± 5 vs. 273 ± 10/169 ± 6 mmHg; 40% = 289 ± 10/176 ± 8 vs. 271 ± 11/154 ± 6 mmHg). Amlodipine blunted the increase in diastolic BP that occurred during the second and third sets of exercise at 40% of 1RM (+75 ± 6 vs. +61 ± 5 mmHg and +78 ± 7 vs. +64 ± 5 mmHg, respectively). Amlodipine was effective in reducing the absolute values of systolic and diastolic BP during resistance exercise and in preventing the progressive increase in diastolic BP that occurs over sets of low‐intensity exercise. These results suggest that systemic vascular resistance is involved in BP increase during resistance exercise, and imply that hypertensives receiving amlodipine are at lower risk of increased BP during resistance exercise than non‐medicated patients.     

Stratification of complexity in congenital heart surgery: comparative study of the Risk Adjustment for Congenital Heart Surgery (RACHS-1) method, Aristotle basic score and Society of Thoracic Surgeons-European Association for Cardio- Thoracic Surgery (STS-EACTS) mortality score

Objective

To determine whether stratification of complexity models in congenital heart surgery (RACHS-1, Aristotle basic score and STS-EACTS mortality score) fit to our center and determine the best method of discriminating hospital mortality.

Methods

Surgical procedures in congenital heart diseases in patients under 18 years of age were allocated to the categories proposed by the stratification of complexity methods currently available. The outcome hospital mortality was calculated for each category from the three models. Statistical analysis was performed to verify whether the categories presented different mortalities. The discriminatory ability of the models was determined by calculating the area under the ROC curve and a comparison between the curves of the three models was performed.

Results

360 patients were allocated according to the three methods. There was a statistically significant difference between the mortality categories: RACHS-1 (1) - 1.3%, (2) - 11.4%, (3)-27.3%, (4) - 50 %, (P<0.001); Aristotle basic score (1) - 1.1%, (2) - 12.2%, (3) - 34%, (4) - 64.7%, (P<0.001); and STS-EACTS mortality score (1) - 5.5 %, (2) - 13.6%, (3) - 18.7%, (4) - 35.8%, (P<0.001). The three models had similar accuracy by calculating the area under the ROC curve: RACHS-1- 0.738; STS-EACTS-0.739; Aristotle- 0.766.

Conclusion

The three models of stratification of complexity currently available in the literature are useful with different mortalities between the proposed categories with similar discriminatory capacity for hospital mortality.     

Exenatide and Sitagliptin Decrease Interleukin 1β, Matrix Metalloproteinase 9, and Nitric Oxide Synthase 2 Gene Expression But Does Not Reduce Alveolar Bone Loss in Rats With Periodontitis

Background: New drugs for the treatment of diabetes, glucagon‐like peptide‐1 (GLP‐1) receptor agonists and inhibitors of dipeptidyl peptidase‐4 (DPP‐4) have shown pleiotropic effects on bone metabolism and anti‐inflammatory properties. The aim of this study is to evaluate the effects of exenatide (GLP‐1 agonist) and sitagliptin (DPP‐4 inhibitor) during periodontitis induction by ligature insertion in rats. Methods: Forty rats were divided into four groups: 1) animals with induced periodontitis that received exenatide (EG); 2) animals with induced periodontitis that received sitagliptin (SG); 3) animals with induced periodontitis and without drug treatment (LG); and 4) animals without induced periodontitis and without drug treatment (controls). The drugs were administered for 28 days. On the day the animals were sacrificed, blood was collected for analysis of glucose and DPP‐4 levels. The gene expressions of prostaglandin‐endoperoxide synthase 2, tissue inhibitor of metalloproteinase 1, Dpp4, nitric oxide synthase 2 (Nos2), interleukin 1β (Il1b), and matrix metalloproteinase 9 (Mmp9) in the gingiva; support and alveolar bone loss; connective tissue attachment; and the quantity of gingival collagen were evaluated. Results: Exenatide and sitagliptin treatments have led to a lower percentage of weight gain but did not influence glycemia. Sitagliptin reduced the serum concentration of DPP‐4. Interestingly, although the gene expression profile has revealed a downregulation of Mmp9, Nos2, and Il1b in both EG and SG compared to LG, a significant protective effect was not observed on alveolar bone and collagen tissue in this model. Conclusion: Regardless of the reduction of the expression of Il1b, Nos2, and Mmp9, the drugs were not effective in the stabilization or reduction of alveolar bone loss and collagen degradation in rats.     

Hydrolysis of Clavulanate by Mycobacterium tuberculosis β-Lactamase BlaC Harboring a Canonical SDN Motif

Combinations of β-lactams with clavulanate are currently being investigated for tuberculosis treatment. Since Mycobacterium tuberculosis produces a broad spectrum β-lactamase, BlaC, the success of this approach could be compromised by the emergence of clavulanate-resistant variants, as observed for inhibitor-resistant TEM variants in enterobacteria. Previous analyses based on site-directed mutagenesis of BlaC have led to the conclusion that this risk was limited. Here, we used a different approach based on determination of the crystal structure of β-lactamase Bla_MAb of Mycobacterium abscessus, which efficiently hydrolyzes clavulanate. Comparison of Bla_MAb and BlaC allowed for structure-assisted site-directed mutagenesis of BlaC and identification of the G¹³²N substitution that was sufficient to switch the interaction of BlaC with clavulanate from irreversible inactivation to efficient hydrolysis. The substitution, which restored the canonical SDN motif (SDG→SDN), allowed for efficient hydrolysis of clavulanate, with a more than 10⁴-fold increase in k_cat (0.41 s⁻¹), without affecting the hydrolysis of other β-lactams. Mass spectrometry revealed that acylation of BlaC and of its G¹³²N variant by clavulanate follows similar paths, involving sequential formation of two acylenzymes. Decarboxylation of the first acylenzyme results in a stable secondary acylenzyme in BlaC, whereas hydrolysis occurs in the G¹³²N variant. The SDN/SDG polymorphism defines two mycobacterial lineages comprising rapidly and slowly growing species, respectively. Together, these results suggest that the efficacy of β-lactam–clavulanate combinations may be limited by the emergence of resistance. β-Lactams active without clavulanate, such as faropenem, should be prioritized for the development of new therapies.     

Unilateral Plantar Flexors Static-Stretching Effects on Ipsilateral and Contralateral Jump Measures

The aim of this study was to evaluate the acute effects of unilateral ankle plantar flexors static-stretching (SS) on the passive range of movement (ROM) of the stretched limb, surface electromyography (sEMG) and single-leg bounce drop jump (SBDJ) performance measures of the ipsilateral stretched and contralateral non-stretched lower limbs. Seventeen young men (24 ± 5 years) performed SBDJ before and after (stretched limb: immediately post-stretch, 10 and 20 minutes and non-stretched limb: immediately post-stretch) unilateral ankle plantar flexor SS (6 sets of 45s/15s, 70-90% point of discomfort). SBDJ performance measures included jump height, impulse, time to reach peak force, contact time as well as the sEMG integral (IEMG) and pre-activation (IEMG_{pre-activation}) of the gastrocnemius lateralis. Ankle dorsiflexion passive ROM increased in the stretched limb after the SS (pre-test: 21 ± 4° and post-test: 26.5 ± 5°, p < 0.001). Post-stretching decreases were observed with peak force (p = 0.029), IEMG (P<0.001), and IEMG_{pre-activation} (p = 0.015) in the stretched limb; as well as impulse (p = 0.03), and jump height (p = 0.032) in the non-stretched limb. In conclusion, SS effectively increased passive ankle ROM of the stretched limb, and transiently (less than 10 minutes) decreased muscle peak force and pre-activation. The decrease of jump height and impulse for the non-stretched limb suggests a SS-induced central nervous system inhibitory effect.

Key points

• When considering whether or not to SS prior to athletic activities, one must consider the potential positive effects of increased ankle dorsiflexion motion with the potential deleterious effects of power and muscle activity during a simple jumping task or as part of the rehabilitation process.
• Since decreased jump performance measures can persist for 10 minutes in the stretched leg, the timing of SS prior to performance must be taken into consideration.
• Athletes, fitness enthusiasts and therapists should also keep in mind that SS one limb has generalized effects upon contralateral limbs as well.

Key words: Athletic training, exercise performance, exercise training, crossover, cross-education