Several investigators have demonstrated that diabetes is associated with autonomic and myocardial dysfunction. Exercise training is an efficient non-pharmacological treatment for cardiac and metabolic diseases. The aim of the present study was to investigate the effects of exercise training on hemodynamic and autonomic diabetic dysfunction. After 1 week of diabetes induction (streptozotocin, 50 mg/kg, iv), male Wistar rats (222 ± 5 g, N = 18) were submitted to exercise training for 10 weeks on a treadmill. Arterial pressure signals were obtained and processed with a data acquisition system. Autonomic function and intrinsic heart rate were studied by injecting methylatropine and propranolol. Left ventricular function was assessed in hearts perfused in vitro by the Langendorff technique. Diabetes (D) bradycardia and hypotension (D: 279 ± 9 bpm and 91 ± 4 mmHg vs 315 ± 11 bpm and 111 ± 4 mmHg in controls, C) were attenuated by training (TD: 305 ± 7 bpm and 100 ± 4 mmHg). Vagal tonus was decreased in the diabetic groups and sympathetic tonus was similar in all animals. Intrinsic heart rate was lower in D (284 ± 11 bpm) compared to C and TD (390 ± 8 and 342 ± 14 bpm, respectively). Peak systolic pressure developed at different pressures was similar for all groups, but +dP/dt max was decreased and -dP/dt max was increased in D. In conclusion, exercise training reversed hypotension and bradycardia and improved myocardial function in diabetic rats. These changes represent an adaptive response to the demands of training, supporting a positive role of physical activity in the management of diabetes.

The objective of the present study was to evaluate and compare the neuromuscular, morphological and functional adaptations of older women subjected to 3 different types of strength training. 58, healthy women (67?5 year) were randomized to experimental (EG, n=41) and control groups (CG, n=17) during the first 6 weeks when the EG group performed traditional resistance exercise for the lower extremity. Afterwards, EG was divided into three specific strength training groups; a traditional group (TG, n=14), a power group (PG, n=13) that performed the concentric phase of contraction at high speed and a rapid strength group (RG, n=14) that performed a lateral box jump exercise emphasizing the stretch-shortening-cycle (SSC). Subjects trained 2 days per week through the entire 12 weeks. Following 6 weeks of generalized strength training, significant improvements occurred in EG for knee extension one-repetition (1RM) maximum strength (+19%), knee extensor muscle thickness (MT, +15%), maximal muscle activation (+44% average) and onset latency (???31% average) for vastus lateralis (VL), vastus medialis (VM) and rectus femoris (RF) compared to CG (p<0.05). Following 6 more weeks of specific strength training, the 1RM increased significantly and similarly between groups (average of +21%), as did muscle thickness of the VL (+25%), and activation of VL (+44%) and VM (+26%). The onset latency of RF (TG=285?109?ms, PG=252?76?ms, RG=203?43?ms), reaction time (TG=366?99?ms, PG=274?76?ms, RG=201?41?ms), 30-s chair stand (TG=18?3, PG=18?1, RG=21?2) and counter movement jump (TG=8?2?cm, PG=10?3?cm, RG=13?2?cm) was significantly improved only in RG (p<0.05). At the end of training, the rate of force development (RFD) over 150?ms (TG=2.3?9.8?N?s???1, PG=3.3?3.2?N?s???1, RG=3.8?6.8?N?s???1, CG=2.3?7.0?N?s???1) was significantly greater in RG and PG than in TG and CG (p<0.05). In conclusion, rapid strength training is more effective for the development of rapid force production of muscle than other specific types of strength training and by consequence, better develops the functional capabilities of older women.

O interesse acerca dos mecanismos de geração e adaptação de radicais livres de oxigênio (RLO) ao exercício aumentou significativamente a partir da demonstração de sua relação com o consumo de oxigênio. Os RLO são formados pela redução incompleta do oxigênio, gerando espécies que apresentam alta reatividade para outras biomoléculas, principalmente lipídios e proteínas das membranas celulares e, até mesmo, o DNA. As injúrias provocadas por estresse oxidativo apresentam efeitos cumulativos e estão relacionadas a uma série de doenças, como o câncer, a aterosclerose e o diabetes. O exercício físico agudo, em função do incremento do consumo de oxigênio, promove o aumento da formação de RLO. No entanto, o treinamento físico é capaz de gerar adaptações capazes de mitigar os efeitos deletérios provocados pelos RLO. Estas adaptações estão relacionadas a uma série de sistemas, dos quais os mais importantes são os sistemas enzimáticos, compostos pela superóxido dismutase, catalase e glutationa peroxidase, e o não enzimático, composto por ceruloplasmina, hormônios sexuais, coenzima Q, ácido úrico, proteínas de choque térmico e outros. Tais adaptações, apesar das controvérsias sobre os mecanismos envolvidos, promovem maior resistência tecidual a desafios oxidativos, como aqueles proporcionados pelo exercício de alta intensidade e longa duração. As técnicas de avaliação de estresse oxidativo, na maioria das vezes, não são capazes de detectar injúria em exercícios de curta duração. Dessa forma, esforços estão sendo feitos para o estudo de esforços físicos realizados por longos períodos de tempo ou efetuados até a exaustão. Novos marcadores de lesão por ação dos RLO estão sendo descobertos e novas técnicas para sua determinação estão sendo criadas. O objetivo deste trabalho é discutir os mecanismos da formação dos RLO e das adaptações ao estresse oxidativo crônico provocado pelo treinamento físico.

In this study, we investigated the effect of biological maturation on maximal oxygen uptake ([Vdot]O(2max)) and ventilatory thresholds (VT(1) and VT(2)) in 110 young soccer players separated into pubescent and post-pubescent groups.. Maximal oxygen uptake and [Vdot]O(2) corresponding to VT(1) and VT(2) were expressed as absolute values, ratio standards, theoretical exponents, and experimentally observed exponents. Absolute [Vdot]O(2) (ml · min(-1)) was different between groups for VT(1), VT(2), and [Vdot]O(2max). Ratio standards (ml · kg(-1) · min(-1)) were not significantly different between groups for VT(1), VT(2), and [Vdot]O(2max). Theoretical exponents (ml · kg(-0.67) · min(-1) and ml · kg(-0.75) · min(-1)) were not properly adjusted for the body mass effects on VT(1), VT(2), and [Vdot]O(2max). When the data were correctly adjusted using experimentally observed exponents, VT(1) (ml · kg(-0.94) · min(-1)) and VT(2) (ml · kg(-0.95) · min(-1)) were not different between groups. The experimentally observed exponent for [Vdot]O(2max) (ml · kg(-0.90) · min(-1)) was different between groups (P = 0.048); however, this difference could not be attributed to biological maturation. In conclusion, biological maturation had no effect on VT(1), VT(2) or [Vdot]O(2max) when the effect of body mass was adjusted by experimentally observed exponents. Thus, when evaluating the physiological performance of young soccer players, allometric scaling needs to be taken into account instead of using theoretical approaches.

PurposeTo explore whether compensatory responses to acute energy deficits induced by exercise or diet differ by sex.MethodsIn experiment one, 12 healthy women completed three 9-h trials (control, exercise-induced (Ex-Def) and food restriction–induced energy deficit (Food-Def)) with identical energy deficits being imposed in the Ex-Def (90-min run, ∼70% of V˙O2max) and Food-Def trials. In experiment two, 10 men and 10 women completed two 7-h trials (control and exercise). Sixty minutes of running (∼70% of V˙O2max) was performed at the beginning of the exercise trial. The participants rested throughout the remainder of the exercise trial and during the control trial. Appetite ratings, plasma concentrations of gut hormones, and ad libitum energy intake were assessed during main trials.ResultsIn experiment one, an energy deficit of approximately 3500 kJ induced via food restriction increased appetite and food intake. These changes corresponded with heightened concentrations of plasma acylated ghrelin and lower peptide YY3–36. None of these compensatory responses were apparent when an equivalent energy deficit was induced by exercise. In experiment two, appetite ratings and plasma acylated ghrelin concentrations were lower in exercise than in control, but energy intake did not differ between trials. The appetite, acylated ghrelin, and energy intake response to exercise did not differ between men and women.ConclusionsWomen exhibit compensatory appetite, gut hormone, and food intake responses to acute energy restriction but not in response to an acute bout of exercise. Additionally, men and women seem to exhibit similar acylated ghrelin and PYY3–36 responses to exercise-induced energy deficits. These findings advance understanding regarding the interaction between exercise and energy homeostasis in women.

Strength training seems to be an interesting approach to counteract decreases that affect knee extensor strength, muscle mass and muscle quality (force per unit of muscle mass) associated with ageing. However, there is no consensus regarding the changes in muscle mass and their contribution to strength during periods of training and detraining in the elderly. Therefore, this study aimed at verifying the behaviour of knee extensor muscle strength, muscle volume and muscle quality in elderly women in response to a 12-week strength training programme followed by a similar period of detraining. Statistical analysis showed no effect of time on muscle quality. However, strength and muscle volume increased from baseline to post-training (33 and 26 %, respectively). After detraining, the knee extensor strength remained 12 % superior to the baseline values, while the gains in muscle mass were almost completely lost. In conclusion, strength gains and losses due to strength training and detraining, respectively, could not be exclusively associated with muscle mass increases. Training-induced strength gains were partially maintained after 3 months of detraining in elderly subjects.

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This study aimed to compare the effect of high-intensity interval training (HIIT) with moderate-intensity continuous training (MCT) on endothelial function, oxidative stress and clinical fitness in patients with type 1 diabetes. Thirty-six type 1 diabetic patients (mean age 23.5 ± 6 years) were randomized into 3 groups: HIIT, MCT, and a non-exercising group (CON). Exercise was performed in a stationary cycle ergometers during 40 min, 3 times/week, for 8 weeks at 50–85% maximal heart rate (HR max ) in HIIT and 50% HR max in MCT. Endothelial function was measured by flow-mediated dilation (FMD) [endothelium-dependent vasodilation (EDVD)], and smooth-muscle function by nitroglycerin-mediated dilation [endothelium-independent vasodilation (EIVD)]. Peak oxygen consumption (VO 2peak ) and oxidative stress markers were determined before and after training. Endothelial dysfunction was defined as an increase < 8% in vascular diameter after cuff release. The trial is registered at ClinicalTrials.gov , identifier: NCT03451201. Twenty-seven patients completed the 8-week protocol, 9 in each group (3 random dropouts per group). Mean baseline EDVD was similar in all groups. After training, mean absolute EDVD response improved from baseline in HIIT: + 5.5 ± 5.4%, ( P = 0.0059), but remained unchanged in MCT: 0.2 ± 4.1% ( P = 0.8593) and in CON: −2.6 ± 6.4% ( P = 0.2635). EDVD increase was greater in HIIT vs. MCT ( P = 0.0074) and CON ( P = 0.0042) (ANOVA with Bonferroni). Baseline VO 2peak was similar in all groups ( P = 0.96). VO 2peak increased 17.6% from baseline after HIIT ( P = 0.0001), but only 3% after MCT ( P = 0.055); no change was detected in CON ( P = 0.63). EIVD was unchanged in all groups ( P = 0.18). Glycemic control was similar in all groups. In patients with type 1 diabetes without microvascular complications, 8-week HIIT produced greater improvement in endothelial function and physical fitness than MCT at a similar glycemic control.