Untrained Research Articles

Influence of Exercise Modality on the Cerebrovascular Response to Physiological Stressors

BackgroundHabitual exercise has previously been shown to alter the cerebrovascular response to hypercapnia. Similar to hypercapnia, increases in the brain’s metabolic activity result in local augmentation of cerebral blood flow; however, the mechanisms governing the cerebrovascular response to these two stimuli likely differ. Although, previous studies have examined the influence of aerobic exercise on the cerebrovascular response to hypercapnia, little is known about the influence of habitual resistance training on cerebrovascular function. Therefore, the purpose of this study was to evaluate the cerebrovascular response to both hypercapnia and a metabolic stimulus (cognitive challenge) in resistance trained (RT), aerobic trained (AT), and untrained (UT) adults.MethodsWe recruited 13 RT (women: n = 2, age: 24 ± 4 y), 12 AT (women: n = 2, age: 28 ± 6 y), and 13 UT (women: n = 2, age: 27 ± 5 y) healthy young adults. Middle cerebral artery velocity (MCAv), beat‐to‐beat mean arterial blood pressure (MAP) and end‐tidal carbon dioxide (ETCO2) were continuously monitored during hypercapnia and a Stroop Color and Word Test. Cerebrovascular conductance index (CVCi) was calculated as MCAv/MAP. Reactivity to hypercapnia was calculated as the slope of the relationship between each variable of interest (MCAv or CVCi) and ETCO2. Responses to the Stroop test were calculated as the absolute change from baseline to the 3‐beat peak of each variable during the test.ResultsThere were no significant differences in MCAv reactivity and CVCi reactivity to hypercapnia between groups. Despite all groups having a similar change in MAP and ETCO2 during the Stroop test, RT individuals had a greater increase in MCAv (RT: 18.1 ± 1.9 cm/s, AT: 9.7 ± 1.5 cm/s, UT: 15.7 ± 2.0 cm/s; AT vs. RT p < 0.01; AT vs. UT p = 0.07) and CVCi (RT: 0.15 ± 0.02 cm/s/mmHg, AT: 0.08 ± 0.02 cm/s/mmHg, UT: 0.12 ± 0.02 cm/s/mmHg; AT vs. RT p = 0.05; AT vs. UT p = 0.28) compared with AT individuals during the Stroop test. While there was a positive association between the MCAv response to hypercapnia and the MCAv response to the Stroop test in AT individuals (r = 0.67, p < 0.05), and a trend for association in UT individuals (r = 0.49, p = 0.09), there was no relationship between the two variables in RT individuals (r = 0.18, p = 0.56).ConclusionWhile exercise modality did not influence the cerebrovascular response to hypercapnia, it did influence the response to a metabolic stimulus, such that RT individuals had a greater MCAv and CVCi response to a cognitive challenge, compared with AT individuals. Further, exercise modality may influence the mechanisms by which the cerebrovasculature of young adults responds to physiological stimuli.Support or Funding InformationSupported by National Institute of Health grant HL118154

What makes long-term resistance-trained individuals so strong? A comparison of skeletal muscle morphology, architecture, and joint mechanics.

The greater muscular strength of long-term resistance-trained (LTT) individuals is often attributed to hypertrophy, but the role of other factors, notably maximum voluntary specific tension (ST), muscle architecture, and any differences in joint mechanics (moment arm), have not been documented. The aim of the present study was to examine the musculoskeletal factors that might explain the greater quadriceps strength and size of LTT vs. untrained (UT) individuals. LTT (n = 16, age 21.6 ± 2.0 yr) had 4.0 ± 0.8 yr of systematic knee extensor heavy-resistance training experience, whereas UT (n = 52; age 25.1 ± 2.3 yr) had no lower-body resistance training experience for >18 mo. Knee extension dynamometry, T1-weighted magnetic resonance images of the thigh and knee, and ultrasonography of the quadriceps muscle group at 10 locations were used to determine quadriceps: isometric maximal voluntary torque (MVT), muscle volume (QVOL), patella tendon moment arm (PTMA), pennation angle (QΘP) and fascicle length (QFL), physiological cross-sectional area (QPCSA), and ST. LTT had substantially greater MVT (+60% vs. UT, P < 0.001) and QVOL (+56%, P < 0.001) and QPCSA (+41%, P < 0.001) but smaller differences in ST (+9%, P < 0.05) and moment arm (+4%, P < 0.05), and thus muscle size was the primary explanation for the greater strength of LTT. The greater muscle size (volume) of LTT was primarily attributable to the greater QPCSA (+41%; indicating more sarcomeres in parallel) rather than the more modest difference in FL (+11%; indicating more sarcomeres in series). There was no evidence in the present study for regional hypertrophy after LTT.NEW & NOTEWORTHY Here we demonstrate that the larger muscle strength (+60%) of a long-term (4+ yr) resistance-trained group compared with untrained controls was due to their similarly larger muscle volume (+56%), primarily due to a larger physiological cross-sectional area and modest differences in fascicle length, as well as modest differences in maximum voluntary specific tension and patella tendon moment arm. In addition, the present study refutes the possibility of regional hypertrophy, despite large differences in muscle volume.

The origins and early developments of the UN Training Program for Interpreters and Translators in Beijing

Abstract This paper fills the missing the link in the research on the history of interpreter and translator training in the P. R. China. After the restoration of China’s seat in the United Nations on October 25, 1971, the UN Secretariat suggested, as early as in 1972, to the P. R. C. Permanent Mission in New York, that a training course be established to train interpreters and translators. But it was not until 1979 that the UN Training Program for Interpreters and Translators (译训班) was established at Beijing Foreign Studies University. What happened during the period of 1972–1978 and how the first cohort of students were recruited and trained remain, to a large extent, unexplored areas. By combining newly-discovered historical materials and interviews with former staff members and students of the program, this paper presents details about the preparatory work carried out in mid-1970s that laid the foundations for the establishment of the program, the month-long negotiations between Chinese and the UN representatives in 1978 that led to the founding of the program, as well as the recruitment and training of the first cohort of students.

Aerobic training and vascular protection: Insight from altered blood flow patterns.

What is the central question of this study? This study sought to determine whether prior upper limb aerobic training can attenuate the vascular dysfunction resulting from negative alteration of blood flow patterns. What is the main finding and its importance? We demonstrated that the microvasculature of young men with prior upper limb aerobic training (rowing) was equally susceptible to negatively altered blood flow patterns when compared with untrained control subjects. This finding reveals that aerobic training does not provide adequate protection against this type of vascular insult, highlighting the importance of reducing known vascular insults regardless of training status. Acute alteration of blood flow patterns can substantially reduce blood vessel function and, if consistently repeated, may chronically reduce vascular health. Aerobic exercise training is associated with improved vascular health, but it is not well understood whether aerobic training-induced vascular adaptations provide protection against acute vascular insults. This study sought to determine whether prior upper limb aerobic training can attenuate the vascular dysfunction resulting from an acute vascular insult (increased retrograde/oscillatory shear). Ten young arm-trained (AT) men (rowers; 22±1 years of age) and 10 untrained (UT) male control subjects (21±3 years of age) were recruited for this study. Subjects completed two brachial artery (BA) flow-mediated dilatation (FMD) tests separated by an acute bout of subdiastolic cuff inflation (SDCI) of the distal forearm. Brachial artery dilatation (normalized for the shear stimulus) and reactive hyperaemia evaluated during the BA FMD test were used to determine conduit artery and microvascular function, respectively. Data were presented as mean values±SD. The AT group reported significantly greater whole body (peak oxygen uptake; P=0.01) and forearm aerobic capacity (P<0.001). The SDCI intervention significantly increased retrograde (P<0.001) and oscillatory shear (P<0.001) in both groups. After the SDCI, microvascular function (post-cuff release hyperaemia), but not conduit artery function (shear-induced BA dilatation), was significantly reduced from pre-SDCI values (P=0.001) independent of group. This study revealed that young men with prior upper limb aerobic training, when compared with untrained control subjects, were equally susceptible to the microvascular dysfunction associated with an acute increase in retrograde/oscillatory shear.

Exercise Mediated Nrf2 Signaling Protects the Myocardium From Isoproterenol-Induced Pathological Remodeling.

Although exercise derived activation of Nrf2 signaling augments myocardial antioxidant signaling, the molecular mechanisms underlying the benefits of moderate exercise training (MET) in the heart remain elusive. Here we hypothesized that exercise training stabilizes Nrf2-dependent antioxidant signaling, which then protects the myocardium from isoproterenol-induced damage. The present study assessed the effects of 6 weeks of MET on the Nrf2/antioxidant function, glutathione redox state, and injury in the myocardium of C57/BL6J mice that received isoproterenol (ISO; 50 mg/kg/day for 7 days). ISO administration significantly reduced the Nrf2 promoter activity (p < 0.05) and downregulated the expression of cardiac antioxidant genes (Gclc, Nqo1, Cat, Gsr, and Gst-μ) in the untrained (UNT) mice. Furthermore, increased oxidative stress with severe myocardial injury was evident in UNT+ISO when compared to UNT mice receiving PBS under basal condition. Of note, MET stabilized the Nrf2-promoter activity and upheld the expression of Nrf2-dependent antioxidant genes in animals receiving ISO, and attenuated the oxidative stress-induced myocardial damage. Echocardiography analysis revealed impaired diastolic ventricular function in UNT+ISO mice, but this was partially normalized in the MET animals. Interestingly, while there was a marginal reduction in ubiquitinated proteins in MET mice that received ISO, the pathological signs were attenuated along with near normal cardiac function in response to exercise training. Thus, moderate intensity exercise training conferred protection against ISO-induced myocardial injury by augmentation of Nrf2-antioxidant signaling and attenuation of isoproterenol-induced oxidative stress.

Psychophysiological and performance-related responses of a potentiation activity in swimmers of different competitive levels

Athletes' competitive level has an effect on several psychophysiological parameters during the execution of sports-related tasks. This study analyzed the acute effect of a potentiation activity (PAP), composed by 5 loaded box jumps, on specific psychological, physiological and performance-related parameters in 22 trained (COM) and untrained (UNT) adult male swimmers. A control condition was also evaluated. Measurements included the Competitive State Anxiety Inventory, rate of perceived exertion, lower limbs muscle oxygenation, exercise heart rate, vertical jumping ability, 3 different split times and total time-trial performance during an all-out 50-m swim test executed using the breaststroke technique. In addition, total swim strokes and the optimal individual response after the potentiation activity were measured. No significant differences among the two testing conditions were found for all psychological, physiological and performance-related parameters (p > .05) with the exception of total performance time in the UNT group after the PAP condition (41.5 ± 5.3 vs. 41.9 ± 5.5 s; p = .023; ES = 0.6). As expected, the COM group showed enhanced swimming performance during all split times and total time, compared to the UNT group. These results suggest that (i) independently of the training level, psychological responses during sports-related tasks are probably not evident under non-competitive situations and, (ii) competitive level athletes may need more challenging activation stimulus, compared to their less competitive counterparts, to induce the desirable adaptations on the subsequent main activity.

Effects of one-legged high-intensity interval training on insulin-mediated skeletal muscle glucose homeostasis in patients with type 2 diabetes.

To examine the effect of high-intensity interval training (HIIT) on glucose clearance rates in skeletal muscle and explore the mechanism within the muscle. Ten males with type 2 diabetes mellitus (T2DM) and ten matched healthy subjects performed 2weeks of one-legged HIIT (total of eight sessions, each comprised of 10×1minute ergometer bicycle exercise at >80% of maximal heart rate, interspersed with one min of rest). Insulin sensitivity was assessed by an isoglycaemic, hyperinsulinaemic clamp combined with arteriovenous leg balance technique of the trained (T) and the untrained (UT) leg and muscle biopsies of both legs. Insulin-stimulated glucose clearance in T legs was ~30% higher compared with UT legs in both groups due to increased blood flow in T vs UT legs and maintained glucose extraction. With each training session, muscle glycogen content decreased only in the training leg, and after the training, glycogen synthase and citrate synthase activities were higher in T vs UT legs. No major changes occurred in the expression of proteins in the insulin signalling cascade. Mitochondrial respiratory capacity was similar in T2DM and healthy subjects, and unchanged by HIIT. HIIT improves skeletal muscle insulin sensitivity. With HIIT, the skeletal muscle of patients with T2DM becomes just as insulin sensitive as untrained muscle in healthy subjects. The mechanism includes oscillations in muscle glycogen stores and a maintained ability to extract glucose from the blood in the face of increased blood flow in the trained leg.

Effects of different frequencies of physical training on electron transport chain and oxidative damage in healthy mice

Abstract Aims: The present study investigated the effect of different frequencies (three and five times a week) on electron transport chain and oxidative stress after 8 weeks of run training. Methods: Eighteen male mice (CF1, 30-35g) were distributed into the following groups (n=6): untrained (UT); trained three-time per week (T3) and trained five- time per week (T5). All training sessions were at the same intensity and duration (45min/day) in a treadmill for small animals. Forty-eight hours after the last training session, the animals were killed by decapitation and quadriceps (red portion) was removed and stored at -70oC. Succinate dehydrogenase (SDH), complexes I, II, II-III, IV and hydroperoxides were measured. Results: Training sessions for five times per week were more effective in increasing the mitochondrial respiratory chain enzyme activities (SDH, complexes I, II, II-III, IV) as well as in decreasing the formation hydroperoxides than sessions performed for three times training per week (p<0.05). Conclusion: Our findings clearly showed that a higher the frequency of training session promotes a greater activity of the electron transport chain and consequently reduces the oxidative stress in healthy animals.

Resistance Exercise on Pulse Wave Reflection and Arterial Stiffness Between Trained and Untrained Individuals

Pulse wave reflection [augmentation index (AIx), augmentation pressure (AP)], and arterial stiffness [pulse wave velocity (PWV)] are indicative of cardiovascular health. Acute resistance exercise (RE) alters pulse wave reflection, and arterial stiffness, but responses in resistance-trained individuals is unclear. PURPOSE: To examine the responses in pulse wave reflection and arterial stiffness after RE in resistance-trained (RT) versus untrained (UT) individuals. METHODS: Twenty-one (RT: n=14; UT: n=7) individuals volunteered. Pulse wave reflection and arterial stiffness were collected at rest, and 10min following a control, or RE consisting of 3 sets of 10 repetitions at 75% 1-repetition maximum (1RM) on the leg press, lat pulldown, leg extension, chest press and leg curl. A 2x2x2 ANOVA was used to examine group (RT, UT) differences across conditions (RE, control) and time (Rest, Recovery). RESULTS: The groups were similar (p>0.05) for age, height, and BMI, but not weight (p<0.05). The 1RMs for all exercises, except leg extension (p=0.26), were different between groups. At rest, the groups were statistically different for the tension-time index [TTI (RT: 1999±282ms; UT: 2192±209ms, p=0.04)], diastolic pressure-time index [DPTI (RT: 2817±316ms; UT: 3047±171ms, p=0.003)], and PWV (RT: 5.5±0.7m/s; UT: 6.3±0.4m/s, p=0.0001). There were significant time by condition interactions for aortic pulse pressure (Rest: 34±6mmHg; Recovery: 37±8mmHg, p=0.01), AP (Rest: 5±3mmHg; Recovery: 6±5mmHg, p=0.003), AIx normalized at 75bpm (Rest: 8.7±12.6%; Recovery: 16.4±6.0%, p=0.004), and TTI (Rest: 2084.6±273.4ms; Recovery: 2760.9±463.3ms, p=0.0001) such that they increased during recovery, compared to rest after RE, and the control. There were condition by time interactions for DPTI (Rest: 2889.6±297.0ms; Recovery: 2394.9±458.3ms, p=0.005) and subendocardial viability ratio SEVR (Rest: 138.4±19.3%; Recovery: 86.6±33.0%, p=0.006) such that they increased after acute resistance exercise, compared to rest and the control. There were no significant changes in arterial stiffness. CONCLUSION: These data suggest that resistance-trained individuals have reduced workload of the heart and lower arterial stiffness at rest, but are similar to untrained individuals after acute resistance exercise.

Acute Resistance Exercise Effects on Blood Flow in Resistance-Trained Versus Untrained Individuals

Data suggests that an acute bout of resistance exercise (ARE) increases forearm blood flow (FBF) and vasodilatory capacity compared to rest. However, the effects of training status on FBF and vasodilatory capacity at rest and during recovery from ARE are uncertain. PURPOSE: To compare the effects of resistance exercise training status on measures of vascular function at rest and recovery from ARE. METHODS: Fifteen resistance-trained (RT) individuals, and seven untrained (UT) individuals volunteered to participate. Measurements were taken after a 10min supine rest and 20min after ARE, or a control. Venous occlusion plethysmography was used to measure FBF and vasodilatory capacity, with 5min of occlusion (220mmHg) to induce reactive hyperemia. Area under the curve (AUC) was utilized to determine differences in blood flow. The ARE consisted of 3 sets of 10 repetitions at 75% 1-repetition maximum (1RM) on the leg press, leg curl, leg extension, lat pulldown, and chest press, with 2min of rest between sets and exercises. A 2x2x2 repeated measures ANOVA was used to evaluate group (RT, UT) across condition (ARE, control) and time (rest, recovery). If the ANOVA was significant, t-tests were used for post-hoc comparisons. RESULTS: Groups were similar (p>0.05) for age, height, and BMI, but not for weight (RT: 74.5±13.0kg; UT: 61.9±10.8kg, p=0.04). The 1RMs for chest press, leg curl, leg press, and lat pulldown were significantly different between groups (p<0.05), but not for leg extension (p=0.26). The total volume of exercise for the ARE was similar between groups (p=0.10). There were no significant (p>0.05) group differences at rest for FBF or vasodilatory capacity. There were no significant (p>0.05) 3-way interactions for FBF or vasodilatory capacity. There was a significant condition by time interaction for FBF (RT: rest: 2.9±1.1ml/100ml of tissue/min, recovery: 8.9±4.0ml/100ml of tissue/min; UT: rest: 3.1±1.1ml/100ml of tissue/min, recovery: 8.9±2.9ml/100ml of tissue/min; p<0.001) and AUC (RT: rest: 56.8±20.2units, recovery: 139.0±66.5units; UT: rest: 53.8±20.2units, recovery: 116.6±25.1units; p<0.001). CONCLUSION: These data demonstrate that acute resistance exercise significantly increases forearm blood flow and vasodilatory capacity regardless of training status.

Aerobic Training Status and Fatty Acid-Induced hTERT mRNA Expression Following Maximal Exercise

PURPOSE: Telomeres protect the ends of cellular chromosomes from degradation. Although telomere length within immune cells shorten naturally with age, increasing risk of disease and all-cause mortality, physical activity preserves telomere length by increasing mRNA expression of the telomerase component, telomerase reverse transcriptase (hTERT). Therefore, this study examined the influence of aerobic training status on the capacity of peripheral blood mononuclear cells (PBMCs) to express hTERT mRNA following palmitate stimulation. METHODS: PBMCs were isolated from 12 trained (T) and 11 untrained (UT) subjects pre- and post-maximal exercise, and stimulated with or without palmitate (4 hours) to examine changes in hTERT mRNA expression. RESULTS: hTERT mRNA expression remained unaltered following palmitate stimulation in T subjects at rest and in response to maximal exercise. To the contrary, palmitate- induced hTERT mRNA expression was elevated at rest relative to unstimulated PBMCs in UT subjects and following maximal exercise was suppressed relative to unstimulated PBMCs and pre-exercise expression levels (F [1, 81] = 7.874, p = 0.006). In addition, cardiorespiratory fitness (VO2max) was negatively associated with the percent change in hTERT mRNA expression in unstimulated PBMCs (r = -0.496, p = 0.022) and positively associated with the percent change in hTERT mRNA expression following palmitate stimulation (r = 0.468, p = 0.032). CONCLUSION: This data suggests that aerobic training may preserve the capacity of immune cells to protect against inflammatory-induced telomere shortening following acute physiological stress.

The Effects of Cherry Juice Supplementation on Antioxidant Capacity, Hydrogen Peroxide and Creatine Kinase Following an Exhaustive Aerobic Exercise in Non-athlete Men

Introduction: Oxidative stress is a condition in which the reactive oxygen species production exceeds the antioxidant system capacity to neutralize these peroxidases. In these situations, proteins, lipids, and nucleic acids are damaged. In this regard, the cherry can be noted as a food antioxidant which leads an increasing antioxidant capacity and reducing inflammation and damage muscle. Therefore, The purpose of this study was to determine the effect of cherry juice supplementation on total antioxidant capacity (TAC), creatine kinase (CK), hydrogen peroxide (H 2 O 2 ) in non-athlete men after an exhaustive aerobic exercise. Method: In this quasi-experimental research, ten untrained (UT) men were randomly selected. Then, they were divided into two equal groups: supplement group (cherry juice) and placebo group (commercial Cherry juice diluted with natural water). After eight days of supplementation period, all subjects were participated in aerobic exercise protocol (Bruce test run to the point of exhaustion) on the treadmill. Primary blood samples in the baseline were taken. The second was immediately after the Bruce test, third and fourth were six and twenty-four hours later were taken (5 ml). For analysis of the results. Analysis of variance with repeated measures was used at the significant level. Result: A significant effect of short-term cherry juice supplementation on TAC, H 2 O 2, and CK was observed (p≤0.05). Conclusions: In general, it can be concluded that probably eight days of cherry juice supplementation probably cannot prevent the adverse effects of oxidative stress caused by acute aerobic exercise.

Effect of different resistance-training protocols on the extracellular matrix of the calcaneal tendon of rats

The calcaneal tendon extracellular matrix (ECM) is composed of collagen, non-collagenous glycoproteins and proteoglycans, and able to adapt to various biomechanical stimuli. The objective of this study was to analyze the response of different resistance-training protocols, such as hypertrophy, strength and resistance, on the organization of the calcaneal tendon after training. Wistar rats were divided into four groups: untrained (UT), resistance training (RT), hypertrophy training (HT), and strength training (ST). The protocol in a vertical climbing platform was performed thrice per week over twelve weeks. For biochemical study, the tendons of each group were minced and analyzed for gelatinases, quantification of non-collagenous proteins, sulfated glycosaminoglycans, and hydroxyproline. For morphological analysis, sections were stained with HE and toluidine blue. Non-stained sections were used for birefringence analysis under polarization microscopy. The highest hydroxyproline concentrations were found in HT (154.8±14.2) and RT (173.6±25.2) compared with UT (122.4±27.0). A higher concentration of non-collagenous proteins was detected in the RT group (14.98mg/g) compared with the other groups. In polarization microscopy, major birefringence was observed in HT and the lowest in ST compared with UT, indicating higher organization of collagen bundles in HT. In analysis for zymography, the presence of latent MMP-9 was more prominent in the ST group and the active MMP-9 more prominent in the HT group. For MMP-2, significant differences in the latent isoform between the HT (184,867±6765) and UT (173,018±9696) groups were found. In sections stained with toluidine blue (TB), higher metachromasia was observed in the tendon’s distal region in HT and RT groups, indicating a greater amount of proteoglycans. We conclude that the different training protocols produced different responses in the ECM. The remarkable presence of MMP-2 and -9 in the hypertrophy training group may be related to the highest organization of collagen bundles and possibly a more efficient remodeling process, observed in that group, as demonstrated by images and measurements of birefringence.

Abstract 458: Moderate Exercise Training Attenuates Isoproterenol-Induced Myocardial Injury by Activating Nrf2-Signaling

Background: Nuclear erythroid-2 like factor-2 (Nrf2), a master transcriptional regulator of antioxidants, is critical to maintain cellular redox homeostasis. We recently reported that exercise training activates Nrf2/antioxidant signaling in the heart. Isoproterenol (ISO) mediated structural, and functional changes in the heart involve oxidative stress. Here, we tested a hypothesis that moderate exercise training will protect the myocardium from isoproterenol-induced injury by augmenting Nrf2-dependent antioxidant defense system. Methods: Age- and sex-matched WT (C57/BL6) mice (6-8 months old) were subjected to moderate exercise training (MET) on a treadmill for 6 weeks (60 min/day; 10m/min; 0% grade). Randomly assigned untrained (UNT) and trained (MET) animals were intraperitoneally injected (at the start of 6 th week) with 50 mg of isoproterenol/kg.bw./day for 7 consecutive days. MET was continued during ISO administration and the animals (UNT + PBS, UNT + ISO; MET + ISO) underwent echocardiography analysis. Heart tissues were collected for histopathology, Nrf2-ARE promoter binding assay (Active-motif TransAM kit), antioxidant gene (qPCR) and protein (Immunoblotting) levels, and glutathione redox status. Results: ISO administration significantly reduced the Nrf2 promoter activity (p&lt;0.05) and downregulated the expression of cardiac antioxidant genes ( Gclc, Nqo1, Cat, Gsr and Gst-μ ) in UNT mice. Further, increased oxidative stress with severe myocardial injury was evident in UNT+ISO when compared to UNT mice receiving PBS under basal condition. Interestingly, MET stabilized the Nrf2-promoter activity and promoted the expression of Nrf2-dependent antioxidant genes and proteins animals receiving ISO, and thereby attenuated the oxidative stress-induced myocardial damage. Echocardiography analysis showed impaired systolic/diastolic ventricular volumes coupled with decreased cardiac output in UNT+ISO mice, but this was normalized in exercise-trained animals. Conclusion: Thus moderate exercise training conferred protection against ISO-induced myocardial injury by augmentation of Nrf2-antioxidant signaling and attenuation of redox perturbations.

Muscle Mass and Training Status Do Not Affect the Maximum Number of Repetitions in Different Upper-Body Resistance Exercises

Background: Data investigating the factors that influence the relationship between different percentages of one repetition maximum (1RM) and the maximum number of repetitions (RM’s) performed are scarce when the movement velocity of each repetition is controlled during the RM’s test. Objective: To evaluate the RM’s performed at 60, 75, and 90% of 1RM in 4 different upper-body free weight exercises: bench press, barbell triceps extension, unilateral dumbbell elbow flexion, unilateral bent knee dumbbell row. Method: Thirty participants, 15 trained (T) and 15 untrained (UT) men, volunteered to participate in this study and attended six separate occasions, each separated by at least 48 h. In the first three sessions, familiarization and 1RM tests were evaluated. The last three sessions were designed to assess the performance of the RM’s at 60%, 75%, and 90% 1RM. The exercise order and intensities performed in each session were randomized. Muscle action velocity for each repetition was controlled by an electronic metronome. Results: There was no significant difference between T and UT in any of the exercises at a given exercise intensity. Moreover, there was no significant difference in the number of repetitions performed when exercises with different muscle mass (i.e., bench press vs. triceps extension, and dumbbell row vs. elbow flexion) at different intensities (i.e., 60%, 75%, and 90%) were compared. Conclusion: Using the same percentage of 1RM, the participants performed a similar number of repetitions in the four free weight upper-body exercises evaluated.

Exercise training decreases NADPH oxidase activity and restores skeletal muscle mass in heart failure rats.

We have recently demonstrated that NADPH oxidase hyperactivity, NF-κB activation, and increased p38 phosphorylation lead to atrophy of glycolytic muscle in heart failure (HF). Aerobic exercise training (AET) is an efficient strategy to counteract skeletal muscle atrophy in this syndrome. Therefore, we tested whether AET would regulate muscle redox balance and protein degradation by decreasing NADPH oxidase hyperactivity and reestablishing NF-κB signaling, p38 phosphorylation, and proteasome activity in plantaris muscle of myocardial infarcted-induced HF (MI) rats. Thirty-two male Wistar rats underwent MI or fictitious surgery (SHAM) and were randomly assigned into untrained (UNT) and trained (T; 8 wk of AET on treadmill) groups. AET prevented HF signals and skeletal muscle atrophy in MI-T, which showed an improved exercise tolerance, attenuated cardiac dysfunction and increased plantaris fiber cross-sectional area. To verify the role of inflammation and redox imbalance in triggering protein degradation, circulating TNF-α levels, NADPH oxidase profile, NF-κB signaling, p38 protein levels, and proteasome activity were assessed. MI-T showed a reduced TNF-α levels, NADPH oxidase activity, and Nox2 mRNA expression toward SHAM-UNT levels. The rescue of NADPH oxidase activity induced by AET in MI rats was paralleled by reducing nuclear binding activity of the NF-κB, p38 phosphorylation, atrogin-1, mRNA levels, and 26S chymotrypsin-like proteasome activity. Taken together our data provide evidence for AET improving plantaris redox homeostasis in HF associated with a decreased NADPH oxidase, redox-sensitive proteins activation, and proteasome hyperactivity further preventing atrophy. These data reinforce the role of AET as an efficient therapy for muscle wasting in HF.NEW & NOTEWORTHY This study demonstrates, for the first time, the contribution of aerobic exercise training (AET) in decreasing muscle NADPH oxidase activity associated with reduced reactive oxygen species production and systemic inflammation, which diminish NF-κB overactivation, p38 phosphorylation, and ubiquitin proteasome system hyperactivity. These molecular changes counteract plantaris atrophy in trained myocardial infarction-induced heart failure rats. Our data provide new evidence into how AET may regulate protein degradation and thus prevent skeletal muscle atrophy.

Left Ventricular Mechanics in Untrained and Trained Males with Tetraplegia.

Reduced left ventricular (LV) function is common in tetraplegia, yet it is unknown whether intrinsic myocardial function is attenuated. This study examined the effect of SCI and exercise-training status on LV mechanics (intrinsic function) and LV systolic/diastolic function by comparing untrained (UT) and trained (TT) individuals with tetraplegia and able-bodied (AB) individuals. Individuals with tetraplegia had a traumatic, chronic, motor-complete cervical spinal cord injury. Nine UT males (40 ± 10 years), 8 TT males (30 ± 5 years), and nine AB males (37 ± 9 years) participated in the study. LV indices were assessed using two-dimensional transthoracic echocardiography, with speckle-tracking analysis for the determination of LV mechanics. For systolic function, stroke volumes were lower in both UT (59 ± 9 mL; p < 0.001) and TT (63 ± 9 mL; p < 0.001) relative to AB (82 ± 11 mL), whereas systolic mechanics were similar across groups. Diastolic function was only reduced in UT, including a lower ratio of early-to-late transmitral filling velocity (1.55 ± 0.28) relative to TT (2.07 ± 0.42; p < 0.05) and AB (2.44 ± 0.61; p < 0.01) and longer isovolumetric relaxation times in UT (101 ± 7 ms) relative to TT (88 ± 11 ms; p < 0.05) and AB (85 ± 6 ms; p < 0.01). Diastolic mechanics (apical circumferential strain rate) were significantly enhanced in TT (3.03 ± 0.83 s-1) compared to AB (1.85 ± 0.65 s-1; p < 0.05). There was a trend (p = 0.062) for a between-group difference in apical radial diastolic strain rate (UT: -2.51 ± 0.83 s-1; TT: -3.92 ± 1.96 s-1; AB: -1.84 ± 0.46 s-1). In tetraplegia, attenuated LV systolic function is not attributed to intrinsic dysfunction, whereas exercise-training status appears to improve both global LV diastolic function and LV mechanics.

Carotid Artery Wall Mechanics During Lower Body Resistance Exercise In Strength Trained and Untrained Men.

PURPOSE: To investigate the impact of double-leg press exercise on arterial wall mechanics (peak circumferential strain, systolic and diastolic strain rate) in the common carotid arteries (CCA) of strength trained (ST) and untrained (UT) men. METHODS: Short-axis ultrasound images of the CCA were collected in 9 ST (age: 23 ± 3 yrs; stature: 177.5 ± 5.5 cm; body mass; 89.3 ± 11.3 kg; 8 repetition maximum (8RM): 264 ± 42.5 kg) and 9 UT (age: 24 ± 4 yrs; stature: 179.5 ± 6.6 cm; body mass; 83.0 ± 11.9 kg; 8RM: 152 ± 19.9 kg) men at rest, and during double-leg press exercise at 40% and 80% of 8RM. Images were analysed for peak circumferential strain (PCS), peak systolic and diastolic strain rate (S-SR and D-SR, respectively), as well as systolic and diastolic carotid diameter (DiamSYS and DiamDIAS respectively). Systolic and diastolic brachial blood pressures (SBP and DBP, respectively) were also assessed at rest and during exercise. In addition, apical five chamber echocardiography was used to examine stroke volume (SV) in a subset of ten participants (n = 6 ST, n = 4 UT). RESULTS: Whilst S-SR and SV were not influenced by exercise intensity (P = 0.86 and P = 0.08, respectively), PCS and D-SR decreased significantly from rest to 40% 8RM (-2.7 ± 0.79 %, 95% CI: 1.0 - 4.4, P < 0.01 and -0.26 ± 0.08 1/s, 95% CI: 0.10 - 0.422, P < 0.01, respectively). There was however, no significant difference in PCS or D-SR from 40% to 80% 8RM (P = 0.126 and P = 0.467, respectively). In contrast, systolic and diastolic diameter (0.06±0.01 cm, 95% CI: 0.35 - 0.75, P < 0.01 and 0.07±0.01, 95% CI: 0.06 - 0.09, P < 0.01 respectively), SBP and DBP (31±2.3 mmHg, 95% CI: 25.9 - 35.5, P < 0.01 and 18.0±1.7 mmHg, 95% CI: 14.3 - 21.6, P < 0.01, respectively) all increased significantly from rest to 40% 8RM, but continued to increase further between 40% and 80% 8RM (all P < 0.01). No significant differences were found between ST and UT men (all P > 0.05). CONCLUSION: Acute changes in carotid arterial wall mechanics occur with the onset of lower body resistance exercise, irrespective of strength training status. Additionally, during double-leg press exercise, changes in carotid arterial wall mechanics do not occur simultaneously with changes in other haemodynamic variables, and therefore might be reflective of modifications to the intrinsic properties of the vessel wall.

Velocity Drives Greater Power Observed During Back Squat Using Cluster Sets.

This investigation compared the kinetics and kinematics of cluster sets (CLU) and traditional sets (TRD) during back squat in trained (RT) and untrained (UT) men. Twenty-four participants (RT = 12, 25 ± 1 year, 179.1 ± 2.2 cm, 84.6 ± 2.1 kg; UT = 12, 25 ± 1 year, 180.1 ± 1.8 cm, 85.4 ± 3.8 kg) performed TRD (4 × 10, 120-second rest) and CLU (4 × (2 × 5) 30 seconds between clusters; 90 seconds between sets) with 70% one repetition maximum, randomly. Kinematics and kinetics were sampled through force plate and linear position transducers. Resistance-trained produced greater overall force, velocity, and power; however, similar patterns were observed in all variables when comparing conditions. Cluster sets produced significantly greater force in isolated repetitions in sets 1-3, while consistently producing greater force due to a required reduction in load during set 4 resulting in greater total volume load (CLU, 3302.4 ± 102.7 kg; TRD, 3274.8 ± 102.8 kg). Velocity loss was lessened in CLU resulting in significantly higher velocities in sets 2 through 4. Furthermore, higher velocities were produced by CLU during later repetitions of each set. Cluster sets produced greater power output for an increasing number of repetitions in each set (set 1, 5 repetitions; sets 2 and 3, 6 repetitions; set 4, 8 repetitions), and the difference between conditions increased over subsequent sets. Time under tension increased over each set and was greater in TRD. This study demonstrates greater power output is driven by greater velocity when back squatting during CLU; therefore, velocity may be a useful measure by which to assess power.

Physical Training Status Determines Oxidative Stress and Redox Changes in Response to an Acute Aerobic Exercise.

Objective. To assess the influence of different physical training status on exercise-induced oxidative stress and changes in cellular redox state. Methods. Thirty male subjects participated in this study and were assigned as well-trained (WT), moderately trained (MT), and untrained (UT) groups. The levels of cortisol, creatine kinase, plasma reduced glutathione to oxidized glutathione (GSH/GSSG), cysteine/cystine (Cys/CySS), and GSH/GSSG ratio in red blood cells (RBCs) were measured immediately and 10 and 30 min after exercise. Results. Following the exercise, plasma GSH/GSSG (p = 0.001) and Cys/CySS (p = 0.005) were significantly reduced in all groups. Reduction in plasma GSH/GSSG ratio in all groups induced a transient shift in redox balance towards a more oxidizing environment without difference between groups (p = 0.860), while RBCs GSH/GSSG showed significant reduction (p = 0.003) and elevation (p = 0.007) in UT and MT groups, respectively. The highest level of RBCs GSH/GSSG ratio was recorded in MT group, and the lowest one was recorded in the WT group. Conclusion. Long term regular exercise training with moderate intensity shifts redox balance towards more reducing environment, versus intensive exercise training leads to more oxidizing environment and consequently development of related diseases.