Carbohydrate refeed does not modify GVT-performance following energy restriction in bodybuilders.

Bodybuilding is a sport in which competitors' physiques are judged on their muscular size, symmetry, and leanness, as displayed in a number of different poses. In the pre-competitive period, bodybuilders attempt to reduce body fat stores as much as possible while maintaining fat-free mass (FFM). This is achieved via a sustained negative energy balance, generally induced by a combination of decreased energy intake and increased energy expenditure. This study aimed to assess the ability of bodybuilders to resist fatigue during resistance exercise based German Volume Training (GVT), as well as the affective response after carbohydrate refeed following four weeks of moderate or severe energy restriction. Eleven male bodybuilders (28.4 ± 2.3 years old) with experience in competitions were randomized into two groups: Moderate Energy Restriction (MER; n = 6) or Severe Energy Restriction (SER; n = 5). On the 2nd day (during energy restriction) and 7th day (during refeed) of the fourth week, both groups completed two leg press protocols involving the GVT method. After the first and last workout protocol subjects were assessed for muscle soreness using the visual-analog scale (VAS), rating of perceived exertion (RPE), affective response, lactate, and creatine kinase. Anthropometric analysis indicated that a reduction of 3.7 and 3.2% in body mass corresponded to a loss of 16.0 and 17.6% of fat mass for the MER and SER groups, respectively, with both groups maintaining FFM. Blood CK and VAS values were reduced only in SER. Our results suggest that a carbohydrate refeed may help to attenuate the perception of muscle soreness and maintain exercise performance, especially when severe energy restriction is combined with an intense training protocol such as GVT.

Oxidative stress, inflammation, psychological status, and severity of respiratory infections are negatively affected during the pre-contest period in amateur bodybuilders.

We examined whether off-season (OffS) and pre-contest (PreC) periods affect blood oxidative stress, inflammatory, immunological, and psychological markers in 20 bodybuilders. The athletes recorded their food intake (3-day record), physical activities, mood states (Profile of Mood States, POMS), recovery-stress (Recovery-Stress Questionnaire for Athletes, RESTQ-Sport), and upper respiratory symptoms (Wisconsin Upper Respiratory Symptom Survey, WURSS-21), and blood was obtained for biochemical analysis. Almost all athletes were in positive energy balance during OffS, while bodybuilders presented markedly restricted energy intake (∼45%) leading to loss of weight (-9%) and fat mass (-45%) with preservation of fat-free mass in PreC. Protein intake was high during both periods, while lipid and carbohydrate intakes were reduced ∼50% in PreC. Almost all athletes consumed 100% of the Recommended Dietary Allowance (RDA) for micronutrients in OffS, while 45% and 75% of the athletes had intakes below the RDA for vitamins A and E in PreC. Oxidative damage to lipids (thiobarbituric acid reactive substances, TBARS), protein carbonyls, and the TBARS/total antioxidant capacity ratio increased in PreC (32%, 27%, 60%), as did plasma tumor necrosis factor α (4-fold) and WURSS-21 scores (25%). There were no significant changes in serum catalase, glutathione reductase, and superoxide dismutase activities nor in interleukin 1ß and immunoglobulins. In PreC, POMS showed negative changes in vigor (-20%), fatigue (23%), and total mood disturbance (35%), and RESTQ-Sport showed alterations for general and sport stress (34% and 50%, respectively) and sport recovery (-23%). Thus, PreC negatively affects nutrient intake, which may worsen oxidative stress, inflammation, psychological status, and the severity of respiratory infections in bodybuilders.

Comparison of the acute effects of traditional versus high velocity resistance training on metabolic, cardiovascular, and psychophysiological responses in elderly hypertensive women.

OBJECTIVES: The aim of the present study was to compare the acute effects of traditional resistance training (RT) versus high velocity RT (HVRT) on metabolic, cardiovascular, and psychophysiological responses in elderly hypertensive women. METHODS: Fifteen elderly women (mean age ± standard deviation, 67.1±6.9 years) classified as having hypertension stage 1 or 2 were randomly allocated to complete traditional RT or HVRT; 1 week later, subjects allocated to RT completed the HVRT session and vice-versa. Heart rate, blood pressure, affective response, perceived effort, and blood samples analyzing lactate, nitrate, nitrite, oxidative damage (thiobarbituric acid reactive substances [TBARS]), and 6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid equivalent antioxidant capacity (TEAC) collected before and after training sessions were assessed. Nutritional counseling was provided regarding nutrients that could affect cardiovascular and nitrate/nitrite analysis. RESULTS: Systolic blood pressure was not statistically different (p>0.05) between conditions at the beginning and during 30 minutes after sessions. Diastolic blood pressure, rate pressure product, and heart rate were not statistically different (p>0.05) between conditions at the beginning and during 45 minutes after sessions. Nitric oxide was significantly higher (p<0.0005) for HVRT compared to RT after 30 minutes of exercise. TBARS and TEAC were significantly higher (p<0.05) for HVRT compared with RT only immediately after exercise. There were no differences for psychophysiological variables between protocols. CONCLUSION: The acute cardiovascular and metabolic responses, including oxidative stress, are transient and within normal values. Taken together with the positive affective responses, both HVRT and RT with this intensity and volume seem to be safe for elderly hypertensive women under medication.

Resistance training-induced gains in muscle strength, body composition, and functional capacity are attenuated in elderly women with sarcopenic obesity.

OBJECTIVES: The purpose of this study was to compare the effects of resistance training (RT) on body composition, muscle strength, and functional capacity in elderly women with and without sarcopenic obesity (SO). METHODS: A total of 49 women (aged ≥60 years) were divided in two groups: without SO (non-SO, n=41) and with SO (n=8). Both groups performed a periodized RT program consisting of two weekly sessions for 16 weeks. All measures were assessed at baseline and postintervention, including anthropometry and body composition (dual-energy X-ray absorptiometry), muscle strength (one repetition maximum) for chest press and 45° leg press, and functional capacity (stand up, elbow flexion, timed "up and go"). RESULTS: After the intervention, only the non-SO group presented significant reductions in percentage body fat (-2.2%; P=0.006), waist circumference (-2.7%; P=0.01), waist-to-hip ratio (-2.3; P=0.02), and neck circumference (-1.8%; P=0.03) as compared with baseline. Muscle strength in the chest press and biceps curl increased in non-SO only (12.9% and 11.3%, respectively), while 45° leg press strength increased in non-SO (50.3%) and SO (40.5%) as compared with baseline. Performance in the chair stand up and timed "up and go" improved in non-SO only (21.4% and -8.4%, respectively), whereas elbow flexion performance increased in non-SO (23.8%) and SO (21.4%). Effect sizes for motor tests were of higher magnitude in the non-SO group, and in general, considered "moderate" compared to "trivial" in the SO group. CONCLUSION: Results suggest that adaptations induced by 16 weeks of RT are attenuated in elderly woman with SO, compromising improvements in adiposity indices and gains in muscle strength and functional capacity.

Aerobic exercise training rescues protein quality control disruption on white skeletal muscle induced by chronic kidney disease in rats.

We tested whether aerobic exercise training (AET) would modulate the skeletal muscle protein quality control (PQC) in a model of chronic kidney disease (CKD) in rats. Adult Wistar rats were evaluated in four groups: control (CS) or trained (CE), and 5/6 nephrectomy sedentary (5/6NxS) or trained (5/6NxE). Exercised rats were submitted to treadmill exercise (60 min., five times/wk for 2 months). We evaluated motor performance (tolerance to exercise on the treadmill and rotarod), cross-sectional area (CSA), gene and protein levels related to the unfolded protein response (UPR), protein synthesis/survive and apoptosis signalling, accumulated misfolded proteins, chymotrypsin-like proteasome activity (UPS activity), redox balance and heat-shock protein (HSP) levels in the tibialis anterior. 5/6NxS presented a trend towards to atrophy, with a reduction in motor performance, down-regulation of protein synthesis and up-regulation of apoptosis signalling; increases in UPS activity, misfolded proteins, GRP78, derlin, HSP27 and HSP70 protein levels, ATF4 and GRP78 genes; and increase in oxidative damage compared to CS group. In 5/6NxE, we observed a restoration in exercise tolerance, accumulated misfolded proteins, UPS activity, protein synthesis/apoptosis signalling, derlin, HSPs protein levels as well as increase in ATF4, GRP78 genes and ATF6α protein levels accompanied by a decrease in oxidative damage and increased catalase and glutathione peroxidase activities. The results suggest a disruption of PQC in white muscle fibres of CKD rats previous to the atrophy. AET can rescue this disruption for the UPR, prevent accumulated misfolded proteins and reduce oxidative damage, HSPs protein levels and exercise tolerance.

Dexamethasone-induced cardiac deterioration is associated with both calcium handling abnormalities and calcineurin signaling pathway activation.

Dexamethasone is a potent and widely used anti-inflammatory and immunosuppressive drug. However, recent evidences suggest that dexamethasone cause pathologic cardiac remodeling, which later impairs cardiac function. The mechanism behind the cardiotoxic effect of dexamethasone is elusive. The present study aimed to verify if dexamethasone-induced cardiotoxicity would be associated with changes in the cardiac net balance of calcium handling protein and calcineurin signaling pathway activation. Wistar rats (~400 g) were treated with dexamethasone (35 µg/g) in drinking water for 15 days. After dexamethasone treatment, we analyzed cardiac function, cardiomyocyte diameter, cardiac fibrosis, and the expression of proteins involved in calcium handling and calcineurin signaling pathway. Dexamethasone-treated rats showed several cardiovascular abnormalities, including elevated blood pressure, diastolic dysfunction, cardiac fibrosis, and cardiomyocyte apoptosis. Regarding the expression of proteins involved in calcium handling, dexamethasone increased phosphorylation of phospholamban at threonine 17, reduced protein levels of Na+/Ca2+ exchanger, and had no effect on protein expression of Serca2a. Protein levels of NFAT and GATA-4 were increased in both cytoplasmic and nuclear faction. In addition, dexamethasone increased nuclear protein levels of calcineurin. Altogether our findings suggest that dexamethasone causes pathologic cardiac remodeling and diastolic dysfunction, which is associated with impaired calcium handling and calcineurin signaling pathway activation.

Impact of leucine supplementation on exercise training induced anti-cardiac remodeling effect in heart failure mice.

Leucine supplementation potentiates the effects of aerobic exercise training (AET) on skeletal muscle; however, its potential effects associated with AET on cardiac muscle have not been clarified yet. We tested whether leucine supplementation would potentiate the anti-cardiac remodeling effect of AET in a genetic model of sympathetic hyperactivity-induced heart failure in mice (α2A/α2CARKO). Mice were assigned to five groups: wild type mice treated with placebo and sedentary (WT, n = 11), α2A/α2CARKO treated with placebo and sedentary (KO, n = 9), α2A/α2CARKO treated with leucine and sedentary (KOL, n = 11), α2A/α2CARKO treated with placebo and AET (KOT, n = 12) or α2A/α2CARKO treated with leucine and AET (KOLT, n = 12). AET consisted of four weeks on a treadmill with 60 min sessions (six days/week, 60% of maximal speed) and administration by gavage of leucine (1.35 g/kg/day) or placebo (distilled water). The AET significantly improved exercise capacity, fractional shortening and re-established cardiomyocytes' diameter and collagen fraction in KOT. Additionally, AET significantly prevented the proteasome hyperactivity, increased misfolded proteins and HSP27 expression. Isolated leucine supplementation displayed no effect on cardiac function and structure (KOL), however, when associated with AET (KOLT), it increased exercise tolerance to a higher degree than isolated AET (KOT) despite no additional effects on AET induced anti-cardiac remodeling. Our results provide evidence for the modest impact of leucine supplementation on cardiac structure and function in exercised heart failure mice. Leucine supplementation potentiated AET effects on exercise tolerance, which might be related to its recognized impact on skeletal muscle.

Aerobic exercise training improves oxidative stress and ubiquitin proteasome system activity in heart of spontaneously hypertensive rats.

The activity of the ubiquitin proteasome system (UPS) and the level of oxidative stress contribute to the transition from compensated cardiac hypertrophy to heart failure in hypertension. Moreover, aerobic exercise training (AET) is an important therapy for the treatment of hypertension, but its effects on the UPS are not completely known. The aim of this study was to evaluate the effect of AET on UPS's activity and oxidative stress level in heart of spontaneously hypertensive rats (SHR). A total of 53 Wistar and SHR rats were randomly divided into sedentary and trained groups. The AET protocol was 5×/week in treadmill for 13 weeks. Exercise tolerance test, non-invasive blood pressure measurement, echocardiographic analyses, and left ventricle hemodynamics were performed during experimental period. The expression of ubiquitinated proteins, 4-hydroxynonenal (4-HNE), Akt, phospho-Akt(ser473), GSK3ß, and phospho-GSK3ß(ser9) were analyzed by western blotting. The evaluation of lipid hydroperoxide concentration was performed using the xylenol orange method, and the proteasomal chymotrypsin-like activity was measured by fluorimetric assay. Sedentary hypertensive group presented cardiac hypertrophy, unaltered expression of total Akt, phospho-Akt, total GSK3ß and phospho-GSK3ß, UPS hyperactivity, increased lipid hydroperoxidation as well as elevated expression of 4-HNE but normal cardiac function. In contrast, AET significantly increased exercise tolerance, decreased resting systolic blood pressure and heart rate in hypertensive animals. In addition, the AET increased phospho-Akt expression, decreased phospho-GSK3ß, and did not alter the expression of total Akt, total GSK3ß, and ubiquitinated proteins, however, significantly attenuated 4-HNE levels, lipid hydroperoxidation, and UPS's activity toward normotensive group levels. Our results provide evidence for the main effect of AET on attenuating cardiac ubiquitin proteasome hyperactivity and oxidative stress in SHR rats.

Effects of creatine supplementation on muscle wasting and glucose homeostasis in rats treated with dexamethasone.

We aimed to investigate the possible role of creatine (CR) supplementation in counteracting dexamethasone-induced muscle wasting and insulin resistance in rats. Also, we examined whether CR intake would modulate molecular pathways involved in muscle remodeling and insulin signaling. Animals were randomly divided into four groups: (1) dexamethasone (DEX); (2) control pair-fed (CON-PF); (3) dexamethasone plus CR (DEX-CR); and (4) CR pair-fed (CR-PF). Dexamethasone (5 mg/kg/day) and CR (5 g/kg/day) were given via drinking water for 7 days. Plantaris and extensor digitorum longus (EDL) muscles were removed for analysis. Plantaris and EDL muscle mass were significantly reduced in the DEX-CR and DEX groups when compared with the CON-PF and CR-PF groups (P<0.05). Dexamethasone significantly decreased phospho-Ser473-Akt protein levels compared to the CON-PF group (P<0.05) and CR supplementation aggravated this response (P<0.001). Serum glucose was significantly increased in the DEX group when compared with the CON-PF group (DEX 7.8±0.6 vs. CON-PF 5.2±0.5 mmol/l; P<0.05). CR supplementation significantly exacerbated hyperglycemia in the dexamethasone-treated animals (DEX-CR 15.1±2.4 mmol/l; P<0.05 vs. others). Dexamethasone reduced GLUT-4 translocation when compared with the CON-PF and CR-PF (P<0.05) groups and this response was aggravated by CR supplementation (P<0.05 vs. others). In conclusion, supplementation with CR resulted in increased insulin resistance and did not attenuate muscle wasting in rats treated with dexamethasone. Given the contrast with the results of human studies that have shown benefits of CR supplementation on muscle atrophy and insulin sensitivity, we suggest caution when extrapolating this animal data to human subjects.