Eight weeks of resistance training in conjunction with glutathione and L-Citrulline supplementation increases lean mass and has no adverse effects on blood clinical safety markers in resistance-trained males.

BACKGROUND: Supplementation of combined glutathione (GSH) with L-citrulline in response to a single bout of resistance exercise has been shown to increase plasma nitric oxide metabolites, nitrite and nitrate and cyclic guanosine monophosphate (cGMP), which may play a role in muscle protein synthesis. As a result, in response to resistance training (RT) these responses may establish a role for GSH + L-citrulline to increase muscle mass. This study attempted to determine the effects of an 8-week RT program in conjunction with GSH (Setria®) + L-citrulline, L-citrulline-malate, or placebo supplementation on lean mass and its association with muscle strength. The secondary purpose was to assess the safety of such supplementation protocol by assessing clinical chemistry markers. METHODS: In a randomized, double-blind, placebo-controlled design, 75 resistance-trained males were randomly assigned to ingest GSH + L-citrulline (GSH + CIT), L-citrulline-malate, or cellulose placebo daily while also participating in 8 weeks of RT. The full dose of each supplement was delivered in capsules that were identical in weight, size, shape, and color. Participants completed testing sessions for body composition and muscle strength before and after 4 and 8 weeks of RT and supplementation. Venous blood samples were obtained before and after 8 weeks. RESULTS: Leg press was increased with RT but was not significantly different between groups (p > 0.05); however, bench press strength was not increased with RT (p > 0.05). There were no significant changes in total body mass, fat mass, or total body water during 8 weeks of RT and supplementation. Lean mass increased in both GSH + CIT when compared to PLC; however, the increase was significant only after 4 weeks. Lean mass and strength were positively correlated (p < 0.05) in GSH + CIT, but not CIT-malate or PLC. Neither RT nor supplementation had any significant effects on blood clinical chemistry variables (p > 0.05). CONCLUSION: Compared to PLC, supplementation of GSH + CIT during resistance training increased lean mass after 4 weeks of RT and was positively associated with muscle strength. However, after 8 weeks of RT there were no significant differences in any of the measured variables.

Resistance Training-Induced Elevations in Muscular Strength in Trained Men Are Maintained After 2 Weeks of Detraining and Not Differentially Affected by Whey Protein Supplementation.

Hwang, PS, Andre, TL, McKinley-Barnard, SK, Morales Marroquín, FE, Gann, JJ, Song, JJ, and Willoughby, DS. Resistance training-induced elevations in muscular strength in trained men are maintained after 2 weeks of detraining and not differentially affected by whey protein supplementation. J Strength Cond Res 31(4): 869-881, 2017-Resistance training (RT) with nutritional strategies incorporating whey protein intake postexercise can stimulate muscle protein synthesis and elicit hypertrophy. The early phases of training-induced anabolic responses can be attenuated with longer-term training. It is currently unknown if short-term detraining (DT) can restore these blunted anabolic responses during a subsequent retraining (ReT) period. Twenty resistance-trained men (age 20.95 ± 1.23 years; n = 20) were randomized into one of 2 groups (PRO or CHO; 25 g) in a double-blind manner. Participants followed a 4-day per week RT program (4-week RT; 2-week DT; 4-week ReT) while consuming their respective supplement only on workout days during RT and ReT, but every day during DT. At baseline, 4 weeks after RT (post-RT), 2 weeks after DT (post-2-week DT), and after 4 weeks of ReT after DT (post-ReT), leg press strength (LPS) was assessed and rectus femoris cross-sectional area and lean mass changes were assessed by ultrasonography and dual-energy x-ray absorptiometry, respectively. A factorial 2 × 4 (group by time) analyses of variance with repeated measures were used with a probability level at ≤0.05. LPS was elevated throughout the 10-week training study (p = 0.003) with no decrease in LPS after DT in both groups. Although not statistically significant, both groups retained lean mass after DT. A 2-week period of DT appeared to retain muscular strength in resistance-trained men. Therefore, a short-term period of DT can potentially retain lower-body strength in young resistance-trained men irrespective of supplementing with 25 g of whey protein postexercise.

Enhanced oxidative stress sensitizes the mitochondrial permeability transition pore to opening in heart from Zucker Fa/fa rats with type 2 diabetes.

AIMS: Obesity and diabetes mellitus type 2 (DM2) frequently coexist and increase the propensity of cardiovascular dysfunction by numerous mechanisms. Chief among them are oxidative stress and Ca(2+) dysregulation, and both are inducers of the mitochondrial permeability transition pore (MPTP). Nevertheless, it is unknown whether MPTP formation is triggered in DM2 animals, and thereby contributing to cardiac dysfunction. We assessed MPTP sensitivity and reactive oxygen species production in cardiac mitochondria, as well as cytosolic Ca(2+) handling in ventricular myocytes from rats with DM2. MAIN METHODS: Male Zucker Fa/fa rats (Fa/fa) 32weeks old presenting DM2, concentric hypertrophy, and diastolic dysfunction were used. MPTP formation was evaluated in isolated mitochondria and Ca(2+) handling in ventricular myocytes, by spectrophotometric and confocal microscope techniques, respectively. KEY FINDINGS: We found that the systolic Ca(2+) transient relaxation was ~40% slower, while mitochondrial H2O2 production increased by ~6-fold. MPTP opening in isolated mitochondria from Fa/fa (mFa/fa) was more sensitive to Ca(2+) than in mitochondria from lean rats (mLean), and correlated with increased thiol group exposure. The mFa/fa showed decreased oxidative phosphorylation capacity. The ATP content decreased in myocytes, while the PCr/ATP ratio remained unchanged and caspase 9 activity largely increased in myocytes from Fa/fa animals. SIGNIFICANCE: Our results showed that oxidative stress and diastolic Ca(2+) dysregulation increased MPTP sensitivity leading to mitochondrial dysfunction and apoptosis. Mitochondrial dysfunction could compromise ATP synthesis, and lower ATP could be linked to decreased SERCA2 activity, which might underlie diastolic dysfunction. Prolonged Ca(2+) transients might further exacerbate mitochondrial dysfunction.