Carbohydrate Loading Practice in Bodybuilders: Effects on Muscle Thickness, Photo Silhouette Scores, Mood States and Gastrointestinal Symptoms.

A common practice among bodybuilders is the use of carbohydrate loading to improve physical appearance during competition, while limited documented data is available about this issue. The aim of the present study was to evaluate muscle thickness, mood states, gastrointestinal symptoms and subjective silhouette assessment following carbohydrate loading in bodybuilders. Twenty-four male bodybuilders were evaluated at the weighing period following three days of carbohydrate depletion (M1), and 24h of carbohydrate loading leading up to the competition (M2), stratified into: no carbohydrate load (NC, n = 9) and carbohydrate loading (CL, n =1 5). The silhouette scale, Brunel mood scale (BRUMS), muscle thickness (ultrasound), circumferences, and gastrointestinal symptoms (GIS) were evaluated at M1 and M2. The NC displayed no differences in muscle thickness and circumferences between M1 and M2. Body mass, muscle thickness (elbow flexors, a combination of biceps brachii/ brachialis muscle, and triceps brachii) and circumferences (chest, hip, thigh, arm, calves, and forearm) increased significantly (p < 0.05) in the CL at M2. There was a significant increase in photo silhouette scores (p < 0.05) in the CL at M2. There was no significant difference in mood states between groups or time. The most reported GIS was constipation: 7/9 (NC) and 9/15 (CL) during M1 and 6/9 (NC), and 5/15 (CL) at M2 with symptoms described as 'moderate' or 'severe'. Diarrhea was reported by 7/15 CL (4/15 as severe). These data suggest that carbohydrate loading may contribute to an acute increase in muscle volume and physical appearance, however, it needs to be better planned to minimize gastrointestinal symptoms in bodybuilders.

Vinegar (acetic acid) intake on glucose metabolism: A narrative review.

Vinegar intake is considered a food item that improves blood glucose in humans. This review aimed to discuss studies that investigated the impact of vinegar intake on the glycemic profile in humans and the putative mechanistic cellular pathways in both human and animal models. A search of literature was performed on the Cochrane, MEDLINE and Web of Science databases for articles published between 1995 and 2018. There is considerable support for vinegar having a positive acute effect on blood glucose levels when combined with carbohydrate-rich meals. Conversely, there are few chronic interventions analyzing the impact of vinegar intake on blood glucose. Based on available evidence, we hypothesize three pathways by which vinegar may improve blood glucose: The inhibition of α-amylase action; increased glucose uptake; and mediation by transcription factors. When evaluating the current body of literature, daily vinegar intake in amounts of ∼10-30 mL (∼2-6 tablespoons) appear to improve the glycemic response to carbohydrate-rich meals; however, there is a paucity of studies investigating chronic effects of vinegar intake.

Akt/mTOR pathway contributes to skeletal muscle anti-atrophic effect of aerobic exercise training in heart failure mice.

BACKGROUND: Exercise intolerance is one of the main clinical symptoms of heart failure (HF) and is associated with skeletal muscle wasting due to an imbalance between proteolysis and protein synthesis. In this study, we tested whether aerobic exercise training (AET) would counteract skeletal muscle atrophy by activating IGF-I/Akt/mTOR pathway in HF mice. METHODS: Sympathetic hyperactivity induced HF mice were assigned into 8-week moderate intensity AET. Untrained wild type and HF mice were used as control. Soleus cross sectional area was evaluated by histochemistry and motor performance by rotarod. 26S proteasome activity was assessed by fluorimetric assay, and components of IGF-I/Akt/mTOR pathway or myostatin pathway by qRT-PCR or immunoblotting. A different subset of mice was used to evaluate the relative contribution of mTOR inhibition (rapamycin) or activation (leucine) on AET-induced changes in muscle mass regulation. RESULTS: AET prevented exercise intolerance and impaired motor performance in HF mice. These effects were associated with attenuation of soleus atrophy. Rapamycin treatment precluded AET effects on soleus mass in HF mice suggesting the involvement of IGF signaling pathway in this response. In fact, AET increased IGF-I Ea and IGF-I Pan mRNA levels, while it reduced myostatin and Smad2 mRNA levels in HF mice. At protein levels, AET prevented reduced expression levels of IGF-I, pAkt (at basal state), as well as, p4E-BP1 and pP70(S6K) (leucine-stimulated state) in HF mice. Additionally, AET prevented 26S proteasome hyperactivity in HF mice. CONCLUSIONS: Taken together, our data provide evidence for AET-induced activation of IGF-I/Akt/mTOR signaling pathway counteracting HF-induced muscle wasting.

Effects of leucine supplementation and resistance exercise on dexamethasone-induced muscle atrophy and insulin resistance in rats.

OBJECTIVE: We aimed to evaluate the effects of resistance exercise (RE) and leucine (LEU) supplementation on dexamethasone (DEXA)-induced muscle atrophy and insulin resistance. METHODS: Male Wistar rats were randomly divided into DEXA (DEX), DEXA + RE (DEX-RE), DEXA + LEU (DEX-LEU), and DEXA + RE + LEU (DEX-RE-LEU) groups. Each group received DEXA 5 mg · kg(-1) · d(-1) for 7 d from drinking water and were pair-fed to the DEX group; LEU-supplemented groups received 0.135 g · kg(-1) · d(-1) through gavage for 7 d; the RE protocol was based on three sessions of squat-type exercise composed by three sets of 10 repetitions at 70% of maximal voluntary strength capacity. RESULTS: The plantaris mass was significantly greater in both trained groups compared with the non-trained groups. Muscle cross-sectional area and fiber areas did not differ between groups. Both trained groups displayed significant increases in the number of intermediated fibers (IIa/IIx), a decreased number of fast-twitch fibers (IIb), an increased ratio of the proteins phospho(Ser2448)/total mammalian target of rapamycin and phospho(Thr389)/total 70-kDa ribosomal protein S6 kinase, and a decreased ratio of phospho(Ser253)/total Forkhead box protein-3a. Plasma glucose was significantly increased in the DEX-LEU group compared with the DEX group and RE significantly decreased hyperglycemia. The DEX-LEU group displayed decreased glucose transporter-4 translocation compared with the DEX group and RE restored this response. LEU supplementation worsened insulin sensitivity and did not attenuate muscle wasting in rats treated with DEXA. Conversely, RE modulated glucose homeostasis and fiber type transition in the plantaris muscle. CONCLUSION: Resistance exercise but not LEU supplementation promoted fiber type transition and improved glucose homeostasis in DEXA-treated rats.