Short-term creatine supplementation changes protein metabolism signaling in hindlimb suspension.

The effect of a short-term creatine supplementation on hindlimb suspension (HS)-induced muscle atrophy was investigated. Creatine monohydrate (5 g/kg b.w. per day) or placebo, divided in 2 daily doses, was given by oral gavage for 5 days. Rats were maintained in HS with dietary supplementation concomitantly for 5 days. Body weight, soleus and EDL muscle masses, and cross-sectional areas (CSA) of the muscle fibers were measured. Signaling pathways associated with skeletal muscle mass regulation (FST, MSTN, FAK, IGF-1, MGF, Akt, mTOR, atrogin-1, and MuRF1 expressions, and Akt, S6, GSK3B, and 4EBP1 proteins) were evaluated in the muscles. Soleus muscle exhibited more atrophy than the EDL muscle due to HS. Creatine supplementation attenuated the decrease of wet weight and increased p-4EBP1 protein in the EDL muscle of HS rats. Also, creatine increased mTOR and atrogin-1 expressions in the same muscle and condition. In the absence of HS, creatine supplementation increased FAK and decreased MGF expressions in the EDL muscle. Creatine attenuated the increase in FST expression due to HS in the soleus muscle. MuRF1 expression increased in the soleus muscle due to creatine supplementation in HS animals whereas atrogin-1 expression increased still further in this group compared with untreated HS rats. In conclusion, short-term creatine supplementation changed protein metabolism signaling in soleus and EDL muscles. However, creatine supplementation only slightly attenuated the mass loss of both muscles and did not prevent the CSA reduction and muscle strength decrease induced by HS for 5 days.

Short-term creatine supplementation changes protein metabolism signaling in hindlimb suspension

The effect of a short-term creatine supplementation on hindlimb suspension (HS)-induced muscle atrophy was investigated. Creatine monohydrate (5 g/kg b.w. per day) or placebo, divided in 2 daily doses, was given by oral gavage for 5 days. Rats were maintained in HS with dietary supplementation concomitantly for 5 days. Body weight, soleus and EDL muscle masses, and cross-sectional areas (CSA) of the muscle fibers were measured. Signaling pathways associated with skeletal muscle mass regulation (FST, MSTN, FAK, IGF-1, MGF, Akt, mTOR, atrogin-1, and MuRF1 expressions, and Akt, S6, GSK3B, and 4EBP1 proteins) were evaluated in the muscles. Soleus muscle exhibited more atrophy than the EDL muscle due to HS. Creatine supplementation attenuated the decrease of wet weight and increased p-4EBP1 protein in the EDL muscle of HS rats. Also, creatine increased mTOR and atrogin-1 expressions in the same muscle and condition. In the absence of HS, creatine supplementation increased FAK and decreased MGF expressions in the EDL muscle. Creatine attenuated the increase in FST expression due to HS in the soleus muscle. MuRF1 expression increased in the soleus muscle due to creatine supplementation in HS animals whereas atrogin-1 expression increased still further in this group compared with untreated HS rats. In conclusion, short-term creatine supplementation changed protein metabolism signaling in soleus and EDL muscles. However, creatine supplementation only slightly attenuated the mass loss of both muscles and did not prevent the CSA reduction and muscle strength decrease induced by HS for 5 days.

Effects of acute caffeine ingestion on resistance training performance and perceptual responses during repeated sets to failure.

AIM: The aim of the present study was to evaluate the effect of oral caffeine ingestion during repeated sets of resistance. METHODS: Fourteen moderately resistance-trained men (20.9 ± 0.36 years and 77.62 ± 2.07 kg of body weight) ingested a dose of caffeine (5 mg.kg-1) or placebo prior to 3 sets of bench press and 3 sets of leg press exercises, respectively. The study used a double-blind, counterbalanced, crossover design. Repetitions completed and total weight lifted were recorded in each set. Readiness to invest in both physical (RTIPE) and mental (RTIME) effort were assessed prior each set, and rating of perceived exertion (RPE) was recorded after each set. Rest and peak heart rates were determined via telemetry. RESULTS: Caffeine ingestion result in increased number of repetitions to failure in bench press (F[1,13]=6.16, P=0.027) and leg press (F[1,13]=9.33, P=0.009) compared to placebo. The sum of repetitions performed in the 3 sets was 11.60% higher in bench press (26.86 ± 1.74; caffeine: 30.00 ± 1.87; P=0.027) and 19.10% in leg press (placebo: 40.0 ± 4.22; caffeine: 47.64 ± 4.69; P=0.009). Also, RTIME was increased in the caffeine condition both in bench press (F[1,13]=7.02, P=0.02) and in leg press (F[1,13]=5.41, P=0.03). There were no differences in RPE, RTIPE and HR (P>0.05) across conditions. CONCLUSION: Acute caffeine ingestion can improve performance in repeated sets to failure and increase RTIME in resistance-trained men.

The effect of caffeine ingestion on functional performance in older adults.

UNLABELLED: Caffeine is a widely used nutritional supplement which has been shown to enhance both physical and cognitive performance in younger adults. However, few studies have assessed the effect of caffeine ingestion on performance, particularly functional performance in older adults. The present study aims to assess the effect of acute caffeine ingestion on functional performance, manual dexterity and readiness to invest effort in older adults. METHODS: 19 apparently healthy, volunteers (10 females and 9 males aged 61-79; 66 ± 2 years) performed tests of functional fitness and manual dexterity post ingestion of caffeine (3mg*kg-1) or placebo in a randomised order. Pre and 60 minutes post ingestion, participants also completed measures of readiness to invest physical (RTIPE) and mental (RTIME) effort. RESULTS: A series of repeated measures ANOVAS indicated enhanced performance in the following functional fitness tests; arm curls (P = .04), 8 foot up and go (P = .007), six minute walk (P = .016). Manual dexterity was also improved in the presence of caffeine (P = .001). RTIME increased (P = .015) pre to post ingestion in the caffeine condition but not in the placebo condition. There were no significant main effects or interactions for RTIPE or gender in any analysis (all P > .05). CONCLUSIONS: The results of this study suggest that acute caffeine ingestion positively enhances functional performance, manual dexterity and readiness to invest effort in apparently healthy older adults.

Beta hydroxy beta methylbutyrate supplementation impairs peripheral insulin sensitivity in healthy sedentary Wistar rats.

AIM: Investigate, in healthy sedentary rats, the potential mechanisms involved on the effects of beta hydroxy beta methylbutyrate (HMB) supplementation upon the glycaemic homeostasis, by evaluating the insulin sensitivity in liver, skeletal muscle, and white adipose tissue. METHODS: Rats were supplemented with either beta hydroxy beta methylbutyrate (320 mg kg(-1)  BW) or saline by gavage for 4 weeks. After the experimental period, the animals were subjected to the glucose tolerance test (GTT) and plasma non-esterified fatty acids (NEFA) concentration measurements. The soleus skeletal muscle, liver and white adipose tissue were removed for molecular (western blotting and RT-PCR) and histological analysis. RESULTS: The beta hydroxy beta methylbutyrate supplemented rats presented: (i) higher ratio between the area under the curve (AUC) of insulinaemia and glycaemia during glucose tolerance test; (ii) impairment of insulin sensitivity on liver and soleus skeletal muscle after insulin overload; (iii) reduction of glucose transporter 4 (GLUT 4) total and plasma membrane content on soleus; (iv) increased hormone-sensitive lipase (HSL) mRNA and protein expression on white adipose tissue and plasma NEFA levels and (v) reduction of fibre cross-sectional area of soleus muscle. CONCLUSION: The data altogether indicate that beta hydroxy beta methylbutyrate supplementation impairs insulin sensitivity in healthy sedentary rats, which, in the long-term, could lead to an increased risk of developing type 2 diabetes.

Chronic supplementation of beta-hydroxy-beta methylbutyrate (HMß) increases the activity of the GH/IGF-I axis and induces hyperinsulinemia in rats.

OBJECTIVE: Beta-hydroxy-beta-methylbutyrate (HMß) is a metabolite of leucine widely used for improving sports performance. Although HMß is recognized to promote anabolic or anti-catabolic effects on protein metabolism, the impact of its long-term use on skeletal muscle and/or genes that control the skeletal protein balance is not fully known. This study aimed to investigate whether chronic HMß treatment affects the activity of GH/IGF-I axis and skeletal muscle IGF-I and myostatin mRNA expression. DESIGN: Rats were treated with HMß (320mg/kg BW) or vehicle, by gavage, for 4 weeks, and killed by decapitation. Blood was collected for evaluation of serum insulin, glucose and IGF-I concentrations. Samples of pituitary, liver, extensor digitorum longus (EDL) and soleus muscles were collected for total RNA or protein extraction to evaluate the expression of pituitary growth hormone (GH) gene (mRNA and protein), hepatic insulin-like growth factor I (IGF-I) mRNA, skeletal muscle IGF-I and myostatin mRNA by Northern blotting/real time-PCR, or Western blotting. RESULTS: Chronic HMß treatment increased the content of pituitary GH mRNA and GH, hepatic IGF-I mRNA and serum IGF-I concentration. No changes were detected on skeletal muscle IGF-I and myostatin mRNA expression. However, the HMß-treated rats although normoglycemic, exhibited hyperinsulinemia. CONCLUSIONS: The data presented herein extend the body of evidence on the potential role of HMß-treatment in stimulating GH/IGF-I axis activity. In spite of this effect, HMß supplementation also induces an apparent insulin resistance state which might limit the beneficial aspects of the former results, at least in rats under normal nutritional status and health conditions.