We concluded that LIR was able to induce gains in 1RM and quadriceps CSA similar to those observed after traditional HI. These responses may be related to the concomitant decrease in MSTN and increase in FLST isoforms, GASP-1, and SMAD-7 mRNA gene expression.

We describe a novel, and likely the first, nonpharmacological therapeutic tool that might be able to counteract the muscle atrophy and the declining strength that usually occur in IBM.

This study investigated the chronic effects of concurrent training (CT) on morphological and molecular adaptations. 37 men (age=23.7?5.5 year) were divided into 4 groups: interval (IT), strength (ST) and concurrent (CT) training and a control group (C) and underwent 8 weeks of training. Maximum strength (1RM) and muscle cross-sectional area (CSA) were evaluated before and after training. Muscle samples were obtained before the training program and 48?h after the last training session. VO2max improved in 5?0.95% and 15?1.3% (pre- to post-test) in groups CT and IT, respectively, when compared to C. Time to exhaustion (TE) improved from pre- to post-test when compared to C (CT=6.1?0.58%; IT=8.3?0.88%; ST=3.2?0.66%). 1RM increased from pre-to post-test only in ST and CT groups (ST=18.5?3.16%; CT=17.6?3.01%). Similarly, ST and CT groups increased quadriceps CSA from pre-to post-test (6.2?1.4%; 7.8?1.66%). The p70S6K1 total protein content increased after CT. The ST group showed increased Akt phosphorylation at Ser473 (45.0?3.3%) whereas AMPK phosphorylation at Thr172 increased only in IT group, (100?17.6%). In summary, our data suggest that despite the differences in molecular adaptations between training regimens, CT did not blunt muscle strength and hypertrophy increments when compared with ST.

In this study, we analyzed the effect of aerobic exercise training (AET) and of a single bout of exercise on plasma oxidative stress and on antioxidant defenses in type 2 diabetes mellitus (DM) and in healthy control subjects (C). DM and C did not differ regarding triglycerides, high-density lipoprotein cholesterol (HDL-c), insulin, and HOMA index at baseline and after AET. To measure the lag time for low-density lipoprotein (LDL) oxidation (LAG) and the maximal rate of conjugated diene formation (MCD), participants' plasma HDL(2) and HDL(3) were incubated with LDL from pooled healthy donors' plasma. In the presence of HDL(3), both LAG and MCD were similar in C and DM, but only in DM did AET improve LAG and reduce MCD. In the presence of HDL(2), the lower baseline LAG in DM equaled C after AET. MCD was unchanged in DM after AET, but was lower than C only after AET. Furthermore, after AET plasma thiobarbituric acid-reactive substances were reduced only in DM subjects. Despite not modifying the total plasma antioxidant status and serum paraoxonase-1 activity in both groups, AET lowered the plasma lipid peroxides, corrected the HDL(2), and improved the HDL(3) antioxidant efficiency in DM independent of the changes in blood glucose, insulin, and plasma HDL concentration and composition.

Creatine supplementation combined with an exercise program improves glycemic control in type 2 diabetic patients. The underlying mechanism seems to be related to an increase in GLUT-4 recruitment to the sarcolemma.