The purpose of our study was to determine if vascular occlusion produced an additive effect on muscle hypertrophy and strength performance with high strength training loads. Sixteen physically active men were divided into two groups: high-intensity (HI = 6 RM) and moderate-intensity training (MI = 12 RM). An occlusion cuff was attached to the proximal end of the right thigh, so that blood flow was reduced during the exercise. The left leg served as a control, thus was trained without vascular occlusion. Knee extension 1 RM and quadriceps cross-sectional area (MRI) were evaluated pre- and post-8 weeks of training. We only found a main time effect for both strength gains and quadriceps hypertrophy (p < 0.001). Therefore, we conclude that vascular occlusion in combination with high-intensity strength training does not augment muscle strength or hypertrophy when compared to high-intensity strength training alone.

The purpose of this investigation was to examine the effects of diet on muscle triglyceride and endurance performance. Seven endurance-trained men completed a 120-min cycling bout at 65% of maximal oxygen uptake. Each subject then ingested an isocaloric high-carbohydrate (Hi-CHO; 83% of energy) or a high-fat (Hi-Fat; 68% of energy) diet for the ensuing 12 h. After a 12-h overnight fast, a 1,600-kJ self-paced cycling bout was completed. Muscle triglyceride measured before (33.0 +/- 2.3 vs. 37.0 +/- 2.1 mmol/kg dry wt) and after (30.9 +/- 2.4 vs. 32.8 +/- 1.6 mmol/kg dry wt) the 120-min cycling bout was not different between the Hi-CHO and Hi-Fat trials, respectively. After the 24-h dietary-fasting period, muscle triglyceride was significantly higher for the Hi-Fat (44.7 +/- 2.4 mmol/kg dry wt) vs. the Hi-CHO (27.5 +/- 2.1 mmol/kg dry wt) trial. Furthermore, self-paced cycling time was significantly greater for the Hi-Fat (139.3 +/- 7.1 min) compared with the Hi-CHO (117.1 +/- 3.2 min) trial. These data demonstrate that there was not a significant difference in muscle triglyceride concentration before and after a prolonged moderate-intensity cycling bout. Nevertheless, a high-fat diet increased muscle triglyceride concentration and reduced self-paced cycling performance 24 h after the exercise compared with a high-carbohydrate diet.

This study determined the contribution of extracellular matrix (ECM) remodeling to the protective adaptation of human skeletal muscle known as the repeated-bout effect (RBE). Muscle biopsies were obtained 3 hours, 2 days, and 27 days following an initial bout (B1) of lengthening contractions (LCs) and 2 days following a repeated bout (B2) in 2 separate studies. Biopsies from the nonexercised legs served as controls. In the first study, global transcriptomic analysis indicated widespread changes in ECM structural, deadhesive, and signaling transcripts, 3 hours following LC. To determine if ECM remodeling is involved in the RBE, we conducted a second study by use of a repeated-bout paradigm. TNC immunoreactivity increased 10.8-fold following B1, was attenuated following B2, and positively correlated with LC-induced strength loss (r 2 = 0.45; P = 0.009). Expression of collagen I, III, and IV (COL1A1, COL3A1, CO-L4A1) transcripts was unchanged early but increased 5.7 6 2.5-, 3.2 6 0.9-, and 2.1 6 0.4-fold (P < 0.05), respectively, 27 days post-B1 and were unaffected by B2. Likewise, TGF-b signaling demonstrated a delayed response following LC. Satellite cell content increased 80% (P < 0.05) 2 days post-B1 (P < 0.05), remained elevated 27 days post-B1, and was unaffected by B2. Collectively, the data suggest sequential ECM remodeling characterized by early deadhesion and delayed reconstructive activity that appear to contribute to the RBE

These data demonstrate that during a common isokinetic strength testing protocol a between set rest period of at least 60 s is sufficient for recovery before the next test set.