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Background: Resistance exercise leads to net muscle protein accretion through a synergistic interaction of exercise and feeding. Proteins from different sources may differ in their ability to support muscle protein accretion because of different patterns of postprandial hyperaminoacidemia. Objective: We examined the effect of consuming isonitrogenous, isoenergetic, and macronutrient-matched soy or milk beverages (18 g protein, 750 kJ) on protein kinetics and net muscle protein balance after resistance exercise in healthy young men. Our hypothesis was that soy ingestion would result in larger but transient hyperaminoacidemia compared with milk and that milk would promote a greater net balance because of lower but prolonged hyperaminoacidemia. Design: Arterial-venous amino acid balance and muscle fractional synthesis rates were measured in young men who consumed fluid milk or a soy-protein beverage in a crossover design after a bout of resistance exercise. Results: Ingestion of both soy and milk resulted in a positive net protein balance. Analysis of area under the net balance curves indicated an overall greater net balance after milk ingestion (P < 0.05). The fractional synthesis rate in muscle was also greater after milk consumption (0.10 [+ or -] 0.01%/h) than after soy consumption (0.07 [+ or -] 0.01%/h; P = 0.05). Conclusions: Milk-based proteins promote muscle protein accretion to a greater extent than do soy-based proteins when consumed after resistance exercise. The consumption of either milk or soy protein with resistance training promotes muscle mass maintenance and gains, but chronic consumption of milk proteins after resistance exercise likely supports a more rapid lean mass accrual. KEY WORDS Skeletal muscle, protein synthesis, dietary protein, feeding, hypertrophy

Results indicate that blood pressure, renal function, or plasma creatine kinase activity are not affected by the administraion of acute creatine monohydrate. However, fat-free mass is significantly increased and is more evident in men than in women.

Research indicates that the standard prediction method for estimating the mean arterial blood pressure (MAP) during exercise is valid. Results are based on comparisons of MAP predictions and actual MAP during exercise of 27 males and 2 women.

The sensitivity and specificity of a modified forearm ischemic test (FIT) are described in the diagnosis of glycogen storage disease, myoadenylate deaminase deficiency, and mitochondrial disease. FIT and muscle biopsy results were reviewed from 99 patients (glycogen storage disease [GSD], myoadenylate deaminase deficiency [AMPD], mitochondrial disease [MITO], miscellaneous neuromuscular disorders, and controls). The influence of catheter placement and an antecedent sugar bolus were also assessed in healthy young men. The FIT had a sensitivity of 1.00 and a specificity of 1.00 for a diagnosis of GSD, whereas the corresponding values were 1.00 and 0.37 for AMPD deficiency. A baseline lactate of >2.5 mmol/L provided the highest sensitivity (0.62) and specificity (1.00) for MITO disease. A baseline and +1 min sample provided optimal sensitivity and specificity for GSD and AMPD deficiency. Catheter placement in any vein other than the ipsilateral antecubital resulted in attenuated lactate responses (P &lt; 0.0001). A pre-FIT sugar bolus did not alter the postexercise lactate or ammonia response. Thus, a modified FIT was helpful in the diagnosis of GSD and excluding AMPD deficiency, but not in the diagnosis of MITO disease. Catheter placement is critical to the interpretation of a FIT, whereas pretesting diet is less important. Muscle Nerve 27: 359–366, 2003

Our purposes were (1) to examine resting arterial blood pressure following an acute bout of resistance exercise and submaximal dynamic exercise, (2) to examine the effects of these exercises on the plasma concentrations of atrial natriuretic peptide ([ANP]), and (3) to evaluate the potential relationship between [ANP] and post-exercise blood pressure. Thirteen males [24.3?±?(2.4)?years] performed 15?min of unilateral leg press exercise (65% of their one-repetition maximum) and, 1?week later, ˜15?min of cycle ergometry (at 65% of their maximum oxygen consumption). Intra-arterial pressure was monitored during exercise and for 1?h post-exercise. Arterial blood was drawn at rest, during exercise and at intervals up to 60?min post-exercise for analysis of haematocrit and [aANP]. No differences occurred in blood pressure between trials, but significant decrements occurred following exercise in both trials. Systolic pressure was ˜20?mmHg lower than before exercise after 10?min, and mean pressure was ˜7?mmHg lower from 30?min onwards. Only slight (non-significant) elevations in [aANP] were detected immediately following exercise, with the concentrations declining to pre-exercise values by 5?min post-exercise. We conclude that post-exercise hypotension occurs following acute bouts of either resistance or submaximal dynamic exercise and, in this investigation, that this decreased blood pressure was not directly related to the release of aANP.

Our purpose was to examine the effects of sprint interval training on muscle glycolytic and oxidative enzyme activity and exercise performance. Twelve healthy men (22 ± 2 yr of age) underwent intense interval training on a cycle ergometer for 7 wk. Training consisted of 30-s maximum sprint efforts (Wingate protocol) interspersed by 2–4 min of recovery, performed three times per week. The program began with four intervals with 4 min of recovery per session in week 1and progressed to 10 intervals with 2.5 min of recovery per session by week 7. Peak power output and total work over repeated maximal 30-s efforts and maximal oxygen consumption (V˙o2 max) were measured before and after the training program. Needle biopsies were taken from vastus lateralis of nine subjects before and after the program and assayed for the maximal activity of hexokinase, total glycogen phosphorylase, phosphofructokinase, lactate dehydrogenase, citrate synthase, succinate dehydrogenase, malate dehydrogenase, and 3-hydroxyacyl-CoA dehydrogenase. The training program resulted in significant increases in peak power output, total work over 30 s, andV˙o2 max. Maximal enzyme activity of hexokinase, phosphofructokinase, citrate synthase, succinate dehydrogenase, and malate dehydrogenase was also significantly (P< 0.05) higher after training. It was concluded that relatively brief but intense sprint training can result in an increase in both glycolytic and oxidative enzyme activity, maximum short-term power output, andV˙o2 max.