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ABSTRACT: 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.
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.
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.
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 +/- 0.01%/h) than after soy consumption (0.07 +/- 0.01%/h; P = 0.05).
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.
American Journal of Clinical Nutrition 04/2007; 85(4):1031-40. · 6.67 Impact Factor
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ABSTRACT: Mitochondrial disorders share common cellular consequences: (1) decreased ATP production; (2) increased reliance on alternative anaerobic energy sources; and (3) increased production of reactive oxygen species. The purpose of the present study was to determine the effect of a combination therapy (creatine monohydrate, coenzyme Q(10), and lipoic acid to target the above-mentioned cellular consequences) on several outcome variables using a randomized, double-blind, placebo-controlled, crossover study design in patients with mitochondrial cytopathies. Three patients had mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes (MELAS), four had mitochondrial DNA deletions (three patients with chronic progressive external ophthalmoplegia and one with Kearns-Sayre syndrome), and nine had a variety of other mitochondrial diseases not falling into the two former groups. The combination therapy resulted in lower resting plasma lactate and urinary 8-isoprostanes, as well as attenuation of the decline in peak ankle dorsiflexion strength in all patient groups, whereas higher fat-free mass was observed only in the MELAS group. Together, these results suggest that combination therapies targeting multiple final common pathways of mitochondrial dysfunction favorably influence surrogate markers of cellular energy dysfunction. Future studies with larger sample sizes in relatively homogeneous groups will be required to determine whether such combination therapies influence function and quality of life.
Muscle & Nerve 03/2007; 35(2):235-42. · 2.37 Impact Factor
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Anne L Friedlander,
Barry Braun,
Margaret Pollack, Jay R MacDonald,
Charles S Fulco,
Steve R Muza,
Paul B Rock,
Gregory C Henderson,
Michael A Horning,
George A Brooks,
Andrew R Hoffman,
Allen Cymerman
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ABSTRACT: The effects of prolonged caloric restriction (CR) on protein kinetics in lean subjects has not been investigated previously. The purpose of this study was to test the hypotheses that 21 days of CR in lean subjects would 1) result in significant losses of lean mass despite a suppression in leucine turnover and oxidation and 2) negatively impact exercise performance. Nine young, normal-weight men [23 +/- 5 y, 78.6 +/- 5.7 kg, peak oxygen consumption (Vo2 peak) 45.2 +/- 7.3 ml.kg(-1).min(-1), mean +/- SD] were underfed by 40% of the calories required to maintain body weight for 21 days and lost 3.8 +/- 0.3 kg body wt and 2.0 +/- 0.4 kg lean mass. Protein intake was kept at 1.2 g.kg(-1).day(-1). Leucine kinetics were measured using alpha-ketoisocaproic acid reciprocal pool model in the postabsorptive state during rest and 50 min of exercise (EX) at 50% of Vo2 peak). Body composition, basal metabolic rate (BMR), and exercise performance were measured throughout the intervention. At rest, leucine flux (approximately 131 micromol.kg(-1).h(-1)) and oxidation (R(ox); approximately 19 micromol.kg(-1).h(-1)) did not differ pre- and post-CR. During EX, leucine flux (129 +/- 6 vs. 121 +/- 6) and R(ox) (54 +/- 6 vs. 46 +/- 8) were lower after CR than they were pre-CR. Nitrogen balance was negative throughout the intervention ( approximately 3.0 g N/day), and BMR declined from 1,898 +/- 262 to 1,670 +/- 203 kcal/day. Aerobic performance (Vo2 peak, endurance cycling) was not impacted by CR, but arm flexion endurance decreased by 20%. In conclusion, 3 wk of caloric restriction reduced leucine flux and R(ox) during exercise in normal-weight young men. However, despite negative nitrogen balance and loss of lean mass, whole body exercise performance was well maintained in response to CR.
AJP Endocrinology and Metabolism 10/2005; 289(3):E446-55. · 4.75 Impact Factor
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ABSTRACT: Patients with muscular dystrophy may be prone to nutrient deficiency due to mobility limitations or oropharyngeal weakness. Patients with myotonic muscular dystrophy (DM1) may be particularly prone to nutritional deficiencies from associated dysmotility of the entire gastrointestinal tract. We prospectively evaluated nutritional intake, body composition, and muscle strength in adult patients with DM1 (n = 29) and other muscular dystrophies (n = 22) on two occasions separated by approximately 6 months. Handgrip was significantly lower and knee extension higher for DM1 compared to other dystrophies, with no between-group differences in nutritional intakes. Many patients in both groups demonstrated inadequate nutrient intake of protein, energy, vitamins (water and fat soluble), and minerals (calcium and magnesium). Significant correlations were found between measures of strength and certain individual nutrients (e.g., copper and water-soluble vitamins). These data indicate that a substantial number of adults with muscular dystrophy do not meet current dietary intake recommendations. The potential clinical implications of these findings are discussed.
Muscle & Nerve 07/2005; 31(6):713-8. · 2.37 Impact Factor
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ABSTRACT: 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 < 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 04/2003; 27(3):359-66. · 2.37 Impact Factor
