Effects of G-trainer, cycle ergometry, and stretching on physiological and psychological recovery from endurance exercise.

The purpose of this study was to compare the effectiveness of 3 treatment modes (Anti-Gravity Treadmill [G-trainer], stationary cycling [CompuTrainer], and static stretching) on the physiological and psychological recovery after an acute bout of exhaustive exercise. In a crossover design, 12 aerobically trained men (21.3 ± 2.3 years, 72.1 ± 8.1 kg, 178.4 ± 6.3 cm, (Equation is included in full-text article.): 53.7 ± 6.3 ml·kg·min) completed a 29-km stationary cycling time trial. Immediately after the time trial, subjects completed 30 minutes of G-trainer or CompuTrainer (40% (Equation is included in full-text article.)) or static stretching exercises. A significant time effect was detected for plasma lactate (p = 0.010) and serum cortisol (p = 0.039) after exercise. No treatment or treatment by time interaction was identified for lactate or cortisol, respectively. No main effects for time, treatment, or treatment by time interaction were identified for interleukin 6 (IL-6) and tumor necrosis factor α (TNF-α). No differences were observed among treatments in skeletal muscle peak power output, mean power output, time to peak power, and rate to fatigue at 24 hours postexercise bout. Finally, no significant changes in mood status were observed after exercise and between treatment groups. When compared with stationary cycling and static stretching, exercise recovery performed on the G-trainer was unable to reduce systemic markers of stress and inflammation, blood lactate, or improve anaerobic performance and psychological mood states after an exhaustive bout of endurance exercise. Further research is warranted that includes individualized recovery modalities to create balances between the stresses of training and competition.

Method for controlled mitochondrial perturbation during phosphorus MRS in children.

UNLABELLED: Insulin resistance is increasingly prevalent in children and may be related to muscle mitochondrial dysfunction, necessitating development of mitochondrial assessment techniques. Recent studies used phosphorus magnetic resonance spectroscopy (P-MRS), a noninvasive technique appealing for clinical research. P-MRS requires exercise at a precise percentage of maximum volitional contraction (MVC). MVC measurement in children, particularly in those with a disease, is problematic because of variability in perception of effort and motivation. We therefore developed a method to predict MVC using maximal calf muscle cross-sectional area (MCSA) to assure controlled and reproducible muscle metabolic perturbations. METHODS: Data were collected from 66 sedentary 12- to 20-yr-old participants. Plantarflexion MVC was assessed using an MRI-compatible exercise treadle device. MCSA of the calf muscles were measured from magnetic resonance images. Data from the first 26 participants were used to model the relation between MVC and MCSA (predicted MVC = 24.763 + 0.0047 MCSA). This model was then applied to the subsequent 40 participants. RESULTS: MVC versus model-predicted mean MVC was 43.9 ± 0.8 kg versus 44.2 ± 1.81 (P = 0.90). P-MRS results when predicted and MVC were similar showed expected changes during MVC-based exercise. In contrast, MVC was markedly lower than predicted in four participants and produced minimal metabolic perturbation. Upon repeat testing, these individuals could perform their predicted MVC with coaching, which produced expected metabolic perturbations. CONCLUSIONS: Compared with using MVC testing alone, using magnetic resonance imaging to predict muscle strength allows for a more accurate and standardized P-MRS protocol during exercise in children. This method overcomes a major obstacle in assessing mitochondrial function in youths. These studies have importance as we seek to determine the role of mitochondrial function in youths with insulin resistance and diabetes and response to interventions.

Oligogenic combinations associated with breast cancer risk in women under 53 years of age.

Common, but weakly penetrant, functional polymorphisms probably account for most of the genetic risk for breast cancer in the general population. Current polygenic risk models assume that component genes act independently. To test for potential gene-gene interactions, single nucleotide polymorphisms in ten genes with known or predicted roles in breast carcinogenesis were examined in a case-control study of 631 Caucasian women diagnosed with breast cancer under the age of 53 years and 1,504 controls under the age of 53 years. Association of breast cancer risk with individual genes and with two- and three-gene combinations was analyzed. Sixty-nine oligogenotypes from 37 distinct two- and three-gene combinations met stringent criteria for significance. Significant odds ratios (ORs) covered a 12-fold range: 0.5-5.9. Of the observed ORs, 17% differed significantly from the ORs predicted by a model of independent gene action, suggesting epistasis, i.e., that these genes interact to affect breast cancer risk in a manner not predictable from single gene effects. Exploration of the biological basis for these oligogenic interactions might reveal etiologic or therapeutic insights into breast cancer and other cancers.