Cytokines and growth factors during and after a wrestling season in adolescent boys

PurposeBrief periods of aerobic exercise training lead to reductions, rather then the expected increases in circulating IGF-I. We hypothesized that intense exercise training in adolescents initially leads to simultaneous increases in proinflammatory cytokines and decreases in activity of the GH/IGF-I axis; and that as exercise training proceeds, levels of proinflammatory cytokines become reduced, and a rebound in IGF-I ensues leading to the higher IGF-I levels.MethodTo test this, we evaluated the GH/IGF-I axis and levels of inflammatory cytokines (IL-6, TNF-alpha, IL-1beta, IL-1ra), body composition, and fitness in 13 healthy adolescent boys (mean age 15.9 +/- 0.3 yr) over the course of a high-school wrestling season. Subjects were tested preseason, midseason (6 wk), peak season (12-14 wk), and 4 wk postseason.ResultsNo significant weight loss was noted throughout the season. During the wrestling season (mid and peak) both total (P < 0.046) and free (P < 0.002) IGF-I levels decreased, whereas proinflammatory cytokines (IL-1ra, P < 0.005; IGFBP-1, P < 0.013; and IGFBP-2, P < 0.025) increased. GHBP (P < 0.018) levels also decreased during the season. In the postseason, there were significant increases in GHBP, and free and total IGF-I, whereas proinflammatory cytokines decreased.ConclusionsAn initial catabolic-type hormonal response occurs with intense exercise training in adolescents. This is followed by a rebound in circulating growth factors when the period of heavy training ceases

Exercise, caloric restriction, and systemic oxidative stress.

BackgroundIn humans, the main sources of reactive oxygen species (ROS), the molecules causing oxidative stress, are mitochondrial superoxide ions and neutrophil-derived oxidative radicals. Circulating antioxidants contribute to the protection against oxidative stress. Although the formation of ROS and secretion of antioxidants are independently regulated by exercise and diet, little is known about their combined effect. We hypothesized that relatively brief, intense exercise training may reduce systemic oxidation via an intrinsic mechanism, independent of changes in circulating antioxidants and of neutrophil-derived enzymes (as may be caused by concomitant caloric restriction).MethodsNineteen volunteers exercised for 7 days, 3 hours/day at 75% of oxygen uptake. Caloric intake was either 110% of caloric expenditure (high calorie, n=10) or 75% of caloric expenditure (low calorie, n=9). Blood samples for F2-isoprostanes, catalase, myeloperoxidase (MPO), interleukin-x (IL-x), white blood cells (WBCs), and other metabolic variables were taken at baseline, at the end of training, and 1 week after completion of the study.ResultsSerum F2-isoprostanes (microg/mL), markers of lipid peroxidation, were similarly reduced after 7 days of exercise in the high-calorie (from 35+/-4 to 27+/-2) and low-calorie (from 35+/-3 to 24+/-2) groups. Similar reductions were observed in IL-x concentrations. Conversely, no change was observed in circulating concentrations of the antioxidant catalase. Whereas total WBCs and neutrophil counts were significantly reduced in the low-calorie group only, no difference in neutrophil-derived MPO was measured between groups.ConclusionA significant reduction in systemic oxidation may occur relatively early during intense exercise training in healthy young men, independent of caloric intake. The potential contribution to these effects of circulating antioxidants and neutrophil-derived oxidative enzymes will require further investigation

Exercise, caloric restriction, and systemic oxidative stress.

BackgroundIn humans, the main sources of reactive oxygen species (ROS), the molecules causing oxidative stress, are mitochondrial superoxide ions and neutrophil-derived oxidative radicals. Circulating antioxidants contribute to the protection against oxidative stress. Although the formation of ROS and secretion of antioxidants are independently regulated by exercise and diet, little is known about their combined effect. We hypothesized that relatively brief, intense exercise training may reduce systemic oxidation via an intrinsic mechanism, independent of changes in circulating antioxidants and of neutrophil-derived enzymes (as may be caused by concomitant caloric restriction).MethodsNineteen volunteers exercised for 7 days, 3 hours/day at 75% of oxygen uptake. Caloric intake was either 110% of caloric expenditure (high calorie, n=10) or 75% of caloric expenditure (low calorie, n=9). Blood samples for F2-isoprostanes, catalase, myeloperoxidase (MPO), interleukin-x (IL-x), white blood cells (WBCs), and other metabolic variables were taken at baseline, at the end of training, and 1 week after completion of the study.ResultsSerum F2-isoprostanes (microg/mL), markers of lipid peroxidation, were similarly reduced after 7 days of exercise in the high-calorie (from 35+/-4 to 27+/-2) and low-calorie (from 35+/-3 to 24+/-2) groups. Similar reductions were observed in IL-x concentrations. Conversely, no change was observed in circulating concentrations of the antioxidant catalase. Whereas total WBCs and neutrophil counts were significantly reduced in the low-calorie group only, no difference in neutrophil-derived MPO was measured between groups.ConclusionA significant reduction in systemic oxidation may occur relatively early during intense exercise training in healthy young men, independent of caloric intake. The potential contribution to these effects of circulating antioxidants and neutrophil-derived oxidative enzymes will require further investigation

Neuromotor noise limits motor performance, but not motor adaptation, in children.

Children do not typically appear to move with the same skill and dexterity as adults, although they can still improve their motor performance in specific tasks with practice. One possible explanation is that their motor performance is limited by an inherently higher level of movement variability, but that their motor adaptive ability is robust to this variability. To test this hypothesis, we examined motor adaptation of 43 children (ages 6-17) and 12 adults as they reached while holding the tip of a lightweight robot. The robot applied either a predictable, velocity-dependent field (the "mean field") or a similar field that incorporated stochastic variation (the "noise field"), thereby further enhancing the variability of the subjects' movements. We found that children exhibited greater initial trial-to-trial variability in their unperturbed movements but were still able to adapt comparably to adults in both the mean and noise fields. Furthermore, the youngest children (ages 6-8) were able to reduce their variability with practice to levels comparable to the remaining children groups although not as low as adults. These results indicate that children as young as age 6 possess adult-like neural systems for motor adaptation and internal model formation that allow them to adapt to novel dynamic environments as well as adults on average despite increased neuromotor or environmental noise. Performance after adaptation is still more variable than adults, however, indicating that movement inconsistency, not motor adaptation inability, ultimately limits motor performance by children and may thus account for their appearance of incoordination and more frequent motor accidents (e.g., spilling, tripping). The results of this study also suggest that movement variability in young children may arise from two sources--a relatively constant, intrinsic source related to fundamental physiological constraints of the developing motor system and a more rapidly modifiable source that is modulated depending on the current motor context

Neuromotor noise limits motor performance, but not motor adaptation, in children.

Children do not typically appear to move with the same skill and dexterity as adults, although they can still improve their motor performance in specific tasks with practice. One possible explanation is that their motor performance is limited by an inherently higher level of movement variability, but that their motor adaptive ability is robust to this variability. To test this hypothesis, we examined motor adaptation of 43 children (ages 6-17) and 12 adults as they reached while holding the tip of a lightweight robot. The robot applied either a predictable, velocity-dependent field (the "mean field") or a similar field that incorporated stochastic variation (the "noise field"), thereby further enhancing the variability of the subjects' movements. We found that children exhibited greater initial trial-to-trial variability in their unperturbed movements but were still able to adapt comparably to adults in both the mean and noise fields. Furthermore, the youngest children (ages 6-8) were able to reduce their variability with practice to levels comparable to the remaining children groups although not as low as adults. These results indicate that children as young as age 6 possess adult-like neural systems for motor adaptation and internal model formation that allow them to adapt to novel dynamic environments as well as adults on average despite increased neuromotor or environmental noise. Performance after adaptation is still more variable than adults, however, indicating that movement inconsistency, not motor adaptation inability, ultimately limits motor performance by children and may thus account for their appearance of incoordination and more frequent motor accidents (e.g., spilling, tripping). The results of this study also suggest that movement variability in young children may arise from two sources--a relatively constant, intrinsic source related to fundamental physiological constraints of the developing motor system and a more rapidly modifiable source that is modulated depending on the current motor context

Effect of muscle fatigue on internal model formation and retention during reaching with the arm.

The motor system adapts to novel dynamic environments by forming internal models that predict the muscle forces needed to move skillfully. The goal of this study was to determine how muscle fatigue affects internal model formation during arm movement and whether an internal model acquired while fatigued could be recalled accurately after rest. Twelve subjects adapted to a viscous force field applied by a lightweight robot as they reached to a target. They then reached while being resisted by elastic bands until they could no longer touch the target. This protocol reduced the strength of the muscles used to resist the force field by approximately 20%. The bands were removed, and subjects adapted again to the viscous force field. Their adaptive ability, quantified by the amount and time constant of adaptation, was not significantly impaired following fatigue. The subjects then rested, recovering approximately 70% of their lost force-generation ability. When they reached in the force field again, their prediction of the force field strength was different than in a nonfatigued state. This alteration was consistent with the use of a higher level of effort than normally used to counteract the force field. These results suggest that recovery from fatigue can affect recall of an internal model, even when the fatigue did not substantially affect the motor system's ability to form the model. Recovery from fatigue apparently affects recall because the motor system represents internal models as a mapping between effort and movement and relies on practice to recalibrate this mapping

Effect of muscle fatigue on internal model formation and retention during reaching with the arm.

The motor system adapts to novel dynamic environments by forming internal models that predict the muscle forces needed to move skillfully. The goal of this study was to determine how muscle fatigue affects internal model formation during arm movement and whether an internal model acquired while fatigued could be recalled accurately after rest. Twelve subjects adapted to a viscous force field applied by a lightweight robot as they reached to a target. They then reached while being resisted by elastic bands until they could no longer touch the target. This protocol reduced the strength of the muscles used to resist the force field by approximately 20%. The bands were removed, and subjects adapted again to the viscous force field. Their adaptive ability, quantified by the amount and time constant of adaptation, was not significantly impaired following fatigue. The subjects then rested, recovering approximately 70% of their lost force-generation ability. When they reached in the force field again, their prediction of the force field strength was different than in a nonfatigued state. This alteration was consistent with the use of a higher level of effort than normally used to counteract the force field. These results suggest that recovery from fatigue can affect recall of an internal model, even when the fatigue did not substantially affect the motor system's ability to form the model. Recovery from fatigue apparently affects recall because the motor system represents internal models as a mapping between effort and movement and relies on practice to recalibrate this mapping