There are a number of symptoms, both neurological and behavioral, associated with a single episode of r mild traumatic brain injury (mTBI). Neuropsychological testing and conventional neuroimaging techniques are not sufficiently sensitive to detect these changes, which adds to the complexity and difficulty in relating symptoms from mTBI to their underlying structural or functional deficits. With the inability of traditional brain imaging techniques to properly assess the severity of brain damage induced by mTBI, there is hope that more advanced neuroimaging applications will be more sensitive, as well as specific, in accurately assessing mTBI. In this study, we used resting state functional magnetic resonance imaging to evaluate the default mode network (DMN) in the subacute phase of mTBI. Fourteen concussed student-athletes who were asymptomatic based upon clinical symptoms resolution and clearance for aerobic exercise by medical professionals were scanned using resting state functional magnetic resonance imaging. Nine additional asymptomatic yet not medically cleared athletes were recruited to investigate the effect of a single episode of mTBI versus multiple mTBIs on the resting state DMN. In concussed individuals the resting state DMN showed a reduced number of connections and strength of connections in the posterior cingulate and lateral parietal cortices. An increased number of connections and strength of connections was seen in the medial prefrontal cortex. Connections between the left dorso-lateral prefrontal cortex and left lateral parietal cortex showed a significant reduction in magnitude as the number of concussions increased. Regression analysis also indicated an overall loss of connectivity as the number of mTBI episodes increased. Our findings indicate that alterations in the brain resting state default mode network in the subacute phase of injury may be of use clinically in assessing the severity of mTBI and offering some insight into the pathophysiology of the disorder.

As a consequence of the physiological demands experienced during a competitive soccer season, the antagonistic relationship between anabolic and catabolic processes can affect performance. Twenty-five male collegiate soccer players were studied throughout a season (11 weeks) to investigate the effects of long-term training and competition. Subjects were grouped as starters (S; n = 11) and nonstarters (NS; n = 14). Measures of physical performance, body composition, and hormonal concentrations (testosterone [T] and cortisol [C]) were assessed preseason (T1) and 5 times throughout the season (T2-T6). Starters and NS participated in 83.06% and 16.95% of total game time, respectively. Nonstarters had a significant increase (+1.6%) in body fat at T6 compared to T1. Isokinetic strength of the knee extensors (1.05 rad.sec(-1)) significantly decreased in both S (-12%) and NS (-10%; p < or = 0.05) at T6. Significant decrements in sprint speed (+4.3%) and vertical jump (-13.8%) were found at T5 in S only. Though within normal ranges (10.4-41.6 nmol.L(-1)), concentrations of T at T1 were low for both groups, but increased significantly by T6. Concentrations of C were elevated in both groups, with concentrations at the high end of the normal range (normal range 138-635 nmol.L(-1)) at T1 and T4 in NS and T4 in S, with both groups remaining elevated at T6. Data indicate that players entering the season with low circulating concentrations of T and elevated levels of C can experience reductions in performance during a season, with performance decrements exacerbated in starters over nonstarters. Soccer players should therefore have a planned program of conditioning that does not result in an acute overtraining phenomenon prior to preseason (e.g., young players trying to get in shape quickly in the 6 to 8 weeks in the summer prior to reporting for preseason camp). The detrimental effects of inappropriate training do not appear to be unloaded during the season and catabolic activities can predominate.

The purposes of this investigation were to see whether free radical production changed with high intensity resistance exercise and, secondly, to see whether vitamin E supplementation would have any effect on free radical formation or variables associated with muscle membrane disruption. Twelve recreationally weight-trained males were divided into two groups. The supplement group (S) received 1200 IUs of vitamin E once a day (3 x 400 IU x d[-1]) for a period of 2 wk. The placebo group (P) received cellulose-based placebo pills once a day for the same period of time. Creatine kinase activity was significantly elevated between preexercise and immediately postexercise, 6 h postexercise, and 24 h postexercise for both groups. The placebo group also had a significant increase in creatine kinase activity at 48 h postexercise. There was a significant difference in creatine kinase activity between the groups at 24 h after exercise. Plasma malondialdehyde significantly increased from preexercise levels for the P group at 6 and 24 h postexercise. Plasma malondialdehyde concentrations significantly increased in the S group between preexercise and immediately postexercise levels. This study indicates that high intensity resistance exercise increases free radical production and that vitamin E supplementation may decrease muscle membrane disruption.

These data indicate that a weight-loss dietary regimen in conjunction with aerobic and resistance exercise prevents the normal decline in fat-free mass and muscular power and augments body composition, maximal strength, and maximum oxygen consumption compared with weight-loss induced by diet alone.