News & Views from the Editor-in-Chief - L. Bruce Gladden
Our journal consistently has excellent papers, and this month is no exception; as usual, I am highlighting three of them. First, Aaltonen and colleagues examined the association between physical activity behavior and academic performance from adolescence to young adulthood by using a genetically informative twin study design with four repeated measurement waves. Their results showed for the first time that familial background (including genetic and shared environmental factors) may be responsible for creating an association between physical activity behavior and academic performance. These results challenge a potential causal relationship between these traits. In light of their study, the most important implication for increasing a child's physical activity behavior and academic performance may be that an intervention in a child's family environment is required rather than an intervention that is directly aimed at promoting physical activity or academic performance.
Second, Tseng et al. compared the effects of unilateral progressive (10%–100% of maximal strength over 5 weeks: 1 session/week) eccentric versus concentric training of the elbow flexors on muscle function and damage of the contralateral elbow flexors. They found that the eccentric training produced greater increases in strength for both trained (19%) and untrained arms (10%) when compared with the concentric training (11%, 5%). The magnitude of muscle damage induced by maximal eccentric exercise of the contralateral arm performed at 1 week post-training was reduced (>50%) after the eccentric training only. These results suggest that eccentric training provided a greater cross-education effect to increase muscle function and prevent muscle damage on the nontrained contralateral muscles than concentric training, and that eccentric training was more effective for maximizing these effects.
Finally, Baumann and colleagues reported that eccentric contraction-induced strength loss is due to plasmalemma electrophysiological dysfunction in mdx muscle but not that of wildtype muscle. A key feature of the mdx mouse, an animal model of Duchenne muscular dystrophy, is hypersensitivity to eccentric contraction-induced strength loss. In this current paper, the researchers demonstrate that mdx muscle possesses a remarkable ability to recover plasmalemmal excitability and subsequently strength. Their data indicate that dystrophin is necessary for complete excitation to occur at the plasmalemma during eccentric contractions, but not essential for plasmalemmal excitability or muscular strength to fully recover. Importantly, these results demonstrate that eccentric contraction-induced injury is mechanistically different between wildtype and mdx mice, and that proposed treatments for dystrophic muscle should consider this fact.
L. Bruce Gladden
School of Kinesiology