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Repetitive, monotonic, and effortful voluntary muscle contractions performed for just a few weeks, i.e., resistance training, can substantially increase maximal voluntary force in the practiced task and can also increase gross motor performance. The increase in motor performance is often accompanied by neuroplastic adaptations in the central nervous system. While historical data assigned functional relevance to such adaptations induced by resistance training, this claim has not yet been systematically and critically examined in the context of motor performance across the lifespan in health and disease. A review of muscle activation, brain and peripheral nerve stimulation, and imaging data revealed that increases in motor performance and neuroplasticity tend to be uncoupled, making a mechanistic link between neuroplasticity and motor performance inconclusive. We recommend new approaches, including causal mediation analytical and hypothesis-driven models to substantiate the functional relevance of resistance training-induced neuroplasticity in the improvements of gross motor function across the lifespan in health and disease.
Remodeling of the extracellular matrix is a key component of the metabolic adaptations of adipose tissue in response to dietary and physiological challenges. Disruption of its integrity is a well-known aspect of adipose tissue dysfunction, for instance, during aging and obesity. Adipocyte regeneration from a tissue-resident pool of mesenchymal stem cells is part of normal tissue homeostasis. Among the pathophysiological consequences of adipogenic stem cell aging, characteristic changes in the secretory phenotype, which includes matrix-modifying proteins, have been described. Here, we show that the expression of the matricellular protein periostin, a component of the extracellular matrix produced and secreted by adipose tissue-resident interstitial cells, is markedly decreased in aged brown and white adipose tissue depots. Using a mouse model, we demonstrate that the adaptation of adipose tissue to adrenergic stimulation and high-fat diet feeding is impaired in animals with systemic ablation of the gene encoding for periostin. Our data suggest that loss of periostin attenuates lipid metabolism in adipose tissue, thus recapitulating one aspect of age-related metabolic dysfunction. In human white adipose tissue, periostin expression showed an unexpected positive correlation with age of study participants. This correlation, however, was no longer evident after adjusting for BMI or plasma lipid and liver function biomarkers. These findings taken together suggest that age-related alterations of the adipose tissue extracellular matrix may contribute to the development of metabolic disease by negatively affecting nutrient homeostasis.