Living high - training low model applied to C57BL/6J mice: Effects on physiological parameters related to aerobic fitness and acid-base balance.

There is a scarcity of data regarding the acclimation to high altitude (hypoxic environment) accompanied by training at low altitude (normoxic conditions), the so-called "living high-training low" (LHTL) model in rodents. We aimed to investigate the effects of aerobic training on C57BL/6J mice living in normoxic (NOR) or hypoxic (HYP) environments on several parameters, including critical velocity (CV), a parameter regarded as a measure of aerobic capacity, on monocarboxylate transporters (MCTs) in muscles and hypothalamus, as well as on hematological parameters and body temperature. In each environment, mice were divided into non-trained (N) and trained (T).

SIRT3 deficiency decreases oxidative metabolism capacity but increases lifespan in male mice under caloric restriction.

Mitochondrial NAD -dependent protein deacetylase Sirtuin3 (SIRT3) has been proposed to mediate calorie restriction (CR)-dependent metabolic regulation and lifespan extension. Here, we investigated the role of SIRT3 in CR-mediated longevity, mitochondrial function, and aerobic fitness. We report that SIRT3 is required for whole-body aerobic capacity but is dispensable for CR-dependent lifespan extension.

Monocarboxylate transporters (MCTs) in skeletal muscle and hypothalamus of less or more physically active mice exposed to aerobic training.

Aims: The synthesis of monocarboxylate transporters (MCTs) can be stimulated by aerobic training, but few is known about this effect associated or not with non-voluntary daily activities. We examined the effect of eight weeks of aerobic training in MCTs on the skeletal muscle and hypothalamus of less or more physically active mice, which can be achieved by keeping them in two different housing models, a small cage (SC) and a large cage (LC).

Main Methods: Forty male C57BL/6J mice were divided into four groups.

The Lung Elastin Matrix Undergoes Rapid Degradation Upon Adult Loss of Function.

genes encode transcription factors that are critical for embryonic skeletal patterning and organogenesis. The , , and paralogs are expressed in the lung mesenchyme and function redundantly during embryonic lung development. Conditional loss-of-function of these genes during postnatal stages leads to severe defects in alveologenesis, specifically in the generation of the elastin network, and animals display bronchopulmonary dysplasia (BPD) or BPD-like phenotype.