Fatiguing high-intensity intermittent exercise depresses maximal Na-K-ATPase activity in human skeletal muscle assessed using a novel NADH-coupled assay.

The Na-K-ATPase is a critical regulator of ion homeostasis during contraction, buffering interstitial K accumulation, which is linked to muscle fatigue during intense exercise. Within this context, we adopted a recently reported methodology to examine exercise-induced alterations in maximal Na-K-ATPase activity. Eighteen trained healthy young males completed a repeated high-intensity cycling protocol consisting of three periods (EX1-EX3) of intermittent exercise.

Mitochondrial bioenergetics are not associated with myofibrillar protein synthesis rates.

Background: Mitochondria represent key organelles influencing cellular homeostasis and have been implicated in the signalling events regulating protein synthesis.

Methods: We examined whether mitochondrial bioenergetics (oxidative phosphorylation and reactive oxygen species (HO) emission, ROS) measured in vitro in permeabilized muscle fibres represent regulatory factors for integrated daily muscle protein synthesis rates and skeletal muscle mass changes across the spectrum of physical activity, including free-living and bed-rest conditions: n = 19 healthy, young men (26 ± 4 years, 23.4 ± 3.

Stimulation of fat oxidation in rat muscle by unacylated ghrelin persists for 2-3 hours, but is independent of fatty acid transporter translocation.

While a definitive mechanism-of-action remains to be identified, recent findings indicate that ghrelin, particularly the unacylated form (UnAG), stimulates skeletal muscle fatty acid oxidation. The biological importance of UnAG-mediated increases in fat oxidation remains unclear, as UnAG peaks in the circulation before mealtimes, and decreases rapidly during the postprandial situation before increases in postabsorptive circulating lipids. Therefore, we aimed to determine if the UnAG-mediated stimulation of fat oxidation would persist long enough to affect the oxidation of meal-derived fatty acids, and if UnAG stimulated the translocation of fatty acid transporters to the sarcolemma as a mechanism-of-action.