Is maximal muscle strength and fatigability of three lower limb muscle groups associated with walking capacity and fatigability in multiple sclerosis? An exploratory study.

Background: Both muscle fatigability and walking fatigability are prevalent in persons with MS (pwMS), but their associations remains unclear. The aim of this study was to examine the association of muscle strength and fatigability from both isometric and concentric protocols of three different muscle groups, and their association to walking capacity and walking fatigability.

Methods: Twenty-seven pwMS and 13 Healthy Controls (HC) were included in this exploratory study.

Periodized versus classic exercise therapy in Multiple Sclerosis: a randomized controlled trial.

Background: Periodizing exercise interventions in Multiple Sclerosis (MS) shows good high intensity exercise training adherence. Whether this approach induces comparable training adaptations with respect to exercise capacity, body composition and muscle strength compared to conventional, linear progressive training programs however is not known.

Methods: Thirty-one persons with MS (all phenotypes, mean EDSS 2.

Periodized home-based training: A new strategy to improve high intensity exercise therapy adherence in mildly affected patients with Multiple Sclerosis.

Introduction: Although high intensity exercise therapy (HIT) in Multiple Sclerosis (MS) induces substantial effects, longer term compliance to such a training program is not evident. When embedded in a periodized, home-based training strategy, high intensity exercise therapy adherence may improve. This is explored first in mildly affected persons with MS.

Muscle carnosine in experimental autoimmune encephalomyelitis and multiple sclerosis.

Background: Muscle carnosine is related to contractile function (Ca handling) and buffering of exercise-induced acidosis. As these muscular functions are altered in Multiple Sclerosis (MS) it is relevant to understand muscle carnosine levels in MS.

Methods: Tibialis anterior muscle carnosine was measured in an animal MS model (EAE, experimental autoimmune encephalomyelitis, n = 40) and controls (CON, n = 40) before and after exercise training (EAE, CON, 10d, 1 h/d, 24 m/min treadmill running) or sedentary conditions (EAE, CON).

Mice deficient in the respiratory chain gene Cox6a2 are protected against high-fat diet-induced obesity and insulin resistance.

Oxidative phosphorylation in mitochondria is responsible for 90% of ATP synthesis in most cells. This essential housekeeping function is mediated by nuclear and mitochondrial genes encoding subunits of complex I to V of the respiratory chain. Although complex IV is the best studied of these complexes, the exact function of the striated muscle-specific subunit COX6A2 is still poorly understood.

Force depression and relaxation kinetics after active shortening and deactivation in mouse soleus muscle.

After active shortening, isometric force production capacity of muscle is reduced (force depression, FD). The mechanism is incompletely understood but increasing cross-bridge detachment and/or decreasing attachment rate might be involved. Therefore we aimed to investigate the relation between work delivered during shortening (W), and change in half-relaxation time (Δ0.

The effect of muscle length on force depression after active shortening in soleus muscle of mice.

Isometric muscle force after active shortening is reduced [force depression (FD)]. The mechanism is incompletely understood but work delivered during shortening has been suggested to be the main determinant of FD. However, whether muscle length affects the sensitivity of FD to work is unknown, although this information might add to the understanding of the phenomenon.

Shortening amplitude affects the incomplete force recovery after active shortening in mouse soleus muscle.

Compared to isometric contraction, the force producing capacity of muscle is reduced (force depression, FD) after a work producing shortening phase. It has been suggested that FD results from an inhibition of cross-bridge binding. Because the rate constants of the exponential force (re)development are thought to be primarily determined by cross-bridge attachment/detachment rate, we aimed to investigate the components of force redevelopment (REDEV) after 0.

Deficiency or inhibition of oxygen sensor Phd1 induces hypoxia tolerance by reprogramming basal metabolism.

HIF prolyl hydroxylases (PHD1-3) are oxygen sensors that regulate the stability of the hypoxia-inducible factors (HIFs) in an oxygen-dependent manner. Here, we show that loss of Phd1 lowers oxygen consumption in skeletal muscle by reprogramming glucose metabolism from oxidative to more anaerobic ATP production through activation of a Pparalpha pathway. This metabolic adaptation to oxygen conservation impairs oxidative muscle performance in healthy conditions, but it provides acute protection of myofibers against lethal ischemia.