Physiopathological mechanism of sarcopenia

The etiology of sarcopenia is multifactorial but still poorly understood, and the sequelae of this phenomenon represent a major public health issue. Age-related loss of muscle mass can be counteracted by adequate metabolic interventions including nutritional intake and exercise training. Other strategies including changes in daily protein pattern, the speed of protein digestion, or specific amino acid supplementation may be beneficial to improve short-term muscle anabolic response in elderly people. A multimodal approach combining nutrition, exercise, hormones, and specific anabolic drugs may be an innovative treatment for limiting the development of sarcopenia with aging.     

Recent data on the physiology of pain

Along the time, the relation between a painful stimulus and the created perception keeps on evolving. The distortion between stimulation and perception concerns all the steps of the painful messages transmission, from the peripheral level to the supraspinal sites. At the peripheral level, C or A delta fibres are excited by noxious stimuli. Involved molecules are released from cellular lysis, inflamed surrounding tissues and C or A delta fibres themselves. The progresses of molecular biology have once again enriched this peripheral inflammatory mix, which composition becomes more and more complicated: ATP and P2X3 purinergic receptor, bradykinin and B2 bradykinin receptor, H+ and ASIC proton receptor, vanillo?d receptor activated by heat, inflammation and increase in synthesis of sodic channels resistant to the tetradotoxine (TTXr).... The first synapses are modulated by excitatory amino-acids and many peptides, at the end of the peripheral nerves in the dorsal horn of the spinal cord A lot of supraspinal sites are activated: the brain stem, the pontomesencephalic regions, the thalamic sites and the cortex. Along the way, multiple mechanisms modulate the pain transmission: the painful perception depends on the balance between both exciting and inhibitory effects. Descending inhibitory controls triggered by noxious stimuli would play a decisive role in the extraction of the painful characteristic of information and would give it priority over other stimuli.     

Hypothyroid myopathy. Physiopathological approach]

Patients with thyroid deficiency often complain of muscular weakness, exercise intolerance, cramps and excessive fatiguability. Hypothyroidism induces a metabolic myopathy, with a fall of the energetic production, and especially of the mitochondrial metabolism. This is due to a global inhibition of the main oxidative pathways (substrate incorporation, substrate oxidation) and of the respiratory chain. A diminished energetic consumption is partially related to a transition in the myosin isoforms, which express a slower ATPase, and to an impairment of the trans-sarcolemic transports. Exercise intolerance could be due to an abnormal recruitment of several metabolic pathways, such as glycolysis, related to the mitochondrial metabolism impairment, and including an abnormal accumulation of protons and monovalent phosphate ions, which are involved in the alteration of the actin-myosin interaction, and also by an abnormal Ca++ metabolism. The decreased number of NA+/K+ ATPase dependent pumps could imply an abnormal intracellular Na+ level and explain the frequent disorders of the membrane excitability.