Exercise-induced muscle injury in humans frequently occurs after unaccustomed exercise, particularly if the exercise involves a large amount of eccentric (muscle lengthening) contractions. Direct measures of exercise-induced muscle damage include cellular and subcellular disturbances, particularly Z-line streaming. Several indirectly assessed markers of muscle damage after exercise include increases in T2 signal intensity via magnetic resonance imaging techniques, prolonged decreases in force production measured during both voluntary and electrically stimulated contractions (particularly at low stimulation frequencies), increases in inflammatory markers both within the injured muscle and in the blood, increased appearance of muscle proteins in the blood, and muscular soreness. Although the exact mechanisms to explain these changes have not been delineated, the initial injury is ascribed to mechanical disruption of the fiber, and subsequent damage is linked to inflammatory processes and to changes in excitation-contraction coupling within the muscle. Performance of one bout of eccentric exercise induces an adaptation such that the muscle is less vulnerable to a subsequent bout of eccentric exercise. Although several theories have been proposed to explain this "repeated bout effect," including altered motor unit recruitment, an increase in sarcomeres in series, a blunted inflammatory response, and a reduction in stress-susceptible fibers, there is no general agreement as to its cause. In addition, there is controversy concerning the presence of sex differences in the response of muscle to damage-inducing exercise. In contrast to the animal literature, which clearly shows that females experience less damage than males, research using human studies suggests that there is either no difference between men and women or that women are more prone to exercise-induced muscle damage than are men.

Exercise-induced muscle damage in humans.

Neuromuscular diseases have been in the limelight for many years, mainly because of the growing interest in muscle and the application of new techniques, such as muscle histochemistry and electron microscopy. This book should be of great interest to muscle histochemists, and should appeal to clinical neurologists and neuropathologists who have more than a fleeting interest in muscle disease. In addition, technicians can use it as a manual for appropriate technical procedures. The authors are known authorities in the field of neuromuscular disease. The book is divided into three sections, each containing illustrations, basic pathology, and case histories—a beautiful integration of the clinical with the pathologic. The first section deals with the muscle biopsy procedure, histochemical stains and reactions, and details of normal and pathologic changes of biopsied muscle. The second section deals with pathologic and clinical aspects of individual neuromuscular disease drawn mainly from the authors' experience, and a

Muscle Biopsy: A Modern Approach

https://www.thelancet.com/pdfs/journals/lancet/PIIS0140-6736(97)09408-7.pdf

Familial Mediterranean fever.

We have examined the development of specific muscle fiber types in zebrafish axial muscle by labeling myogenic precursor cells with vital fluorescent dyes and following their subsequent differentiation and fate. Two populations of muscle precursors, medial and lateral, can be distinguished in the segmental plate by position, morphology and gene expression. The medial cells, known as adaxial cells, are large, cuboidal cells adjacent to the notochord that express myoD. Surprisingly, after somite formation, they migrate radially away from the notochord, becoming a superficial layer of muscle cells. A subset of adaxial cells develop into engrailed-expressing muscle pioneers. Adaxial cells differentiate into slow muscle fibers of the adult fish. We have named the lateral population of cells in the segmental plate, lateral presomitic cells. They are smaller, more irregularly shaped and separated from the notochord by adaxial cells; they do not express myoD until after somite formation. Lateral presomitic cells remain deep in the myotome and they differentiate into fast muscle fibers. Thus, slow and fast muscle fiber types in zebrafish axial muscle arise from distinct populations of cells in the segmental plate that develop in different cellular environments and display distinct behaviors.

Identification of separate slow and fast muscle precursor cells in vivo, prior to somite formation

Inhibition of mitochondrial beta-oxidation as a mechanism of hepatotoxicity.

Muscles and Their Neural Control

The effect of 2 hours of exercise on the serum creatine kinase (CK) level was investigated in 11 men and 9 women. The mean increase of CK 24 hours after exercise was significantly greater in men. The relative lack of CK elevation in women may: (1) indicate that female muscle is less susceptible to damage by adverse factors; and (2) explain discrepancies in previous reports.

Increased serum creatine kinase after exercise A sex‐linked phenomenon

Four patients with ptosis, external ophthalmoplegia, and ragged-red fibers on muscle biopsy were found to have decreased ventilatory responses to hypoxia and hypercapnia. Respiratory muscle weakness was not responsible for these findings since these responses were normal in muscle disease control patients. An altered metabolic state also can cause diminished ventilatory response, but overall oxygen consumption data in the ragged-red fiber patients were normal. The decreased ventilatory responses may be clinically significant because two of the ragged-red fiber patients had episodes suspicious of hypoventilation with poor response to hypoxia.

Depressed ventilatory response in oculocraniosomatic neuromuscular disease

Long-term colchicine prophylaxis in children with familial Mediterranean fever (recurrent hereditary polyserositis)

Infant mice (2 to 4 days old) received valproate (100 or 200 mg per kilogram body weight) subcutaneously once daily for 5 days. Both dosages decreased plasma beta-hydroxybutyrate levels to about one-third of the control value, in the face of normal free fatty acid and glycerol levels. At 200 mg per kilogram of valproate, there were significant decreases in brain weight and brain K content. Both doses produced metabolite changes in brain compatible with a reduced metabolic flux through the glycolytic pathway and the citric acid cycle. Valproate reduced brain aspartate but did not increase brain GABA levels in infant mice. At 200 mg per kilogram of valproate, brain glutamate decreased and taurine levels increased. Two hundred milligrams per kilogram of valproate caused a profound reduction of liver glycogen stores. The apparent decrease in cerebral metabolic rate, reduced glutamate and aspartate, and increased levels of taurine in brain may relate to the anticonvulsant action of valproate. Together with the decreased brain weight and K content, the findings are also compatible with maturational delay. Decreased ketonemia and liver glycogen content may relate to the hepatic toxicity associated with valproate administration in infants and children.

Chronic valproate administration produces hepatic dysfunction and may delay brain maturation in infant mice

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