Conduction velocity of nerve and muscle fiber action potentials after a space mission or a bed rest

Effect of 23-day muscle disuse on sarcoplasmic reticulum Ca2+ properties and contractility in human type I and type II skeletal muscle fibers

“…Although the loss of skeletal muscle mass induced by the disuse is widely acknowledged to contribute to this impairment, it has become increasingly evident that contractile dysfunction is disproportionately greater than decrements in cross-sectional area (CSA), as indicated by a decrease of specific force, suggesting a significant role played by decreased muscle "quality" in the dysfunction (4,9,15,33,51). It has been recently reported that the reduction of muscle quality can be attributed to a complex interaction of many factors that can affect neuromuscular transmission (4,24,42), muscle architecture (8, 9), muscle fiber phenotype (14,38), and contractile apparatus properties (20,21).Studies examining human muscle biopsies following a longterm period of muscle disuse have reported an overall shift in myosin heavy chain (MHC) isoforms from I to IIa to IIx (51), though this is not seen with shorter term disuse (6, 30). Interestingly, measures of contractile function of single fibers collected from human muscle biopsies have shown a decrease in Ca 2ϩ sensitivity and a loss of specific force, indicating the presence of single-fiber intrinsic qualitative changes (6,20,21).…”

“…Although the loss of skeletal muscle mass induced by the disuse is widely acknowledged to contribute to this impairment, it has become increasingly evident that contractile dysfunction is disproportionately greater than decrements in cross-sectional area (CSA), as indicated by a decrease of specific force, suggesting a significant role played by decreased muscle "quality" in the dysfunction (4,9,15,33,51). It has been recently reported that the reduction of muscle quality can be attributed to a complex interaction of many factors that can affect neuromuscular transmission (4,24,42), muscle architecture (8,9), muscle fiber phenotype (14,38), and contractile apparatus properties (20,21).…”

Descripción de los cambios en la velocidad media de flujo sanguíneo cerebral en posición supino y sedente, en pacientes con hemorragia subaracnoidea aneurismática con vasoespasmo asintomático o sin vasoespasmo: Serie de casos

“…Esta respuesta autónoma estaría permitiendo mantener VMFSC sin diferencias significativas entre el supino y sedente, incluso en aquellos pacientes con VEA basal. El esfuerzo cardiovascular durante el sedente se debe a que el reposo prolongado produce un deterioro en la respuesta cardiovascular al ejercicio 16 , cuyos efectos se ha visto que pueden ser disminuidos con una intervención física de movilización y activación en cama precoz 18,21 . Analizando los promedios en las VMFSC, existe una tendencia a la disminución con el cambio ortostático; y sólo en aquellos pacientes que posteriormente hicieron VE se observó una leve tendencia al aumento en la VMFSC.…”

“…Los pacientes que generaron VE posterior fueron sentados en los días de mayor riesgo de VE (día 7 ± 5) 7 , siendo en su mayoría mujeres, lo que se condice con la literatura 1,3 . Al analizar el nivel de sangrado mediante escala Fisher y la presencia de VE, los pacientes conVEA basal presentaban distintos niveles Fisher (I-IV); y aquellos que generaron VE posterior presentaban niveles de sangrado mayores (III y IV) 2 y se encontraban en el período de mayor riesgo de generación de VE 16 . Sin embargo, 52,3% de los sujetos con VMFSC normal basal no presentaron VE días posteriores al sedente, a pesar de presentar niveles escala Fisher III-IV.…”

What Is Being Trained? How Divergent Forms of Plasticity Compete To Shape Locomotor Recovery after Spinal Cord Injury

“…Clinical studies have shown that both long-term prolonged bed rest without traumatic CNS injury and microgravity in spaceflight may induce slower axonal conduction velocity in the branching axon terminals. 95 Furthermore, 4-week lower extremity unloading without traumatic CNS injury induces substantial maladaptive spinal plasticity contributing transient neurological dysfunction, suggesting that the muscle deconditioning due to disuse decreases afferent input and proprioceptive feedback in consequence of adaptation to unloading condition. 96 While these findings suggest that hindlimb unloading may induce locomotor impairments, little is known about the direct effect of HU on spinal plasticity after SCI.…”