Association of Pain History and Current Pain With Sagittal Spinal Alignment and Muscle Stiffness and Muscle Mass of the Back Muscles in Middle-aged and Elderly Women

[Study Design] A cross-sectional study. [Objective] To investigate the association of low back pain history (LBPH) and LBP with sagittal spinal alignment, stiffness assessed using ultrasonic shear wave elastography, and mass of the back muscle in community-dwelling middle-aged and elderly women. [Summary of Background Data] The association of LBPH and LBP with sagittal spinal alignment, stiffness, and mass of the back muscles remains unclear in middle-aged and elderly women. [Participants and Methods] The study comprised 19 asymptomatic middle-aged and elderly women [control (CTR) group], 16 middle-aged and elderly women with LBPH (LBPH group), and 23 middle-aged and elderly women with LBP (LBP group). Sagittal spinal alignment in the standing and prone positions (kyphosis angle in the thoracic spine, lordosis angle in the lumbar spine, and anterior inclination angle in the sacrum) was measured using a Spinal Mouse. The stiffness of the back muscles (lumbar erector spinae and multifidus) in the prone position was measured using ultrasonic shear wave elastography. The mass of the back muscles (thoracic and lumbar erector spinae, lumbar multifidus, and quadratus lumborum) was also measured. [Results] Multiple logistic regression analysis with a forward selection method showed that the stiffness of the lumbar multifidus muscle was a significant and independent factor of LBPH. The stiffness of the lumbar multifidus muscle was significantly higher in the LBPH group than in the CTR group. Multiple logistic regression analysis also indicated that lumbar lordosis angle in the standing position was a significant and independent factor of LBP. The lumbar lordosis angle was significantly smaller in the LBP group than in the CTR group. [Conclusions] Our results suggest that LBPH is associated with increased stiffness of the lumbar multifidus muscle in the prone position, and that LBP is associated with the decreased lumbar lordosis in the standing position in community-dwelling middle-aged and elderly women

Deficient of a Clock Gene, Brain and Muscle Arnt-Like Protein-1 (BMAL1), Induces Dyslipidemia and Ectopic Fat Formation

A link between circadian rhythm and metabolism has long been discussed. Circadian rhythm is controlled by positive and negative transcriptional and translational feedback loops composed of several clock genes. Among clock genes, the brain and muscle Arnt-like protein-1 (BMAL1) and circadian locomotor output cycles kaput (CLOCK) play important roles in the regulation of the positive rhythmic transcription. In addition to control of circadian rhythm, we have previously shown that BMAL1 regulates adipogenesis. In metabolic syndrome patients, the function of BMAL1 is dysregulated in visceral adipose tissue. In addition, analysis of SNPs has revealed that BMAL1 is associated with susceptibility to hypertension and type II diabetes. Furthermore, the significant roles of BMAL1 in pancreatic β cells proliferation and maturation were recently reported. These results suggest that BMAL1 regulates energy homeostasis. Therefore, in this study, we examined whether loss of BMAL1 function is capable of inducing metabolic syndrome. Deficient of the Bmal1 gene in mice resulted in elevation of the respiratory quotient value, indicating that BMAL1 is involved in the utilization of fat as an energy source. Indeed, lack of Bmal1 reduced the capacity of fat storage in adipose tissue, resulting in an increase in the levels of circulating fatty acids, including triglycerides, free fatty acids, and cholesterol. Elevation of the circulating fatty acids level induced the formation of ectopic fat in the liver and skeletal muscle in Bmal1 -/- mice. Interestingly, ectopic fat formation was not observed in tissue-specific (liver or skeletal muscle) Bmal1 -/- mice even under high fat diet feeding condition. Therefore, we were led to conclude that BMAL1 is a crucial factor in the regulation of energy homeostasis, and disorders of the functions of BMAL1 lead to the development of metabolic syndrome

Association between physical function and the load pattern during stepping-up motion in community-dwelling elderly women

Objective: Stepping-up motion is challenging task for elderly people in daily life. The present study investigated the relationship between the load pattern during stepping-up motion at maximum speed and physical function in elderly women. Methods: The subjects comprised 109 community-dwelling elderly women (age 72.5 ± 5.3 years). The load pattern (maximum load, rate of load production, and stepping-up time) during ascending a 30 cm step at maximum speed was measured, using a step up platform that measures the load at the lower and upper level. Physical function, including hip and knee extensor strength and performance on the vertical jump test, one-legged stance test, timed “Up & Go” (TUG) test, and stepping test were measured. Results: Pearson’s correlation analysis showed that stepping-up time was correlated with the maximum load at the lower level (r = −0.51), but not with the maximum load at the upper level. A multiple regression analysis showed that hip extensor strength and performance on the vertical jump, TUG, and stepping tests were significant determinants of the load pattern during stepping-up motion in the elderly women. Conclusions: Our study revealed that rapid stepping-up ability was more closely related to the maximum load during push-off at the lower level rather than that during weight loading on the upper level, and that the load pattern during stepping-up motion in elderly women was associated with various physical functions such as the hip extensor strength, leg muscle power, dynamic balance function, and agility

Deletion of Bmal1 Prevents Diet-Induced Ectopic Fat Accumulation by Controlling Oxidative Capacity in the Skeletal Muscle

Brain and muscle arnt-like protein 1 (BMAL1), is a transcription factor known to regulate circadian rhythm. BMAL1 was originally characterized by its high expression in the skeletal muscle. Since the skeletal muscle is the dominant organ system in energy metabolism, the possible functions of BMAL1 in the skeletal muscle include the control of metabolism. Here, we established that its involvement in the regulation of oxidative capacity in the skeletal muscle. Muscle-specific Bmal1 KO mice (MKO mice) displayed several physiological hallmarks for the increase of oxidative capacity. This included increased energy expenditure and oxygen consumption, high running endurance and resistance to obesity with improved metabolic profiles. Also, the phosphorylation status of AMP-activated protein kinase and its downstream signaling substrate acetyl-CoA carboxylase in the MKO mice were substantially higher than those in the Bmal1flox/flox mice. In addition, biochemical and histological studies confirmed the substantial activation of oxidative fibers in the skeletal muscle of the MKO mice. The mechanism includes the regulation of Cacna1s expression, followed by the activation of calcium—nuclear factor of activated T cells (NFAT) axis. We thus conclude that BMAL1 is a critical regulator of the muscular fatty acid level under nutrition overloading and that the mechanism involves the control of oxidative capacity