Low-magnitude Mechanical Signals Research Articles

Adipogenesis is inhibited by brief, daily exposure to high-frequency, extremely low-magnitude mechanical signals.

Obesity, a global pandemic that debilitates millions of people and burdens society with tens of billions of dollars in health care costs, is deterred by exercise. Although it is presumed that the more strenuous a physical challenge the more effective it will be in the suppression of adiposity, here it is shown that 15 weeks of brief, daily exposure to high-frequency mechanical signals, induced at a magnitude well below that which would arise during walking, inhibited adipogenesis by 27% in C57BL/6J mice. The mechanical signal also reduced key risk factors in the onset of type II diabetes, nonesterified free fatty acid and triglyceride content in the liver, by 43% and 39%, respectively. Over 9 weeks, these same signals suppressed fat production by 22% in the C3H.B6-6T congenic mouse strain that exhibits accelerated age-related changes in body composition. In an effort to understand the means by which fat production was inhibited, irradiated mice receiving bone marrow transplants from heterozygous GFP+ mice revealed that 6 weeks of these low-magnitude mechanical signals reduced the commitment of mesenchymal stem cell differentiation into adipocytes by 19%, indicating that formation of adipose tissue in these models was deterred by a marked reduction in stem cell adipogenesis. Translated to the human, this may represent the basis for the nonpharmacologic prevention of obesity and its sequelae, achieved through developmental, rather than metabolic, pathways.

Low-level mechanical signals and their potential as a non-pharmacological intervention for osteoporosis

exercise is recognised as a critical regulatory signal to the skeletal system, but which specific aspects of exercise are responsible for influencing bone mass and morphology and resisting fractures remains unknown. Recent data indicate that extremely low-level mechanical signals are anabolic to bone, and thus may be used, non-invasively, as a form of 'passive' exercise to positively influence skeletal status. to summarise recent experimental studies on the effect of low-level mechanical signals (hypothesised to serve as a surrogate for the spectral content of muscle contractility) as a potential non-pharmacological intervention for osteoporosis. low magnitude mechanical signals are anabolic to bone if applied at a high frequency (15-90 Hz). Long-term animal studies (1 year) show that these low-magnitude mechanical signals can increase cancellous bone volume fraction, trabecular thickness, trabecular number and enhance bone stiffness and strength. Studies in the mouse have shown that these low-level signals will stimulate bone formation rate and labelled surface in cortical and cancellous bone, but the molecular and genetic regulation of this mechanosensitivity is extremely complex. Preliminary studies in children with disabling conditions and post-menopausal women indicate that such signals can be efficacious in reversing and/or preventing bone loss. considering that the strains (deformations) that result from these low-level vibrations are far below (<1/1000th) those which may cause damage to the bone, we believe they represent a unique, non-pharmacological prophylaxis for osteoporosis. Given that so many physiologic systems are tuned to specific frequencies, such as sight, hearing and touch, it should not be entirely surprising that the musculoskeletal system would be responsive to frequency as well.

Low-magnitude mechanical signals that stimulate bone formation in the ovariectomized rat are dependent on the applied frequency but not on the strain magnitude

There is growing evidence that extremely small mechanical signals, if applied at a sufficiently high frequency, can serve as anabolic signals to bone tissue. To determine if the responsiveness of bone to low-magnitude, high-frequency parameters is modulated by endocrine imbalance, ovariectomized (OVX) Sprague–Dawley rats were subjected to whole body vibrations (WBV, 0.15 g) at 45 Hz ( n = 6 ) or 90 Hz ( n = 6 ) for 10 min/day, and compared to OVX age-matched controls ( n = 6 ). Five additional rats were used, in vivo, to establish the induced bone surface strain magnitudes (and strain rates). Following a 28 d protocol, bone formation rates in the metaphysis of the proximal tibia were 159% greater in 90 Hz rats when compared to age-matched controls, but 45 Hz rats were not significantly different from controls. Bone morphology of 90 Hz rats indicated significantly greater trabecular bone volume (22% and 25%) and thicker trabeculae (11% and 12%) over either controls or 45 Hz rats in the epiphysis of the distal femur, respectively. Despite the enhanced sensitivity of the skeleton towards the 90 Hz signal, the strain magnitudes and strain rates induced by this frequency were significantly lower than during 45 Hz vibration, suggesting that factors other than matrix strain are driving the anabolic response. Ideally, such mechanical signals represent a non-pharmacologic means of controlling bone mass and morphology in spite of systemic pressures for bone resorption.

The anabolic activity of bone tissue, suppressed by disuse, is normalized by brief exposure to extremely low-magnitude mechanical stimuli.

It is generally believed that mechanical signals must be large in order to be anabolic to bone tissue. Recent evidence indicates, however, that extremely low-magnitude (<10 microstrain) mechanical signals readily stimulate bone formation if induced at a high frequency. We examined the ability of extremely low-magnitude, high-frequency mechanical signals to restore anabolic bone cell activity inhibited by disuse. Adult female rats were randomly assigned to six groups: baseline control, age-matched control, mechanically stimulated for 10 min/day, disuse (hind limb suspension), disuse interrupted by 10 min/day of weight bearing, and disuse interrupted by 10 min/day of mechanical stimulation. After a 28 day protocol, bone formation rates (BFR) in the proximal tibia of mechanically stimulated rats increased compared with age-matched control (+97%). Disuse alone reduced BFR (-92%), a suppression only slightly curbed when disuse was interrupted by 10 min of weight bearing (-61%). In contrast, disuse interrupted by 10 min per day of low-level mechanical intervention normalized BFR to values seen in age-matched controls. This work indicates that this noninvasive, extremely low-level stimulus may provide an effective biomechanical intervention for the bone loss that plagues long-term space flight, bed rest, or immobilization caused by paralysis.