Sunday, March 28, 2010

Can we build our muscles in such a way as to make us taller?

Unfortunately, their are no muscles on the top of the head so we can't gain height via hypertrophy there.  Their are however several muscles in the feet so it could be possible to gain height by having your muscles act sort of like lifts making you taller.

Source: Southwest Orthopedics

The plantar surface refers to the bottom of the foot.  The feet do have an arch(unless you are flat footed) but as evidenced by high heels if any part if the feet is elevated the whole body is elevated.  If we can cause hypertrophy(muscle growth) in say our adductor hallicus and abductor hallicus we will be slightly taller!

The abductor hallicus moves our big toe away from the body so if we say wore toe weights and abducted our toes from side to side we would build up our abductor hallicus.  The foot is not as adapt as the hand(huge understatement) is at gripping but I have lifted a ten pound dumbell by placing it between my big toe and the toe next to my big toe.  This isn't quite as optimal as wearing toe weights and just moving your toes around but most exercises involve the usage of several muscles.

We all know that muscle mass correlates with bone mass but their are determinants of bone mass that are not accounted for by increased muscle masses(determinants that we try to create by say laterally loading the ends of the long bones).  Increasing muscle mass cannot hurt however...

And an increased muscle mass may have systematic effects that aid in bone building.

Muscle may also modulate myostatin activity which inhibits cellular proliferation.  Muscle also provides direct stimulation to the bone.

Is bone formation induced by high-frequency mechanical signals modulated by muscle activity?

"Bone formation and resorption are sensitive to both external loads arising from gravitational loading as well to internal loads generated by muscular activity. The question as to which of the two sources provides the dominant stimulus for bone homeostasis and new bone accretion is arguably tied to the specific type of activity and anatomical site but it is often assumed that, because of their purportedly greater magnitude, muscle loads modulate changes in bone morphology. High-frequency mechanical signals may provide benefits at low- (<1g) and high- (>1g) acceleration magnitudes[so a stimulus that occurs frequently and the peak point of the stimulus is achieved very rapidly]. While the mechanisms by which cells perceive high-frequency signals are largely unknown, higher magnitude vibrations can cause large muscle loads and may therefore be sensed by pathways similar to those associated with exercise. Here, we review experimental data to examine whether vibrations applied at very low magnitudes may be sensed directly by transmittance of the signal through the skeleton or whether muscle activity modulates, and perhaps amplifies, the externally applied mechanical stimulus. Current data indicate that the anabolic and anti-catabolic effects of whole body vibrations on the skeleton are unlikely to require muscular activity to become effective. Even high-frequency signals that induce bone matrix deformations of far less than five microstrain can promote bone formation in the absence of muscular activity[but these stimulus may generate a lot of hydrostatic pressure for instance]. This independence of cells on large strains suggests that mechanical interventions can be designed that are both safe and effective."

"Cortical surface bone strains generated in the proximal tibia during a 0.3g, 45Hz vibratory regime were measured in two adult BALB/cByJ mice16. Under isoflurane anesthesia, a miniature single-element strain gage (1mm gage length) was implanted on the antero-medial surface of the proximal tibia. Upon recovery from surgery and with the animal standing on the vibrating plate, strain data were collected at a resolution of approximately 0.5 microstrain (με). The vibratory oscillations induced peak bone strain oscillations at the antero-medial surface of the tibia on the order of approximately 10με. In the rat, decreasing the acceleration of the signal to 0.15g and increasing the frequency to 90Hz reduces the strain magnitude at the cortical surface to about 2με"<-the acceleration of the signal is more important than frequency.

"subjects subject to 10min/d low-level whole body vibrations (30Hz, 0.3g). A per protocol (PP) analysis demonstrated that women had to stand on the vibrating plate for at least 2 min/d to achieve a gain in bone mass, including a 3.9% net benefit in cancellous bone of the spine or a 3.0% net benefit in cortical bone of the femur. In this study and in contrast to the previous two, muscle was included as an outcome measure. The low-level mechanical signal elevated muscle mass, with a 7.2% net benefit in the total paraspinous musculature, a 5.2% net benefit in the psoas muscle and a 7.9% net benefit in the erector spinae"<-the increase in muscle mass was greater than that of the bone.

"the study which demonstrated anabolism in both muscle and bone of young women employed a frequency of 30Hz. Excitation frequencies of at least 400Hz are required for maximal power output when the muscle itself is stimulated. In contrast, when a muscle dynamically oscillates without any electrical stimulation, its natural frequency is between 10-50Hz"<-dynamic muscle contraction is within the range of frequencies to stimulate bone but we're not sure if this applies to stem cells and chondrocytes as well or just osteoblasts.

"Following a 28d protocol, bone formation rates in the metaphysis of the proximal tibia were 159% greater in 90Hz rats when compared to age-matched controls, but 45Hz rats were not significantly different from controls"<-so to induce bone formation with vibration the frequency has to be greater than that caused by normal muscle contraction 45Hz is less than 50.

"During treatment, mice were anesthesized and therefore, all muscle tone was removed. Mice were allowed to freely ambulate between treatments. After 3wk, trabecular metaphyseal bone formation rates were 88% greater in tibiae accelerated at 0.3g than in their contralateral control, similar to the 66% increase in formation rates of bones accelerated at 0.6g. Stimulated tibiae also displayed significantly greater cortical area (+8%) and thickness (+8%), together suggesting that tiny acceleratory motions – independent of direct loading of the matrix"<-So bone formation can occur independent of muscle activity but myostatin regulation by muscle could still potentially play a role.

Muscle contraction controls skeletal morphogenesis through regulation of chondrocyte convergent extension

"Convergent extension driven by mediolateral intercalation of chondrocytes is a key process that contributes to skeletal growth and morphogenesis. Using the zebrafish as a model system, we found abnormal pharyngeal cartilage morphology in both chemically and genetically paralyzed embryos, demonstrating the importance of muscle contraction for zebrafish skeletal development. The shortening of skeletal elements was accompanied by prominent changes in cell morphology and organization. While in control the cells were elongated, chondrocytes in paralyzed zebrafish were smaller and exhibited a more rounded shape, confirmed by a reduction in their length-to-width ratio. The typical columnar organization of cells was affected too, as chondrocytes in various skeletal elements exhibited abnormal stacking patterns, indicating aberrant intercalation. Finally, we demonstrate impaired chondrocyte intercalation in growth plates of muscle-less Spd mouse embryos, implying the evolutionary conservation of muscle force regulation of this essential morphogenetic process."

However, this doesn't provide evidence that enhanced muscular contration may further elongate chondrogenic cells.

"During endochondral ossification, the mediolateral intercalation of chondrocytes into columns is an important module that facilitates elongation and contributes to bone morphology"

"Cell intercalation is a morphogenetic process, which occurs in epithelial or mesenchymal cells and leads to tissue narrowing, known as convergence, and its elongation, or extension. During convergent extension, the intercalating cell moves to separate neighboring cells, while staying in the same plane. During intercalation, cells increase their length-to-width ratio, perpendicularly to the direction of tissue elongation"

" in mice, unlike in zebrafish, columns are formed in the absence of muscle contraction indicates that the first step of intercalation is mostly muscle independent."

"Muscle and bone are inextricably linked genetically, molecularly, and mechanically. The intertwining of the connections at the different organizational levels (subcellular, cellular, and supracellular) makes it difficult to tease out the relative contributions of each connection. For instance, a change in the molecular communication between the tissues on the cellular level will likely also change their mechanical linkage at the supracellular (i.e., tissue and organ) level and vice versa."

"oscillatory muscle stimulation to tail-suspended rats for 10 min per day for 4 weeks to show that stimulation at 20 or 50 Hz was able to maintain trabecular bone mass, whereas stimulation introduced at 1 Hz was ineffective. The stimulation at 20 Hz resulted in minimal matrix deformation (<100 microstrain), but resulted in a ninefold increase in oscillatory (peak-to-peak) intramedullary pressure (ImP)"

"IFF can result from bone matrix deformation (i.e., strain) associated with muscle forces during locomotion which give rise to local pressure gradients within the matrix and drive interstitial fluid through the lacunocanalicular system. Alternatively, IFF can be generated through elevations in ImP. Pressurization of the intramedullary cavity causes an outward pressure gradient from the intramedullary cavity to the periosteal surface to also induce IFF within the lacunocanicular system "

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