Tuesday, June 21, 2011

Growing Taller with Heat

We know that water is a key component of growing taller.  Temperature alters the state of water thus it has the ability to alter hydrostatic pressure.  Something like LIPUS also increases temperature and the speed of chemical reactions.  Studying temperature and the effects of temperature on water and in turn on hydrostatic pressure will help us in our plans for growing taller.

Exercise mitigates the stunting effect of cold temperature on limb elongation in mice by increasing solute delivery to the growth plate.

"Ambient temperature and physical activity modulate bone elongation in mammals. Cartilaginous [growth] plates receive nutritional support via delivery of solutes from the vasculature. We [increased] solute delivery to the growth plate{this doesn't mean that cold and warm temperature modulate hydrostatic pressure too}. We housed 68 weanling female mice at cold (16°C) or warm (25°C) temperatures and allowed some groups voluntary access to a running wheel. Exercise mitigates the stunting effect of cold temperature on limb elongation after 11 days of wheel running. All runners had significantly lengthened limbs, regardless of temperature, while nonrunning mice had shorter limbs that correlated with housing temperature. Tail length was impacted only by temperature, indicating that the exercise effect was localized to limb bones and was not a systemic endocrine reaction{This could be a growth rate only effect however only a small change in temperature was studied}.  [There was] enhanced solute delivery to tibial growth plates in wheel-running mice{Cartilage is negatively charged which helps it attract positive ions which makes it absorb more water so enhanced solute delivery is related to water}, measured under anesthesia at rest. There was a minimal effect of rearing temperature on solute delivery when measured at an intermediate room temperature (20°C), suggesting that a lasting increase in solute delivery is an important factor in exercise-mediated limb lengthening but may not play a role in temperature-mediated limb lengthening{exercise may lead to permanent adaptions in vascularity in the surrounding tissues if not directly in the growth plates in contrast to a temperature change}."

"Growth plate cartilage does not have a penetrating blood supply. Growth plates receive nutritional support via delivery of solutes from the vasculature located in and around the adjacent bone"<-But the efficiency of the surrounding vasculature can impact the delivery of solutes to the growth plate.

"Environmental temperature and exercise may modify extremity growth by inducing changes in limb vasculature"<-Vasculature could also influence hydrostatic pressure too.

"High temperature, exercise, and stimulated muscle contractions increase blood supply to bone" <-This is why flexing may help improve LSJL results.

"Exercise markedly increased fluorescein tracer[fluorescin is a mechanism of measuring solute absorption] intensities in the growth plate and metaphyseal vasculature of wheel-running mice. There was no appreciable effect of temperature on fluorescein levels in the growth plate or vasculature" <-So the increase in vasculature can explain  height grain in the exercise groups but it can't in the temperature groups so likely hydrostatic pressure plays a role there.

"Moderate compression of articular cartilage has an anabolic effect on chondrocytes by stimulating changes in cell matrix, fluid flow, and biochemical activity. Since growth plate cartilage is composed of the same resident cell type, it is possible that increased compression of the long bones stimulates the same changes in growth plate cartilage to enhance its growth potential, whereas temperature acts through alternate mechanisms"<-That mechanism likely being hydrostatic pressure.

"Bone perfusion was only reduced in mice housed at their coldest study temperature (7°C) and did not differ between two warmer-housed groups (21°C and 27°C), even though limb lengths differed. It is possible that the temperatures used in the present study (16°C and 25°C) were above a similar cold threshold that maintains normal solute delivery to cartilage."<-However, the cold temp and warm temperature mice still differed in terms of limb length.

"To increase solute delivery to the growth plate, increase the total volume of blood arriving at a bone by increasing flow rate, enlarging vessel diameter (vasodilation), and/or increasing vessel numbers (angiogenesis)."<-Flow rate being the mechanism likely to enhance hydrostatic pressure.

"The WW[warm wheel] mice had slightly lower levels of fluorescein in the vasculature, yet their relative growth plate levels did not differ from their CW[cold wheel] counterparts."<-So the warm wheel had to be getting their solutes from another source than the vasculature.  However, it could be that cold temperature reduces bone density resulting in less fluorescein per square inch.

So therefore, vascularity explains the increase in bone growth due to exercise but not during temperature changes.  Changes in the composition of water may play a role in temperature differences.  There is very little change in density of water between 0 and 25 degrees celsius so the density of water is not likely to play a role.  The density decreases slightly from 0 to 25 degrees celsuis.  From 0 to 45 degrees celsius the amount of compression water does decreases.  After 45 degrees celsius it starts to rise again.  From cold to warm in the study water would be less compressible.  Less compression of water could lead to higher hydrostatic pressure.

Temperature regulates limb length in homeotherms by directly modulating cartilage growth.

"[A] strong positive correlations exist among latitude, ambient temperature, and limb length in mammals{of course the difference could be due to genotypic selection rather than adaptions in phenotype}. Although genetic selection for thermoregulatory adaptation is frequently presumed to be the primary basis of this phenomenon, important but frequently overlooked research has shown that appendage outgrowth is also markedly influenced by environmental temperature{but is this influence only in growth rate or does it affect adult stature}. Alteration of limb blood flow via vasoconstriction/vasodilation [partially explains] this growth plasticity{Water is likely involved and we can see what properties of water are involved by seeing what happens to the growth at which temperatures which correlate with different properties of water}. Peripheral tissue temperature closely reflects housing temperature in vivo, and chondrocyte proliferation and extracellular matrix volume strongly correlate with tissue temperature in metatarsals cultured without vasculature in vitro{Chondrocyte proliferation increase can still be inhibited by a limit in proliferative capacity so temperature increase wouldn't affect adult stature.  ECM volume could impact adult stature but does ECM volume always increase with increasing temperature}. Vasomotor changes likely modulate extremity growth indirectly, via their effects on appendage temperature, rather than vascular nutrient delivery{appendage temperature affecting the properties of the compounds inside the appendeges like water}."

"Impairment of bone growth by disruption of blood flow is well-known, as are correlations of enhanced blood flow with bone elongation and ear enlargement"

"The ears, limbs, and tails of warm-reared mice were significantly longer than those of siblings raised in the cold, with no change in total body mass"<-If cellular proliferation was impacted then you'd think there would be an increase in cellular proliferation everywhere.

"Differences in core organ size appeared to account for the latter—hearts and kidneys were enlarged in cold-reared mice—{you'd think you'd need more than enlarged heart and kidneys to compensate for limb length gain} but differences in limb length were not explicable by diet and/or activity level, because cold-reared mice consumed substantially more food and were more active than their warm and control counterparts"

"Blood not only provides developing limbs with a reservoir of essential growth factors, nutrients, and oxygen, it is also an important source of heat"<-The larger the blood vessals the more heat available for the chondrocytes for chemical reactions.

"growth of neonatal mouse metatarsals (MTs) in culture maintained at cold (32 °C), control (37 °C) or warm (39 °C) temperatures"

"MTs from all three groups showed increases in length from baseline at two- and four-day time intervals, but total accrued growth was strikingly temperature dependent. Interestingly, although the control and warm groups differed only slightly in temperature (2 °C), this small increase was still sufficient to produce significantly greater growth in warm MTs compared with both other groups"

So temperature seems to be beneficial at least up to 39 degrees Celsius.  Room Temperature is usually between 15 to 25 degrees celsius.  Saunas are typically between 70 and 100 degrees celsius.  A hot tub can go to 99 or 104.  If the growth benefits are related to water and compressibility you'd expect to see a decline in benefits around 45 degrees celsius.  It's also unclear whether the benefits of heat need to be sustained or can they be intermittent.  For example, a heating pad or the hot tub/jacuzzi.   Increased muscle mass could lead to elevated temperatures.

Increased blood vessel size and larger ECM could lead to higher growth during puberty as well as during LSJL.  As the temperature could impact the ability of stem cells to differentiate into chondrocytes.

Hindlimb heating increases vascular access of large molecules to murine tibial growth plates measured by in vivo multiphoton imaging.

"Dense extracellular matrix and lack of penetrating blood vessels create a semi-permeable "barrier," which hinders molecular transport at the vascular-cartilage interface. To overcome this obstacle, we employed a hindlimb heating model to manipulate bone circulation in 5-week-old female mice. Temperatures represented a physiological range of normal human knee joints. We used in vivo multiphoton microscopy to quantify temperature-enhanced delivery of large molecules into tibial growth plates. We tested the hypothesis that increasing hindlimb temperature from 22C to 34C increases vascular access of large systemic molecules, modeled using 10-, 40-, and 70 kDa dextrans that approximate sizes of physiological regulators. Vascular access was quantified by vessel diameter, velocity, and dextran leakage from subperichondrial plexus vessels and accumulation in growth plate cartilage. Growth plate entry of 10 kDa dextrans increased over 150% at 34C. Entry of 40- and 70 kDa dextrans increased < 50%, suggesting a size-dependent temperature enhancement. Total dextran levels in the plexus increased at 34C, but relative leakage out of vessels was not temperature-dependent. Blood velocity and vessel diameter increased 118% and 31%, respectively, at 34C. These results demonstrate that heat enhances vascular carrying capacity and bioavailability of large molecules around growth plates, suggesting that temperature could be a non-invasive strategy for modulating delivery of therapeutics to impaired growth plates of children."

But can this be used to increase height?

"There are two components of the vascular-cartilage barrier that determine solute availability in growth plates: 1) ability of molecules to exit the vasculature and 2) ability to enter the cartilage matrix. The endpoint of interest is total uptake in the growth plate since this is what ultimately impacts chondrocyte performance. Molecular size [is] a limiting factor for entry of fluoresceinated dextrans into mouse tibial growth plates.  A transport block [exists] at the metaphyseal chondro-osseous junction and molecules over 10 kDa [are] essentially size-excluded from the growth plate."

"heat increases 107 small solute (< 500 Da) uptake in growth plate cartilage in vivo"

One question is where there is any large molecules produced by the human body naturally or are available in foods and supplements that affect height?

No comments:

Post a Comment