Thursday, June 28, 2012

Do you grow when you sleep?

Getting more sleep is one of the most commonly cited ways to grow taller but does it actually help you grow?  Does it only affect growth rate or can it increase adult stature?  Microgravity has been found to be pro-chondrogenic.  When you lay down there's less load on the bone.

Growing pains: are they due to increased growth during recumbency as documented in a lamb model?

"The rate and patterns of longitudinal bone growth are affected by many different local and systemic factors; however, uncompromised growth is usually considered to be smoothly continuous, with predictable accelerations and decelerations over periods of months to years. The authors used implanted microtransducers to document bone growth in immature lambs. Bone length measurements were sampled every 167 seconds for 21 to 25 days. The authors show that at least 90% of bone elongation occurs during recumbency and almost no growth occurs during standing or locomotion[so the more you are recumbant the faster you'll grow but that doesn't mean that your adult height will be larger]. The authors hypothesize that growth may also occur in children during rest or sleep, thus supporting the concept of nocturnal growth and perhaps a relationship to growing pains."

"Within a brief 1- to 3-day interval, children grew 1 cm or more, and this was followed by a much longer period of 10 to 50 days when no demonstrable growth occurred."<-This supports the theory that growth involves a build up and than an explosion where bone is pushed apart.  A build up of hypertrophic chondrocytes followed by apoptosis which pushes the bones apart allowing for new bone to be filled in.

"we found that overall growth consists of a period of rapid elongation with low-amplitude fluctuations. This pattern alternates with high-frequency fluctuations with no or negative growth as measured by microtransducers. The oscillations recorded by both transducers are thought to represent strains at the growth plate and in diaphyseal bone. We interpret these larger oscillations as growth plate compression (negative direction) and elastic recoil and/or growth plate tension (positive direction). Similarly, the oscillations in the diaphyseal transducer signal, while much smaller, are synchronous with oscillations from the growth plate transducer."<-Now just because most growth occurs during recumbancy doesn't mean that other activities can't benefit growth.  LSJL and other activities help with the build up phase before the explosive push that occurs during the recumbant phase.  It makes sense that the push comes during the recumbant phase as there is less force to overcome so the hypertrophic chondrocytes apoptosis' can push the bone apart farther to allow for more bone growth to occur in between.

" including increased growth at rest [may be] due to elevations in growth hormone (GH) and insulin growth factor (IGF-1)"<-this is a confounding variable as to whether recumbancy is the only factor affecting growth.

"when growth plate chondrocytes are stimulated by mechanical strain, the inhibitory loop may prevent bone elongation. It is possible that recumbency leads to decreased strain in the growth plate, with subsequent decreased synthesis of Ihh. Therefore, the Ihh-PTHrP inhibitory pathway is turned off and a cohort of growth plate chondrocytes would proceed to terminal differentiation characterized by hypertrophy, the phase during which most bone growth occurs."<-a mechanism as to how reduced load may trigger hypertrophy and in turn apoptosis.

Here's an article that explains how genes are altered during sleep and height is affected by genes:

A metabolic-transcriptional network links sleep and cellular energetics in the brain.

AMPK may mediate the inhibition of Lin28 activity and Lin28 is pro-height.

"When the AMP/ATP ratio increases due to consumption of ATP (a decrease in cellular “energy charge”), AMPK is phosphorylated by upstream kinases and initiates changes in the cell that slow ATP consumption. This mechanism appears to be at work in the brain in association with sleep; temporal patterns of AMPK phosphorylation provide evidence that this metabolic sensor reacts to changes in sleep/wake states. AMPK phosphorylation in the brain is reduced during times of day when sleep predominates. Enforced wake caused an increase in phosphorylated AMPK (pAMPK)"<-this should be true in non-brain areas like the bone.

NADPH oxidase 2 and 4 are required for chondrogenic differentiation.

"A high rate of ATP production will alter the NAD(P)H:NAD(P) + ratio."  However, the study mentions that sleep deprivation increases oxidative stress thus likely increasing NOX2 and NOX4.  However, Nox2/4 are important for the early stages of chondrogenesis.  Thus, loading, which induces oxidative stress, may be important for the initial stages of chondrogenesis and sleep may be important for later stages of chondrogenesis where there's less oxidative stress.

" GSK3β, like AMPK, is sensitive to cellular metabolic status and enforced wakefulness, and affects sleep. The phosphorylation of GSK3β increases in synaptosomes during enforced wakefulness"

"Overexpression of GSK3β shortens circadian period in cultured mammalian cells while pharmacological inhibition lengthens it."

phosphorylation of GSK3Beta promotes chondrocyte hypertrophy.  GSK3Beta degrades Beta-Catenin. Runx2 expressing cells must have virtually no Beta-Catenin.  This is not consistent with our theory as phosphorylation of GSK3Beta increases during wakefullness and GSK3Beta phosphorylation promotes chondrocyte hypertrophy.  However, the phosphorylation of GSK3Beta was increased in synaptosomes and this may or may not be true for stem cells or chondrocytes.

PPARgamma stimulates adipogenesis and thus less likely to stimulate chondrogenesis.

"PPARs, a family of transcriptional regulatory nuclear receptors, are sensitive to the endogenous sleep-promoting lipids anandamide and oleylethanolamide"

Sleep, ghrelin, leptin and changes in body weight during a 1-year moderate-intensity physical activity intervention.

"We randomly assigned 173 post-menopausal sedentary overweight (body mass index >or=24.0 kg/m(2) and >33% body fat) women aged 50-75 years living in western Washington State to either a facility- and home-based moderate-intensity physical activity intervention or a stretching control group. Fasting plasma ghrelin, leptin, measured height, weight and self-reported sleep were assessed at baseline and 12 months.
There were no consistent cross-sectional patterns between self-reported sleep measures and ghrelin or leptin at baseline. The weight loss differences between exercisers and stretchers were greater for those who slept less at follow-up than at baseline compared to those whose sleep duration did not change (-3.2 kg, 95% confidence interval (CI) -5.8, -0.5). Improvements in sleep quality were associated with significantly greater differences between exercisers and stretchers for ghrelin increases (improved vs same sleep quality: +115 pg/ml, 95% CI +25, +206) and leptin decreases (improved vs worsened sleep quality: -5.7 ng/ml, 95% CI -9.5, -1.5).
There was only limited evidence that changes in sleep duration or quality modified exercise-induced changes in weight, ghrelin or leptin. Moreover, the observed differences were not in the directions hypothesized. Future longitudinal studies including population-based samples using objective measures of sleep and long follow-up may help to clarify these relationships."

<-So sleep enhances exercise increases in Ghrelin and decreases in Leptin.  Remember though that Leptin is growth stimulating.  Ghrelin is expressed in the growth plate.

Now the one most commonly associated with sleep HGH:

Complexity and non-linear description of diurnal cortisol and growth hormone secretory patterns before and after sleep deprivation.

"The circadian secretory profiles of cortisol and growth hormone (hGH) in normal subjects are interrelated. Slight alterations in cortisol secretion are paralleled by similar ones of hGH secretion. Under physiological conditions an inhibitory effect of glucocorticoids on hGH secretion is more potent than a stimulatory one, while in normal young subjects the nychtohemeral cortisol and hGH levels are lower and higher, respectively, post 24 hours total sleep-deprivation, compared to baseline values. The aim of the present work was to further assess the qualitative characteristics of the 24-hour secretory patterns of these two hormones before and after 24 hours total sleep deprivation, by studying their non-linear profiles using fractal analysis.
Cortisol and hGH were measured in 24-hour samples drawn from 10 healthy men (mean age SD: 24 +/- 1 yr, mean BMI SD: 25 +/- 1 kg/m2) before and after 24 hours total sleep deprivation. Twenty-four hour blood sampling was performed serially every 30 min the day before and the day after total sleep deprivation. The 24-hour hormone profiles were analyzed by Fourier spectrum, in order to verify periodicities; the corresponding attractors were drawn and their respective fractal dimensions were calculated using the box counting method.
Diurnal cortisol levels before sleep deprivation gave rise to a fractal attractor with a D0 fractal dimension of 2.65 +/- 0.03, which decreased, post-sleep deprivation, to D0: 2.18 +/- 0.04. Growth hormone before sleep deprivation gave rise to a fractal attractor with a D0 dimension of 1.96 +/- 0.60, which increased to 2.24 +/- 0.60 post-sleep deprivation. These post-sleep deprivation changes of the fractal dimensions of cortisol and hGH, suggest that sleep deprivation leads to a more regular secretory profile of cortisol, while it tends to render hGH secretory profile less regular. Additionally, these changes of the fractal dimensions parallell the previously described quantitative overall changes of these hormones.
The post-sleep deprivation decrease of cortisol fluctuation might reflect the mechanism by which sleep deprivation temporarily improves mood in melancholic depression, a condition associated with hyperactivity of the hypothalamic-pituitary-adrenal axis."

So yes sleep raises HGH and lowers Cortisol.  No genes have yet been found directly linking HGH to height.  There's SOCS2 which affects the HGH/IGF-1 access.  But you'd expect there to be a gene enhancing HGH secretion to increase height if HGH has such a large influence.  However, HGH transgenic mice have been found to be twice as large as their littermates.

So sleep affects load(which is why you shouldn't sleep with ankle weights), AMPK, NADPH, GSK3Beta, PPAR, Ghrelin, Leptin, HGH, and Cortisol.  All of these may have varying effects on height.  However, these hormones may have different effects on stem cells and chondrocytes in different stages of differentiation which is why it is important to cycle recumbancy and activity.  It's possible that a deeper sleep or more recumbancy(weightless sleeping) could have more effects on height.

No comments:

Post a Comment