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Finals Readings Notes.pdf

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Department
Kinesiology
Course
Kinesiology 3347A/B
Professor
T.Olver
Semester
Fall

Description
Finals Readings Notes Lecture 6 – 160-178 - Fat cells distributed in clusters called fat depots (large number of adipose cells or adipocytes held together by a scaffold-like structure of collage and other structural molecules) o Abundant neural connections and rich network of blood vessels o Involved in endocrine, autocrine, and paracrine actions - LPL – regulates lipid storage in adipocytes by transport to the capillary endothelium and hydrolysation of fatty acids from circulating triglycerides, allowing for FA uptake by adipocyte o Synthesized by adipocyte and regulated by hormones - Leptin – peptide released by adipocyte, regulates food intake, energy expenditure, glucose and lipid metabolism, puberty, reproductive functions, angiogenesis, and other processes - Fat cells also secrete IGF-1 and PAI-1 (high levels ▯ increase blood clotting) - Angiotensinogen – may be involved in adipogenesis - ASP – stimulates triglyceride synthesis in adipose tissue, results from enzymatic modification of C3a which is secreted by adipocytes in the adipsin-ASP pathway - TNF-a – may be involved in a feedback loop limiting growth of adipocytes Stages and mechanisms of adipogenesis - Multipotent mesenchymal cells ▯ adipoblasts ▯ fate commitment ▯ preadipocytes ▯ very small adipocytes ▯ mature adipocytes - Originally thought that mature adipocytes contribute to adipose tissue hyperplasia, no in vitro or in vivo studies support this, however, we know that PPAR-y, CCAAT/C/EBP, ADD-1 and SREBP-1 have been marked as important - Fat cell size is augmented after exposure to excess insulin and glucocorticoids or deficient growth hormone + testosterone - Fat cells become smaller when the cell is exposed to high levels of growth hormone, thyroid hormone or TNF-a - Fat cell # increases with high levels of insulin, cortisol, growth hormone and thyroid hormone White and brown adipose cells - White – fat cells with one large droplet of lipid, well innervated and vascularized - Brown – several small lipid droplets, nucleus not compressed, more mitochondria, main purpose not to store lipids, but to generate heat, usually smaller than white adipocyte, only present around the kidney, back of the neck, interscapular region of the back in newborns, disappears after infancy, highly vascularized and innervated, Prenatal/postnatal life - Prenatal life – no sex differences, earliest indication at 14 week of gestation, after the 23 week, multiplication for adipocytes and vascularization for adipose tissue are predominant, differences in body fat content between babies ha to do with triglyceride content, not cell #, body fat is essential to sustain baby between birth and first feeding - Postnatal life – increases from 5 billion to 30-50 billion in non-obese young adult, hyperplasia + hypertrophy o Adipocyte size – increase 2-3 times during first year of postnatal life and increase again for females during puberty o Adipocyte number – exact mechanism of adipogenesis is unknown, cell number increase 2-3 times from 1-2 years, then doubles with the onset of puberty and plateaus o Obese subjects indicated in below graph, open circle is obese, closed circle is normal, obesity is due to increased cell number Metabolic properties of fat cells - Storage of lipid and breakdown of triglycerides through LPL pathway Metabolic variation among fat depots - Differences in surface receptos, regualtion in gene expression, activites of key metabolic enzymes, sex hormones, etc., no studies on children or adolescents, only adults - Two major findings: 1) is not a single entity 2) differences inf at topography (allocation of fat) are associated with individual differences - Gender trends durign puberty support that males accumulate fat in trunk while bitches just accumualte fat everywhere Subcutaneous fat dsitribution during growth Radiographic data - Girl have more subcutaneous fat than boys at all ages from infancy to 18yrs - Rapid rise in both sexes during first 6months of life then reduction through 6-7 years with linear increase after through puberty for girls and slight increase from 7-12 yrs in boys and decrease through puberty Skinfold thickness - Girls have more subcu fat There are more but just go to page 170-171 for graphs Abdominal visceral fat ring growth - Can be detect as early as 4 years of age at ~10% of visceral fat area commonly seen in normal- weight young adults, most visceral fat is believed to be extrapetoneal or surrounds the kidneys - In adults, amount of abdominal visceral fat is strongly ocrrelated with total adiposity Lecture 6B – 137-157 – Muscle - Three types: skeletal, cardiac, smooth Chemical composition of muscle - Fetus – small, few in number, separated by extracellular material - Postnatal – small, greater in number, more closely packed - Adult – fibers are larger in diamete, little space between them - These changes are due to: o ↓extracellular ions (Na, Cl), ↑intracellular cosn▯tuents (K, P) o ↑nonprotein + protein nitrogen Molecular architecture of muscle Myofibrillar and contractile system - Muscle fiber has 100-1000 myofibrils, myofibril is the contractile unit of the muscle, myofilaments are the contractil eelements of the myofibril - Myofilament – dark lines are z-line/disk, white area is sarcomere - Sarcomere – thick filament with myosin and thin filament with actin/tropponin/tropomyosin anchored to the Z-line/disk - Myosin is the molcule responsible for contraction, made of two heavy chains and four light chains, two MLC bound to each MHC, MHC is composed of light meromyosin and heavy meromyosin, HMM is hinge region and contains S1 and S2, S1 hydrolyzes ATP and is the motor Muscle connective tissue system Three layers – endomysium (muscle fiber), perimyseium (fiber bundle), epimysium (whole muscle), not much is known about development of these layers Myogenesis - Require inhibition and promotion from various transcription factors, if Myf5 or MyoD are absent at 8 and 11 days of embryonic phase, no skeletal muscle ▯ DEATH - GDF-8 (mysotatin or growth and differentiation factor 8) is a strong negative regulator of embryonic muscle growth, knockout of GDF-8 ▯ twofold increase in muscle mass - Over expression of mysotatin during embryonic phases reduce myogenesis - Testosterone and IGF-1 exposure may increase cell differentiation (Bhasin)th - Skeletal msuclecontractiona s early as 8 week of gestation - Lecture 6c – 121-135 – Bone Osteocyte - Mature bone cell, osteoblasts that become embedded in bone matrix, contains inorganic (hydroxyapatite derived from calcium and phosphate) and organic compounds (collagen), surround Haversian system (canals that run parallel with the shaft that innervate and vascularizes bone) Osteoblast - Bone forming cells, differentiated mesenchymal/osteoprogenitor cells from mesoderm, periosteummarrow, secretes osteon, osteocalcin, osteonectin, osteopontin - Osteoblast produces collagen and ground substance, becoming osteocyte which them mineralizes collagen with hydroxyapatite Osteoclast - Resorb bone tissue, differentiated monocyte macrophages, removes mineralized matrix and collagen, reside in resorption bays, contains lysosomes (acid phosphatases for resorption) - Requires the presence of RANKL and is inhibited by OPG secreted by osteoblasts Bone formation - Two processes – intramembranous ossification and endochondral ossification o Intramembranous ossification – flat bones of skull, maxilla, mandible clavicle, non-cartilaginous from mesenchymal cells o Endochondral ossification – postcranial skeleton, develops from cartilage Notes on bone growth - At week 8 hyaline cartilage begins ossification - Ossification of the CO in long bones occurs prenatally - Ossification of the SCO in long bones occurs prenatally and postnatally (infancy) - SOC occurs and completes earlier in females than in males - Femur and tibia increase in length by ~60% during first year of life (0-1 years), declines it ~30% (1-2), ~15% (2-3), `7% (3-4) - Takes 20 years for total shift from cartilage model ▯ mature skeleton - Parathyroid hormone – bone resorption responds to low Ca+ conc in blood - Glucocotricoiods: promote bone resorption - Clitriol - ↑Ca absorp▯on, ↓PTH - Estrogen – protects from excessive bone turnover - Vitamin K - ↓osteoblast apoptosis - IGF-1/GH – stimulate bone formation - NB – relationships are tentative/complex and multifactorial - BMC follows similar growth pattern as height and weight in both sexes (slide 28) - Girls plateau in BMC, BA, and BMD at around 15-16 years, this is not seen in military women Intramembranous ossification 1. Ossification center – MSC replicate around blood vessels and differentiate into osteoprogenitor cells forming a primitive collagen network 2. Calcification – other MSC differentiate to osteoblast and secret osteoid, trapping them and forming osteocyte to enhance the collagen network 3. Trabeculae – primitive collagen network (bone spicule)rearrange to become trabecular bone 4. Periosteum – MSC surrounding the trabecular bone form periosteum, the primary center of ossification is between the periosteum surface and trabecular bone, bone growth occurs here Endochondral ossification - 1. Bone is formed prenatally as a cartilage model and a perichondrial membrane envelops the model to hold shape and provide structure to bone, hypertrophy occurs, collagen fibers appear between cells to further separate them a. Bone collar forms by week 8 in utero b. Outer fibrous layer of fibroblasts that develop to collagen c. Inner chondrogenic/osteo B layer that form cartilage 2. Hypertrophy cartilage cells calcify while osteoblasts from on the outer surface near its center 3. Osteoblasts begin to deposit bone matrix the surfaces of calcified cartilage cells creating a center of ossification, this process also causes vascularization, occurs by week 12 in utero 4. CO is made of cancellous bone with spicules, calcified cartilage and is highly vascularized, continued growth leads to the establishment of marrow cavity and growth plate a. Marrow cavity is formed by the resorption of cancellous bone by osteoclasts and deposition of compact or cortical bone by osteoblasts beneath the periosteum b. At the growth plate, thin layer of proliferating cartilage cells adjacent to hypertrophying cartilage cells resulting in bidirectional growth 5. The epiphysis is formed from the secondary center of ossification (pre/post natally) which develops at the ends of long bones, as both centers grow, cartilage layer becomes thinner and thinner and disappears in adulthood 6. Bone growth begins to slow or stop when ossification exceeds chondrocyte proliferation at the growth plate, proliferation is outmatched by cartilage cell degeneration and ossification/remodeling a. NB – bone remodeling is ongoing b. Growth plate disappears and the diaphysis and epiphysis mold together Bone Graphs BL – males do not level off as much as females, as you age, your bones get bigger and content increases BL – increase weight, increase mineral content, Girls have slightly higher BMD due to earlier growth spurt Lecture 7a – 283-336 Biological maturation - Skeletal vs. sexual vs. somatic Skeletal maturation – cartilage model entirely replaced by bone - Initial ppearnace of bone centers on x- ray + characterization + union of epi- diaphyses = predict skeletal age by entering into a model - Computer images of x-rays will qualitatively compare against averages - Note that skeletal maturation is separate from chronological age, sexual maturation, etc. Sexual maturation - Acontinuous process that begins with embryonic sexual differentiation ▯ puberty ▯ sexual maturity/fertility - Three indicators: o Secondary sex characteristic – breast growth + menarche in females, penis and testes development in males, used to assess stages of sexual maturity o Maturation of reproductive system – development of ovum and capable of carrying pregnancy to term, development of mature sperm, used to assess stages of sexual maturity o Adolescent growth spurt - Tanner-Whitehouse Stages of sexual maturation o Stage 1 – prepubertal (B1, G1, PH1) o Stage 2 – elevation for breasts, enlarged genetials, PH (little) o Stage 3&4 – more of 2, difficult to differentiate o Stage 5 – adult, mature state o Stage 6 – not a requirement and only applies to increase PH - The issues with the Tanner-Whitehouse method is that assessments must be done in a clinical setting, assessments are also very qualitative in that it is usually by direct comparison of the subject to pictures, self-rating can be used, but data suggests a tendency of youngsters to overestimate early stages and to underestimate later stages of sexual development - Menarche – first menstrual cycle, age at menarche is common indicator of F maturity, requires adequate bf% of`17%, majority of cycle during the first year of/post menarche do not contain the release of an oocyte o Age of menarche is decreasing Somatic maturation - Growth curves - Height velocity curve o Two main parameters – takeoff (TO) which gives the sense of timing and peak height velocity (PHV) gives the sense o Early maturers have a higher PHV to compensate for decreased period of growth o Age at PHV is an indicator of somatic maturity Biological maturation - B2>PH2>PHV(cm/y)>B3>PH3>PH4>B4>Menarche>PH5>B5 o ~80% begin with B2 - G2G3>PH2>G4>PH3>PHV(cm/y)>PH4>G5>PH5 o ~98% begin with G2 - Systems develop simultaneously but at different rate, so how do we create a standard of comparison? - Here we have two curves, height velocity and BMC, what we see is that bones are growing faster than they are replacing their density resulting in imbalances and periods for development that are prone to weakness - PHV is noted to be before peak BMC velocity leaving children ages 5-10 susceptible to more bone breaks - Girls who have a higher age at menarche tend to have lower peak BMC velocity - - Know this Lecture 7b – 399-402 Hormonal regulation - Intracrine – internal hormone-like molecule becomes active - Autocrine – secreted hormones impacts producing cells - Paracrine – secreted hormone impacts neighbouring cells - Endocrine – hormones are transports in the blood and act on many different tissues in proportion to receptor density Endocrine - Organs that can produce/secrete active hormones: pituitary, thyroid, parathyroid, pineal body, thymus, adrenals, pancreas, ovaries, testes, liver, kidney, stomach GIT, adipose tissue, etc. - For each hormone there are specific receptors located throughout the body in different densities - Pituitary, parathyroid, pancreas o Release protein/protein derivatives o Bind to membrane receptors (signal transduction) - Gonads, adrenals (cortex) o Steroid hormones (sex and adrenal) o Bypass membrane through diffusion, bind to receptors in cytoplasm o Hormone-receptor complex translocates into nucleus to elicit a response (ex. gene expression) - Adrenal medulla, thyroid o Amines from AA o Cell surface receptor mechanism (EPI) o Nuclear receptor (thyroxine) Growth hormone - Produced in anterior pituitary, decreases rate of CHO uptake at muscle, enhances lipid mobilization, stimulates production of IGF in liver ▯↑LBM - General trends: o Released diurnally, bursts occur at night o GH pulses increase during puberty o Increase is not due to increased number of pulses (c, but rather increase magnitude of pulses (b) o IGF-1 - Primarily produced in the liver and is stable during the day and mediate GH - Stimulates cell proliferation including cartilage cells at growth plates – linear growth - Stimulates protein synthesis and nitrogen retention Luteinizing hormone - Produced in anterior pituitary - Promotes maturation of ovarian follicle/ovulation, estrog/progesterone release from ovaries, testosterone production from testes from Leydig cells - LH concentration increases throughout puberty with females having higher concentration in the end - FSH stimulates growth of ovarian follicles, LH promotes maturation of follicle, FSH spikes after onset of menopause and is relatively stable beforehand (both males and females) - FSH promotes growth of the seminiferous tubules and production of sperm, LH stimulates interstitial cells of Leydig to enlarge and produce testosterone Estrogen and testosterone - Estrogen/progesterone – released from ovarian follicles/adrenal cortex, acts on primary and secondary sex characteristics, increases nitrogen retention and fat mass in women - Testosterone – released from testes/adrenal cortex, acts on primary/secondary characteristics, promotes LBM/growth spurt and skeletal maturation Leptin - Produced from adipocytes, reaches CNS and acts on several hypothalamic neuron centers (high receptor density) - Overall effect is to regulate energy balance by decreasing food intake/increasing energy output - Supposedly increased fat mass ▯ ↑leptin▯↓fat mass, but this doesn’t happen due to “leptin insensitivity”, we still do not fully understand leptin - You need a certain level of leptin to undergo puberty - Leptin goes up in puberty and drops for boys - Leptin itself is not sufficient to trigger the advent of puberty, however, the absence of leptin prevents sexual maturation - Leptin is also involved in the regulation of the hypothalamic- pituitary-adrenal axis Physical outcomes - Hormonal changes ▯ changes in LBM, strength, aerobic fitness - PHV = peak height velocity, what we see is that gains in body weight is guided by fat free mass, not fat
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