Presentation on theme: "1 Principles of Skeletal Muscle Adaptation Brooks ch 19 p 401-420 Outline Myoplasticity Protein turnover Fiber Type Training adaptations Adaptations with."— Presentation transcript:
1 Principles of Skeletal Muscle Adaptation Brooks ch 19 p Outline Myoplasticity Protein turnover Fiber Type Training adaptations Adaptations with inactivity, injury Age associated changes
2 Myoplasticity Altered gene expression - resulting in an increase or decrease in amount of specific protein –tremendous potential to alter expression in sk ms –molecular basis for adaptations that occur due to exercise tx in sk ms proteins 20%of sk ms is protein, balance is water, ions... –All types of protein can be regulated by altering gene expression Fig 19-1 cascade of regulatory events - impacting gene expression
3 Myoplasticity cont. myoplasticity - change either quantity (amount) or quality (type) of protein expressed Eg. Responses to training type IIb - hypertrophy (enlargement) - inc amount of protein in fiber –larger fast II b fiber Another fiber - hypertrophy –also repress gene for fast II b myosin HC, turn on fast IIa myosin HC –not only enlarged, but change in contractile phenotype –larger, slower contracting fiber.
4 Protein turnover Protein Turnover reflects 1/2 life of protein - time frame for existence –protein transcribed (DNA-mRNA) –translated then degraded level of protein in cell governed by –synthesis / degeneration ratio –precise regulation of content through control of transcription rate –and/or degradation rate capacity to regulate structural and functional properties of the ms –applies to both structural and contractile proteins and regulatory proteins –as well as enzymes involved in metabolism
5 Adaptation Sk ms adaptation characterized by –morphological –biochemical –molecular –variables that alter the functional attributes of fibers in specific motor units adaptations readily reversible when stimulus is diminished or removed Fig 19-2 intracellular and extracellular influences - reg gene pool expression –stimuli of sufficient amount for sufficient time- overload –lead to changes in expression of specific proteins - specificity
6 Signals for Adaptation Insufficient energy balance nutrition can also influence endocrine system - insulin endocrine system influence independent of nutrition – thyroid hormone –IGF-1 - insulin like growth factor 1 –mediates Growth Hormone effects power developed by motor unit –load against which fibers contract –specific responses to demands each result in acute changes in cellular environment –changes can lead to altered rates of protein synthesis and degradation –changes [ ] or activity of proteins
7 Hormonal Influences(cont) IGF-1 - GH stimulates release from liver hours –also muscle mediated release Autocrine/paracrine MGH - mechanogrowth factor –Training inc IGF-1 mRNA expression GH dependant and independant Endurance Training –GH- no change at rest –Less dramatic rise during exercise Unless training above lactate inflection Resistance Training –Testosterone and GH - two primary hormones that affect adaptations –Inc secretion with training –Testosterone - augments GH release Inc muscle force production - Nervous system influence
8 Phenotype When protein structure of muscle is altered - phenotype change –outwardly observable characteristics of muscle –reflects underlying genes (genotype) and their regulation by several factors (exercise) –altered phenotypes - affect cellular environment as well eg. Receptors, integrating centers, signal translocation factors and effectors - mechanisms not fully understood.
9 Muscle Fiber Types Elite athletes - specialized fiber typing –sprinter II b, endurance I Fig elite - ends of spectrum genetics - strong influence on fiber type disposition Training studies - alter biochemical and histological properties - not fiber type distinction - (myosin isoform) evidence, however, that intermediate transitions can occur in MHC expression - not detected with conventional techniques
10 Endurance Adaptations Occurs with large increase in recruitment frequency and modest inc in load –minimal impact on X-sec area –significant adaptations to metabolic –Inc mitochondrial proteins –HK inc, LDH dec(cytosol), inc mito 2 fold inc in ox metabolism –degree of adaptation depends on pre training status, intensity and duration Table 19-1 Succinate DH (Krebs) –response varies with fiber type - involvement in training –inc max blood flow, capillary density, and potential for O2 extraction
11 Adaptations to Resistance Training Increased recruitment frequency and load Hypertrophy - inc X-sec area Hyperplasia - inc cell number –major adaptation is with hypertropyhy - inc max force generating capacity Fig 17-28b - Force velocity after tx –move sub max load at higher velocity of shortening –enhanced power capacity Fiber type specific adaptation –inc X-sec area of both type I and II –Fig month longitudinal study –II - 33%, I - 27% increase
12 Resistance Training Fastest MHC’s repressed, inc in expression of intermediate MHC isoforms II x - II a mito volume and cap density reduced with resistance tx Fig % dec in mito protein Fig cap density dec 13% Adaptation with decreased activity large reduction in recruitment frequency and /or load reduction in ms and ms fiber X-sec area - dec in metabolic proteins Fig 19-8
13 Injury and Regeneration Induced by a variety of insults trauma, ischemia, excessive stretch eccentric exercise, dennervation active lifestyle - continuous population of regenerating fibers two phases immediate - mechanical secondary - biochemical - several days Gender differences Table size and strength Table strength vs. X-sec area