Principles of Skeletal Muscle Adaptation

1. Principles of Skeletal Muscle Adaptation • Brooks ch 19 p 401-420 • 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 - 8-30 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 19-3 - 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 19-4 5-6 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 19-5 - 25 % dec in mito protein • Fig 19-6 - 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 19-2 - size and strength • Table 19-3 - strength vs. X-sec area