Principles of Skeletal Muscle Adaptation

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Presentation transcript:

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

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

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 Iiz myosin HC not only enlarged, but change in contractile phenotype larger, slower contracting fiber.

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

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

Signals for Adaptation Insufficient energy balance nutrition can also influence endocrine system - insulin endocrine system independent influence thyroid hormone IGF-1 - insulin like growth factor 1 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

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.

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

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

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

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

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

Age Changes in Muscle Reduction with age in ability to produce and sustain ms power physical inactivity may contribute to this decline, but not predominant explanation 65 yrs muscle mass dec by 25-30 % peak at 25 - 30 yrs possible explanations Fiber diameter diameter quite consistent until 70 Fiber number varied results - X-sec designed studies (measure subjects from different age groups)

Age changes Motor Unit remodeling with age - alteration in normal turnover of synaptic junction old - aggregation of type I Fig 19-9 - Motor units and age 47 % dec in both genders Muscle Function strength - dec 8% per decade after 30 atrophy (refer back to fig 19-3) power and endurance 30 % less in old - atrophy and other factors Fig 19-10,11

Response to Training Muscle and fiber hypertrophy and performance improvements can occur together with resistance training in aged Fig 19-12,13,14 following 12 weeks 110% increase in force (1 rep max) 9% inc in quadriceps area 34% inc X-xec area type I 28% inc X-sec area type II