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SR-334 > RESISTANCE > Flashcards

RESISTANCE Flashcards

1
Q

Contraction Types - Isometric

A
  • activation of muscle when the joints spanned by the muscle are held in fixed positions
  • entails some stretching of tendinous connection and stabilise joint complexes during locomotion and maintenance of posture
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2
Q

Contraction Types - Concentric

A
  • the muscle is activated and shortens, power is generated and work is done
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3
Q

Contraction Types - Eccentric

A
  • the muscle is activated and lengthens due to an external force which exceeds that generated by the degree of activation
  • occurs during daily activities (e.g. walking down stairs) as work is done on the muscle and energy is absorbed, muscle acts as a brake
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4
Q

Contraction Types - Stretch-Shortening and Other Pre-Activation Contractions

A
  • combination of different types of contraction occur
  • ‘stretch shortening cycle’ = eccentric contraction of the muscle immediately prior to a concentric, power generating phase in running
  • leg extensor muscles generate power by concentric contractions but also act as a brake or shock absorber on landing, absorbing some of the Ep and Ek generated in the previous push off by the opposite leg
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5
Q

Sargeant, 1999 - Human Muscle Fibre Types

A
  • muscles meet demands for different mechanical output by variations in the contractile and metabolic properties of fibres
  • human fibres divided into 3 main types, Type I, Type IIa, and Type IIb
  • more of a continuum than 3 discrete types they currently are
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6
Q

Sargeant, 1999 - Fundamental Muscle Properties

A
  • maximum velocity of shortening of muscle fibres = Vmax
  • continuum of Vmax values between various types, and also within each type of isoform there is a considerable variability
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7
Q

Fundamental Muscle Properties - Length-Tensioning Relationship

A
  • isometric tension a muscle can generate depends on its length
  • tension is due to the interaction actin and myosin myofilaments within each sarcomere
  • as muscle lengthens to its limit, there is an increasing level of passive tension due to stretching
  • passive stretch tension is subtracted form active tension
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8
Q

Sargeant, 1991 - Muscle Length and Active & Passive Tension

A

Amount of actin-myosin overlap is indicated by:
- short length where A-filaments from opposite ends of sarcomere overlap and force is reduced
- optimum length where the greatest active force is generated due to maximum number of cross bridges
- at long length where there is no overlap and no cross bridges are formed

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9
Q

Sargeant, 1991 - Force-Velocity and Power-Velocity Relationships

A
  • force varies with the velocity of shortening or lengthening
  • as velocity of shortening increases, the force generated falls in hyperbolic fashion, eventually reaching zero at max muscle velocity
  • during lengthening, force increases above that attained at zero velocity (isometric) before plateauing
  • max power is generated at optimum velocity (Vopt), ~30% of Vmax when force is zero
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10
Q

Determinants of Maximal Strength and Power

A
  • muscle activation
  • muscle size and isometric strength
  • muscle size and maximal power
  • body dimensions and muscle function
  • muscle fibre type and power output
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11
Q

Muscle Activation

A
  • pre-requisite in determining max force is if the muscle is fully activated
  • muscle can be tested for MVC by applying electrical stimulation to muscle or nerve
  • can achieve almost-maximal VC’s in isometric exercise
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12
Q

Muscle Strength is Determined by Sarcomeres in Parallel NOT in Series

A
  • cross bridges act as force generators but are arranged in sarcomere units with opposing forces
  • no matter how many sarcomeres are arranged in series the net force will be equivalent to only one sarcomere
  • if the muscle is arranged with same number of sarcomeres arranged side by side all contribute to force production
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13
Q

Muscle Power and Muscle Size

A
  • Power = force x velocity
  • total distance will be 4x that of sarcomeres in parallel
  • muscular power should be normalised by number of sarcomeres in series and in parallel
  • reflected in measurements of muscle volume
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14
Q

Muscle Function, Body Dimensions and Performance

A
  • sometimes useful to express muscle function in terms of body dimensions (J/kg-1 BM)
  • important when body mass must be overcome by the exercising muscle
  • this method of scaling is often considered simplistic based on the pattern of muscle use, size and intrinsic function of the muscle group
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15
Q

Muscle Fibre Type and Power Output

A
  • Vmax and F-V relationship of muscle fibres is strongly determined by the MHC expression
  • force and power in relation to velocity for a type I and II fibre population that generate some isometric force but whose Vmax varies
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16
Q

Sargeant, 1987 - Muscle Fibre Type and Power Output

A
  • larger power output in type II fibres is reflected in data comparing untrained subjects (50% type II) vs ultra distance marathon runners (4% type II)
  • endurance athletes max power is only half of the UT subjects even though data was normalised for upper leg muscle mass
17
Q

Sargeant, 1987 - Acute and Chronic Plasticity

A
  • exercise can modify muscle properties
  • when ex continued to fatigue muscle contractile properties may be acutely transformed towards slower characteristics (Vmax is reduced and muscle becomes less powerful)
  • muscle fatigue may be greater at fast movement frequencies
  • increase in Tm also modify contractile and metabolic properties
  • effect of temp is velocity dependant so increases in Tm will also make muscle faster and more powerful at higher velocities
  • greater XBC rate and energy turnover reduce economy
18
Q

Effects of Caffeine Ingestion on Power

A
  • member of the methylxanthine family, chemical formula = C8H10N4O2
  • common in cola drinks (25-50mg Caffeine per serving)
  • energy drinks contain much more ( ~80mg)
  • present in chocolate and cocoa products
19
Q

Lopes et al., 1983 Caffeine Ingestion and MVC Performance

A
  • significant difference between placebo and caffeine at lower frequencies (10,20 and 50 Hz) but not 100Hz
  • caffeine consumption significantly affected performance of muscle contractions at slow to moderate speeds but not higher speeds
20
Q

Methodological Considerations of Caffeine Ingestion Studies

A
  • dosages
  • participant numbers
  • exercise protocols (max, sub-max)
  • control of environments (temp, humidity, biometric pressure)
  • control of subjects (caffeine users, sensitivity/tolerance to caffeine, age, etc)
21
Q

Mechanisms of Action - Excitation-Contraction Coupling

A
  • with excessive caffeine intake there is a heightened SR CA2+ release
  • effect may be greater in slow twitch vs fast twitch fibres
  • muscles contract in the presence of Ca2+
22
Q

Mechanisms of Action - Blocking Adenosine Receptors in the Brain

A
  • adenosine binds to A-receptors that cause nerves to release inhibitory signals that lead to drowsiness and sleep
  • caffeine blocks A-receptors and promotes continued nerve activity
  • caffeine antagonises adenosine (blocks the receptors), reducing adenosine actions so maintains/increases Ach release leading to continued release of brain cell NA and over-rides fatigue
23
Q

Bird et al., 2005 - Strength Training

A
  • many studies show a significant increase in performance with resistance training of sufficient training volume
  • but most training studies are short duration (<3 month) and use untrained subjects
24
Q

Factors That Interact to Affect Development and Maintenance of Muscle Mass

A
  • exercise
  • nutrition
  • genetics
  • endocrine
  • nervous system activation
  • environment
25
Q

Andersen et al., 2005 - Nutriton and Resistance Training on Muscle Fibre Size and Strength

A
  • protein group showed significant fibre hypertrophy of trained leg muscles (Type I=18.5±5%; Type II 26±5%), no change in CHO group
  • Protein group increased SJ by 9±2%
  • protein group improved CMJ by 10±2%, CHO group 7±6%
  • isometric and isokinetic eccentric and concentric peak torque at slow velocities increaesed 11-20%, no diff between groups
26
Q

Muscle Growth with Resistance Training

A
  • can be used clinically to treat muscle wasting (cancer, AIDS, burns)
  • muscle hypertrophy caused by increase in protein synthesis or reduction in protein breakdown
  • net protein accretion = protein synthesis - breakdown
  • protein synthesis and breakdown can vary 50-100% over a day due to age, diet and activity (Price et al., 1994)
27
Q

Lexell et al., 1988 - Human Resistance Training

A
  • large variability in number of fibres in a muscle
  • between 393,000-903,000 fibres in vastus lateralis
  • individual’s number is fixed, but size can be increased w resistance training
28
Q

Muscle Protein Synthesis Post-Ex

A
  • remains elevated for more than 48h post-ex in untrained (Rennie and Tipton, 2000)
  • protein breakdown also increases (Philips et al., 1997)
  • net protein breakdown may occur unless protein is consumed (Tipton et al., 1999)
  • mixed meal will increase appearance of AA (increased protein gain) and glucose (insulin decrease protein loss) (Rennie and Tipton, 2000)
29
Q

Muscle Growth and Resistance Training

A
  • max rate of protein synthesis by feeding alone requires 10g EAA’s i.e. ~20g total AAs or protein
  • need to eat protein and exercise to increase muscle hypertrophy
  • Philips, 2004 - upper safe limit of protein intake 1.33g.kg-1BM.d-1
30
Q

Factors Leading to Muscle Hypertrophy

A
  • first messengers binding to receptors causing propagation of cellular signals that activate a network of signal transduction pathways
  • cell nucleus TFs change expression of major muscle growth regulators IGF-1/MGF and myostatin or rRNA
  • IGF-1/MGF and insulin activate the PI3K-PKB/AKT-mTor pathway, enhances protein synthesis via increased translational initiation and the synthesis of ribosomal proteins for ribosome biogenesis

SR-334 (7 decks)

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