1
Q
What is a strength and conditioning coach
A
someone that makes strategic decisions about stress allocation across biological systems over time
goals
- optimize stress and recovery to improve performance at the right time
- reduce injury/re-injury risk
2
Q
What is a personal trainer
A
someone who provides individualised exercise programming and client instruction
goals
- helps clients meet their personal goals
- provide external motivation and accountability
- educate on health and wellness
3
Q
What are the 3 pillars of the scientist coach
A
- mechanist understanding
- measurement literacy
- strategic judgement
4
Q
What does evidence based mean
A
using the best, high quality, systematic evidence available to make decisions about care and treatment
5
Q
EBP
A
Evidence Based Practice
6
Q
Step by Step EBP
A
- define the problem you wish to investigate PICOT
ASK QUESTION - search peer-reviewed literature, discuss with other coaches or academics
SEARCH - determine the quality and applicability of what you find in you search. pay attention to reproducibility and sources of bias
CRITICALLY APPRAISE - decision should be base on the strength of research, athlete needs, budgetary restrictions and professional judgment
IMPLEMENT - assessment of the effectiveness of the application
EVALUTE
7
Q
Does load determine adaption
ie same weight but smith machine vs free weight
A
no
- they are performed different ways and follow a different trajectory
- the smith machine is fixed limiting ROM
- depends on the technique of how one preforms their squat
8
Q
Does squat position alters torque
A
different position will produce different results as they target different muscle groups
however neither is right or wrong it just depends on what you are trying to achieve
9
Q
Does load determine adaption
A
no
load is external and is used in a way of adding stress to the body (stressor)
torque distribution follows imposed stress, it is the internal resistance in the muscle system (resistance)
adaption follows imposed stress
10
Q
Adaption follows the
A
stress
11
Q
Load does not determine
A
adaption
12
Q
What determines adaption
A
imposed stress
the same external load can produce difference joint moments, which creates different force vector which produces different adaptions
the load is the stressor but the stress stimulus comes from the internal resistance
13
Q
Does technique alter torque distribution
A
yes, how you do the exercise can determine which muscle groups you target, through changing the force trajectory changing the torque and therefore the adaptions in the muscle groups
14
Q
How technique modifies mechanical stimulus
A
- technique factors modify constraints
- altered joint moments
- altered force vector
- altered stimulus
- different adaption
15
Q
Specificity
A
is the degree to which training matches the mechanical and energetic demands of performance
specificity operates at the level of motor control
16
Q
Free Weights vs Machine
A
machines are safer due to being more stable and allow to target or isolate specific muscle groups but rely on the quality of the equipments
free weight allow for more global muscle activation, and greater control of the movement tempo, and testosterone production
17
Q
Core stability scientific basis
A
the spine is unstable and having poor core stability leads to low back pain
through strengthening the core this allows the spine to stiffen and decrease back pain
18
Q
Stability
A
refers to the state of equilibrium, where mobility and control of the spine are at an optimal balance. when we are stable we have fluid movement with the muscle activating at the optimal time and amplitude for the movement
19
Q
Back Pain
A
most common pain globally
the back pain is often caused by excessive/hyper active muscles around the spine which are working harder than usual to stabilise the spine so they fatigue faster
but this also depends on ones pain barrier
20
Q
Benefit of core exercises
A
when you strengthen you core muscles you have greater control and stiffen your trunk.
however when you stiffen your trunk you decrease motility which can be bad in some movements so it is important to find the optimal stability for the specific task at hand
21
Q
Stability Control
A
is the task specific control of the COM relative to the BOS which
- limits around the COM
- limits result from the interaction between velocity and position of the COM with respect to the BOS
- other factors can affect our ability to expand our limits of stability
22
Q
Core exercise importance
A
it is important that the core exercise are able to reflect and benefit the task one it training for. it should be dynamic by using similar muscles and tempo for both
23
Q
Core Should
A
- enhance force transfer
- improve inter-muscular coordination
- improve proximal to distal sequencing
- be context dependent
24
Q
Posture and Stability
A
the ideal posture has optimal stability. you don’t have to use your muscles to hold you up, making it more efficient
25
Posture and Muscle Synergies
posture can alter the way we use muscle synergies, when posture change, synergy selection changes.
26
What is 'good' posture
posture is the relationship between segments that optimises force transmission for the task
27
Should you do core exercises or assistance exercises first
core exercises ie lunges or squats before assistance exercise ie russian twists so you are warmed up
28
Specificity lives in
motor control
29
before prescribing load identify
the limiting constraints
if adaption follows imposed stress then as coaches our job is not to add load it is to shape stress
30
What is symmetry
we are all asymmetrical by the nature of laterality. there anatomical and behavioural asymmetries such as dominants hands reflect cerebral organisation in our brain
31
Bilateral deficit
when the summed unilateral force (adding the right and then left side of the body force) is greater than the bilateral force (adding the total body force)
32
Sticking Point
is the position where the strength of the muscles can't overcome the resistance
occurs when the muscles are either to shortened or enlarged so they are weaker as the actin and myosin can't bind do produce a large enough force to overcome the resitance
33
Asymmetry and Sticking Point
this sticking point can be overcome through the asymmetry of the body through mechanical advantage and inter-muscle coordination
because the muscles do not have the mechanical advantage and cannot over come the sticking point. therefore we reposition ourselves to create an asymmetry to change the load on your muscle to engage other muscle group that have a mechanical advantage in this position to overcome the resistance
34
Regional hypertrophy
is when the bulk of the muscle tissue sits within the length of that muscle which often different to either side of the body reflecting how we favour that muscle
35
Is asymmetry correlated with injury
reasons finding are inconsistent
because it is highly task specific , calculation issues or validility
36
Is asymmetry associated with reduced performance
no
- bowlers with greater flexion angle depending on what arm the bowl with allows them to generate more force
- cyclists push harder with their stronger leg even though they sit symmetrically on the bike frame
- didn't effect sprinters, Usain Bolt had different leg length
37
Functional Asymmetry - Tennis
studies on tennis player from using the same arm found that muscle mass, bone length (only for those who played before puberty) and density of the bone differs
those who started playing tennis before puberty show stronger asymmetry and fewer injuries in racket arm
puberty made a difference because mechanical stress stimulate protein synthesis leading to tissue growth which then the bone adapted leading to better adaptions and become more anatomically adapted to their sports
38
Functional asymmetry and injury
asymmetrical sports that require high speed or ballistic movement should be a little asymmetrical to protect the spine some asymmetry is necessary
39
Unilateral vs Bilateral Training
both improve performance
bilateral is better for absolute strength and maximal force development
unilateral is better for acceleration and COD
40
When to do what type of training
General Preparation Phase - bilateral emphasis - focus on growing the muscle fibre
Development Phase - blend both uni/bilateral training
Performance Phase - still blending both but more unilateral as reflects a but closer to performance
41
The programming principle
capacity is often developed bilaterally
capacity is often expressed unilaterally
42
What are the three types of of athlete assessment
screening
monitoring
testing
43
Athlete assessment: screening
identifies risk or dysfunction
ie mobility screen
44
Athlete assessment: testing
measure performance capacity
ie, sprint time
45
Athlete assessment: monitoring
track changes over time
ie, GPS load
46
Athlete assessments history
in the early 1980s research showed that training variables influence the type of adaptions and performance improvements
- acute training variables
-specificity
then the concept of a needs analysis was born, enabling exercise prescription to reflect informed choices for program variables based on specific needs
47
The needs analysis
is a two stage process that include
stage one - an evaluation of the requirements and characteristics of the sport
stage two - an assessment of the athletes
(define sport constraints then once you put the athlete into the sport more constraints occur)
the ultimate goal is to design athlete specific training programme that improves performance and reduces injury risk
48
Steps for needs analysis vs injury prevention
establish injury risk vs perform needs analysis
identify mechanisms vs test selection
design testing battery and assess vs baseline testing
implement training intervention vs implement training programme
retest vs retest
essentially they mirror each other
49
Evaluation of the characteristic of the sport
- physical capacity/demands
- movement quality/biomechanics
- injury risk, what are the common injuries
50
Evaluation of the characteristic of the sport - injury profile
knowledge required
- define injury (grade, tissues, onset, complexity)
- what are the risk factors for injury
- prioritising risks for your sport
51
Depending on the characteristics of the injury depends on how
it gets treated
52
Defining sports injury: severity
an injury is any event occurring as a result of sport participation
this injury needs medical attention and time is lost off sport
time lost is usually equivalent to the amount of tissue magnitude of tissue damage. more time off = more time to rehab which is important as a SNC
53
Defining sports injury: injury risk
injury risk is the probability of injury occurring for any given athlete
risk fact is something that increases your chances of experiencing an injury
the epidemiology of the injury can be categorized in the determining of its characteristics
54
Injury Risk Factors
risk factors are the factors suspected to modify the likelihood of injury to an athlete
intrinsic - related to the athlete
extrinsic - related to environment
modifiable - something we can change to lower the risk
non-modifiable - something we cannot change to lower the risk (ie age)
55
Injury Surveys vs Surveillance
surveys are usually one time events that are method to report injuries
surveillance is an ongoing activity that can be built into the day to day operations of an agency
56
Epidemiologic Measures of Injury Risk
measures of injury frequency/rate represent the burden in a population
prevalence is the proportion of the total number of cases to the total population at risk with no regard to time at risk
incidence a measure of the risk developing some new condition within a specified period of time usually expressed as proportion or a rate with a denominator
57
Mechanism of Injury
describe the inciting event in biomechanics terms by defining the specific loading characteristics that lead to the tissue damage
- tissue fails due to acute stress or reduced failure tolerance
- acute load exceed tissue tolerance
- overuse tissue tolerance is reduced due to repetitive overload and inadequate remodelling
58
Evaluation of characteristics of the athlete
Key Performance Indicators (KPI) asses performance gaps within athletes
gapes
- metabolic condition
- speed and strength
- movement quality
59
Athlete screening
is used to identify risk factors
testing or screening
60
Testing vs Screening
testing = benchmarking: systematically measuring an athletes physical, physiological and psychological attributes
screening = safety and competency: determines the level or preparedness for loading patterns required by training sporting stressors
61
Who/when should we screen
- new athletes
- return to sport
- pre season
- after periods of significant growth
- new modalities
62
Practical screening skills
- observational skills, experiences and knowledge of loading patterns required of the sport
- use of video
- understanding how the mechanics of the body as a whole is important
- keeping good records and performing screening in a standardised fashion
63
Are testing and screening the same
no
64
What is the purpose of athlete testing
to identify performance gaps or intrinsic risks
65
What are the main 4 ways to athlete test
- physical capacity testing
- skill based movement quality testing
- physiological testing
psychological testing
66
Baseline Testing: What is the best way to test the exercises
this is important as the order of testing may influence the results of the test
- do the most fatiguing tests last in sequence
- put results on graph and find where the performance bottle neck is
67
Why monitor an athletes workload
- manual residual training effects
- dose response
- reduce risk of injury and enhance competition readiness
- making informed coaching choices
68
What are the 4 type of stretching
- static stretching = holding
- dynamic stretching/activation exercises = pulsing/swinging
- PNF Stretching = another person pushes against a muscle to activate the stretch
- fascia release = not very researched
69
What does stretching actually do
- Increase ROM
- Reduce injury risk
- improve performance
it is all about what stimulus we want to get, the response we want from the stretch
70
What limits our ROM in terms of structure
active structures - muscle fascicles
passive structures - tendons, joint capsules and ligaments restrict ROM with passive muscle elongation
viscosity - as the composition of a human can range from 50-78% water depended on many factors the viscosity of the tissue can substantially affect flexibility
central nervous system - furthermore, a highly activated CNS could increase muscle tonus and with a less relaxed muscle inhibit flexaility
discomfort - pushing a joint to its maximum ROM can be uncomfortable or painful and this the ability to tolerate this discomfort or pain may allow some individuals to stretch further than other more pain sensitive individuals
71
Is muscle stretching anatomically possible
biarticular muscles are easily stretched ie hammys
monoarticular muscle are anatomically impossible
72
How many skeletal muscles are in human body
640 skeletal
73
What part of the muscle is stretched
myofibrils can be stretched twice their resting length without damage
- titin = one of the most flexiable part of the muscle fibre
- coiled = meant for stretching allowing the actin and myosin seperate but still hold itself and protects the muscle from going to far
- fibronectin = the protein that will stimulate synthesis within the muscle as a response to stretch, which stimulates synthesis of growth in the tissue in response to mechanical deconstruction
74
What part of the muscle is stretched
actively produced force through shortening muscle and passively produced through lengthening muscle
as we shorted the muscle we reduce force producing but increase the tension on the tendon causing the bone to move causing ROM to change
as lengths increases we get a decrease in the force production but the total tension in the muscle will still increase through the passive tension
75
Does Stretching increase ROM
yes both acute and chronic increases in ROM have been observed in hamstring and gastroc but the trivial results regarding impact to muscle stiffness
76
How does stretching increase ROM - Acute
1. decrease viscosity - thixotropic effects which can be achieved from any stretch easily
- a decrease in viscosity leads to a decrease in fluid resistance through heating it up. this is the warmth you feel when you stretch the first response stimulated. Lowering the thixotropicity of the fluid in the muscle structures which means the fluid will move around a bit more easily reducing the resistance of the muscle to the stretch stimulus
2. alter muscle tone
- muscle spindle sensitivity
- golgi tendon organ activation
- alpha motor neuron firing rate
- CNS mediated changes in excitability
this is a CNS res`ponse through the muscle relaxing from heating up the muscle
77
Static Stretching Acute Mechanisms - Thixotropic Effects
thixotrophy is a time dependent property of materials where they become less viscous (more fluid like) when subjected to movement or stress but return to a more gel like state when left undisturbed. in the context of muscles, tendons and connective tissue the thixtropic effects influence stiffness, flexibility, and resistance to movement. without movement, tissues come stiffer due to the gel-like behaviour of intracellular and extracellular components, including actin-myosin cross bridges and connective tissue ground substance
78
Stress v Strain Curve
when we load the the muscle we stretch the muscle but when we release the load the muscle doesn't return to its resting length through the same path so the length and strain relationship changes between tension and release
the gap in between the curve is the energy that is returned back to the system after load is released the lost energy goes to the heat during the stretch
if we perform a stretch multiple times and the viscosity decreases so the thixocity decreases and we decrease the amount of energy we lose to heat each cycle as the fluid is looser. however after immobility tissues become more viscous/stiff leading to increased hysteresis when movement resumes
79
Static stretching acute mechanisms: muscle spindles
prolonged static stretching leads to a gradual desensitisation of muscle spindles, reducing the stretch reflex and decreasing muscle excitation. this lowers muscle stiffness and enhances ROM but may reduce force output and reaction speed.
- have to hold for longer than 30 secs to get this response so when prescribing stretching you need to say how long for. this is because when you stretch the spindle sends a response to the spinal cord then back to the muscle to create a muscle tone to decrease this tone we need to hold the stretch for long enough to flood the muscle spindle holding it in tension so long that the loo keeps running and turns itself off.
80
Stretch relaxation response
this is because wehn you stretch the spindle sends a response to the spinal cord then back to the muscle to create a muscle tone to decrease this tone we need to hold the stretch for long enough to flood the muscle spindle holding it in tension so long that the loo keeps running and turns itself off.
81
Static stretching acute mechanisms: golgi tendons
historically it was those that holding a static stretch activates the GTP meditated inhibitory response, leading to muscle relaxation. this reduces motor unit recruitment contributing to decreased muscle excitation
however this is likely not the case
the GTOs respond mainly to active tension they are much more sensitive during muscle contraction not passive stretch, the autogenic inhibition occurs too quickly the reflex occurs within ms but the relaxation seen during static stretching develops over 10-60 secs.
they contribute to spinal inhibitory feedback but they are one part of a larger inhibitory network not the main driver of stretching adaptations
82
Static stretching acute mechanisms: CNS mediated changes in excitability
static stretching may reduce cortical drive from the CNS reducing the excitability of motor neuron. this contributes to short-term decreases in neuromuscular performance follow static stretching.
the initial discomfort your brain stimulates when you stretch disappears when you keep holding the stretch as your brain decreases the excitations from the muscle and reduces the tone as the brain sees this as pain which it protects against
83
Static stretching acute mechanisms: alpha motor neuron
- normally a motor neuron fires only when it receives continuous excitatory input from the CNS. so if the brain stops sending signals the motor neuron stops firing the muscle relaxes
- persistent inward currents are ion currents inside motor neurons that amplify and sustain neural signals which sodium helps initiate firing and calcium helps sustain firing
- once activated the motor neuron keeps firing even when the original signal decreases so the neruon behaves like a self-sustaining switch
- this means more muscle activation, tone and reflex responsiveness
these persistant inward current contributes to muscle tone, reflex sensitivity and sustained muscle activation when PIC is high the muscle stays more switched on, reflexes are stronger and muscle resist lengthening more
84
PIC and Static stretching
so by holding a static stretch this decreases PIC which decreases motorneruon excitability, but depends on intensity and duration
85
Summary. Why does static stretching increase ROM
there are four neural mechanisms that can reduce muscle activation
1. muscle spindle desensitisation decreases stretch reflex
2. reduced PIC activity decrease motor neuron amplification
3. central inhibition decreases alpha motor neuron excitability
3. GTO input decreases inhibitory inter neurons
5. leading to a mechanical mechanism through a decrease in viscosity
lower neural drives decreases muscle tone increase stretch tolerance therefore increasing ROM
86
Static stretching and power performance
don't static stretch before power performance as you are decreasing neural drive decreasing excitability and therefore force they produce
87
Dynamic stretching acute mechanisms
1. decrease viscosity - thixotropic effects
- same heat response but we don't get the decrease in neural drive and it actually enhances excitability
2. alter muscle tone
- muscle spindle sensitivity enhanced
- golgi tendon organ activation limited
- increased alpha motor neuron excitability/recruitment
- CNS mediated increases in excitability
= through the excitability and activation of the muscle the name is changing to muscle activation as they increase power and strength output
88
Chronic Adaptions of static stretching
permanent changes to ROM
1. increased stretch tolerance
- inhibition of E reflexes
2. structural adaptions
- increase fascicle length when you do high volume stretching
- muscle thickness (CSA)
3. promote increased collagen turnover and remodelling in tendon
- static reduces muscle stiffness
- dynamic increases tendon stiffness
4. improved collagen alignment and fibroblast activity in other connective tissue
89
Chronic adaptions to static stretching: muscle structure
increase in muscle length = sarcomerogenesis
- more sarcomeres in series allow for greater elongation without excessive tension improving functional ROM
- greater contraction velocity due to series contraction
- this adaption is particularly notable in postural and biarticular muscles
changes in muscle pennation angle
- chronix stretching can decrease pennation angle leading to longer more parallel muscle fibres
- this improves muscle extensibility but may slightly reduce force production as force is typically maximised in more pennated
90
Stretching Type: static stretching g(acute, pre-exercise)
mechanism - reduces muscle stiffness and inhibit reflex activity
effect on injury risk - no strong evidence for injury prevention
91
Stretching Type: static stretching g(chronic, long term)
mechanism - increases muscle length, improves tissue compliance
effect on injury risk - some indirect evidence for reduced injury risk especially in high ROM sports
92
Stretching Type: dynamic stretching (pre-exercise)
mechanism - increases blood flow, maintains muscle stiffness
effect on injury risk - improves performance and may prevent injuries
93
Stretching Type: PNF stretching
mechanism - enhances neuromuscular control and increases flexibility
effect on injury - limited direct evidence but may help in rehab settings
94
Stretching Type: ballistic stretching
mechanism - mimics sport specific movements
effect on injury risk - only beneficial for sports requiring ballistic actions
95
Other health benefits of poor flexibility
poor flexibility has been associated with
- difficulty when performing your daily activities
- joint stiffness, muscle tightness, lower back pain and other postural and health related problems
- greater arterial stiffening which influences how hard you heart has to work to pump you blood around your body.
96
Stretching summary
stretching will acutely and chronically increase ROM in muscles that we can anatomically stretch
stretching may plausibly reduce risk of injury in hamstring muscles in sprinting athletes
you should stretch to increase ROM for those wanting to improve flexibility, athletes who require a large ROM, hamstring protection and may benefit speed strength due to increased contractile components
97
Does stretching increase ROM
yes -
acute does through changing excitation, physiological mechanisms and decreasing viscosity of tissue
chronic alters the tuning of the neuromuscular system to stretch stimulus, increasing tolerance to stretch stimulus and stiffness may be affected but stiffness provides trivial results to ROM
98
Stretch modality based on adaption required
always keep in mind the reason for performing the stretch
- relaxation (static)
- flexibility (static, PNF)
- activation
- pain relief (foam rolling)
99
Muscle to Tendon Stretch Relationship (calve example)
in every movement this is some stretch we do
there is a force through the segment is by shortening or lengthening the muscle transmitting the force onto the tendon as they are coupled. but they don't always have to be coupled as we can manipulate them by stretching.
the tendon stores energy that will be passed back to the system when it recoils
when the muscle shortens the tendon stretches or when the muscle lengths the tendon shortens
when the muscle elongates it relaxes so is less powerful and less efficient as its going to lose more energy giving less back to the system when it recoils.
100
How does types of stretching effect performance
acute static stretching is bad before performance but PNF has even worse effect
therefore there is a dose response that highlight that deficits are associated with longer duration stretching, short duration stretching do not have significant effects
101
Sprinting impairment and sprinting
it can have a 1-5% effect on performance when static stretching when in sprinting can effect performance greatly effecting outcome
102
Chronic stretching and hysteresis curve
chronic stretching can alter the hysteresis of the tendon which effects the behaviour between amount of force required to elongate the muscle and when you release the stress how it returns back. the gap in the curve is the energy loss and the area underneath the curve is the energy that is maintain or given back to the loop
a period of chronic stretching reduced the hysteresis curve for the achillies curve highlight less energy lost and giving more energy back under the curve due to changing the viscosity ot the tend. this means a less compliant muscle unit able to store more energy and give more energy back so benefits a very short contact time.
103
What does MTU stiffness/viscosity do
decrease tendon hysteresis = rapid elastic recoil
104
Muscle tendon compliance and performance
a very stuff MTU absorbs the reaction forces over a very short period and returns the energy to the muscles very quickly = good economy
if the system is very stiff, the mechanical and reflex energy return would occur while the slower runner is still in the landing phase and not ready to propel themself into the next stride
= poor economy
want less stiff muscle for more contact time
105
Muscle-Tendon Injury in Running
stiff gastrocnemius with a high load puts a lot of strain on the hamstring so need to have a very compliant hammy in sprinters
to reduce hammy injury we need flexibility training is much greater than just training ROM
106
Muscle-Tendon Summary
muscle-tendon mechanics is important for sport performance and can be complex. compliance or stiffness of either tissue may affect the stretch shortening cycle and energy return
107
Considerations for Stretch Programming
1. the answer to the question why drives the method, greater ROM, relation, pre-performance activation and pain relief
2. how are the bi-articular muscles used by the athlete? do we require greater compliance or stiffness which muscle groups
we must understand the reasons and apply our knowledge to the mechanisms we engage for a desired outcome
108
Prescribing Stretching: NSCA Pre event Static Stretching
NSCA does not endorse static stretching Pre-event. pre SS may adversely affect athletic performance particularly in spots that involve strength and power unless they are athletes who require high levels of flexibility ie gymnasts
SS should be done during cool down due to the potential benefits of SS form ROM and injury prevention
109
Stretching Duration
minimum of 15s of stretch is required to increase active ROM
30-60s of SS provided the greatest increase in passive ROM
greatest length changes to muscle/tendon unit occurs within the first 4 repetitions
2 x 30 sec minimum required to decrease stiffness
minimum of 5min/week for each muscle group to achieve chronic adaptions of ROM
sets of 2-4 repetitions within 15-30 sec rests
110
Stretching Intensity
overload principle - the thought that you must stretch to the point of discomfort or pain
reccomendation stretch 6-80% intensity
111
Stretching - Time of Day
diurnal variations in performance, strength, power, VO2 are larger than day to day variations
- may be athlete specific
- dynamis stretches are recc at times of day when performance is lowest (am)
- static stretching of the spine is not recc in the morning
112
Stretching: periodised or non-periodised
periodization is defined as strategic implementation or specific training phases based on increasing and decreasing volume and intensity - plan out what stretching to do when
- increasing ROM stretch training should include early training phases either pre season or early season
- if require ROM athletes should use RNF stretch for the first 4 weeks of training block than SS for next 4 weeks
113
Stretching for relaxation or recovery
a higher parasympathetic reactivation and faster HR recovery after exercise are commonly associated with lower risk of CVD.
performing 5 min of SS can change the predominance of the autonomic nervous system to increase predominance of parasympathetic
high intensity stretching is not recc post exercise due to muscle fatigue and potential for injury to the muscle
114
Stretching and Breathing
breathe out as you lean into the stretch
there is a gender effect in the way we breathe during stretching
115
Sports Injury Definition
damage to the tissues of the body that occurs as a result of sport or exercise
- we need to classify the injury to assist with the surveillance which there are many ways to do so
116
Time is related to tissue trauma: acute vs overuse
acute is a sudden overload of tissue ie sprain
overuse occurs over a period of time excessive and repetitive loading of the tissue, the symptoms appear gradually ie stress fracture
116
Time and Injury Mechanism
time is often related to the cause of mechanism
there are two types of injury related to time
acute - stress exceeds tolerance, 1 event
chronic - insidious onset, overuse over long time
117
Wound healing
1. bleeding: the initial trauma that lasts a couple of hours
2. inflammatory: take up to 0-6 days depending on the severity, but this stage helps the body respond to trauma by stopping the bleeding a clot and clean the debris
3. proliferative: takes 3 days to 6 weeks, this stage fills in the wound proliferating cell repair, which we can see happening as the scar tissue forms
4. remodeling: (6 weeks to a year) which is when the tissue remodeling gets back to the normal make up of our healthy normal tissue
118
Wound Healing: 2. Inflammation Phase
we want this phase to go ahead so don't try to stop it
roles it has
1. clot bleeding tissue to stop the bleeding
2. prevent the spread of damaging agents to nearby tissues
3. disposes of cell debris and pathogens - so the damage cells don't effect the rest of the body
4. sets the stage for the repair process
119
Inflammatory Response
1. increased blood flow: the blood vessels near the injury site dilate allowing increased blood flow to the area which can cause redness, warmth and swelling to the affected areas
2. migration of wbcs: the immune system specifically wbcs migrate to the injured or infected site. neutrophils are typically the first wbc cells to arrive followed by macrophages. these cells help clear out any damaged tissues, debris and invading pathogens.
3. release of chemicals: the damaged tissue and the wbc release chemicals called cytokines and chemokines. these chemicals signal other cells to come to the injured site and help with the repair process
4. formation of blood clots: blood clotting factors are activated to prevent further blood loss at the injury site
5. pain: nerve endings around the injury site are stimulated resulting in pain
120
What are the 5 cardinal signs of inflammation
1. heat
2. redness
3. pain
4. swelling
5. loss of function
121
Swelling during the inflammatory response
approx 1 hour post injury and occurs as the vascular walls become more permeable and increased pressure within the vessels forces a plasma exudate into the interstitial
this helps dilute harmful substances, brings necessary nutrients for increased metabolism required during healing and allows entry of clotting proteins
122
Swelling and Reponse
swelling follows gravity and pools at the bottom doesn't mean theirs trauma there
RICE, ice dulls the nerve ending reducing pain but the ice can disrupt inflammatory response so just elevate and compress
123
What is the most important inflammatory reponse
elevate followed by compression
124
Muscle healing and rice
applying ice to an inflamed area actually slows down the healing process, reduced fibre area and greater muscle of collagen fibres in iced muscles. greater number of centrally nucleated muscle fibres and greater number of collagen in iced muscle signal proliferation phase of healing
- delayed muscle healing
do do not ice muscles
125
How to treat inflammatory phase 1
Phase 1 = acute phase 1-7 days
goal is to minimize inflammation and pain
treatment - protect, optimal loading, compression and elevation, resistance to unaffected areas
no heat or message physio
pain meds can be recc
126
How to treat inflammatory phase 2
proliferation 3-21 days
1. formation of the granulation tissue which contains new blood vessels and fibroblasts which produces collagen the main structural protein in the body
2. angiogensis - new blood vessels are formed in the granulation tissue, supplying oxygen and nutrients to the new tissue
3. collagen - fibrioblasts produce and deposit new collagen fibres which help strengthen the new tissue
4. epithelialization - if theinjury invovles the skin or mucous membranes new epithelial cells migrate across the surface of the wound to cover it and prevent
5. contraction - in some types of injuries such as cuts or wounds the edges of the wound may contract bringing the wound closer together
this phase starts when the signs of inflammation begin to reduce. inflammation signs are heat, swelling, redness and pain
the goal is to prevent muscle atrophy, reconditioning, restore ROM develop NMK control, build and endurance through the brain reconnecting
127
Collagen and Inflammatory Response
type 3 collagen fibres mostly reside and proliferate quickly and not a strong as type one.
if the tissue is disrupted then the scar tissue will fill the gap and try bring them back in together in a highly organised parelle to the line of stress in the body to resist loading. type 3 collagen fills in the type 1 collagen area after the trauma to hold it together whilst they are healing
128
Appearance of a healing ligament
1 week post = initial proliferation
6 weeks post = fibres become thicker
14 weeks post = becomes more organised from being used/stretched contributing to growth/proliferation
129
How to treat inflammatory phase 3
= strength accumulation (after 3 weeks)
design a progression of exercises that safely stressess the maturing connective tissue
goals
- improve NMJ control, CV endurance, progress to functional activity
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How to treat inflammatory phase 4
maturation (6 wks)
- decreased fibroblast activities
- type 3 to 1 collagen
- realignment/remodelling of collagen
any injury is like a 6 week injury the body can heal almost anything in about 6 weeks to where you can start exercising again where the tissue is moving back into organised from dis-organised
131
Tendon and ligament organization tell us how to strengthen
fibroblasts
- maintain the structural integrity of connective tissue
- continuously secret precursors of the extracellular matrix
- fibroblast bodies are drawn out in the primary direction of loading
progressing stress and strain in the main direction of loading may help the realignment of fibres and strengthening or injured tissue
132
Adaption to mechanical loading
effects of immobilisation are things such as tendon stiffness, water content etc
this doesn't only happen to the injured leg but also in the uninjured leg as your good side will be not used as much so it will also lose muscle if immobilised. we know the muscle will be strong but more inclined to sprains
133
How to treat remodelling phase
goal is to realignment of scar tissue/promote tissue strengthening
- stretching to avoid a decrease in flexibility
- increased concentric strengthening
- begin eccentric strengthening
- know the risk of the re-injury
in simple increase stress to get back to sport conditions
134
What are the primary goals of resistance training
peripheral adaption - hypertrophy
strength is an outcome of adaption
135
What are the 3 factors that effect muscle size
1. correct stimulus
2. nutrition
3. hormonal status
136
What is the primary site of hypertrophy
myofibril
137
Muscle hypertrophy - myofibrils
is primarily occurs in the myofibrils which are contractile units of the muscle fibre, composed of repeating sarcomeres. with training the number of myofibrils increases or existing ones become thicker (added in parallel). this increases the CSA and force generating capacity of the fibre
this can all be achieved through strength training
138
Types of myofiber growth
1. myofiber hypertrophy - gets thicker
2. myofiber splittle - more myofibres
3. longitudinal growth - increase in length
139
4 parts involved in muscle hypertrophy
1. myofibrils
2. sarcomeres
3. sarcoplasm
4. satellite cells and myonuclei
140
Muscle Hypertrophy - Sarcomeres
the basic unit of muscle contraction, made of actin, myosin, titin and other protiens
in hypertrophy more sarcomeres are added in parallel contributing to increased fibre diameter and strength. series addition is more common in longitudinal growth.
141
Muscle Hypertrophy - Sarcoplasm
the cytoplasm of the muscle cell where the hypertrophy actually occurs, with the mitochondria here providing energy.
in sarcoplasmic hypertrophy, volume of non contractile elements like fluid increases which is more common with high volume lower load training. through not a primary drivers of hypertrophy both mitochondria and capillaries can increase in number volume and number especially type 1 fibres.
this only increases the volume not meaning more force but the additional fluid/energy increases the endurance of the muscle to get larger
142
Muscle hypertrophy - satellite cells and myonuclei
satellite cells are activated with overload which donates nuclei to growing fibres and then increased myonuclear number which gives the muscle more capacity to regulate protein synthesis across a larger fibre
143
Hypertrophy types
larger muscle fibre volume but not increasing force generating ability
increase myofibril number or size will increase force generating ability
144
Muscle Adaption Continuum
the body doesn't choose hypertrophy or endurance it adapts best on the dominant signal in the training programme
145
Dominant Signal
the dominant signal in the training programme your body won't stimulate to all the signal you get in the programme only the dominant one/s. therefore it is important we create with a stimulus we want to achieve a dominant signal at the right time of the exercise we want
146
Primary Mechanisms of Muscle Hypertrophy
1. mechanical tension: which is generated during forceful contractions, which drives mechanotransduction leading to increased muscle protein synthesis.
2. metabolic stress: increases fibre recruitment and cellular swelling, more promiment in mod-high training.
3. muscle fibre recruitment: recruitment of high-threshold motor units is critical which is achieved by heavy loads or training close to failure
these can be influenced by
- muscle damage
- hormonla environment
- energetic stress
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Hypertrophy Cellular Mechanisms
1. start with the trigger: heavy loading, muscle fibres experience strain + micro damage
2. translate that into signal
3. activate the satellite cells: lead into proliferation (multiply)
4. fusion: increase myonuclear number
5. outcome" more nuclei, more protein synthesis, supports continued hypertrophy
148
Hypertrophy Mechanism to Training Application
for myofibrillar adaption/max force production = long rest, do not train to failure, high load/tension
for sarcoplasmic/metabolic adaption = short rest, train to failure, high volume higher fatigue
149
Why shorter rest periods for hypertrophy
1. maximise metabolic stress: short rests create a buildup, the metabolic stress contributes to cell swelling, anabolic signalling and muscle fibre recruitment, pump effect.
2. greater time under tension: shorter rests force muscle to work harder with incomplete rest increase TUT, essential for hypertrophy.
3. Increase muscle fibre recruitment: short rests mean as main muscle targeting fatigue faster we adapt to using a wider range of muscles groups
4. elevate hormonal responses
- increase in testosterone and growth hormonal
150
Morphological Implications: Changes in Muscle Pennation Angles
adding more muscles with lots of directions will increase angle, so you can add more fibres in parallel changing this angle increase CSA in these muscles
151
Morphological Implications: Changes in Length
- high force training increases in a muscles CSA by adding sarcomeres in parallel.
- high velocity training may add sarcomeres in series
152
Type 1 vs 2A vs 2X
type 1 - slow twitch = must be stimulated first
type 2A - fast twitch= next to be stimulates
type 2X = engaged last, hardest to stimulate
153
How stimulus affects different types of muscle fibres: Type 1
primary function - endurance and fatigue resistance
hypertrophy potential - lower than type 2 but they do hypertrophy esp under high volume lower training load
training stimuli - respond better to moderate load and higher repetitions
adaptions - increase mitochondrial content, capillarization, aerobic activity
- modest increase in CSA
154
How stimulus affects different types of muscle fibres: Type 2A
primary function - force and power with some endurance capacity
hypertrophy potential - very responsive to resistance training esp, mod-high loads
training stimuli - benefit from both strength and hypertrophy
adaptions -
- significant increase in CSA
- enhanced use of energy
155
How stimulus affects different types of muscle fibres: Type 2X
primary function - explosive power, low fatigue resistance
hypertrophy potential - high
- these fibres tend to shift towards type 2A with regular resistance training.
- type 2X fibers have high theoretical hypertophy potential they often convert to type 2A before hypertrophy is fully expressed
training stimuli - respond to heavy, explosive, or ballistic training
adaptions - in trained individuals tyep 2X are rare as transition back to 2A
156
Fibre Type Transition
its the process by which muscle fibres change their phenotype meaning their contractile and metabolic properties, in response to stimuli like resistance training, endurance training or inactivity
- many fibre express more than one myosin heavy chain isoform during training
resistance training 2X to 2A
endurance 2S to 2A to 1
inactivity 1 to 2A to 2X
157
Mechanisms behind Fibre Type Transitions
neural drive - changes in motor neuron firing patterns influence gene expression of MHC isoforms
mechanical load - load and contraction affect signalling
metabolic stress - alters energy demands and mitochondrial adaptions
hormonal signals - testosterone, growth hormone
158
During inactivity why does the fibre change from type 1 to 2A to 2X
less neural drive input decreases motor unit recruitment
decreased mechanical loading, due to less activation of growth pathways
reduced mitochondrial demand
159
Fibre type transition - retraining after inactivity
due to the more amount of 2x shows why we see an inital jump in performance
160
Fibre type transition - aging and sarcopenia
with aging we lose muscle quality but have lots of 2 x fibre as lowest energy demand
161
Implication for shape of muscle - regional hypertrophy
the most active compartment of a muscle in any exercise will grow the most due to the biggest CSA increase
this belly/compartment depends on the task specific movement
162
What are peripheral muscle adaptions
changes in
1. metabolic capacity
2. muscle size
3. ratio of fibre types
4. architecture of the muscles
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CNS intermuscular adaptions
inter coordination and cross education = task specificity
- motor cortex adaptions
- corticospinal tract
164
CNS adaptions: corticospinal tract
- excitability
- feedback, feed-foward loops
- improved anticipation
- muscle synergy
- precision
through increasing the stimulus to the tract, increases the drive to the muscle, determining the amount of muscle activation.
task-specific training improves precision of muscle timing in these pathways
165
Initial Strength Gain
the initial strength gain when we first start doing strength training, these is a big jump in progress not cause of muscle growth but we have trained that motor plan/specific task so when we know the muscle connecting and timing you get stronger just due to the intermuscular connection and strengthening that pathway
166
Movements with and without visual feedback
when you can predict the movement you can come up with a predatory postural control plan to change the activation of the muscle giving us information. when you can't predict the movement there isn't previous movement which requires you to use a lot more activation of the muscle
167
What is neural drive
refers to the collective output from the CNS to motor neurons which directly controls how a muscle behaves, how strongly, how quickly, and how consistently it contracts
- excitability down the spinal tract to the muscle system sending signals with intent to move
- external cues are best to increase force production
- as a SNC it is important to use intent to move as a factor in training
168
What does neural influence
- force production
- rate of force development: the faster the drive the faster the activation of the muscle
- muscle coordination and timing
- fatigue resistance
169
What happens when neural drive is impaired
when neural drive is altered these patterns become
- less efficient
- delayed or premature
- poorly sequenced
- overly co-contracted
leading to
- reduced force or power output
- poor coordination
- compensatory movement patterns
- increased injury risk
170
Pain and Neural Drive
pain effects neural drive involuntary, if you think you are going to have pain, you brain will lower the force driving out of those muscle to help control the pain which leads to poor sequencing and coordination to changing drive
171
Neural inhibition
reduction in voluntary neural drive of given muscle group
- centrally: at the brain or spinal cord level
- peripherally: via spinal reflexes
172
Central intramuscular adaption - resistance
resistance training will create adaption in muscle control that is task specific
173
What is a motor unti
its the basic function unit of movement control
- one motor neuron and all the muscle fibres it innervates
- there are multiple motor unit within a muscle and each motor unit controls multiple muscle fibres but each individual muscle fibre belongs to only one motor unit
- when the neuron fires all its fibres contract together
174
Motor unit recruitment - henneman's size principle
in order to contract a particular muscle, motor neurons with small cell bodies are recruited before motor neuron with large cell bodies
small to large
as activity increases we engage more motor units we recruit units depending on demand and based of the external stimulus to the muscle
175
Motor unit recruitment - size principle
lower stimulus means that only type 1 fibres are activated for a long period of time
type 2A fibres require a high amount of stimulus to engage
type 2x fibres require a even higher stimulus but we have to go through the other fibres first. these fibre only fire for a short amount of time as they fatigue fast
= we just continue to use type 1 fibres until they fatigue after a very long time, you then engage the other fibres when deplete the other ones
176
Idea of strength training and motor recruitment
when we are training our fibres we are not training the type 2 fibres for endurance but we are wanting to make them less sensitive to lower the stimulus to engage them to get from type 1 to 2x faster
177
Does low intensity training to failure work
yes and no
it doesn't increase force production
training to failure is not necessary as you want to engage more fibres which is achieved by high load not fatigue
178
Recruitment - subgroups of motor units
neuromechanical matching - neural system matches the recruitment of mechanically advantageous muscle fibres to a specific
implication - variety = more consistent growth
but task specific growth may alter the shape of muscle
the more we use muscles for a specific movement we will get more hypertrophy
179
Control of muscle force: rate coding
- recruitment operated together with rate coding
- rate coding refers to the frequency at which a motor neuron sends action potentials to its muscle fibers
180
Rate coding - why volume alters velocity
when a muscle contracts it is a combination of type 1 and type 2 fibers
type 1 fibers reduce/inhibit contraction velocity of type 2
goal for strength or power training you only want to train on rested muscles so can have velocity in the trainings
181
Changes in motor unit discharge with strength training
increase discharge rate of the muscles and shift the curve
182
Control of muscle force - synchronization
motor unit discharge behaviour
- the brain normally protects muscle by inhibiting high synchronisation of large numbers of motor unit with training there is a reduction in this inhibition
183
Discharge Rate
how fast a motor neuron fires determining twitch stimulation and force output
184
What is adapting
neural (CNS) - determine how the force is produced ie unit recruitment
peripheral (muscular) - determine how much force is produced ie hypertrophy
185
How to programme strength-power continuum
it is a continuum when endurance at one end and max RM at the other highlighting what you are trying to target
ie more endurance you would do more reps
ie more rests lengths for strength
186
Why you can't maximise everything at once
1. cross bridge cycle time limits velocity
2. motor unit recruitment limits force
3. length tension limits force over full ROM
4. force and velocity relationship
187
Cross bridges time limits velocity
this cross bridging cycle takes time which is the biggest limitation, which is based on the time it take for the chemical binding and release of the actin and myosin
188
Motor unit recruitment limits force
muscle fibre make up is unique to every individuals and therefore there is a genetic component to but we can train these and/or work within each persons fibre type
ie Usain Bolt had lots of type 2 fibres so training as a sprinter will benefit him
189
Lenght-tension limits force over full ROM
this highlights the force we produce isn't consistent across a movement/ROM. this is because as the joint changes so does the length/tension relationship so their is certain points where we will be stronger and some where we will be weakers
190
Force-Velocity Curve
the faster we move the lower the force output we can produce. if we want max force then we to move slowly as we want to engage as many motor units that we can
- most athletes are in the middle of this curve but the idea with training is to lift it up and produce more force in a short amount of time in which to achieve this we need to target the other 4 limitations
191
Force, velocity, adaptions, programming
to increase force we need to work on the length v tension for a muscular adaption then increase motor unit recruitment leading to a neural adaption. then we work on the time constraint making a sport specific adaption
192
Programming goals continuum
PREPARATORY PHASE
1. strength endurance (general preparatory period)
2. maximum strength (specific preparatory period)
COMPETITIVE PHASE
3. strength-power (pre comp moving to main competitive period)
4. peak RFD and power (taper and peaking
193
3 Programming Goals
1. increase force capacity
2. increase rate of force development
3. increase transfer/expression to sporting tasks
programming for power = training force, time and intent
so the programming must address force ceiling, speed of force expression, task specificity
194
3 Programming Goals: increase force capacity
we want to do this for late RFD and overall force production are strongly supported by maximal strength
implication
- heavy resistance training raises the athletes force ceiling
- this matters because a higher max force gives more force available within short time windows
- particularly important for weaker or less trained athletes
- high load
- low reps
- full recovery
- intent to move fast
- heavy compound lifts
- eccentric training
- cluster sets
195
Accentuated Eccentric Loading (AEL) - eccentric training
greater mechanical tension, increased muscle damage, heightened satellite cell activation, and enhanced hypertrophic signalling pathways
- load selection, safety- benefits for strength enhancement and targeted hypertrophy
- 3-4 day recovery or if even higher does then up to 2 weeks
196
Cluster Sets
allows someone to maintain the same velocity of the movement for all the reps and set without fatiguing
197
3 Programming Goals: Increase RFD
sport usually does not allow time to reach maximal force
implication
- RFD is the ability to produce force rapidly
- early RFD is more neural
- later RDF is influenced by strength and contractile capacity
- so RFD training should include high intent, high movement quality and time sensitive actions
- ballistic training
- plyometrics
- explosive isometrics
198
3 Programming Goals: improve expression/transfer
an athlete can be strong and even explosive in the gym but still fail to express it in sport
implication
- programming must be resemble the time demands, direction of force, and movement constraints of performance task
- move in ways that you don't in the gym as in sport we move in so many different directions
- contrast/complex training so that we have a time constraint, high coordination and sport specific
199
Potentiation of muscle force: calcium sensitivity
heavy contractions of activates myosin light chain kinase which increases calcium sensitivity of the actin-myosin complex
- when you do a heavy lift that stresses the binding site the myosin head is more sensitive to CA which will make it more reactive to another contraction
200
Potentiation of muscle force: enhanced motor unit recruitment
post-tetanic potentiation = twitch force is maximal following a brief tetanus
- faster firing rate
- high threshold primed to to be recruited more easily
201
Potentiation of muscle force: time course
- peak effect occurs within 0-5 minutes
- highly fatiguable sensitive - if fatigue outweighs potentiation performance may decrease instead
202
Potential mechanisms for post activation performance enhancement
an acute but longer latency enhancement in performance following high load resistance, not directly related to myosin phosphorylation
- increased muscle temperature: warmer muscle contract more quickly and improves enzyme activity
- changes in muscle water content and pH: higher cell hydration can increase muscle stiffness and force transfer efficiency
- psychological and neural arousal: heavy lifting acts as a neurological primers increase drive and attentional focus
- time course: peak performance improvement occurs 5-15mins, lasts longer than PAP are more robust to fatigue
- best for: pre-competition warmups, using heavy squats etc
203
Post Activation Potentiation Training - Complex Training
complex training combines strength training exercises with plyometric or explosive movements in a single session. typically a complex training session involves performing a strength exercise followed immediately by a plyometric exercise. the goal is to enhance power and explosiveness by capitalising on the PAP effect where the strength exercise primes the muscle for greater force production during the subsequent explosive movement
204
Post Activation Potentiation Training - Complex Training
also combines strength exercises with plyometrics but it involves alternating between heavy resistance exercises and lighter more explosive movements. you might perform a heavy lift followed by a set of plyometric exercises. the contrast between the heavy lifting and the explosive movements aims to improve both strength and power, leveraging the PAP effect similar to complex training
204
SPEX 305
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