KIN202 L7

FITT-VP model

-frequency

-intensity

-time

-type

-volume

-progression

training principles

-overload

-specificity

-progression

-reversibility

-periodization

-individualization

overload

a stimulis that is greater than the body is accustomed to

specificity

the concept of specifically performing sport related memories or breaking down movements into parts and training using those specific components

progression

the gradual and systemic increases in training stress to maintain tissue overload and to provoke continued training adaptation

reversibility

the reversal or loss of tissue adaption when overload stimulus is removed

periodization

the planned systemic and structured variation of a training program over time

individualization

the development/ modification of a training program to account for the individuals needs/ capabilities/ goals of the athlete

changed in VO2 max following endurance training

-increases as WR max increases

-we assume mechanical efficiency does not change therefore VO2 required at a given absolute WR will not change

determinants of the magnitude of adaptation

-genetics

-initial training status

physiological ceiling

-increasing training volume does not lead to further adaptation

-point where VO2 max no longer increases

endurance training and CO

-increases with WR increasing

-no difference at rest or same absolute submaximal work load

-change in maximal CO max with increase work rate

endurance training and SV

-curve moves up post training

-increased difference at rest, submaximal and maximal work rates

endurance training and HR

-line moves down post training

-decrease resting and submaximal

-no change in HR max

training and O2 extraction

-resting and submaximal O2 extraction similar between trained and untrained

O2 extraction max and training

similar between pre and post training bu toccurs at different max WR

endurance training and VO2 kinetics

-trained individuals reach steady state faster

-reduction in O2 deficit

blood flow kinetics and endurance training at exercise onset

-faster kinetics at exercise onset post training

-contributes to increase in VO2 kinetics

cardiac adaptations to aerobic training

-LV

-increased compliance of LV

-cardiac hypertrophy

aerobic training induced cardiac hypertrophy

-increased ventricular wall thickness and pump strength which lowers ESV

-increased myocyte length and width

cardiac hypertrophy stimuli

-stretch(preload)

-afterload

-neuralhumoral

-metabolic

-many intracellular signalling pathways

blood adaptation to training

-increased plasma, red cell volume

-no change in Hct

-CaO2 does not change

[Hb] adaptation to training

-does not change

-oxygen carrying capacity does not change

how does blood volume change affect VO2 max

-increased stroke volume

-increased blood volume, increased venous return, increased end diastolic volume and preload, decreased end systolic blood volume

angiogenesis

-new capillaries sprout from existing ones

-increased # of capillaries

-increased tortuosity in capillaries

capillary tortuosity

increased tortuosity will prevent short transit of RBC, allowing for oxygen extraction by muscle cells

arteriogenesis

-growth of new or enlargement of existing arterioles and small arteries

-smaller scale than capillary growth

-some new vessel growth possible

function adaptations

-enhanced endothelial cell and vascular smooth muscle function

-finer control of vascular tone

-increased BF max

metabolic control in untrained

-loose metabolic control

-large changes in metabolites like PCr, Pi, ADP and ATP

metabolic control in untrained

-tight metabolic control

-minimal changed in PCr, Pi, ADP and ATP despite large increased in ATP demand and supply

mitochondrial biogenesis

-primary adaption to endurance training in skeletal muscle

-more mitochondria in trained muscle cells

effects of endurance training on substrate utilization at submaximal exercise

-increase in fat oxidation

-decrease in glycolysis

mechanisms for increased FFA oxidation adaptations

-increased mitochondrial content

-more triacyglycerides in skeletal muscle

-enhanced FFA mobilization

RER and endurance training

-curve moves down

-decreases at rest and submaximal

-maximal value may or may not change based on the individual

ventilation and endurance training

-no change at rest and submaximal work loads

-increase in maximal value

blood lactate and endurance training

-no difference at rest

-decreased production and increased removal at submaximal work rate

-OBLA at higher WR

glycogen and endurance training

-glycogen storage enhanced post training

-glycogen depletion delayed post training

glycogen in trained individuals at rest

increased in [ ]

glycogen in trained individuals in exercise

-increased in [ ] with more fat used for fuel

-decreased reliance on CHo means rate of glycogenolysis is reduced

SIT vs endurance training substrate use

-no statistical difference between training methods

-both used more fats in post training

-increased mitochondrial enzyme activity

muscle glycogen in SIT vs endurance

-increased at rest in trained individuals

-reduced breakdown in trained individuals

-no difference in training methods

PCr in SIT vs endurance

-no change in resting [ ]

-reduced breakdown in trained individuals

-no difference in training methods

agonist

muscles mainly responsible for producing force in the intended direction of movment

synergists

muscle that assist in coordinating the movement

antagonists

muscles that supply force in opposite direction of agonists

muscular strength

peak force developed during a maximum voluntary effort

muscular power

-the explosive aspect of strength defined as the rate at which mechanicam work is performed

muscle endurance

ability to sustain repeated muscle actions or to sustain fixed static muscle actions for an extended period of time

adaptations to resistance training

-neural adaptation

-hypertrophy

neural adaptations to resistance training

-initial adaptations

-increased excitability of motor neurons

-reduced antagonist coactivation

-increased rate of force development

-synchronization of agonists within a muscle group and/ or intermuscular coordination

unilateral resistance training adaptation

-trained arm increases strength due to neural adaptations and hypertrophy

-untrained arm increases strength due to neural adaptations

training method and MVC- weighted squats

-large increase in peak force

-not much change in maximum rate of force development

-not much change in muscle activation

training method and MVC- ballistic jumping

-smaller change in peak force

-increased maximum rate of force development

-increased muscle activation

whole muscle size determinants

-fibre size

-genetically determined number of muscle fibres

resistance training induced hypertrophy

-increases muscle fibre cross sectional area

-increase in CSA is associated with large increase in myofibrillar content

stimuli that cause hypertrophy

-hormonal mechanisms hediate both short-term homeostatic control and long-term cellular adaptations to resistance training

-growth hormone, insulin like growth factor, testosterone

-mechanical tension is the primary stimulus

early phase of hypertrophy

-due to muscle protein synthesis

-training shifts balance of MPS and MPB toward synthesis

myonuclei, ribosomes and hypertrophy

-increase ribosomal translational capacity, more protein produced

-satellite cells become myonuclei, more translational machinery

myonuclear domain

area of skeletal muscle cell that is supported by a nucleus through transcription and translation

mitochondrial volume and resistance training

-absolute value increases

-volume does not increase with relative cell volume

capillary density and resistance training

-relatively unchanged following resistance training

-absolute number of capillaries larger