Wk 8 - The physiology of training: effects of aerobic and anaerobic training and effects of resistance training Flashcards
1
Q
What things should be considered when training/ performing?
A
Sources of energy (systems) and fibres used for force production. Energy systems depend upon how long the exercise lasts.
2
Q
What is overload?
A
Training effect occurs when a physiological system is exercised at a level beyond which is normally accustomed. Exercise-induced adaptation/ hormesis.
3
Q
What is specificity and reversibility?
A
-Specificity -> Training effect is specific to: muscle fibres recruited during exercise, energy system involved (aerobic versus anaerobic), velocity of contraction and type of contraction (eccentric, concentric, isometric)
-Reversibility -> Gains are lost when training ceases
4
Q
How to increase VO2 max and the increases in VO2 max with endurance training:
A
-Training to increase VO2 MAX -> Large muscle groups, dynamic activity. 20 to 60 min, >3 times per week, >50% VO2 max.
-Increases in VO2 max with endurance training -> Average = 15-20% increase. Smaller increases in individuals with high initial VO2 max – individuals with high VO2 max may require higher exercise training intensities (>70% VO2 max) to obtain improvements. Up to 50% in those with low initial VO2 max.
5
Q
What are the impacts of genetics on VO2 max and exercise training response?
A
- Heritability (genetics) – determines approximately 50% of VO2 max in sedentary adults. Genetics also plays key role in determining the training response.
- Average improvement in VO2 max is 15-20%. Low responders improve VO2 max by 2-3% and high responders can improve VO2 max by ~50% with rigorous training.
- Large variations in training adaptations reveal that heritability of training adaptations is approximately 47%.
6
Q
Why does exercise training improve VO2 max?
A
- VO2 max is defined by Fick’s equation -> VO2 max = maximal cardiac output X a-Vo2 difference
- Differences in VO2 max between individuals -> Primarily due to differences in SV max. Maximal cardiac output and VO2 max are tightly coupled
- Exercise-induced improvements in VO2 max -> Short duration (approximately 4 months) – increases in SV dominant factor in increasing VO2 max. Longer duration training (approximately 28 months) – both SV and a-vO2 increase to improve VO2 max.
7
Q
What factors contribute to endurance training induced increases in VO2 max?
A
-Oxygen uptake = cardiac output x a-v O2 difference
-Increased maximal CO, increased SV, increased preload
-Increased a-v 02 difference, increased muscle blood flow, increased capillary mitochondria
8
Q
How does endurance training increase SV?
A
- This increases pre load of end diastolic volume (EDV), plasma volume (over days), venous return (over days) and ventricular volume (over months to years). Eccentric hypertrophy – chamber size and wall thickness increases. There is a 12-20% increase in plasma volume occurring after only 3-6 aerobic training sessions.
- A decrease in afterload of (TPR) causes, a decrease in arterial constriction (lowered SNA) and increased maximal muscle blood flow which has no change in mean arterial pressure i.e. increase in CO parallels the decrease in resistance.
- Increased contractility (independent on SNS input and other constant factors of EDV and HR), causes a greater force produced with each contraction (in animal studies) and improved ‘twist mechanics’ of the LV.
- Combined effect – Differences in EDV, ESV and EF (ejection factor)
9
Q
What factors influence stroke volume?
A
-Increased end diastolic volume
-Increased contractility
-Decreased total peripheral resistance
-Increased plasma volume
-Increased filling time and venous return
-Increased ventricular volume
10
Q
Describe maximal CO increases with training
A
CO = SV x HR. Predominantly linear and there is a sub-max reduction in CO in highly trained individuals.
11
Q
Why does sub-maximal workload HR lower following training from increases in HR?
A
- At any given sub-maximal workload heart rate is lower following training due to an increase in SV. Therefore, the required CO can be achieved with fewer beats per min.
- Resting HR lower after training -> vagal tone increased and allows greater filling time (EDV)
- Maximal HR may fall slightly in the highly endurance trained -> intrinsic firing rate of SA node creased
- Reduced metabolic cost for cardiac muscle and longer diastolic time for coronary blood flow
12
Q
What training-induced increases arise from increases in arteriovenous O2 differences?
A
- Muscle blood flow increases -> Decreased SNS vasoconstriction and increased diameter and compliance of arteries. Increased arterial diameter is specific to limb being used and permits greater ‘volume flow per beat’ to limb.
- Improved ability of muscle fibres to extract and utilize O2 from the blood -> Increased capillary density – slower blood flow through muscle. Increased mitochondrial number/ volume.
- Increased capillary supply – slower blood through muscle
- Increased mitochondrial number/ volume
- Increased capillary supply and oxygen delivery in trained muscle -> During contractions, transit time of RBCs decreases. Training increased capillary density, thus reducing diffusion distance. Transit time is increased because with bigger capillary network, RBCs take longer to pass through
13
Q
What is the time course of training/ detraining adaptations in skeletal muscle mitochondrial content?
A
-Endurance training increases the volume of both subsarcolemmal and intermyofibrillar (80% of total) mitochondria in muscle fibers. Results in improved oxidative capacity and ability to utilize fat as fuel
-Muscle mitochondria adapt quickly to training - double within 5 weeks of training
14
Q
What difference do vascular remodelling and muscle metabolic changes make to muscle blood flow in exercise?
A
-During submaximal exercise, blood flow in trained muscles is lower because the A-V difference greater (better oxygen extraction)
-During maximal exercise, blood flow in trained muscles is higher and the A-V difference is greater
15
Q
What are the effects of endurance training on performance and homeostasis?
A
- The ability to perform prolonged, submaximal exercise is dependent on the ability to maintain homeostasis
- Training-induced improvements in homeostatic processes result in a more rapid transition from rest to steady state, a reduced reliance on limited liver and muscle glycogen stores, and numerous cardiovascular and thermoregulatory adaptations that assist in maintaining homeostasis
16
Q
What adaptations result in muscle fibres that maintain homeostasis from endurance exercise training?
A
- Shift in muscle fibre type (fast to slow) and increased number of capillaries
- Increased mitochondrial volume
- Training-induced changes in fuel utilization
- Increased antioxidant capacity
- Improved acid-base regulation
17
Q
Why does endurance training promote a fast to slow shift in muscle fibre type and increased capillarisation?
A
- Fast to slow shift in muscle fibre type – Reduction in fast fibres and increase in number of slow fibres. Increase in slow myosin isoform, which have lower myosin ATPase activity but better efficiency. Magnitude of fibre type change determined by duration of training, type of training and genetics
- Increased number of capillaries surrounding muscle fibres – Enhanced diffusion of oxygen and improved removal of wastes
18
Q
Describe how endurance training increases mitochondrial volume and turnover in skeletal muscle?
A
- Endurance training increases the volume of both subsarcolemmal and intermyofibrillar (80% of total) mitochondria in muscle fibres – Training also increases mitochondrial turnover
- Significance:
- Increased mitochondrial volume results in greater capacity for oxidative phosphorylation
- Increased mitochondrial volume also decreases cytosolic (ADP) due to increased ADP transporters in mitochondrial membrane, which results in less lactate and H+ formation and less PC depletion
- However, during submaximal exercise, the steady state VO2 is not influenced by endurance training
19
Q
How does endurance training induce changes in fuel utilization?
A
- Increased utilization of fast and sparing of plasma glucose and muscle glycogen – Plasma glucose vital source for CNS. Intramuscular fat provides ~50% of lipid oxidized during exercise, plasma FFA provides the remainder
- Endurance training adaptations improve plasma FFA transport and oxidation – Increased capillary density (allows increased transit time for greater transport) and increased fatty acid binding protein and fatty acid translocase (FAT)
- Transport of FFA from the cytoplasm to the mitochondria – Higher levels of carnitine palmitoyl transferase and FAT
- Mitochondrial oxidation of FFA – Increased enzyme of beta oxidation, increased rate of acetyl-coa formation and high citrate levels
20
Q
How does endurance training improve the antioxidant capacity of muscle?
A
- Contracting skeletal muscle produce free radicals – Radicals chemical species that contain unpaired electron, making them highly reactive and can damage proteins, membrane and DNA. Radicals promote oxidative damage and muscle fatigue
- Training increases endogenous antioxidant enzymes – Improves the fibres ability to remove radicals and protects against exercise-induced damage and muscle fatigue
21
Q
How does endurance training improve acid-base balance during exercise?
A
- Lactate production during exercise
- Training adaptations – Increased mitochondrial number (less carbohydrate=less pyruvate formed), increased NADH shuttles (less NADH for lactic acid formation), changes in LDH isoform
22
Q
What are the molecular bases of exercise training adaptations?
A
- Endurance and resistance training promotes protein synthesis in fibres – Exercise ‘stress’ activated gene transcription
- Process of training-induced muscle adaptation – Muscle contraction activated primary and secondary messengers. Results in expression of genes and synthesis of new proteins.
23
Q
What are the process of training-induced muscle adaptations?
A
-Muscle contraction activated primary and secondary messengers
-Results in expression of genes and synthesis of new proteins
-mRNA levels typically peak in 4 to 8 hours, back to baseline within 24 hours
-Daily exercise required for training-induced adaptations
24
Q
Describe intracellular signalling in response to endurance exercise testing:
A
Primary and secondary signalling pathways interact to promote exercise-induced adaptations i.e. increased protein synthesis, mitochondrial biogenesis. Specific muscle adaptive responses depends on exercise stimulus – resistance v endurance training. Primary signals: mechanical stress (resistance training), calcium (endurance training), AMP/ATP (endurance training) and free radicals (endurance training)
25
What are the secondary messengers in skeletal muscle?
-7 points
- AMP kinase (AMPK) -> important signalling molecule activated during endurance exercise; promotes glucose uptake and linked to gene expression by activation of transcriptional activating factors
-Mitogen-activated kinase (p38) -> important signalling
-PGC-1a -> master regulator or mitochondrial biogenesis; promotes angiogenesis and synthesis of antioxidant enzymes. activated by AMPK, p38 and CaMK
-Calmodulin-dependent kinases (CaMK) -> activated by increased in cytosolic calcium - promotes activation of PGC - 1a
-Calcineurin (phosphate) -> participates in numerous adaptive responses of muscle including fiber regeneration and a fast-to-slow shift in fiber type
-Nuclear factor kappa B (NFkB) -> activated by radicals-promotes synthesis of antioxidant enzymes
-mTOR -> protein kinase-major regulator of protein synthesis and muscle size
26
What are the post-exercise molecular responses for endurance training?
-Seconds -> increased calcium, free radicals, AMP/ATP
-Minutes -> increased caclinurium, CaMK, AMPK, p38, NFkB
-Hours -> Increased PGC-1alpha, mitochondrial biogenesis
27
What are the biochemical changes in muscle from endurance training influencing cardio-respiratory responses to exercise?
-> Training-induced reductions in HR and ventilation due to:
* Training results in improved muscle homeostasis during exercise and reduced ‘feedback’ from muscle chemoreceptors to cardiovascular control centre
* Less feedback to cardiovascular control centre from group 3 and group 4 nerve fibres (responsive to temperature and biochemical changes)
* Reduced number of motor units recruited
28
What are the central controls of motor unit recruitment, HR, ventilation and blood flow to liver/ kidneys?
-> Endurance exercise training reduces central command outflow during submaximal exercise that results in a lower heart rate and ventilatory response during exercise – e.g. improvements in muscle fibre oxidative capacity means that fewer motor units required for submaximal work
29
What is detraining and VO2 max for endurance training?
* Rapid decreases in VO2 max – decreases approximately 8% within 12 days; decreased 20% after 84 days
* Decreased SV max – decreased rapid loss of plasma volume
* Decreased maximal a-v O2 difference – decreased mitochondria, oxidative capacity of muscle, type 2a fibres and increase in type 2-x fibres
* Initial decrease in VO2 max due to lowered SV max
* Later decrease due to decrease a-v O2 max
30
What is de/retraining and submax performance for endurance training?
* Primarily due to changes in mitochondria – Muscle mitochondria adapt quickly to training. Double within 5 weeks of training
* Mitochondrial adaptations lost quickly with detraining – Loss of 50% training gain within 1 week of detraining and majority of adaptations lost in 2 weeks
* Required 3 to 4 weeks of retraining to regain mitochondrial adaptations
31
Describe anaerobic exercise:
-Anaerobic exercise -> Refers to short-duration all-out exercise (sprint training):
- Recruits both type 1 and 2 muscle fibres
- During exercise <10 seconds, energy is primarily supplied by ATP-PC system
- During exercise lasting 20 to 30 seconds, 80% of energy needed is provided anaerobically whereas remaining 20% is provided aerobically
32
Describe anaerobic training increasing performance:
- 4 to 10 weeks of sprint training can increase peak anaerobic power by 3 to 28% across individuals
- Sprint training improves muscle buffering capacity by increasing both intracellular buffers and hydrogen ion transporters
- Sprint training also results in hypertrophy of type 2 muscle fibres and elevates enzymes involved in both the ATP-PC system and glycolysis
- High intensity interval training >30 seconds (at near or above VO2 max) promotes mitochondrial biogenesis.
33
What is muscular strength and endurance?
-Muscular strength -> Maximal force that a muscle group can generate. 1-RM.
-Muscular endurance -> Ability to make repeated contractions against a submaximal load
34
Describe strength training:
* High-resistance training (6 to 10 reps till fatigue) – results in strength increases
* Low-resistance (that is 35 to 40 reps till fatigue) – results in increases in endurance
* Compared to the >5000 times active muscle contract at relative low loads during 60 mins of moderate intensity continuous exercise
35
How does ageing result in a loss of muscle mass and strength?
-Ageing results in a loss of muscle mass-greatest decline occurring >age 50 ->
* Loss of muscle mass (termed sarcopenia)
* Atrophy type 2 fibres
* Reduced number of both type one and two fibres (loss of motor neurons)
* Resistance training promotes hypertrophy/ strength gains in older individuals but lower than young individuals
* Annual decline of strength is reported to be ~3 to 4% in men and ~2.5-3% in women
36
What neural adaptations are responsible for early gains in strength?
* Strength gains during first 8 weeks of training are largely due to nervous system adaptations
* As evidenced by ->
- Muscular strength increases in the first 2 weeks of training without increase in muscle fibre size
- Phenomenon of ‘cross education’ – training of one limb results in increases of strength in untrained limb
* Adaptations within muscle fibres occurs later – increased muscle fibre specific tension and increased muscle mass
37
What early gains are related to changes in the nervous system?
* Neural steps leading to muscular contraction – adaptations include ->
- Increased neural drive (measured via EMG)
- Increased number motor units recruited
- Increased firing rate of motor units
- Increased motor unit synchronization
- Improved neural transmission across neuromuscular junction
38
Describe increased muscle fibre specific tension in type 1 fibers?
* Mechanism responsible for training-induced increase in specific tension in type one fibres appears to be linked to increase calcium sensitivity – resulting in greater number of cross-bridges bound to actin. Enables more actin-myosin cross-bridge formation = more force per m. u. Evidence to support strength strength independent of muscle growth.
39
Describe training-induced increased in muscle mass:
- Hyperplasia – increased number of fibres- unclear if hyperplasia occurs in humans
- Hypertrophy – increased cross-sectional area of muscle fibres. Hypertrophy likely the dominant factor in resistance training-induced increases in muscle mass. Hypertrophy due to increased muscle proteins (that is actin and myosin). Evidence of a resistance training-induced transition from Type IIx to Type IIa.
40
Describe resistance training-induced increase in muscle protein synthesis:
-A single bout of resistance exercise promotes increases in both muscle protein synthesis and breakdown
-Muscle growth occurs because protein synthesis exceeds rate of breakdown – relatively slow rate of growth – synthesis must exceed breakdown for 3 or more weeks to achieve significant fibre growth
-Time course of resistance training-induced increase in muscle protein synthesis – increases 50 to 150% with 1-4 hours post exercise, elevated 30 to 48 hour depending on training status.
41
What are the key factors that contribute to resistance training-induced increase in MPS?
-mRNA increases resulting in protein synthesis at the ribosome
-ribosomes increase in number and elevate muscles protein synthesis capacity
-activation of the protein kinase 'mechanistic target of rapamycin' (mTOR) is the key factor accelerating protein synthesis following a bout of resistance training
42
Describe the 2 signalling molecules which stimulate the activation of mTOR:
phosphatidic (PA) and Ras homolog enriched in brain (Rheb)
-Muscle contractions activate a sarcolemmal mechanoreceptor stimualting synthesis of PA
-Contraction-induced activation of sarcolemmal mechanoreceptors also activated extracellular signal-related kinase (Erk)
-Hence, resistance training activates mTOR by synthesizing PA and removing the TSC2 inhibition of Rheb
43
What is the time course of molecular responses to resistance training?
-Seconds - increased Rheb and PA
-Minutes - mTOR activation
-Hours - increased protein synthesis
44
What are the other factors linked to resistance training-induced hypertrophy?
-Both insulin-growth factor-1 (IGF-1) and growth hormone are linked to m TOR activation and have potential to increase muscle protein synthesis ->
* A single bout of resistance training results in small increases in circulating levels of IGF-1 and growth hormone
* Although high circulating levels of these hormones can support resistance training-induced hypertrophy, increases in these hormones are not required to achieve resistance-training-induced hypertrophy
-Many individuals use over-the-counter nonsteroidal anti-inflammatory drugs (e.g. ibuprofen) to combat sore muscles and arthritis -> Animal studies suggest that these drugs blunt resistance training-induced muscle hypertrophy. However, recent human studies reveal that these drugs do not relatively impact strength gains in humans
45
What are the roles of satellite cells in resistance training-induced hypertrophy?
-Satellite cells are stem cells located between the sarcolemma and basal lamina
-* Resistance training activates satellite cells to divide and fuse with adjacent muscle fibres to increase myonuclei
* Resistance training-induced increases in myonuclei results in a constant ratio between number of myonuclei and size of muscle fibre
* Addition of new myonuclei to fibres is likely required to support increases protein synthesis in large muscle fibres – essential to achieve maximal hypertrophy
* Resistance training-induced satellite cells activation is blunted in older individuals – limits resistance training-induced muscle hypertrophy
* Resistance training results in parallel increases in muscle fibre size and number of myonuclei
46
What is the genetic influence on magnitude of resistance training-induced hypertrophy?
-> Approximately 80% of the differences in muscle mass between individuals is due to genetic variation:
* 47 different genes are major contributors to muscle mass
* Many hypertrophy-linked genes are directly linked to the m TOR pathway and are activated via resistance training
* Large differences exist between people in the magnitude of resistance training-induced skeletal muscle hypertrophy (high responders versus low responders)
* These differences are due to variations between people in their ability to activate specific ‘protein synthesis’ genes in skeletal muscle in response to resistance training
47
Explain detraining following strength training:
* Cessation of resistance training results in muscle atrophy and a loss of strength
- Compared to endurance training, the rate of detraining (strength loss) is slower
- Moreover, recovery of dynamic strength loss can occur rapidly (within 6 weeks) with retraining
* Gym folklore holds that, even after prolonged periods of inactivity, previously trained individuals can make a rapid recovery during retraining
- This ability for a rapid recovery is called ‘muscle memory’
- Mechanism responsible for muscle memory remains controversial
- Recent research suggests that muscle memory is due to resistance training-induced increases in myonuclei in the trained fibres that are not lost during detraining
- Maintaining myonuclei provides advantage in rapid protein synthesis upon retraining
48
How does prolonged skeletal muscle inactivity lead to rapid fibre atrophy?
-> Prolonged periods of muscle inactivity results in skeletal muscle atrophy:
* 20 to 30 days of muscle inactivity can result in 20 to 30% reduction in muscle fibre size
* Conservation of muscle mass is dependent upon balance between protein synthesis and rates of protein degradation
49
What are the key mechanisms responsible for inactivity-induced muscle atrophy?
. Increased radical production promotes atrophy during prolonged inactivity by depressing protein synthesis and increasing degradation
50
Describe the potential for interference of training adaptations following concurrent strength and endurance training:
- Strength training increases muscle fibre size whereas endurance training does not
- Depends on intensity, volume and frequency of endurance training
- Studies conclude that concurrent strength and endurance training impairs strength gains compared to strength training alone
51
What are the potential mechanisms following concurrent strength and endurance training?
- Neural factors – impaired motor unit recruitment
- Overtraining – no direct evidence exists to prove overtraining contributes
- Depressed protein synthesis – endurance training cells signalling can interfere with protein synthesis – via inhibition of m TOR by activation of AMPK
