Week 8 Flashcards
(28 cards)
Two main considerations when training/performing?
System contribution eg ATP-PC, glycolysis, aerobic, the time exercising usually determines which.
Muscle fibre recruitment eg type 1, 2a and 2x - determined by intensity.
Principles of training ?
- Overload
Training adaptations occur when the body is stressed beyond its normal level
Leads to exercise-induced adaptations (hormesis - see week 1)
- Specificity
Adaptations are specific to the exercise performed, including:
- Type of muscle fibers recruited
- Energy system used (aerobic vs. anaerobic)
- Contraction velocity
- Type of muscle contraction (eccentric, concentric, isometric)
- Reversibility
Training gains are lost when training stops
Detraining happens faster than adaptations are gained
Endurance Training and VO2 Max?
Ability to utilise oxygen effectively
- Training to increase VO2 max. - typical training.
- 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 to 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.
- Individuals with high VO2 max may require higher exercise training intensities (>70% VO2 max) to obtain
- Up to 50% in those with low initial VO2 max.
Average Vo2 Maxes (Males/Females)
Cross country skiers - 84/72
Sedentary (young) - 45 - 38
Severe diseased - 13
Impact of Genetics on VO2max and Exercise Training Response ?
- 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 to 20%.
- Low responders improve VO2 max by 2 to 3%
- 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%.
What is VO2 Max and Why Does Training Improve it?
- VO₂ max = Max cardiac output × arteriovenous O₂ difference (Fick’s equation)
- It reflects how well the body inspires/delivers and uses oxygen during maximal exercise.
Why it Improves with Training:
- Training enhances respiration, muscle metabolism, and central & peripheral circulation.
- Individual VO₂ max differences are mainly due to differences in stroke volume (SV) max, which links to Max CO which is tightly coupled with Vo2 max
- Short-term training (~4 months): Increases VO₂ max mostly via increased SV.
- Long-term training (~28 months): Increases in both SV and a-vO₂ difference.
Adaptations of VO2 max?
VO₂ max improves through adaptations in respiration, muscle metabolism, central circulation, and peripheral circulation:
- Respiration:
- Improved O₂ diffusion across lungs
- Enhanced ventilation efficiency
- Better alveolar ventilation:perfusion ratio
- Optimized hemoglobin (Hb)–O₂ affinity - Muscle Metabolism:
- Increased oxidative enzymes and aerobic capacity
- Enhanced energy stores (e.g., glycogen)
- More myoglobin for O₂ transport in muscle
- Larger and more numerous mitochondria
- Changes in muscle mass and fiber type (shift to more oxidative fibers)
- Improved substrate delivery and utilization - Central Circulation:
- Increased cardiac output (CO = HR × SV)
- Enhanced stroke volume (SV)
- Maintained or slightly increased arterial blood pressure
- Higher hemoglobin concentration for better O₂ transport - Peripheral Circulation:
- Reduced blood flow to non-exercising regions
- Increased muscle blood flow during exercise
- Greater capillary density in muscles
- Improved O₂ diffusion into muscles
- Enhanced muscle vascular conductance
- More efficient O₂ extraction
- Optimized Hb–O₂ affinity at tissue level
Summarised factors that improve VO2 max
VO₂ max = Cardiac Output (CO) × a-vO₂ difference
- Arteriovenous oxygen difference (a-vO₂ difference) is the amount of oxygen extracted by tissues from the blood.
It’s calculated as the difference between the oxygen content of arterial blood and venous blood. - CO is the amount of bloood the heart pumps per minute
- Cardiac Output (CO):
- ↑ Stroke Volume (SV) due to:
- ↑ Preload (more venous return)
- ↓ Afterload (less resistance)
- ↑ SNS activity to heart - a-vO₂ Difference:
- ↑ Muscle blood flow from SNS activity
-↑ Capillary density
- ↑ Mitochondrial number & size
How does endurance training increase Stroke volume? CO and HR recovery.
- ↑ Preload (↑ End-Diastolic Volume / EDV):
- ↑ Plasma volume (↑ 12–20% within 3–6 sessions).
- ↑ Venous return (more blood returning to heart).
- ↑ Ventricular chamber volume (adapts over months to years).
- ↓ Afterload (↓ Total Peripheral Resistance / TPR):
- ↓ Sympathetic nerve activity (SNA) → less arterial constriction.
- ↑ Maximal blood flow without ↑ MAP (mean arterial pressure).
- MAP = CO × TPR → Training allows higher CO with lower resistance.
- ↑ Contractility:
- Greater force of contraction (even without more SNS input).
- Improved “twist mechanics” of the left ventricle (LV).
- Supported by animal studies.
Combined Effects on Stroke Volume (SV):
- ↑ EDV, ↓ ESV, ↑ Ejection fraction during higher work rates.
- SV ↑ due to:
- ↑ Preload (plasma volume, venous return, chamber size)
- ↑ Contractility
- ↓ Afterload
CO and HR Recovery:
- Maximal cardiac output (CO) ↑ with training.
- Resting and submaximal HR ↓, but SV ↑, allowing higher CO with fewer beats.
Faster HR recovery post-exercise due to:
- Quicker parasympathetic reactivation
- More efficient autonomic balance
Training induced Increases in Arteriovenous O2 differences
- Muscle blood flow increases due to
decreased SNS vasoconstriction
Increased diameter and compliance of arteries
Increased diameter is however specific to limb being used. Permitting greater volume of flow per beat to limb
- Improved ability of muscle fibres to extract and utilise O2 from blood due to
Increased capillary density - slower blood flow though muscle
Increased mitochondrial number/volume
Increased capilllary supply and oxygen delivery in trained muscles?
During muscle contractions, red blood cell (RBC) transit time decreases due to faster blood flow
Endurance training increases capillary density, which:
— Reduces diffusion distance for oxygen
— Improves oxygen delivery to muscle fibers
Despite faster flow, overall RBC transit time increases in trained muscles because of the larger capillary network—allowing more time for oxygen exchange
What Difference does vascular remodelling and muscle metabolism changes makes to muscle blood flow in exercise ?
Submaximal Exercise:
- Blood flow to trained muscle is lower despite similar or higher workload.
- Because ↑ a-vO₂ difference (trained muscles extract more oxygen).
- Result: More efficient oxygen use, needing less blood flow.
Maximal Exercise:
- Blood flow to trained muscles is higher.
- Also, a-vO₂ difference is greater because of combined effect of:
— Vascular remodelling (↑ capillary density, vessel dilation).
— Improved mitochondrial/metabolic function (↑ O₂ utilization). - Result: Higher total oxygen delivery and usage → supports higher VO₂max.
Effects of endurance training on Performance and Homeostasis?
The ability to perform prolonged submax exercise is dependent on the ability to maintain homeostasis.
- Training improves homeostasis by:
- Faster transition from rest to steady-state.
- Reduced reliance on muscle glycogen.
- Enhanced cardiovascular and thermoregulatory efficiency.
- Numerous muscle fibre adaptations from training:
1. Shift from fast to slow and increased number of capillaries
2. Increased mitochondrial volume
3. Training induced changes in fuel utilisation
4. Increased antioxidant capacity
5. Improved acid-base regulation
Muscle Fiber Adaptations of training?
Fast-to-slow fiber shift:
- ↓ Type IIx (fast-twitch)
- ↑ Type I (slow-twitch)
- Leads to greater efficiency (more work per ATP used).
Capillary density increases:
- Improves oxygen delivery and waste removal.
Adaptation magnitude depends on:
- Training duration
- Training type
- Genetics
Mitochondrial Changes of endurance training?
- Mitochondrial biogenesis:
- Trainingdoubles mitochondrial volume in 5 weeks.
- Increased mitochondrial turnover(removal of damaged mitochondria viamitophagy).
- Improves metabolic efficiency:
- ↓ Cytosolic ADP.
- ↓ Lactate & H+ accumulation.
Fuel Utilization Adaptations?
- Increased fat utilization:
- ↑ Fatty acid transport proteins.
- ↑ Carnitine palmitoyltransferase (CPT) for mitochondrial FFA transport.
- Glycogen-sparing effect:
- More reliance on fat oxidation.
What comes from an Improved Acid-Base Balance?
With endurance training or adaptations, the body becomes better at handling acid build-up during exercise:
Lactate buffering Mechanisms:
- ↑ Mitochondrial density → more pyruvate and NADH used aerobically → ↓ lactate production.
- LDH isoform shift → favors conversion of lactate → pyruvate instead of puruvate into lactate.
Intracellular Signaling & Exercise Adaptation?
- Primary signals Triggered by exercise:
- Mechanical stretch→ From Resistance training.
- Calcium release→ From Endurance training.
- AMP/ATP ratio→ Indicates low Energy status.
- Free radicals→ Stimulate Antioxidant defense.
- Key Secondary Messengers:
- AMPK→ ↑ Mitochondrial biogenesis, ↑ glucose uptake.
- PGC-1α→ Master regulator of endurance adaptations.
- CaMK→ Activated by Ca²⁺, promotes PGC-1α activity.
- mTOR→ Activated from Resistance training → ↑ Protein synthesis.
- NFκB→ promotes Antioxidant enzyme production.
Muscle Adaptations to Anaerobic Training?
- Sprint training (10-30s)
- ↑ Type 2 fiber hypertrophy.
- ↑ ATP-PC and glycolytic enzymes.
- ↑ Intracellular buffers & H+ transporters.
- HIIT promotes mitochondrial biogenesis.
What is muscle strength and endurance? And what are the training types?
- Muscular Strength: Maximum force a muscle group can generate (measured by 1-RM).
Strength Training Types:
- High-resistance training (6–10 reps to fatigue)→ Increases strength.
- Low-resistance training (35–40 reps to fatigue)→ Increases endurance.
Muscular Endurance:
- Ability to perform repeated contractions against a submaximal load.
Age-Related Muscle Loss ? Causes? Training benefits?
Sarcopenia
- Muscle mass and strength decline with age, especially after50 years.
- Causes:
- Atrophy of Type II fibers.
- Reduction in Type I and II fibers due to motor neuron loss.
- Training Benefits: Resistance training canslow downbut not fully prevent age-related muscle decline.
Neural Adaptations? & Strength Gains?
- In the first ~8 weeks of resistance training, strength gains are primarily due to neural adaptations, not muscle hypertrophy.
Evidence:
- Strength improvements occur without visible muscle fiber growth
Cross-education effect:
- Training one limb also improves strength in the untrained limb
Key Neural Adaptations:
- Increased neural drive (↑ EMG activity)
- Greater motor unit recruitment
- Faster motor unit firing rates
- Improved synchronization of motor units
- Larger neuromuscular junctions (NMJ) and more acetylcholine (ACh) vesicles
Muscle Protein Synthesis & Hypertrophy?
- Muscle growth occurs when protein synthesis exceeds breakdown.
- Resistance Training Response:
- Protein synthesis increases50-150% within 1–4 hourspost-exercise.
- Remains elevated for30-48 hours, depending on training status.
- Faster hypertrophy in untrained individuals.
Muscle Fiber Adaptations?
- Increased Specific Tension in Type I Fibres:
- Due to greater calcium sensitivity
- Leads to more actin–myosin cross-bridge formation
- Muscle Growth Mechanisms:
Hypertrophy:
- ↑ Cross-sectional area of muscle fibres
- Main mechanism of strength gains
Hyperplasia:
- ↑ Number of fibres
- Unclear evidence in humans
- Fibre Type Shifts:
- Training causes a shift from Type IIx → Type IIa
- No shift from Type II → Type I with resistance training
Key Molecular Mechanisms?
- mTOR Pathway – Master regulator of muscle growth
Activated by:
- Phosphatidic Acid (PA): produced during muscle contractions
- Rheb: activated via Erk signalling (by lifting inhibition)
- Stimulates protein synthesis → hypertrophy
- Hormonal Influence:
IGF-1 and Growth Hormone support hypertrophy
- Help regulate satellite cell activity and protein synthesis
- But not essential for muscle growth
NSAIDs:
- May blunt growth in animal studies
- No clear effect in humans
