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?
Defined by Ficks equation - VO2 Max = Maximal cardiac output X a-vO2 difference.
How effectively the body inspires and utilises oxygen during max exercise.
Improves respiration, muscle metabolism, central and peripheral circulation.
Differences in VO2 max between people is often due to differences in SV max, Max CO and VO2 are tightly coupled
Exercise induced improvements in VO2 max can be seen after short duration of training, about 4 months, an increased in SV is the dominant factor and longer durations of about 28 months shows both a SV and a a-VO2 increase
Adaptations of VO2 max?
Improves in Respiration, muscle metabolism, central and peripheral circulation.
Respiration:
O2 diffusion
Ventilation
Alveolar ventilation : Perfusion ratio
Hb - O2 affinity improvements
Muscle metabolism:
Enzymes and oxidative potential
energy stores
Myoglobin
mitochondrial size and numbers
Muscle mass and fibre type
Substrate delivery
Central circulation:
CO = HR, SV
Arterial BP
Hb Conc
Peripheral circulation:
Flow to non exercising regions
Muscle blood flow
Muscle capillary density
O2 diffusion
Muscle vascular conductance
O2 extraction
Hb-O2 affinity
Summarised factors that improve VO2 max
Oxygen uptake = Cardiac output X a-v O2 diff
CO:
Effected by Increased SV which comes from increased Preload and decreased Afterload
(This is also aided by Increased SNS activity to working muscles)
a-VO2 differenc:
Comes from increased blood flow from increased SNS activity to working muscles as well as increased capillaries mitochondria
How does endurance training increase Stroke volume? CO and HR recovery.
↑ Preload (EDV).
• ↑ Plasma volume. (Days) - 12-20% increase after only 3-6 sessions
• ↑ Venous return. (Days)
• ↑ Ventricular volume. (months to years)
Decreased Afterload (TPR)
- Arterial constriction (decreased SNA)
- Increased Max blood flow with no change in MAP eg increase in CO parallels the decrease in resistance
MAP = CO x TPR
Increased Contractility (independent on SNS input and other factors constant (EDV, HR, Afterload))
- Greater force produced with each contraction (animal studies)
- Iprves ‘twist mechanics’ of the LV
Combined effects:
Difference in -
EDV, ESV, Ejection fraction increases with rates of work of individuals
Increased Ventricular volume, filling time, venous return and plasma volume increases EDV.
Increased Contraclity and decreased TPR(Afterload) alongside increased EDV increases SV
Max CO also increases with training, HR decrease but SV increases leading to higher CO achieved in fewer beats.
HR recover also improves
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 contractions, transit time of RBCs ecreases
Training increases capillary density reducing diffusion distance
Transit time is increased overall because bigger capillary networks means RBCs take longer to pass through
What Difference does vascular remodelling and muscle metabolism changes makes to muscle blood flow in exercise ?
During submax exercise, blood flow increases due ttrained muscles is lower because the AV difference is greater (better oxygen extraction)
During MAX exercise blood flow in trained muscles is higher and the AV difference is greater
Effects 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:
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:
- ↓ Fast fibers (Type 2x) and ↑ Slow fibers (Type 1).
- Improved efficiency (more work per ATP used).
- Magnitude of fibre type change is determined by duration of training, type and genetics
- Capillary Density Increases:
- EnhancesO2 diffusionandwaste removal.
Mitochondrial Changes?
- 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.
Improved Acid-Base Balance?
- Lactate buffering:
- ↑ Mitochondria → ↓ Pyruvate and NADH accumulation.
- Shift inLDH isoformsto favorless lactate production.
Intracellular Signaling & Exercise Adaptation?
- Primary signals:
- Mechanical stretch→ Resistance training.
- Calcium release→ Endurance training.
- AMP/ATP ratio→ Energy status.
- Free radicals→ Antioxidant defense.
- Key Secondary Messengers:
- AMPK→ ↑ Mitochondrial biogenesis, glucose uptake.
- PGC-1α→ Master regulator of endurance adaptations.
- CaMK→ Activated by Ca²⁺, promotes PGC-1α.
- mTOR→ Resistance training → ↑ Protein synthesis.
- NFκB→ 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.
- HIITpromotesmitochondrial 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).
- Muscular Endurance: Ability to perform repeated contractions against a submaximal load.
- Strength Training Types:
- High-resistance training (6–10 reps to fatigue)→ Increases strength.
- Low-resistance training (35–40 reps to fatigue)→ Increases endurance.
Age-Related Muscle Loss ?
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?
- First 8 weeks of training: Strength gains are mostly due toneural adaptations.
- Evidence:
- Strength increases occurwithoutmuscle fiber growth in the initial weeks.
- Cross-education effect: Training one limb enhances strength in the untrained limb.
- Neural Adaptations:
- Increasedneural drive(measured via EMG).
- Moremotor units recruited.
- Fastermotor unit firing rate.
- Bettersynchronization of motor units.
- Largerneuromuscular junction (NMJ)and increased 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 Fibers:
- Due to increasedcalcium sensitivity, leading to more actin-myosin cross-bridges.
- Muscle Growth Mechanisms:
- Hypertrophy: Increase in fibercross-sectional area(dominant form of muscle growth).
- Hyperplasia: Increase in fibernumber(uncertain in humans).
- Fiber Type Shifts:
- Resistance training shifts fibers fromType IIx → Type IIa.
- No shift fromType II → Type I.
Key Molecular Mechanisms?
- mTOR Pathway(Master regulator of muscle growth)
- Activated byPhosphatidic Acid (PA)andRas homolog enriched in brain (Rheb).
- PA is synthesized frommuscle contractions.
- Rheb activation isdisinhibitedvia Erk signaling.
- Hormonal Influence:
- IGF-1 and Growth Hormonesupport hypertrophybut are not essential.
- NSAIDsmay blunt muscle growthin animal studies, butnot in humans.
