1/137
Looks like no tags are added yet.
Name | Mastery | Learn | Test | Matching | Spaced | Call with Kai |
|---|
No analytics yet
Send a link to your students to track their progress
Why do we do resistance training?
Increase strength, increase muscle size (hypertrophy), and improve performance/function.
Why does training work?
It increases demands and disrupts homeostasis.
What is progressive overload?
Training at a higher intensity than normal to force adaptation.
Components of a training program?
Exercise choice, intensity (weight), sets & reps, rest periods, order.
Muscular strength?
Max force in one effort (ex: 1-RM).
Muscular endurance?
Ability to perform repeated contractions without fatigue.
Strength training?
Exercise using resistance to increase strength and endurance.
Two components of strength gains?
Neural adaptations & contractile protein adaptations.
What are neural adaptations?
Learning” effects that improve nervous system efficiency.
Examples of neural adaptations?
Recruit more Type II motor units, better synchronization, Less Golgi tendon inhibition, and increased firing frequency
When are strength gains mostly neural?
First 8 weeks.
What is the cross-over effect?
Training one limb increases strength in the untrained limb.
What happens in contractile protein adaptation?
Increased actin & myosin → increased fiber CSA.
Why does increased CSA matter?
Bigger CSA = more force.
What must occur for hypertrophy?
Muscle fibers must experience overload (stress) and then repair/adapt.
Hypertrophy protein balance?
positive protein balance
Atrophy protein balance ?
negative protein balance
What regulates protein balance?
Hormones, diet, mechanical loading.
Anabolism
build up
Catabolism
break down
What is hyperplasia?
Increase in number of cells in tissues or organs.
Is hyperplasia measurable in humans?
No, difficult/impossible to quantify.
What is testosterone?
Hormone regulating growth and development.
What does growth hormone (GH) do?
Increases muscle mass, strength, protein synthesis; decreases breakdown.
Where does IGF-1 come from?
Liver (systemic) & muscle (local).
What is MGF?
Mechano Growth Factor
Where is IGF-1Ec released from
skeletal muscle
What triggers MGF release?
Stretch and overload.
What does MGF do?
Activates satellite cells → muscle growth.
What stimulates anabolic hormone release?
Muscle loading, stretch (eccentric), total muscle mass used.
How does loading stimulate hormone release?
Mechanical stress on sarcolemma → signal inside cell → hormone release.
What is systemic hormone response?
Heavy lifting triggers whole-body hormone release (like GH).
What is up-regulation?
Increased hormone receptors → greater sensitivity.
What are satellite cells?
Muscle stem cells between sarcolemma & basal lamina.
What happens when satellite cells are activated?
Divide and fuse with muscle → add myonuclei.
Why are myonuclei important?
More nuclei = more protein synthesis = maximal hypertrophy.
What is mTOR?
Mechanistic Target of Rapamycin; master growth switch.
Main trigger for mTOR?
Mechanical tension.
How does IGF-1 activate mTOR?
IGF-1 → Akt pathway → mTOR.
Akt Pathway
a cell signaling pathway that helps control muscle growth, protein synthesis, cell survival, and metabolism
What amino acid strongly activates mTOR?
Leucine.
Best combo for mTOR activation?
Protein + resistance training.
What is myostatin?
A protein that blocks muscle growth.
What happens if myostatin is blocked?
Greater muscle growth.
What happens to muscle fiber size during atrophy?
It decreases (both slow & fast fibers shrink)
How does fiber type change with atrophy?
Shifts from slow → fast
What happens to force production during atrophy?
Decreases (more than muscle mass loss)
What happens to protein synthesis during atrophy?
Decreases
What happens to mitochondrial enzymes during atrophy?
Decrease → less endurance
What is metabolism?
Breaking down food → to make energy
Why is metabolism important?
Provides energy for movement + body functions
What is bioenergetics?
Flow of energy in the body
First Law of Thermodynamics?
Energy cannot be created or destroyed, only transformed
What is energy?
Ability to do work
What is ATP?
Main energy source for muscle contraction
Main carb sources?
Glucose + glycogen
Why are fats important?
Store the most energy
When is protein used for energy?
Only when energy is low
What is glycolysis?
Breakdown of glucose → ATP
Where does glycolysis occur?
Cytoplasm
End products of glycolysis?
Pyruvate + ATP (+ lactate if anaerobic)
What is the rate-limiting enzyme?
PFK (phosphofructokinase)
What slows glycolysis?
High ATP, citrate, H⁺
What speeds glycolysis up?
High AMP, ADP
Glycogenesis?
Make glycogen
Glycogenolysis?
Break glycogen → glucose
Gluconeogenesis?
Make new glucose (non-carbs)
Fastest energy system?
Creatine Phosphate (CP)
How long does CP last?
8–20 seconds
Is CP aerobic or anaerobic?
Anaerobic
What does CP do?
Quickly rebuilds ATP
Myokinase reaction?
2 ADP → ATP + AMP
What is lactate threshold?
Point where lactate rises quickly
What causes fatigue?
H⁺ buildup (acid)
What does lactate indicate?
Endurance ability
Main aerobic fuel?
Glucose + fat
Where does aerobic metabolism occur?
Mitochondria
Is aerobic fast or slow?
Slow but long-lasting
Purpose of Krebs cycle?
Make electron carriers (NADH, FADH₂)
Where is ETC located?
Inner mitochondrial membrane
What does ETC do?
Produces most ATP
What controls metabolism speed?
Enzymes
What turns glycolysis OFF?
High ATP/CP (rest)
What turns glycolysis ON?
High AMP/ADP (exercise)
What slows glycolysis during intense exercise?
High H⁺
What does hexokinase do?
Adds Pi to glucose → traps it in the cell
What is succinate dehydrogenase (SDH)?
Enzyme in Krebs cycle → makes FADH₂
Why is SDH important?
SDH activity shows how good a muscle is at using oxygen (oxidative capacity)
What is the CP shuttle?
Moves high-energy phosphate from mitochondria → cytoplasm
Why is the CP shuttle important?
Helps make ATP quickly where it’s needed
What does “nonoxidative” mean?
No oxygen required
What does LDH do?
Converts pyruvate → lactate
When is LDH active?
High energy demand / low oxygen
Which fibers have more LDH?
Fast-twitch fibers
Which fibers have less LDH?
Slow-twitch fibers
What does PDH do?
Converts pyruvate → Acetyl-CoA
Why is PDH important?
Sends fuel into Krebs cycle (aerobic energy)
What activates PDH?
ADP, Ca²⁺, pyruvate
What inhibits PDH?
Free fatty acids (FFA), low glycogen
What controls oxidative metabolism?
Rate of Krebs cycle + ETC