Quiz #1 + Exam #1 Flashcards
(a) What are skeletal muscles comprised of? What are they bundles of?
(b) What are muscles fibers/muscle cells composed of and what can they be subdivided into? What are they also called?
(c) Where are satellitle cells located?
(d) In humans, most skeletal muscles are ____ of muscle fiber types.
(e) What determines where the sliding filament theory occurs?
(a) Skeletal muscles are comprised of fasicles, which are bundles of muscle fibers
(b) Myofibrils, which can be divided into actin and myosin (aka contractile proteins)
(c) Near, or embedded in, the sarcolemma (exterior of the cell)
(d) a mix
(e) Depends on the acitivy of the individual, thus certain muscle fiber types will be activated
What are the three major functions of skeletal muscle?
- Force generation for locomotion and breathing
- Force generation for postural support
- Heat production during cold stress
What is the sarcoplasm?
A connective tissue that wraps around an individual muscle cell/muscle fiber.
(a) What are thin filaments also called?
(b) What consists of the thin filaments?
(c) What is the net charge?
(a) actin
(b) G-actin, troponin, tropomyosin
(c) positive, +
(a) What are thick filaments also called?
(b) What consists of the thick filaments?
(c) What is the net charge?
(a) myosin
(b) Myosin heads, myosin tails
(c) negative, -
How does the net charge of thick and thin filaments help with muscle contraction?
Allows for them to bind to each other with opposite charges.
(a) What are satellite cells?
(b) Where are they located?
(c) What type of training can activate satellite cells? What does it become?
(d) What is it predicted to play a role in?
e) Explain how does training activate satellite cells (HINT! include nuclei)
(f) “____ is the brain of the cells, without it, the cell has nothing to regulate it.”
(a) A type of precursor cell
(b) Located near the sarcolemma
(c) Resistance training, can become most cell types as needed for bodily fucntion and maintenance
(d) Predicted to play a role in muscle growth and repair
(e) Contraction from training causes tension on the surface of a muscle cell, which is where the satellitle cells are located, thus causing them to become activated and dividing, which theoretically could** increase** the number of cellular nuclei
(f) Nuclei!
What is fascia?
A connective tissue that seperates individual muscles from each other, holding them in position
(a) Describe the neuromuscular junction (NMJ). Be detailed in its function.
(b) Which types of exercise training cause positive adaptions to the NMJ?
(c) Describe the 3 adaptations to the NMJ that occur as a result of training. What does this enhance?
(d) T/F: We see change in muscle size before adaption in the NMJ after weeks of optimal training.
(a) Neuromuscular junction: Interface bewteen a motor neruon and muscle cells OR where neurons meet muscle fibers
- Signals are sent from the brain, down the spinal cord to an alpha motor neuron. AP travels dow nthe synaptic bulb to which it will release ACh, which will then bind to the binding sites on the muscle cells
(b) Both resistance and endurance training
(c) 1. ↑ # of vesicles contain ACh
- ↑ # of ACh receptors on motor end plate
- ↑ size of motor end plate
= Overall enhancement of the electrical signal to the muscles
(d) False!
Consider the results of a 16-week resistance training program, where periodization and nutrition are optimal…
(a) Visually, what are we likely to see?
(b) What causes this result?
(c) Why do muscle cells adapt in this manner? (Exercise training is a stressor)
(d) True or false? Only muscle cells adapt to training. Justify your response.
(e) What term describes the situation where the # of muscle fibers increases? What is the misconception?
(a) Hypertrophy
(b) ↑ # of myofibrils
(c) So that future bouts of exercise/activity are less stressful
(d) ALL systems adapt, all cells involved adapt ; Systems that support muscle cells must also grow and adapt, or else it will all fail.
(e) Hyperplasia ; small amt. of evidence in humans, but def. in chicken and cat
Describe what is the “Myonuclear domain.”
- Myonuclear domain is the volume of sarcoplasm surrounding an individual nucleus. The nucleus is considered to be, “the brain of the (muscle) cell” and holds the necessary gene expression, such as for protein production. Without it, the cell will not be able to regulate/function on its own.
- A single nucleus, however, can only manage cellular activities/functions for a fixed volume of sarcoplasm and the ratio of cell volume and per nucleus remains constant.
- If the sarcoplasmic volume increases due to hypertrophy (from training), then the number of nuclei must also increase. Therefore, to remain a constant ratio, the satellite cells will become activated from training, dividing and creating additional nucleus.
Describe “motor unit”
The motor neuron and all the muscle fiber it innervates.
What is the difference in the motor unit recruitment in relfex movements vs. planned movments.
- Reflex movements begin at spinal cord, brain is “informed” after movement has been intitiated
- Planned movements being in the brain
Describe the excitation sequence of the excitation-contraction coupling.
- Action potential (AP) arrives at synaptic bulb or knob.
- Vesicles secrete ACh, a neurotransmitter.
— ACh binds to receptors on the motor end plate, aka post-synaptic membrane -
Ion channels open on sarcolemma, and Na+ floods
into muscle cell, causing depolarization of the muscle cell.
Describe the contraction sequence of the excitation-contraction coupling.
- Waves of depolarization spread across muscle cells, down ** t-tubules ,** which stimulates SR (sarcoplasmic reticulum) to release Ca2+.
- Ca2+ binds to troponin, which then pulls tropomyosin off the myosin binding site on actin.
- Actin and mysoin bind, formin a cross-bridge.
- Pi is released from mysoin head → powerstroke
- ADP is released from mysoin head → rigor state
- New ATP binds to myosin head, which breaks rigor state
- Enzyme Myosin ATPase hydrolyzes the ATP on the myosin head
- Energy, a product of ATP hydrolysis, is used to recock the myosin head back to starting position
Describe the relaxation sequence of the excitation-contraction coupling.
- Brain stops generating AP
- The release of neurotransmitter, ACh, from vesicles within muscle cells stops
- Muscle cells repolarize
- The Ca2+ that is now within the muscle cell goes back/is pumped back to the SR, which requires ATP
- Troponin blocks the myosin binding site on actin, which breaks apart the crossbridge.
Be familiar with the formula during ATP hydrolysis
*ATP hydrolysis occurs in the presense of water and ATPase!
ATP + H2O (w/ Myosin ATPase) → ADP + Pi + Energy + OH- + H+
Which structure found in skeletal muscle fibers acts the storage location for calcium?
Sarcoplasmic reticulum (SR)
What are the 3 sources of ATP production in muscle during contraction?
- PCr
- Glycolysis
- Oxidative Phosphorylation (Kreb Cycle and Beta Oxidation)
(a) What are human skeletal muscle fiber-type categories based on?
(b) About how many spectrum of fiber type exists?
(c) What are the three types of human skeletal fiber types that will be discussed in class?
(a) Biomechanical properties, mechanical properties, and fucntional characteristics
- Some overlap exists
(b) 12 - 13
(c) - Type I slow-twitch (slow oxidative)
- Type II fast-twitch:
1. Type IIa intermediate (fast oxidative, glycolytic)
2. Type IIx fast glycolytic or fast-twitch
What are the three primary biomechanical properties of skeletal muscle? Explain each one.
- Oxidative capacity:
a) mitochondrial vol. or density
- Relates to cell’s ability to produce ATP aerobically (beta-oxidation) AND fatigue resistance
b) Capillary density: the network of blood vessels that move O2 from lungs to muscle
- ↑capillary density = ↑O2 from lungs to muscle
c) [myoglobin] or [MB]: transports oxygen from through sarcoplasm to mitochondria - Myosin isoform (or type)
- Myosin ATPase
- Type I, IIa, IIx - # actin/mysoin
- per muscle fiber and motor unti
What are the four performance charcteristics of the contractilie properties of a skeletal muscle? Explain each one.
- (346) Max force production or (446) specific tension
- = # of force produced/cross-sectional area of muscle fiber - (346) speed of contraction or (446) max. shortening velocity (aka Vmax)
- Related to:
a) Isoform of ATPase
b) Size of motor neuron
- If the neuron is much bigger, it allows for AP to travel much quicker
c) SR development
- SR is a network that surrounds the muscle fiber that holds Ca2+
- The denser and closer the webbing in a Type IIx allows for Ca2+ to travel a small distance to the troponin, vs. the webbing in a Type I - Max. power output
- = to points #1 and #2 - Effciency of contraction
- = # of ATP used/# of force produced
Distinguish type I fibers vs. type IIA fibers vs. type IIX fibers in terms of the following…
(a) Number of mitochondria
(b) Resistance to fatigue
(c) Predominant energy system
(d) ATPase activity
(e) Vmax (speed of shortening)
(f) Effciency
(g) Specific tension
(a) Number of mitochondria:
- Type I: High
- Type IIa: High/moderate
- Type IIx: Low
(b) Resistance to fatigue:
- Type I: High
- Type IIa: High/moderate
- Type IIx: Low
(c) Predominant energy system:
- Type I: Aerobic
- Type IIa: Combination
- Type IIx: Anaerobic
(d) ATPase activity:
- Type I: Low
- Type IIa: High
- Type IIx: Highest
(e) Vmax (speed of shortening):
- Type I: Low
- Type IIa: High
- Type IIx: Highest
(f) Effciency:
- Type I: High
- Type IIa: Moderate
- Type IIx: Low
(g) Specific tension:
- Type I: Moderate
- Type IIa: High
- Type IIx: High
(a) T/F: Is atheltic performance due only to fiber type distribution? Explain.
(b) What factors in athletic performance?
(c) What are the fiber type distribution in nonathletes?
(d) _ % of fiber types determined prior to birth and _ % determined during first 24 months of life.
(e) What determines a starting point for fiber distribution?
(a) False ; EX: % of Type I fiber distribtuion explains only 40% of VO2 max between individuals
(b) Athletic performance is due to a complex interaction of psychological, neurological, cardiopulmonary, and biomechanical factors
(c) 50% Type I and 50% Type IIa/x
(d) 80% ; 20%
(e) Gene pool
What is the specific term for age-related loss of muscle mass?
Sarcopenia
(a) According to the text, what are muscle cramps?
Consider the two popular theories (Dehydrated and electrolyte imbalance theory and Altered neuromuscular control theory) as to the cause of exercise-associated muscle cramps…
(b1.) Which of the theories is least supported by science? Why
(b2.) What roles might the GTO and muscle spindle play in exercise-associated muscle cramps?
(c) What relieves exercise-associated muscle cramps?
(a) Muscle cramps are spasmodic and involuntary muscle contractions that can be painful
(b1.) Dehydration and electrolyte imbalance theory is least supported by science.
- As dehydration and electrolyte imbalance affect the whole body, cramps should occur in all muscles rather than only the working muscles.
- Second, contraction-induced cramping is caused by a repeated electrical stimulation of a small group of skeletal muscles, in which no change in the blood electrolyte concentration occurs.
- Third, if dehydration caused the cramp, stretching would not relieve the cramps because no fluids or electrolytes relieved the body.
(b2.) Muscle spindles function as length detectors and GTO provides the CNS feedback on the tension/strain across a tendon from a muscle force generation. Prolonged, intense exercises often result in fatigue/injury, which can promote dysfunction of the muscle spindle and/or the golgi tendon. Therefore, rigorous exercise could promote muscle cramps by decreasing the firing of GTO (decreased inhibition of motor neuron firing) and increasing the firing of the muscle spindles (increased motor neuron activation)
(c) Passive stretch of the muscle
(a) When do chemical reactions occur?
(b) What are the starting substances are known as?
(c) What are the ending substances are known as?
(d) What is referred to as all chemical reaction occuring within the body?
(a) Occurs when new bonds form or old bonds break between atoms
(b) Reactants
(c) Products
(d) Metabolism
(a) Chemical reactions that release energy are known as…?
(b) Chemical reactions that require the input of energy are known as…?
(a) Exothermic or Exergonic reactions
(b) Endothermic or Endergonic reactions
(a) Each chemical reaction involves ____ changes. What does it have the capacity to do?
(b) What are the two principle forms of energy? Define each one.
(c) What is chemical energy in a form of?
(d) What are compounds and how does this relate to the body?
(a) Energy, is the capacity to do work
(b) Potential energy: Energy stored by matter due to its position.
Kinetic energy: Energy associate with matter in motion.
(c) Kinetic energy that is stored in the bonds of compounds and molecules.
(d) Compounds: A substance that contains atoms of 2 or more different elements.
- Most atoms in the body are joined into compounds
(a) How are oxidation and reduction reactions different? In other words, how is the movement of hydrogens and electrons different between the two?
(b) What is the oxidation-reduction reactions?
(a)
Oxidation: The process of removing an electron from an atom or molecule
Reduction: The addition of an electron to an atom or molecule
(b) Oxidation-reduction reactions: a coupled reaction that involves the transfer of hydrogen atoms (with their electrons) rather than free electrons alone, because a hydrogen atom contains one electron and one proton in the nucleus
- Therefore, a molecule that loses a hydrogen atom also loses an electron and therefore is oxidized; the molecule that gains the hydrogen (and electron) is reduced.
(a) What type of compound is ATP? What are the elements of ATP?
(b) What do the bonds between each phosphate group store?
(c) In the prescence of H2O, which enzyme is used to break the bond bewteen the second and third phosphate group? What does this release?
(d) During muscle contraction, the energy released by ATP hydrolysis is used to…?
(a) High-energy compund. Consists of Adenine, ribose, 3 phosphate groups
(b) Stores great amt. of energy
(c) Myosin ATPase, releasing energy
(d) Recock/reset the myosin head back to the starting positon
(a) What are enzymes?
(b) What are catalysts?
(c) What is activation energy?
(d) Do enzymes cause a reaction to occur? Explain!
(a) Enzymes: Cellular proteins that act as catalysts to ↑ the speed of chemical reactions
(b) Catalysts: Chemical compounds that ↑ speed of chemical reactions by lowering the activation energy of the reaction
(c) Activation energy: The energy needed to break (or make) the bonds of reactants in a chemical reaction.
(d) NO! But, they do affect the rate or speed of chemical reaction. Having more enzymes available can increase the rate in reaction.
(a) Enzymes that add a phosphate group are known as?
(b) Enzymes that remove a hydrogen atom are known as?
(c) Enzymes that rearrange atoms within a molecule are known as?
(d) Enzymes that catalyze REDOX reactions are known as?
(a) Kinases
(b) Dehydorgenases
(c) Isomerases
(d) Oxidases
(a) What is the important role of enzymes in chemical reactions?
(b) How is enzyme activity measured?
(c) What conditions or factors increase enzyme activity rates?
(d) What is the ideal temp. for enzymes to work faster?
(e) How is pH related to the muscle cell? What happens when [H+] increases vs. decreases
(f) In regards to pH balance, what occurs when exercise intensity increases?
(a) Enzymes will lower the activation energy, making the chemical reaction occur much faster. The number of enzymes asscoiated with a certain activity will increase with long term training, so that future activity is less stressful than it was before.
(b) By the rate of product formation (how fast we get what we want to get)
(c) Body temp., and pH
(d) ~37°C - 40°C
(e) pH is related to [H+] in a muscle cell. Therefore, as [H+] ↑, then pH↓ and vice versa.
(e) As exercise intensity increases, this will cause ATP hydorlysis to increase, creating more products. With H+ being one of the products = ↑ [H+], pH↓
(a) What are the components of CHO (3)?
(b) What is the storage form of CHO called vs the usuable form?
(c) What is the process called to convert the storgae form of CHO to usable form? What is the enzyme used?
(d) What is the process called to convert the usable form of CHO to storage form? What is the enzyme used?
(a) Carbon, Hydrogen, Oxygen (specific ratio)
(b) Storgae form = glycogen, Useable form = glucose
(c) Glycogen → Glucose (via glycogenolysis, w/ glycogen phosphorylase)
(d) Glucose → Glycogen (via glycogenesis, w/ glycogen synthase)
(a) What are the components of Fat (3)? How does this differ from CHO?
(b) What is the storage form of Fat called vs the usuable form?
(c) What is the process called to convert the storgae form of fat to usable form? What is the enzyme used?
(d) What is the process called to convert the usable form of Fat to storage form? What is the enzyme used?
(a) Carbon, Hydrogen, Oxygen (in a certain ratio, but different from CHO); Fats have a greater ratio of carbon to oxygen given their nature of being an ideal fuel source for prolonged exercise.
(b) Storage form = Triglycerides ; Usable form = Fatty acids
(c) TG → Fatty Acids (via lipolysis, w/ hormone sensitive lipase - rate limiting enzyme)
(d) Fatty Acids → TG (via lipogenesis/esterification, w/ many enzymes)
(a) Is more energy stored as CHO or Fat (in terms of kcal)?
(b) Where is most of CHO stored?
(c) Where is least amt. of CHO stored?
(d) Where is most of Fat stored?
(a) Fat!
(b) Muscle (as muscle glycogen)
(c) Blood glucose
(d) Subcutaneous (under skin) and visceral (around internal organs)
(a) How is using CHO for fuel different from using fat? (Consider where its located and the steps it takes to convert)
(b) When converting a macronutrient from storage form to usable form, about how many is the chemical reaction for CHO vs. Fat?
(c) Which macronutrient is being primarily used for high intensity?
(a) CHO is generally stored closest to contractile proteins in the muscle cell. Therfore, the steps to convert CHO is much faster and the rate limiting enzyme is faster
(b) CHO: 2 dozen chemical reactions
Fat: 100+ chemical reactions
(c) CHO (sugar)
Consider the ATP-producing pathways discussed in Chapter 3. Which occur within the mitochondria, and which occur in the sarcoplasm?
- Sarcoplasm: Stored muscle ATP, ATP-PCr, Glycolysis
- Mitochondria: Oxidative phosphorylation of ATP (Krebs Cycle, Beta-Ox., ETC)
(a) What are the components of protein?
(b) What are the building blocks of protein?
(c) How much A.A. is necessary to synthesize all bodily proteins?
(d) What are the two categories of amino acids? How much is in each category and how do they differ?
(e) Do our cells store protein the same as with CHO or Fat? Explain.
(a) Carbon, hydrogen, oxygen, and a nitogen group (NH4) aka amine group
(b) Amino acids
(c) 20
(d) Essential A.A. = 9 (only come from diet) ; Non-essential = 11 (can be synthesized from other amino acids
(e) No! There are 20 “pools” that are filled up for each individual A.A.. With the excess protein, they can either become fat storage OR get lost via urinating.
(a) What are possible sources of protein?
(b) How do we get so many possible results/options from protein digestion/breakdown? In other words… what are the 2 processes?
(a) Chicken, fish, beans, dairy, meat
(b)
1. Transamination: Nitorgen group get transeferred from one amino acid to another
2. Deamination: Nitrogen group removed from A.A., and the ramining carbon skeleton can be used as fuel.
Carbohydrates (CHO) contain a certain ratio of carbon, hydrogen, and oxygen molecules. How is this similar and different to the molecules that make up fats and proteins?
- CHO is similar to the molecules that make up fats as they have the same molecules
- However, the ratio of these molecules differ in these macronutrients as fats have a greater ratio of carbon to oxygen than carbohydrates do, given their nature of being an ideal fuel source for prolonged exercise.
- On the other hand, proteins are composed of many small subunits called amino acids.
How many kcals per gram are provided by CHO, Fat, and protein?
CHO: 1g = 4 kcals
Fat: 1g = 9 kcals
Pro: 1g = 4 kcals
(a) Where do most amino aicd metabolism occur? How about in a smaller degree?
(b) Where else can a few amino acids be metabolized? What amino acids are these and which part of group are they from?
(c) In addition to proteins, what else can amino acids also form?
(a) Liver. Kidneys for smaller degree
(b) Skeletal muscle fibers. Leucine, Isoleucine, Valine (part of Branch-Chain Amino Acids aka BCAAs)
(c) Glucose (usable form of sugar), Pyruvate (end product of slow glycolysis), Acetyl CoA (product when pyruvate enters the mitochondria and starts the Kreb Cycle) and other Kreb Cycle Intermediates
(a) In chemical reactions, the _ point is important.
(b) How does this relate to free energy ladders when combusting CHO?
(c) How much ATP does NADH yield in the ETC vs. FADH?
(a) starting
(b) When combusting CHO, there is a release of free energy. At the start of this reaction, there is a lot more energy. However, during cellular oxidation (Kreb cycle and Beta oxidation), there is less energy. However, you will still get the same end result.
(c) 2.5 ATP/NADH
1.5 ATP/ FADH
Understand the role of the two subpopulations of mitochondria found in skeletal muscle fibers
- The mitochondria consists of two subpopulations, subsarcolemmal mitochondria and intermyofibrillar mitochondria to help supply the muscle with a constant supply of usable energy.
- The subsarcolemmal mitochondria is located beneath the sarcolemma which produces the cellular energy needed to maintain active transport of ions across the sarcolemma.
- The intermyofibrillar mitochondria is found near the myofibrillar proteins where it can provide the energy needed to sustain muscle contractions.
(a) What are the roles of NAD+ and FAD in the chemical reactions related to Bioenergetics?
(b) From which general family of vitamins are NAD+ and FAD derived?
(a) These are two molecules that play an important role in the transfer of electrons:
- The oxidized form of nicotinamide adenine dinucleotide is written as NAD+, whereas the reduced form is written as NADH
- The oxidized form of flavin adenine dinucleotide is written as FAD, whereas the reduced form is written as FADH
(b) NAD+ and FAD are derived from the general family of vitamin B. (NAD+ from vitamin B3 and FAD from vitamin B2)
How do modulators affect the rates of the chemical reactions discussed in Chapter 3?
Modulators are substances that regulate the activity of rate-limiting enzymes whether by increasing or decreasing the enzyme activity.
Identify the rate-limiting enzymes in the aerobic and anaerobic ATP-producing pathways as described in lecture and your textbook.
Anaerobic:
PCr- Creatine kinase
Glycolysis - PFK
Aerobic:
Krebs Cycle - Isocitrate dehydrogense
Beta-ox - HSL
ETC - Cytochrome oxidase
Indicate the following for stored muscle ATP:
(a) _ energy (fuel) source
(b) Cellular compartment:
(c) Rate-limiting enzyme:
(d) Duration at max intensity:
(e) Other info:
(a) **Immediate ** energy (fuel) source
(b) Sarcoplasm
(c) Myosin ATPase
(d) ~ 2 secs
(e) Store only a small amt. of ATP w/ muscle cells
What are the 2 options for ATP synthesis in chemical reaction?
- Substrate-level phosphorylation (aka direct phosphorylation)
- Oxidative phosphorylation (aka indirect phosphorylation)
(a) What is another word for substrate level phosphorylation?
(b) What is a substrate?
(c) What happens during substrate-level phosphorylation?
ii. Where does it occur?
iii. What does it not involve?
(a) Direct phosphorylation
(b) Any molecule that an enzyme acts upon
(c) A substrate can transfer a phosphate to ADP, which forms a new molecule of ATP
ii. Sarcoplasm and mitochondria
iii. Oxygen (though O2 is always present)
(a) What is another word for oxidative phosphorylation?
(b) What happens during oxidative phosphorylation?
ii. Where does it occur?
iii. What does it involve?
(a) Indirect phosphorylation
(b) Creates ATP by transferring electrons from NADH and FADH to oxygen in ETC
ii. Mitochondria (ETC specifically)
iii. ALWAYS require oxygen
Which molecule accepts electrons at the end of the electron transport chain (ETC)?
Oxygen
Indicate the following for ATP-PCr:
(a) Time needed for full-activation?
(b) Cellular compartment:
(c) Rate-limiting enzyme
(d) Duration @ max effort/intensity?
(e) When does ATP-PCr restoration occur within muscle cells?
i. 50% of ATP-PCr is restored within how many secs.?
ii. 90% of ATP-PCr is restored within how many secs.?
iiii. 100% of ATP-PCr is restored within how many secs. or mins. ?
(a) 1-2 secs
(b) Sarcoplasm
(c) Creatine kinase
(d) 8-15 secs
(e) During rest via aerobic metabolism (first few things that get restored during EPOC)
i. 30 secs
ii. 120 secs (2 mins.)
iii. 300 secs or 5 mins.
Answer the follwoing regarding ATP-PCr:
(a) During short-term, high-intensity exercise (100 – 200 m sprint), PCr depletion may _ performance
(b) As cellular [PCr] ______ → ______ rate of ATP production by ATP-PCr system.
(c) Once stored muscle cell ATP is depleted, what can PCr be used for?
(d) How does creatine monohydrate help with high intensity exercises?
i. What is the loading phase?
ii. What is the maintenance phase?
iii. Some evidence: consuming creatine monohydrate along with ____ kcals protein & ____ kcals CHO may improve creatine uptake in muscle cells due to ___ insulin response.
- Know the details!
(e) What are some side effects?
(a) limit
(b) ↓, ↓ (given that its not replaced until you rest)
(c) PCr use allows for reformation of ATP and muscle contraction can continue
(d) It increases the amt. of PCr in the system so that short-high intensity exercises can last longer
i. Loading phase = 5 grams/4x a day, 5-7 days
ii. Maintenance phase = 3-5 grams/day
iii. 100 kcals, 100 kcals, ↑
- Brain releases Ep/Noe and glucagon which breakdown storage form of fuel to usable form that msucles can use.
- At the end of workout, protein will help build muscle, CHO will tell tissues to stop releasing the hormones. ↑ sugar intake = ↑ insulin
- GLUT4 transports that pick up the sugar, will also pick up more creatine
(e) GI distress, water-retention & kidney dysfunction w/ long term use
Know the ATP-PCr diagram that was covered in class.
W/n sarcoplasm of the muscle cell:
Exergonic rxn: PCr + creatine kinase (enzyme) → Creatine, energy, Pi
Stored muscle ATP → ADP, Pi
(Endergonic rxn) New ATP = ADP + Energy + Pi
Indicate the following for Adenylate-Kinase RXN (related to ATP-PCR):
(a) Aka ?
(b) Cellular compartment:
(c) Rate-limiting enzyme:
(d) How does this reaction generate ATP?
(a) Myokinase reaction
(b) Sarcoplasm
(c) Myokinase or adenylate kinase
(d) From hydrolysis of ATP, ADP is floating around cell
ADP (2 Pi) + ADP (2 Pi) → ATP (3 Pi) + AMP* (1Pi)
Indicate the following for Glycolysis:
(a) Cellular compartment:
(b) Rate-limiting enzyme:
(c) Time needed for full activation:
(d) Duration:
(e) Potential end products?
(f) What determines the final product?
(a) Sarcoplasm
(b) PFK
(c) 6-10 secs
(d) 2-3 mins
(e) Pyruvate + H, Lactate + H
(f) Relative glycolytic and mitochondrial activites (i.e., what type of individual is this, what type of acitvity are they doing, is glycolysis fast or slow,is the mito. and ETC availiable)
(a) What are the 2 phases of glycolysis?
(b) 1st phase: How much ATP is invested if it was to begin with blood glucose:
(c) 1st phase: How much ATP is invested if it was to begin with muscle glycogen:
(d) 2nd phase: How much ATP is gained at a substrate-level phosphorylation?
(e) 2nd phase: At a oxidative phosphorylation, each G3P produces how much NADH? Therefore, how many molecules of G3P is produced by G6P, making a total of how many NADH?
(f) Gross (or total #) ATP (before investment):
(g) Net ATP (after investment)
(a) 1. Energy investment phase (Before the split of G6P) ; 2. Energy generation phase (After the split of G6P to pyruvate)
(b) -2 ATP
(c) -1 ATP
(d) +4 ATP
(e) 1 NADH ; 2 G3P = 2 NADH
(f) 9
(g) 7
Know the Glycolysis Diagram that was covered in class.
Blood glucose (-1 ATP) → G6P ← Muscle glycogen (via glucogen phosphorylase)
- 1 ATP↓PFK
(2) G3P
NAD → NADH ↓+2 ATP
(2) Pyruvate
(a) Pyruvic acid is made up of what molecules?
(b) Lactic acid is made up of what molecules?
(c) How are these two related?
i. What enzyme catalyzes this reaction?
(d) What are isoforms?
i. T/F: The enzyme to catalyze this reaction has many isoforms.
(e) How do Type I fibers isoform work vs. Type II fibers isoform?
(f) Which fiber type is more likely to create more lactic acid?
(g) What does the amt. of lactate in the bloodstream determine?
(h) Is there any benefit of lactic acid formation during exercise?
(a) Pyruvate + H
(b) Lactate + H
(c) Pyruvic acid ↔ Lactic acid
i. Lactate dehydrogenase (aka LDH)
(d) Isoforms are made up of the same part but are organized differently, thus having different charcteristics in performance
i. True
(e) Type I: Lactate → Pyruvate
Type II: Pryruvate → Lactate
(f) Type II
(g) Can determine what type of muscle fiber you’re trying to recruit; W/ type II, at the end of gylcolysis, Pryruvate → Lactate
(h) 1. Lactic acid can be used for fuel, 2. Allows for reformation of NAD+ → G3P step to form NADH, glycolysis continues via NADH shuttle
Answer the following regarding the Krebs Cycle:
(a) Compartment:
(b) Activation time:
i. Initial:
ii. Full (able to accept Pyruvate and NADH):
(c) Duration and what does it require:
(d) What is the first product of the Kreb Cycle and what products formed it?
(a) Mitochondrial matrix
(bi.) ~ 10 secs
(bii.) 2.5-3mins
(c) Unlimited; requires O2 and fuel
(d) Citrate = Oxaloacetate + Acetyl-Coa w/ citrate synthase (enzyme)
(a) Distinguish how much each moleucule is produced per molecule of pyruvate in the Krebs Cycle?:
i. NADH
ii. FADH
iii. CO2
iv. ATP (substrate-level):
v. ATP (oxidative phosphorylation):
(b) Distinguish how much each moleucule is produced per molecule of Acetyl Coa in the Krebs Cycle?:
i. NADH
ii. FADH
(ai.) 4 NADH
(aii.) 1 FADH
(aiii.) 3 CO2
(aiv.) 2 ATP
(av.) 11.5 ATP
(bi.) 3 NADH
(bii.) 1 FADH
(a) What is pyruvate the precursor of?
i. Why is this important for the Krebs Cycle?
(b) Which of the three macronutrients is the primary source of pyruvate?
(c) What else pyruvate be synthesized from? How is this important for our diet?
(a) Oxaloacetate and malate
i. These molecules must be maintained at certain concentrations in order for the Kreb Cycle to generate optimally; thus, there must be a certain amt. of pyruvate available
(b) CHO
(c) From amino acids, which are the building blocks of protein, which in term speaks to the importance of adequate protein intake.
Answer the following in regards to using fats for fuel aka Beta-Oxidation:
(a) What is the storage form of fat? What is it composed of?
(b) Where does this process occur?
(c) For ATP synthesis, what must occur and how much ATP is lost?
(d) What occurs during Beta-oxidation?
(a) Triglyceride = glycerol and 3 fatty acids
(b) Mitochondrial matrix
(c) For ATP synthesis, Fatty acids must be activated, which implies they are seperated from glycerol (-2 ATP)
(d) During beta-ox, fatty acids are chopped into H+ and carbon pairs
- H+/e- are removed by NAD+ and FAD, which then shuttle them into ETC within the mitochondria
- The carbon pairs continue through beta-ox, and through a series of chemical reaction “become” Acetyl CoA
- The formation of Acetyl Coa is a common entry point for both CHO and FAT in aerobic ATP synthesis
When considering aerobic ATP synthesis, which substrate acts as the common entry point for both CHO and fats?
Acetyl-CoA
Know the Beta-Oxidation Diagram that was covered in class.
- What does each FFA consists of?
- How many carbons are per FFA?
- Each FFA is a strand of carbon and hydrogen molecules
- Typically 12-20 carbons per FFA
- Consider a 14-carbon:
- At the sarcoplasm: TG → (-2 ATP) glycerol + 3 FFA
CC-CC-CC-CC-CC-CC-CC - At the mitochondrial matrix:
- 6 hydrogen bonds → BETA-OX x 6 (break bonds between the cc)
- 7 carbon pairs → KREBS x 7
Answer the following in regards to the Electron Transport Chain (ETC):
(a) Cellular compartment:
(b) Involves series of structures which include:
(c) Duration and what does it require:
(d) What occurs during this process and what are the two things being formed?
(a) Mitochondria
(b) Pumps and other protein structures
(c) Indefinite; reuqires O2, adequate enzymes, and fuel
(d) Series of REDOX reactions → formation of: water and aerobically-synthesized molecules of ATP
(a) What are ATP generating pathways tightly controlled, catalyzed by?
(b) If substrate abundant & ↑ # enzyme activity, what does this result in chemical rxns and ATP synthesis?
(c) What are rate-limiting enzymes? What are some examples?
(d) What are modulators?
(e) For all enzymes, activity rates increase due to:
(f) What are enzymes regulated by modulators known as?
(g) What are the two catgories of modulators?
(a) specific enzymes (occuring at very specific order)
(b) ↑ rate of chemical rxns → ↑ rate of ATP synthesis.
(c) Rate-limiting enzymes control the overall rate of chemical reactions; EX: Creatine kinase (PCr), PFK (glycolysis), HSL (beta-ox)
(d) Modulators: substances that control enzyme activity of rate-limiting enzymes
(e) ↑ body temp.* and /or ↓ pH*
(f) Allosteric enzyme
(g) Stimulatory modulators: ↑ rate of chemical rxns
Inhibitory modulators: ↓ rate of chemical rxns
Determine the rate-limting enzymes for the following pathways. Be detailed as possible:
Stored muscle ATP (2 secs)
- Rate limiting enzyme: Myosin ATPase
Determine the stimulatory and inhibitory modulators and the rate-limting enzymes for the following pathways. Be detailed as possible:
ATP-PCr (8-15 secs)
- Rate limiting enzyme: Creatine kinase
- Stimulatory: ADP (bypriducts of ATP hydrolysis)
- Inhibitory: ATP (not working as hard)
Determine the stimulatory and inhibitory modulators and the rate-limting enzymes for the following pathways. Be detailed as possible:
Glycolysis (2-3 mins.)
- Rate limiting enzyme: PFK
- Stimulatory: ADP, Pi, AMP (signaling molecule from the myokinase reaction)
- Inhibitory: ATP, PCr, citrate (kreb cycle is working fast, producing lots of it, indicates that glycolysis is working at a faster rate than neccessary), pH↓↓
Determine the stimulatory and inhibitory modulators and the rate-limting enzymes for the following pathways. Be detailed as possible:
Krebs Cycle (unlimited)
- Rate limiting enzyme: Isocitrate dehydrogenase
- Stimulatory: ADP, Ca2+ (assuming that the excitation-contraction process/AP has been occuring for 2-3mins/glycolysis, there is huge quantity of Ca2+ in the muscle cell), NAD (NAD is reforming fast as it’s dropping H+/e- in the mitochondria or pyruvate via NADH shuttle, and glycolysis is working hard)
- Inhibitory: ATP, NADH (suggests NADH shuttle is slow, as well as glycolysis = krebs doesn’t work as hard)
Determine the stimulatory and inhibitory modulators and the rate-limting enzymes for the following pathways. Be detailed as possible:
Electron transport chain
- Rate limiting enzyme: Cytochrome oxidase
- Stimulatory: ADP, Pi
- Inhibitory: ATP
Determine the stimulatory and inhibitory modulators and the rate-limting enzymes for the following pathways. Be detailed as possible:
Beta-oxidation
- Rate limiting enzyme: Hormone sensitve lipase
- Stimulatory: ADP, Pi, and…
- ↑ Epi/NoE: Release from adrenal glands, Epi is the primary stimulator of beta-ox; = ↑ rate of glycogenolysis (breakdown of storage form of sugar in liver and musc.) and ↑ rate of lipolysis (adipose tissue)
- ↑ glucagon: Released by the pancreas, stimulated to release by low blood sugar (CHO stored in liver and muscle) and when the activity is lengthy or intensity is moderate = ↑ rate of liver glycogenolysis and ↑ rate of gluconeogenesis
- Inhibitory: ATP, pH↓↓, ↑↑[H+], insulin
Which of the two pathways have rate-limting enzymes that are sensitive to an acidic environment?
- Glycolysis - PFK
- Beta-oxidation - HSL
Explain as to why the first two minutes of exercise will not feel to great?
The Kreb Cycle and ETC takes 2.5-3 mins for it to become fully activated.
What are the 2 additional pathways to create energy and when does this occur?
- Gluconeogenesis
- Ketogenesis
- Both occur in response to to low CHO availiabilty
(a) What is gluconeogenesis?
(b) What is the downside of this process?
(c) Where does gluconeogenesis occur?
(d) What are the potenital substrates for gluconeogenesis? (skeletal m. lacks necessary enzymes)
(e) What are two molecules that can also be converted into glucose in certain instances?
(a) Gluconeogensis: Formation of glucose from non-CHO substrates
(b) Slow process, have to invest ATP, ineffcient
(c) Primarily in the liver, to a lesser degree in the kidneys
(d)
1. Lactate → glucose: CORI cycle
2. Glycerol → glucose**: Glycerol cycle
3. Alanine (amino acid) → glucose: Alanine cycle
(e) Pyruvate and glutamine
(a) What is ketogenesis?
(b) What is it activated by? What does is lead to and result?
(c) What do skeletal muscles cells do in regards to this process?
(d) What do the liver cells do in regards to this process?
(a) Ketogenesis: Leads to a formation of: KETONES, aka KETONE BODIES, which are acidic.
(b) Activated by LOW CHO availiabilty, which leads to ↑ fat metabolism, which results in ↑ rate of TG breakdown → ↑ #FFAs availiable to oxidize
(c) Skeletal muscles can oxidize FFAs via Beta-oxidation → ↑ amts of Acetyl CoA, which then become citrate, the first product in the Kreb Cycle
(d) Liver cells can oxidize FFAs, which then become KETONES, which can be used as fuel by the brain and skeletal muscles, but not the liver or red blood cells (RBCs)
(a) Why do skeletal muscles have an upper limit to ketone body oxidation? (Consider enzyme activity and the nature of the ketone bodies)
(b) If CHO availabilty is low:
i. What fuel source (macronutrient) must we rely more heavily upon to meet energy demands?
ii. What happens to rates of synthesis of pyruvate & oxaloacetate?
iii. What in turn, happens to rate of ATP synthesis in the Krebs Cycle?
(a) When rates of ketogenesis increase, the acid levels in cells increase, potentially decreasing the acitvity rates of enzymes; a little acidity is helpful, but a lot isn’t)
(bi.) FATS
(bii.) Decrease
(biii.) Decrease
What are some of the long-term effects of a Keto diet (can include but are not limited to)? (3)
- Sever dehydration (as msucles lose CHO, they also lose H2O)
- Electrolyte disturbance (issues w/ +/- charges)
- Hypoglycemia (CNS prefers CHO vs. fat for fuel)
What are the 2 defintions of skeletal muscle fatigue?
- Inability (or decreased ability) to produce force
- A slowing speed of contraction
What are the 3 factors in speed of contraction?
- Size of motor neuron
- SR density
- Isoform of myosin ATPase
What determines force production?
Quantity of contractile proteins/myofibrils (actin and myosin)
= crossbridge → powerstroke!
- Force is produced by powerstroke
Define Fatigue vs. Injury
- Fatigue: Reversible by a few hours rest
- Injury: may require days, weeks, months
What are the 3 possible factors of fatigue and its subcomponent?
- Depletion:
* Metabolites: ATP, PCr
* CHO: Muscle glycogen, blood glucose - Central Fatigue:
* Related to Central Nervous System (CNS) - Peripheral Fatigue:
Within skeletal muscle, at the contractile-level
Answer the following given this primary context:
With very high intensity, short duration exercise
(a) Generally, is the storage of ATP or PCR in the muscle cells small or large?
(b) What causes fatigue in regards to the usage and restoration of ATP/PCr?
(c) What causes ATP and PCr to be depleted? In other words, how does exercise intenstiy/rate affect ATP-PCr usage?
(d) What happens when ATP and PCr are fully depleted?
(a) Small
(b) If rates of ATP/PCr use is greater than ATP/PCr restoration
(c) If workload (or intensity) increases → increases the speed at which ATP and PCr become depleted
(d) Individual is at a point of fatigue
(a) Consider where some, least, and most CHO is stored
(b) Which type of CHO is generally being utilized during the follwoing exercise:
i. Short-term, low-moderate intensity:
ii. Short-term, high-intensity:
iii. Prolonged, sub-max intensity:
(c) Without appropriate CHO intake during prolonged exercise, what occurs to CHO availability?
(d) What are two other substrate options? But how does this relate to fatigue?
(a) Liver glycogen (some) → Blood glucose (least) → Skeletal muscle (most)
(bi.) muscle glycogen
(bii.) Muscle glycogen and blood glucose
(biii.) Muscle glycogen and blood glucose but at a much slower rate
(c) Decrease
(d)
1. Fats: Oxidation is slower than CHO → slowing speed of contraction → FATIGUE
2. Gluconeogenesis (amino acids, glycerol, HLa): Requires energy, energy investment, produces little glucose, slow w/ fatigue = slowing speed of ocntraction
(a) What is the “feedback loops” in regards to CNS fatigue?
(b) What type of exercise can CNS fatigue occur with?
(c) Therefore, what type of mechanism occurs? What does this lead to?
(d) How much does the CNS contribute to fatigue?
(a) Feeback loops: between the motor cortex (brain) and muscles
(b) Prolonged endurance exercise or prolonged high-intensity exercise (86-90% VO2max for 2 hrs)
(c) A self-perservation mechanism (within the brain): CNS generates fewer APs to muscle
- Leads to: ↓ in muscle cell depol. → ↓ in cross-bridge formation
- ↓ # of powerstrokes
- ↓ # of force produced (force is produced by powerstroke)
(d) About 10% of total fatigue
In regards to peripheral fatigue within the skeletal muscle, what are 3 possible factors?
- Conisder how this fatigue relates to Excitation-Contraction Coupling from now on!
- ADP, Pi
- Ca2+
- pH
Answer the following in regards to peripheral fatigue:
(a) What are the products of ATP Hydrolysis?
(b) What event or action causes the “power stroke”?
(c) What event or action causes “rigor state”?
(d) How do molecules move with regard to gradients?
(e) If you are near or in a fatigued state, how much ATP has been hydrolized?
(f) How do these ATP products result in fatigue? Explain!
(a) ATP + H2O → ADP + Pi + OH- + H+ + Energy
(b) Pi is release from myosin head
(c) ADP is released from myosin head
(d) From areas of high pressure/concentration to areas of low pressure/concentration
(e) A LOT!
(f) Considering the gradient of the metabolic products…
- ↑ [Pi] → slows rate of Pi being released from myosin head → ↓ # of powerstroke → ↓ # of force produced (↓ # of force produced by powerstroke and FATIGUE)
- ↑ [ADP] → ADP comes off myosin head slower, slowing down the rate of new ATP binding to myosin head → ↓ speed of contraction
(a) With high concentrations Pi in the skeletal muscle, how does this affect troponin?
(b) In this case, what must occur in the release of Ca2+ in order for the excitation-contraction to occur?
(c) What does this result in corss-bridge formation?
(d) What does this mean for powerstoke?
(a) ↑ [muscle cell Pi] → ↓ in troponin’s sensitivity to Ca2+
(b) This means ↑ Ca2+ must be released from the SR in order to activate troponin, which then moves tropomyosin off the mysoin binding site on actin.
(c) This results in ↓ rate of cross bridge formation
(d) ↓ # of powerstroke → ↓ force produced (force is produced by powerstroke)
(a) What is Ca2+ bound mainly to within a rested muscle? Where is it located?
(b) What occurs in a fatigue muscle? What is the new molecule that is being formed?
(c) What does this result in?
(a) Calsequestrian, located in the SR
(b) Pi enters the Sr, binding to Ca2+ which forms a new molecule known as calcium phosphate (CP)
(c) ↓ # of calcium availiable to bind to troponin, which leads to…
↓ # of cross bridges formed → ↓ # of powerstroke
= ↓ # of force produced = fatigue
(a) If pH drops within muscle cells, is [H+] low or high?
(b) Therefore, what is the environement?
i. What would this mean for enzymes?
(c) What ion competes with Ca2+ for the binding site on troponin?
i. What does this affect?
(d) . Which fiber type show greater force impairment in an acidic environment?
(e) In acidic environment, Type _ fibers may prodice _ % less force than in neutral environment.
(a) High
(b) Acidic
(bi.) Slows enzyme rate → ↓ speed of contraction = “fatigue”
(c) H+
(ci.) Can affect rate at which ↓ cross bridge are formed, which results in…
↓ cross-bridge formation → ↓ # of powerstrokes → ↓ #of force production = “fatigue”
(d) Type II
(e) Type II, 50
Explain the NADH shuttle. Why is this pathway important in relation to glycolysis?
- NADH shuttle occurs if the mitochondria or ETC is unavailiable or relatively full.
- Instead of dropping its H+/e- at the mitochondria, NADH will then have to resort to dropping it to pyruvate → Lactic acid (HLa), dissociating into Lactate (used a fuel via gluconeogenesis) and H+ (factors in fatigue)
- After dropping H+/e- to pyruvate, it reforms back to NAD+, allowing for glycolysis to continue
What is meant by activation energy? How does the presence of enzymes change activation energy?
- Activation energy: The energy required to initiate chemical reaction
- The presence of enzymes will work as catalysts by lowering the activation energy, thus increasing the rate of chemical reaction.
(a) What occurs after a muscle contracts?
(b) Write down the formula of ATP hydrolysis.
(c) Why is this important?
(a) ATP hydrolysis
(b) ATP + H2O → ADP + Pi + OH- + H+ + Energy
(c) While new ATP products can be formed, the Energy that is being rleased will recock the myosin head o continue muscle contraction
