KIN 486 Final Exam Review Guide PDF
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Uploaded by PoignantTulip1820
University of South Alabama
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This document is a review guide for KIN 486, potentially an undergraduate-level kinesiology course. It covers various topics related to muscle function, actions, and responses to exercise. The document includes key concepts like muscle fiber force production and different types of muscle contractions (e.g., isometric, concentric, eccentric).
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KIN 486 Final Exam Review Guide *Chapters 3, 4, 11, & 12* **[Chapter 3]** **3.1** **[\*Discuss the 5 ways in which a muscle fiber can acutely increase force output]** 1. Recruiting more motor units = dependent on load 2. Increasing the firing rate of motor neurons (summation principle) =...
KIN 486 Final Exam Review Guide *Chapters 3, 4, 11, & 12* **[Chapter 3]** **3.1** **[\*Discuss the 5 ways in which a muscle fiber can acutely increase force output]** 1. Recruiting more motor units = dependent on load 2. Increasing the firing rate of motor neurons (summation principle) = if you repeatedly activate a fiber before it can relax you tension can summate and get a supramaximal force output = stronger muscle contraction = greater force output 3. Type of motor unit recruited = type 1 (slow twitch) -\> larger/type 2 (fast twitch) fibers for more force = more power 4. Preloading the muscle (activating stretch reflex) 5. Speed of contraction **[Distinguish between the major types of muscle actions and be able to provide examples of each]** 1. Static (isometric) muscle action = produces force, does not change length (muscle length stays the same) = plank and wall sit 2. Dynamic muscle action = produces force and length changes - Concentric muscle action = muscle shortens while producing force = lifting bar (reps) - Eccentric muscle action = muscle lengthens while producing force = lowering bar 3. Isotonic contractions = force stays the same = bicep curls 4. Isokinetic contractions = speed of the movements stays the same = can be concentric or eccentric = weight machines = hydrolytic exercise and astronauts and gravity **[\*Explain the relationship between force and velocity of contraction]** As speed (velocity) increases, force decreases = inversely related Faster contraction = less force generated = primarily for concentric isotonic contractions (shortening/speed) **[At what general concentric speeds can you generate the most force? What about power?]** Concentric: Slower speeds = more force Size principle = motor units are recruited in order from smallest to largest depending on the intensity of the force being applied Type 1 -\> Type 2 Selective recruitment = override the use of type 1 directly to type 2 in instances like explosive movements, ballistic contractions = jumping All fibers will need to be recruited in order to generate force Power = work/time More force = more work = slower contraction speed = more time = a lot of work in a short amount of time Eccentric: Force is higher here Quick contraction without loss of force generation = somewhere in the middle How does your ability generate force compare for concentric, eccentric, and isometric muscle actions? **[In class notes:]** Larger motor units = more force/power = larger loads = quads Precision = smaller motor units = muscles in your hand/eyes All or none principle = a nerve or muscle fiber will either respond completely or not at all to a stimulus, regardless of the stimulus\'s strength or duration = cannot partially activate **How can you generate more gradation of force without sending a stronger signal?** *Recruiting more motor units to generate more force in that muscle* Summation = adding of tension for maximal contraction ↑frequency of stimuli increases \> fibers do not have time to relax \> "summation" and ↑ force production Taping into different muscle types (type 1 and 2) and summation can garner more force Power is different than force because it has a time component **\*Where on the force velocity curve would you see isometric?** *At 0* Eccentric can be seen in the negatives = doing negatives = lowering the weight Eccentric is strongest (slowly lower it), concentric is weakest, isometric is how much you can hold 3.2 **[Distinguish between muscle spindles and GTOs on their functions and how they are activated]** Muscle spindles = in the muscle = neural fibers that sense changes in length of muscle fibers and send signals to the CNS for the muscle to contract = initiates stretch reflex = important for powerful contractions = minimizing when relaxing muscle Golgi tendon organs = in the tendon = infused in the fibers = increases tension in the tendon = support tendons as muscle tension increases to prevent rupture/injury Lengthen a muscle (stretching) -\> activates muscle spindles -\> triggers contraction of the muscle (negative feedback) Contracting a muscle forcefully (builds too much tension) -\> activates GTOs -\> signals to relax muscles to prevent injury/overstretching (dropping a weight due to overload) **[Distinguish between the neurophysiological model and the mechanical model of the stretch reflex]** Neurophysiological model Activation of muscle spindles = initiates stretch reflex "pre-loading the muscle" 1. Muscle spindle responds to stretch 2. Afferent nerve carries signal to spinal cord 3. Efferent spinal cord motor neuron activates stretched muscle fibers Mechanical model Elastic energy in tendons in muscles = rubber band ideology (eccentric muscle action) Briefly stored Eccentric action must be met with concentric action = will lose elastic energy **[Discuss the 3 phases of the SSC]** Combination of mechanical and physiological mechanisms to generate stronger concentric contractions 1. Eccentric = stretch the muscle 2. Amortization = brief pause = transition = short as possible for stronger force production 3. Concentric = elastic energy is released = motor neuron activated by muscle spindles Example: jumping = squatting down (eccentric) = how long you squat for (amortization) = push upwards (concentric) **[Briefly explain the role of the proprioceptors in stretching]** **[Explain the benefits of GTO activation]** Help relax the muscles = better stretch/better ROM due to relaxed muscles **[In class notes:]** Activated GTOs during eccentric or isometric = to prevent injury/rupture Not enough force concentrically to activate GTOs Stretch reflex (preloading/ssc) -\> neurophysiological model = muscle spindles -\> mechanical model = elasticity **[Chapter 11]** Explain the General Adaptation Syndrome and the importance of progressive overload in relation to a resistance training program For the general adaptation syndrome (GAS), you must first overload the muscle (alarm), which leads to resistance, then lastly, an adaptation or exhaustion period. Rather the muscle adapts or exhausts is dependent on proper recovery. Proper recovery = adaptation while improper recovery = exhaustion. Exhaustion is usually a result of over training. Discuss the significance of neural adaptations in strength increases during a resistance training program Explain how the reps & load of a "Strength" program increase these adaptations Explain at least 7 neural adaptations that were discussed ¬1 central, 2-3 MU, 2-3 NMJ, 2-3 proprioceptor Discuss many of the muscular adaptations that happen in response to anaerobic training Explain the underlying reasons for muscle fiber and thus muscle hypertrophy **[In class notes:]** Reps Load Rest ------------- ------ -------- ------------ Strength \< 6 \>85% 3-5 mins Hypertrophy 6-12 67-85% 30-90 secs Endurance \>12 \ 2. Explain the 5 ways that you can acutely increase force that were discussed in Lecture 3.1. 1. Recruiting more motor units = dependent on load 2. Increasing the firing rate of motor neurons (summation principle) = if you repeatedly activate a fiber before it can relax you tension can summate and get a supramaximal force output = stronger muscle contraction = greater force output 3. Type of motor unit recruited = type 1 (slow twitch) -\ larger/type 2 (fast twitch) fibers for more force = more power 4. Preloading the muscle (activating stretch reflex) 5. Speed of contraction 3. Next, discuss how each of those 5 ways enhanced as part of the neural adaptations to resistance training. 4. Distinguish between the key terms of hypertrophy, atrophy, and hyperplasia. Hypertrophy = an increase in the size of muscle Atrophy = a decrease in the size of muscle Hyperplasia = an increase in the number of cells in a muscle 5. Discuss the 2 main types of muscle fiber hypertrophy and explain the underlying components. 6. Distinguish between what types of training (specific stressors) elicit neural adaptations vs. those that elicit hypertrophic adaptations vs. those that elicit bioenergetic adaptations **[Chapter 12]** 12.1 **[In class notes:]** VO2 = Q (sv x hr) x a-vo2 VO2max = max amount of oxygen used VO2 = oxygen consumption Endurance athletes work at a submaximal exercise intensity To increase VO2max = increase a-vo2 difference = increased mitochondrial density = more mitochondria = increased capillary density = increased oxidative enzymes = increased overall oxygen consumption HR stays the same = SV will increase At submaximal VO2 = lower heart rate as a response to higher SV and higher a-vo2 difference Increased heart function = Q & SV Improved capillary network in endurance athletes = improved oxygen intake = quicker removal of waste products (CO2 and heat) Higher heart rate = higher capillary stress Transcription: - Converts DNA sequence into an mRNA sequence. - Occurs in the nucleus of eukaryotic cells. - Enzyme RNA polymerase is involved. Translation: - Use the mRNA sequence to build a protein chain. - Occurs in the cytoplasm on ribosomes. - Requires transfer RNA (tRNA) molecules to bring specific amino acids to the ribosome. **[Chapter 4:]** 4.3 **[In class notes:]** Acute responses = increased HR & SV, increased respiration, increased sweat production Chronic responses = increased mitochondrial and muscular density Chronic adaptations to acute responses = lower HR at submax intensity because of their higher stroke volume because of their adaptation to exercise intensity Glucose levels during exercise = more energy is required = glucose is utilized by the muscles Glycogen in the liver = increased blood glucose levels by breaking down glycogen and releasing into the blood stream (if not eaten anything) = eating can increase blood glucose levels Pituitary hormones = hypothalamus Hypothalamus releases growth releasing hormone (peptides) to get the pituitary gland to release growth hormones Growth hormone = anabolic properties go to the liver to release insulin like growth hormone from the liver = helps with amino acid transport Negative feedback stimulates release of GRH from the hypothalamus Too much = negative feedback will release GHIH to reduce GRH release GHIH = somastatin = body inhibiting GH = somtropic Cort = most steroid hormones How do catecholamines facilitate so many acute responses to exercise? Stimulation of the beta receptors Breathing rate = beta receptors relax the bronchi and improve air flow Sweat production = alpha receptors will constrict sweat from visceral organs while beta receptors will dilate where sweat is needed (working muscle) Different receptors will change the way the hormone response is needed, getting blood and such to places that need it vs places that do not 4.2 Panopto assignment: 1. What are diurnal variations in regard to hormone secretion? 2. Categorize the following hormones based on their type (peptide, steroid, catecholamine) and name their endocrine organ: 1. Growth hormone -- peptide -- anterior pituitary gland 2. Testosterone -- steroid -- testes 3. Epinephrine -- amine -- adrenal medulla 4. Cortisol -- steroid -- adrenal cortex 3. Compare and contrast the locations of receptors for steroid and peptide hormones. 5. Why can steroid hormones utilize intracellular receptors and peptide cannot? 4. What is a second-messenger system and why is it required by peptide hormones? 3. Panopto Assignment: 6. Briefly explain why epinephrine and norepinephrine increase during a GXT. Epinephrine and norepinephrine both increase during a GXT because they are triggered by the stress the body undergoes from physical activity. As a response to the stress placed on the body during exercise, the sympathetic nervous system is activated and signals for the release of these hormones leading to physiological changes such as increased heart rate = initiates fight or flight. 7. What is IGF-1 and why would GH stimulate its release? GH stimulates the release of IGFs to stimulate fat metabolism. It stimulates IGF-1 specifically to mitigate the effects of GH. IGF-1 being a stabilizer of GH. 8. What 2nd messenger pathway does epinephrine utilize to stimulate fat metabolism? Epinephrine utilizes cAMP to stimulate fat metabolism. 9. Given that cortisol and testosterone are both steroid hormones, how do they facilitate their impacts on protein metabolism? Do they utilize 2nd messengers or have intracellular receptors? Cortisol and testosterone both facilitate their impact in protein metabolism through intracellular receptors as the are both lipid soluble in nature and bind to specific receptors within the cell. **[In class notes:]** 4.4 Panopto Assignment: 1. Discuss how glucagon activates the cyclic AMP pathway to initiate glycogenolysis. Use 5 steps of the pathway to explain the process. 2. Contrast the roles of insulin to that of glucagon. 3. Explain how activating the AMPK pathway during exercise could be useful for a Type 2 diabetic **[Final Exam Review Day:]** Calculate relative torque and ipsilateral imbalances (only calculation for the new material) Exercise endocrinology -- use the table = negative feedback General function for hunger hormones and others Know the process of transcription and translation -- how steroids activate these Know the three pathways and how they are activated Review Fick equation and VO2 Review of energy system changes What are 4 adaptation in response to aerobic training? 1. More mitochondria 2. Increased VO2max 3. Lower EPOC 4. Lower Type 1 fiber recruitment How does it relate to the Fick Equation: Increased VO2max = Increased cardiac output (increased stroke volume (increased preload = increased venous return = increased blood volume = decreased peripheral resistance (diastolic BP)) and HRmax stays the same) = Increased a-VO2 difference (increased capillary density = increased mitochondrial density = increased hemoglobin and myoglobin) think oxygen extraction Cardio adaptation for at rest: 1. Lower EPOC 2. Lower SV 3. Lower HR Faster HR recovery Submax exercise: Lower oxygen deficit Increased SV Lower HR Higher lactate threshold Explain the endocrine organ and function of leptin and ghrelin Leptin = adipose tissue = more fat tissue = more leptin Ghrelin = stomach/GI tract Explain how steroid hormones can stimulate protein synthesis Steroid hormones: 1. Steroid enters cell and binds to intracellular receptor = hydrophobic 2. HRC binds to DNA and initiate gene transcription to mRNA 3. mRNA leaves the nucleus to be translated by the ribosomes to protein Codon's are how the amino acid knows what to add = a start and a stop codon What are the steps of the JAK/STAT pathway? 1. GH binds to the receptor extracellularly 2. JAK phosphorylates STAT = occurs twice = cascade effect 3. Two phosphorylated STATS form a STAT dimer or "sandwich) 4. STAT dimer goes to the nucleus and initiates gene transcription 5. mRNA will be translated by the ribosomes to protein Growth hormone is too water soluble and large and must use a second messenger = JAK/STAT pathway What stimulates the release of growth hormone? What gland? Increased exercise intensity (stress) = sensed by the hypothalamus to release GHRH to release GH from the anterior pituitary = GH tells liver to release IGF-1 (anabolic work) = IGF-1 stimulates/promotes protein synthesis in the muscle (promotes amino acid transport into cell, stimulate gene transcription, & stimulates ribosomal translation) Negative feedback = too much GH is sensed so GHIH is released to stop the release of GH What is an amine hormone? What are two endocrine glands the release amine hormones? Amino acid derivative -- convert amino acids Thyroid and Adrenal medulla cAMP pathway for glycogenolysis & lipolysis) hormones = peptide (glucagon, epinephrine, etc.) Glycogenolysis & Lipolysis 1. Glucagon, Epi & Norepi -\ bind to the receptor and activate adenylate cyclase 2. ATP -adenylate cyclase -\> P + cAMP 3. cAMP activates PKA 4. PKA activates glycogen phosphorylase = PKA activates HSL (hormone-sensitive lipase) 5. Glycogen -glycogen phosphorylase -\> G6P = TAG -HSL-\> glycerol & 3 FFA