SPEX303 FINAL EXAM LATEST 2023-2024 ACTUAL
EXAM 100 QUESTIONS AND CORRECT DETAILED
ANSWERS (VERIFIED ANSWERS) |ALREADY GRADED
A+
Why might testosterone decrease with over-training? - ANSDecreased testicular LH receptor sensitivity
from increased ACTH and cortisol
Enzymatic inhibition or direct on Leydig cells by cortisol
Head trauma?
Increased breakdown of testosterone
Effect on sex hormone binding globulins
What are some Anti-reproductive hormones? - ANSMelatonin, Prolactin, Beta-endorphin, cortisol
Melanin - where is it secreted from? when is it secreted? what can it impair? - ANSPineal glands - high at
night, low during day, increases with exercise in day but not at night
May impair rhythm of release of sex hormones
Prolactin - when does it secrete? - ANSWith exercise
Opiod peptides (beta-endorphins) can be secreted when? Effect on GnRH and LH? - ANSduring long-
lasting exercise, >60mins or highly intensive, anaerobic exercise shorter (30 mins or less)
Decreases GnRH and LH pulsatility
Why is plasma creatine kinase activity an indicator of overtraining? - ANSShouldn't be in the
bloodstream and therefore is an indicator of muscle damage
What are some practical ways of avoiding over-training? - ANSHard day:Easy day principle
Adjust diet to accommodate needs - CHO and protein
,What factor is the quickest to detrain? - ANSStroke volume (diastolic filling) - primary function of
reduced plasma volume
What are the fibre type changes when detraining? - ANSType IIa to IIb
Detraining/Conditioning - adaptations to the environment (recumbent position) - ANSDecrease
hydrostatic pressure to lower extremities
Elimination longitudinal compression long bones, spine
Reduced force all bones
Reduced energy expenditure
Bedrest observations - early work - ANSIncrease: Na+ and Ca++, decrease O2 uptake
Effects on: BMR, muscle atrophy, bone demineralisation, CHO metabolism
Plasma volume decreases with prolonged bedrest - Possible contributors for this? - ANSGauer-Henry
Reflex - headward shift of fluid produces transient increase in BV, compensatory loss of water and
sodium
ANP release
Decreased sensitivity of kidneys to fluid
Decrease plasma protein
Prolonged muscular activation can result in? - ANSFatigue
Define fatigue - ANSInability to maintain a given or expected power output or force production
Central fatigue? - ANSCentral command, motoneurons, conducive pathways to motor endplates
Peripheral fatigue - ANSPeripheral nervous system - excitation (contractile coupling), contractile
processes
Muscle - sarcolemma, myofibril, sarcoplasmic reticulum
,Why do some motor units fatigue before others? - ANSFibre type differences
Why could there be a change in motor unit activation after continued activity? - ANSAltered recruitment
pattern
Support from surrounding units not initially activated
Muscular contractions: Origins of fatigue - ANSLong-lasting endurance exercise, moderate intensity
- central fatigue, neurotransmitter, production (serotonin) or lack of (noradrenaline)
- IL-6
- peripheral fatigue - substrate reduction
High intensity
- peripheral fatigue - metabolite accumulation, Na+/K+ imbalance
Sites of Fatigue - Excitation - ANSNeuromuscular junction, voltage gates Na+/K+ channels, sarcolemma t-
tubules
Sites of Fatigue - Excitation-contraction coupling - ANST-tubules, Ca++ release, binding troponin
Sites of Fatigue - Contractile Processes - ANSBinding actin and myosin, cross-bridge formation, uptake
Ca++ into sarcoplasmic reticulum, relaxation role of ATP
Role of Metabolites in Fatigue - ANSIncreased [H+] decreases Ca++ sensitivity, binding of Ca++ to
troponin
Increased [Pi] also affects Ca++ activated tension
Increased [Mg++] inhibits Ca++ release from SR
Effect of Metabolic Factors in Fatigue - ANSATP necessary for Na+K+ pump and relaxation
ATP resynthesis dependent upon - PCr, glycogenolysis, glycolysis, aerobic metabolism CHO/fat
, IL-6 and Central Fatigue - ANSLarge increase with strenuous exercise and impairs athletic performance,
decreases endurance running
Transcription enhanced with glycogen depletion
Ammonia as a factor of Central Fatigue - ANSAssociated with toxicity when high - altered neuronal
excitability, extreme convulsions
Can deplete GABA and glutamate
Also stimulate PFK
Physiological differences between sexes: Men have higher... - ANSVO2max
Blood volume
Hct
Heart size
Better Hb and oxygen carrying capacity
Absolute strength
Greater muscle mass
VO2max differences between male and female. What does this mean for intensity and performance?
What happens to this difference once made relative to /kg fat free mass - ANSVO2max higher in males
than females
Given absolute intensity is higher %VO2max
Once made relative to /kg FFM, differences nearly disappear
Who has more % body mass (males vs females) and (normal/elite) - ANSMales < Females % body mass
Normal > elite
Hip width performance differences between males and females - ANSWider = less effective
Made relative, differences almost disappear
EXAM 100 QUESTIONS AND CORRECT DETAILED
ANSWERS (VERIFIED ANSWERS) |ALREADY GRADED
A+
Why might testosterone decrease with over-training? - ANSDecreased testicular LH receptor sensitivity
from increased ACTH and cortisol
Enzymatic inhibition or direct on Leydig cells by cortisol
Head trauma?
Increased breakdown of testosterone
Effect on sex hormone binding globulins
What are some Anti-reproductive hormones? - ANSMelatonin, Prolactin, Beta-endorphin, cortisol
Melanin - where is it secreted from? when is it secreted? what can it impair? - ANSPineal glands - high at
night, low during day, increases with exercise in day but not at night
May impair rhythm of release of sex hormones
Prolactin - when does it secrete? - ANSWith exercise
Opiod peptides (beta-endorphins) can be secreted when? Effect on GnRH and LH? - ANSduring long-
lasting exercise, >60mins or highly intensive, anaerobic exercise shorter (30 mins or less)
Decreases GnRH and LH pulsatility
Why is plasma creatine kinase activity an indicator of overtraining? - ANSShouldn't be in the
bloodstream and therefore is an indicator of muscle damage
What are some practical ways of avoiding over-training? - ANSHard day:Easy day principle
Adjust diet to accommodate needs - CHO and protein
,What factor is the quickest to detrain? - ANSStroke volume (diastolic filling) - primary function of
reduced plasma volume
What are the fibre type changes when detraining? - ANSType IIa to IIb
Detraining/Conditioning - adaptations to the environment (recumbent position) - ANSDecrease
hydrostatic pressure to lower extremities
Elimination longitudinal compression long bones, spine
Reduced force all bones
Reduced energy expenditure
Bedrest observations - early work - ANSIncrease: Na+ and Ca++, decrease O2 uptake
Effects on: BMR, muscle atrophy, bone demineralisation, CHO metabolism
Plasma volume decreases with prolonged bedrest - Possible contributors for this? - ANSGauer-Henry
Reflex - headward shift of fluid produces transient increase in BV, compensatory loss of water and
sodium
ANP release
Decreased sensitivity of kidneys to fluid
Decrease plasma protein
Prolonged muscular activation can result in? - ANSFatigue
Define fatigue - ANSInability to maintain a given or expected power output or force production
Central fatigue? - ANSCentral command, motoneurons, conducive pathways to motor endplates
Peripheral fatigue - ANSPeripheral nervous system - excitation (contractile coupling), contractile
processes
Muscle - sarcolemma, myofibril, sarcoplasmic reticulum
,Why do some motor units fatigue before others? - ANSFibre type differences
Why could there be a change in motor unit activation after continued activity? - ANSAltered recruitment
pattern
Support from surrounding units not initially activated
Muscular contractions: Origins of fatigue - ANSLong-lasting endurance exercise, moderate intensity
- central fatigue, neurotransmitter, production (serotonin) or lack of (noradrenaline)
- IL-6
- peripheral fatigue - substrate reduction
High intensity
- peripheral fatigue - metabolite accumulation, Na+/K+ imbalance
Sites of Fatigue - Excitation - ANSNeuromuscular junction, voltage gates Na+/K+ channels, sarcolemma t-
tubules
Sites of Fatigue - Excitation-contraction coupling - ANST-tubules, Ca++ release, binding troponin
Sites of Fatigue - Contractile Processes - ANSBinding actin and myosin, cross-bridge formation, uptake
Ca++ into sarcoplasmic reticulum, relaxation role of ATP
Role of Metabolites in Fatigue - ANSIncreased [H+] decreases Ca++ sensitivity, binding of Ca++ to
troponin
Increased [Pi] also affects Ca++ activated tension
Increased [Mg++] inhibits Ca++ release from SR
Effect of Metabolic Factors in Fatigue - ANSATP necessary for Na+K+ pump and relaxation
ATP resynthesis dependent upon - PCr, glycogenolysis, glycolysis, aerobic metabolism CHO/fat
, IL-6 and Central Fatigue - ANSLarge increase with strenuous exercise and impairs athletic performance,
decreases endurance running
Transcription enhanced with glycogen depletion
Ammonia as a factor of Central Fatigue - ANSAssociated with toxicity when high - altered neuronal
excitability, extreme convulsions
Can deplete GABA and glutamate
Also stimulate PFK
Physiological differences between sexes: Men have higher... - ANSVO2max
Blood volume
Hct
Heart size
Better Hb and oxygen carrying capacity
Absolute strength
Greater muscle mass
VO2max differences between male and female. What does this mean for intensity and performance?
What happens to this difference once made relative to /kg fat free mass - ANSVO2max higher in males
than females
Given absolute intensity is higher %VO2max
Once made relative to /kg FFM, differences nearly disappear
Who has more % body mass (males vs females) and (normal/elite) - ANSMales < Females % body mass
Normal > elite
Hip width performance differences between males and females - ANSWider = less effective
Made relative, differences almost disappear
