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HES 403- Exam 3
| Question | Answer |
|---|---|
| Two ways we determine fiber type | in the lab, what develops? |
| Troponin-c isoforms | higher sensitivity in power athletes |
| Western blot of fiber type was looking at what? | myosin heavy chain |
| Counting fiber type was looking at what? | myosin ATPase |
| Soleus muscle | posture muscle; slow-twitch |
| White vastis lateralis | found only in rodents; very few mitochondria |
| Diaphragm | mix of slow and fast twitch & mosaic fibers |
| Red/white fibers | both FT; red= IIa, white= IIb (rodents only) |
| Slow twitch fiber characteristics | high oxidative capacity, low glycolytic capacity, 110 ms speed, 10-180 fibers per motor neuron, low SR development |
| FT a characteristics | moderate oxidative capacity & moderate fatigue resistance, 50 ms speed, high anaerobic capacity, 300-800 fibers per neuron |
| FT b characteristics | high anaerobic capacity, 50 ms speed, higher peak force, 300-800 per neuron, high SR volume |
| Primary difference in force between FT and ST | number of fibers per neuron, but each fiber does have higher peak power |
| Myosin ATPase Vmax | 3x higher IIa than I; 5x higher IIb than I |
| What determines fiber type? | genetics determine which neuron; become specialized based on that neuron; endurance training can result in small changes; aging FT==>ST |
| Alpha motor neurons | innervate skeletal muscle |
| Gamma motor neurons | aka muscle spindles |
| Muscle spindles; what do they sense? | sense both length and rate of change in length |
| Golgi tension organs | defense against injury; sense tension |
| Ca2+ sensitivity of myofibrilar proteins/fatigue (3) | (troponin C); reduction from Pi, lower pH, or ROS |
| Max Ca2+ activated force/fatigue | reduced by Pi |
| SR Ca2+ released by RyR/fatigue | CaPi precipitation, Mg2+, low ATP, Pi |
| SR Ca2+ reuptake/fatigue | Pi, ADP, low ATP, ROS |
| Size of fast twitch and slow twitch muscles | fast twitch usually larger |
| Glycogen synthase untrained ST/FT & endurance trained? | more in FT than ST; will increase in FT and IIa |
| Plasticity of muscle inside & outside mitochondria | outside= small changes; inside=large |
| Phenotype adaptations in muscle | fiber size, enzymes/ Vmax, gene expression, organelle morphology |
| Interval training adaptations | look like endurance; not sure why |
| Calcium sensitive transcription factors | slow twitch sensitive to low concentration; fast twitch sensitive to high concentration |
| Muscle IGF | paracrine/autocrine; spliced differently |
| Muscle satellite cells | (stem cells); work in muscle repair, can be recruited with exercise, become deaf to signals as we age (may also decrease with age) |
| Myostatin | autocrine/paracrine growth signal |
| Myostatin mutation | huge steer (involved in gigantism) |
| Regulation of skeletal muscle plasticity (5) | nutrition, exercise, endo/exogenous signals, aging, drugs/hormones |
| Progressive overload | progressive increase in training load as body adapts (volume/intensity) |
| Adaptations to resistance training (3) | hypertrophy, increased power, increased 1 rep max (increased performance) |
| VO2 doesn’t decline in de-training, but… | it’s not a good indicator of performance in homogeneous populations (pH threshold is better) |
| Endurance training adaptations (6) | cardiovascular, pulmonary, skeletal muscle, bone/connective tissue, endocrine, renal |
| 5 causes of overtraining syndrome | neuromuscular, sympathetic system, metabolic, psychological, adrenal |
| neuromuscular overload | choline depletion? |
| Sympathetic overload | maladaptive fight or flight |
| Metabolic overload | glycogen or AA depletion |
| Psychological overload | altered hypothalamic pituitary function |
| Adrenal overload | decreased cortisol response |
| Symptoms of overtraining | performance, weight loss, allergies/colds, emotional, HR/BP, muscle tenderness |
| Causes of overtraining | excessive training, emotional, *abnormal autonomic NS, *disturbances in endocrine, *depressed immune (*=probably b/c of overtraining) |
| URTI | highest in sedentary and very high exercise volume/intensity |
| Highest fidelity sign of overtraining? | increased resting heart rate |
| How to predict overtraining? | constant miles per hour, measure heart rate compared to trained |
| How to treat over-training? | decrease intensity for several days, rest 3-5 days, counseling, alternate easy with hard, carbs |
| Excessive training | an unnecessarily high volume or intensity |
| 4 effects of properly tapering | increased muscular strength, reserved energy stores, no loss of VO2 max, performance increases |
| which sport has seen the most tapering research? | swimmers |
| detraining | cessation of regular training due to inactivity or immobilization; loss of muscle strength/size/power, decrease in muscular & cv endurance, loss of speed/agility/flexibility |
| loss of muscle strength during detraining | disrupted fiber recruitment (also happens in sarcopenia), atrophy |
| how to retain training gains if detraining? | training once every 10-14 days (only works ~2x) |
| loss of muscular endurance (5) | ox enzyme, glycolytic unchanged for 84 days, glycogen, acid-base, capillaries |
| loss of cardiorespiratory endurance (4) | greatest in highly trained; plasma volume, stroke volume, endurance performance, VO2 max |
| detraining effects (endurance athletes) can be minimized by | training 3x per week at 70% VO2 max |
| what is considered high altitude? | 1500 m (4921 ft) |
| environmental changes at high altitude | decreased pO2, temp, humidity, increased solar radiation |
| respiratory water loss | exacerbated in dry climates (high altitude); need more body water to moisten air |
| what cognitive things decline with high altitude? (6) | light sensitivity, visual acuity, postural stability, cognition, recall, reaction time |
| 3 metabolic responses to altitude | increased anaerobic metabolism, increased lactate production, decreased lactate at VO2 max |
| respiratory responses to altitude (3) | VE increases, pulmonary diffusion unchanged (if no edema), O2 transport and uptake impaired |
| altitude for sea-level performance | RBCs maintained when return to sea level; not proven; difficult to study since volume reduced at high altitude (live high train low) |
| training for optimal altitude performance | 1500-3000m above sea level 2 weeks before, do not compete within 24 hours, increase VO2 max at sea level to compete at a lower relative intensity |
| symptoms of acute mountain sickness (4) | nausea, vomiting, dyspnea, insomnia |
| when does AMS occur? | within 6-96 hours of arrival at altitude |
| what might be the cause of AMS? | CO2 accumulation (does not match up w/ hyperventilation) |
| how to prevent AMS? | ascend slowly (<300 m per day above 3000m) |
| symptoms of high altitude pulmonary edema (4) | dyspnea, excessive fatigue, cyanosis (blue nails/lips), mental confusion |
| HAPE occurs when? | rapid ascent above 2700m |
| Treat HAPE (3) | administer O2 and move to lower altitude, dexamethasome (synthetic cortisol) |
| High altitude cerebral edema | accumulation in the cranial cavity (>14000 feet); can easily lead to coma/death |
| Nitrogen narcosis | similar to alcohol intoxication; “the rapture of the deep” |
| Heat producing hormones | thyroxine, epinephrine, norepinephrine |
| Most important method of heat loss | evaporation |
| Kcal/mL heat loss? | 0.5 kcal/mL EVAPORATED sweat |
| Internal body temperature (3) | can exceed 40C during exercise; may be 42 in active muscles; small Q10 effect= faster enzymes |
| How is body temp measured? | |
| 2 sensors of heat exchange & 4 regulators | hypothalamus, central/peripheral thermoreceptors; sweat glands, smooth muscle around arterioles, skeletal muscle, endocrine |
| Cardic output in the heat | some will have to go to the skin |
| Rate of heat exchange rest vs. exercise | 1 kcal/min, 15kcal/min |
| Cardiovascular responses to exercise in heat | muscles/skin compete for blood, stroke volume decreases, HR increases because of this (cardiac drift) |
| Metabolic responses to exercise in heat (4) | body temp increases, O2 uptake increases (inefficiency), glycogen depletion hastened, lactate increases (inefficiency) |
| Heat acclimatization (4) | sweating becomes more efficient (where not blocked), blood flow to skin decreases, blood volume increases, glycogen use decreases |
| How to acclimatize to heat? | 1 hour or more for 5-10 days; CV adaptations 3-5 days, sweat mechanics up to 10 |
| How does the body conserve/produce heat? (3) | shivering, nonshivering thermogenesis (BAT), peripheral vasoconstriction |
| 4 factors that affect body heat loss | body side/comp (subcutaneous doesn’t matter much), air temperature, wind chill, water immersion |
| 2 responses to exercise in the cold | muscle fatigue occurs more quickly, FFA release impaired (use glycogen faster) |
| micro/zero gravity | <1g; effects similar to detraining |
| what is a countermeasure to microgravity? | exercise (but must not require power & be light) |
| ground based models of microgravity | supine, walk on treadmill with feet |
| which fiber type declines quicker with microgravity/bedrest? | fast twitch |
| vastis lateralis/soleus muscles | quad/postural calf |
| 28 days on skylab is like | 30 days of bedrest |
Created by:
melaniebeale
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