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UM / Kinesiology / KIN 321 / Why vo2max stays the same at altitude?

Why vo2max stays the same at altitude?

Why vo2max stays the same at altitude?


School: University of Miami
Department: Kinesiology
Course: Introduction to Systemic Exercise Physiology
Professor: Kevin jacobs
Term: Fall 2016
Tags: KIN321 and SystemicPhysiology
Cost: 50
Name: KIN321 Exam 3 Study Guide
Description: These notes cover lecture 13-20
Uploaded: 12/04/2016
30 Pages 197 Views 6 Unlocks

KIN321  Class  Notes  Week  10  (10/24­10/28)

Why vo2max stays the same at altitude?

________________________________________________________________________________ From previous sections

­ Thermoregulation I & II

________________________________________________________________________________ Lecture 13 Altitude

­ Exercise at altitude is stressful due to the low partial pressure of O2(PO2) ­ Partial pressure gradient

­ - Once PaO 2 drops, you deliver less O 2 to tissue -

Does c supp increase protein synthesis and therefore provide basis for increase in strength?

- - [At altitude, Hb/O 2 saturation can drop during exercise (as low as 65%) & sleep (low 70%)] - VO 2max begins to drop at 5000 ft (1500m) and then drop ~3% for each 1000 ft thereafter - UNAFFECTED by acclimatization We also discuss several other topics like What does it mean to be modern? what did “modern” mean in 1876?

- VO 2max would stay suppressed when staying at altitude (doesn’t restore) - Ventilatory Acclimatization

What hr would cause chest pain?

- Peripheral chemoreceptors in aortic arch and carotid bodies sense drop in PaO 2 → ^ ventilatory rate

- Hypoxic ventilatory response → aim is to ^ PAO 2 to partially restore gradient - - [the lower the PO 2 at any given power output = the higher the V E ] We also discuss several other topics like What does the painting titian, diana, and actaeon depict?
If you want to learn more check out Which barriers prevent mating or fertilization between species?

- Acute acclimatization = Hyperventilation = ↑PAO 2 → ↑SaO 2→ ↓PACO 2 (↑blood pH)If you want to learn more check out Why is nullification illegal?


- O 2 Transport Acclimatization

- O 2 transport is the product of arterial O 2 content (CaO 2) and cardiac output -

- - - Oxygen cost of work does not change at altitude, but perception of e៌�ort is much greater We also discuss several other topics like How characters are held as numbers in computers?


- Why VO2max stays the same at altitude? (stay depressed?)


- Hormonal Acclimatization

- - Epinephrine → increase in glycolysis We also discuss several other topics like What are the aspects of athletic training?

- When glycolytic rate > pyruvate oxidation → increased lactate production - Altitude as a training tool

- “Altitude simulation masks” is respiratory training devices but not true altitude simulators

- Reduced V E → slightly reduced SpO2, but not to same extent as actual altitude

- No improvement bene២�t to VO2max over 6 weeks of high-intensity training - “Live High-Train Low”

- Live high enough (6900-9200 ft) for long enough (4 wks) to induce an increase in RBC mass

- Train low enough (<4100 ft) that conditions are near normoxic and power outputs of intense workouts can be maintained

- Avg improvement of 1.5% at sea level (range=0.6%) due primarily to ~8% improvement in RBC mass in well-trained athletes

Lecture 14 Carbohydrate

­ Fuel use during exercise

­ Limited CHO storage + Heavy reliance on carbohydrate during moderate intensity exercise = ­ Need for a high CHO diet and potentially for carbohydrate supplementation before, during, and after sustained moderate/high exercise ≥60min (<60min there is enough muscle glycogen to carry the body)

­ Muscle Glycogen

­ There are only 3 ways to put glucose into the blood: (all through liver)

­ Gluconeogenesis

­ Absorption

­ Liver Glycogen

­ There are only 2 fates for glucose when it enters muscle:

­ Stored as glycogen

­ Oxidized → pyruvate/lactate → TCA Cycle

­ Rate of muscle glycogen use is highly dependent on exercise intensity

­ ^ intensity = ^ rate of muscle glycogen depletion

­ Liver Glycogen

­ Glycogen concentration of the liver is 4­6 fold higher than skeletal muscle → 80­150g CHO ­ Liver (and kidneys to a minor extent) are only tissue capable of producing glucose and releasing it into the bloodstream

­ Liver glycogen content may be <20g following an overnight fast (8­12hr)

­ Hepatic glucose production balances glucose uptake to maintain blood glucose concentration ­ Dietary CHO

­ General population dietary guideline is ~50­55% of total daily calories from CHO

­ Likely sufficient for recreational athletes

­ Endurance athletes with heavy training/competition demands may benefits from 60­70% CHO ­ High CHO diet = high bulk of food

­ More manageable with liquid CHO supped in

­ Flexible CHO recommendation based on body weight → 7­10g CHO/kg BW/day ­ May need to be elevated to 12g following heavy training bouts

­ Lack of clear experimental support

­ 10g vs 5g CHO/kg/day for 7­28 days in cyclists, runners, and rowers → no performance impairments

­ Limitation: duration of these studies are limited


­ CHO before exercise

­ It is part of a sound diet → goal is to assure adequate liver and muscle glycogen stores ­ Ideal maybe 150­300g CHO (3­5g CHO/kg BW) 3­4 hours before

­ Consider low to moderate glycemic foods

­ Reduce absolute intake as start of exercise nears

­ Pre­exercise meal likely causes rebound hypoglycemia at the start of exercise ­ High insulin + muscle contraction causes independent & additive effect on glucose uptake by muscle, → low blood glucose

­ Not likely to reduce performance unless very sensitive

­ Prevention of rebound hypoglycemia:

­ Experiment with amount and timing of pre­exercise CHO ingestion ➙ lower incidence when CHO consumed within 15 min of start of exercise. (insulin has not enough time to spike before epinephrine kicks in from exercise)

­ Low glycemic index foods or fructose.

­ High intensity warm­up sprints ➙ stimulate Hepatic Glucose Production. (^Epi) ­ CHO during exercise

­ Goal is to maintain blood glucose availability (and ∴ CHO oxidation) late in exercise when muscle glycogen stores become depleted ➙ spare liver glycogen.


­ 30­90 g CHO/hour in a 6­8% solution ingested at a rate of 600­1200 ml/hour.

­ Max exogenous CHO oxidation rate is ~ 1.0­1.4 g/min.

­ Clear improvement in performance compared to placebo.

­ If consumed more than 90g, possibly causes GI problem

­ Liquid vs. solid ➙ no clear difference in performance, but liquids have added bonus of replacing sweat loss.

­ Limitations to exogenous CHO oxidation:

­ Intestinal absorption is the most limiting factor


­ Mixture of glucose AND fructose may increase exogenous CHO oxidation

­ Separate means of absorption (they don’t compete with each other)

­ Glucose oxidized at ~1g/min and fructose at ~0.6g/min

­ SGLT­1 Glucose (active)

­ GLUT­5 Fructose (facilitated)

­ ­ Saturated SGLT­1, Glucose absorption plateaus


­ Possible benefit of taste → mouth rinse technique

­ Taste of CHO activates reward center of the brain, allows higher intensity of performance

­ Some evidence that ability to oxidize exogenous CHO during exercise is improved with 28 days of a high CHO diet compared to baseline

­ Suggests trainability of gut.

­ Good portion of endurance training should be done while consuming high CHO diet.

­ CHO After Exercise

­ Rapid phase of muscle glycogen re­synthesis for ~45­60min after exercise

­ → Needs to eat 30min after exercise coz CHO takes ~15min to show up in blood ­ Not reliant on insulin due the residual effect of muscle contraction on glucose uptake ­ Rapid due to low glycogen concentration + residual permeability to glucose

­ Slow phase of muscle glycogen synthesis beyond 60min after exercise

­ 7­10 fold slower than rapid phase

­ Dependent on insulin for glucose uptake

­ Within 48hr muscle glycogen will replete no matter what we eat

­ High insulin sensitivity after exercise

­ Optimal frequency and amount:

­ 1.0­1.5 g CHO/kg BW within 30 min and every 2 hrs up to 6 hrs

­ High glycemic foods optimal

­ Certain amino acids promote insulin secretion

­ Addition of protein to CHO after exercise resulted in ~40% faster rate of muscle glycogen resynthesis

­ Sucrose, glucose → fructose

­ Some fructose should be included → preferentially replenishes liver glycogen

­ Solid = liquid (Unless dehydrated)

­ Glycogen Supplementation

­ Classic studies in the late 1960’s show doubling muscle glycogen after loading protocol ­ Glycogen depletion → 3d low CHO diet → glycogen depletion again → 3 d high CHO diet ­ Strenuous protocol → fatigue, irritability

­ (Due to) Repeating glycogen depletion drives glycogen synthase activity very high ­ Modified protocol just as effective 

­ Taper training 6­7 days before competition + 3d mod CHO (45­50%) diet followed by 3 d high CHO diet (70%)

­ Placebo? Psychological?


KIN321  Class  Notes  Week  11  (10/31­11/04)

________________________________________________________________________________ From previous sections

­ Exercise and altitude, CHO supplementation

________________________________________________________________________________ Lecture 15 Ergogenic Aids and Athletic Performance

­ Ergogenic  =  “work  producing”

­ Ergolytic  =  “work  reducing”

­ Classification  of  ergogenic  aids:

­ Nutritional

­ Macronutrients,  creatine

­ Pharmacological

­ Caffeine,  amphetamines,  anabolic  steroids

­ Physiological

­ Blood  doping,  bicarbonate  loading

­ Mechanical

­ Equipment

­ Biomechanical

­ Efficiency  of  movement,  body  position,  economy

­ Psychological

­ Visualization,  pep  talks,  ^arousal

­ Goals  of  scientific  study  of  ergogenic  aids:

­ Identify  ergogenic/ergolytic  properties

­ Magnitude  (%  improvement  compared  to  placebo)

­ Duration

­ Identify  mechanism(s)  of  action

­ Rate­limiting?  →  importance  of  magnitude

­ Compare  and  rank


­   Fuel  availability                       ­  CHO

­ Hydration  status                      ­   Fluid

­ Studies  that  attempt  to  validate  ergogenic  aids  should  employ  the  following:

­ Decision  to  use  an  ergogenic  aid  →  all  three  of  the  following  must  be  satisfied: ­ Safe?  →  any  short­  or  long­term  effects

­ Risk:Benefit  ratio

­ Legal?  →  may  depend  on  the  event  and  organizing  body

­ Effective?  →  support  of  well­controlled,  published  studies

­ Creatine  Supplementation

­ CP  acts  a  buffer  to  supplement  ATP  and  delay  fatigue.

­ CP  is  a  limited  energy  source  ➙  re­synthesized  during  recovery.

­ C  plays  a  critical  role  during  repeated  bouts  of  high  intensity  exercise.   (<30s,  near maximal)

­ Delay  CP  depletion.

­ Stimulate  CP  synthesis  during  recovery.

­ Total  muscle  C  replenished  at  rate  of  ~2  g/day  →  ~1g  exogenous  intake  and  ~  1g endogenous  production

­ Endogenous  production  by  kidneys,  liver,  and  pancreas

­ Suppressed  when  C  intake  is  high

­ ^  red  meat  (protein)  intake  =  dec.  endogenous  C  production

­ Typical  C  supp  protocol:  20  g/day  for  5  days  followed  by  maintenance  at  2  g/day ­ Greater  than  20%  increase  in  total  muscle  C,  ~4­5%  increase  in  muscle  CP ­ Magnitude  highly  related  to  baseline  [C]

­ Effect  may  be  enhanced  by   CHO  co­ingestion  and  exercise  training

­ Slow  wash­out  →  ~4  weeks

­ Variable  results  →  20­30%  show  little  or  no  increase  in  [C]  →  no  improvement  in performance

­ Greenhaff  et  al.  (1993)  →  PL  or  C  supp  followed  by  five  bouts  of  30  maximal  knee extensions

­ 4mins  rest  between  bouts

­ C  →  5­7%  higher  torque  values  during  last  10  contractions  of  bout  1  and throughout  bouts  2­4

­ →  benefits  doesn’t  kick  in  until  late,  repeated

­ C  supp  improves  performance  by  increasing  CP  availability  mainly  in  fast  twitch fibers

­ Which  are  tapped  in  late  when  slow  twitch  can’t  handle/not  enough

­ C  supp  has  no  effect  on  submaximal  exercise  performance 

­ CP  availability  not  limiting

­ DOES  C  supp  increase  protein  synthesis  and  therefore  provide  basis  for  increase  in strength?

­ ^  workload,  volume,  intensity  →  ^  stress  &  tear  of  muscle  →  ^  muscle  adaptation, protein  synthesis

­ Water  retention  &  swelling  of  muscle  cells  →  increases  protein  synthesis  a  TINY bit

­ Protein  Metabolism  101

­ Nitrogen  Balance  Technique

­ Anabolic/Catabolic  =  +/­  N  balance

­ Disadvantages  of  N  balance  technique:

­ Demanding  of  subjects

­ Labor  intensive  for  investigators

­ Overestimates  N  intake  and  underestimates  N  excretion  →  favors  +  N balance

­ “Black  box”  →  Conveys  protein  balance,  but  does  not  quantify  protein 

degradation  and  synthesis 

­ Tracer  techniques  explore  the  “black  box”:  combination  with  muscle


­ BCAA  Oxidation

­ BCAA  are  preferentially  oxidized  by  skeletal  muscle  during  exercise  compared  to  other amino  acids

­ BCAA  oxidation  is  inversely  proportional  to  carbohydrate  availability

­ Acute  CHO  supplementation  prevents  protein  degradation

­ Protein  for  Endurance  Athletes

­ Might  need  more  protein  than  the  RDA  value  (0.8g/kg/d)  due  to  long  duration  of exercise  and  possibility  of  CHO  depletion

­ Only  those  (untrained  men)  who  consumed  1.5  (rather  than  1.0)  g/kg/d  remained in  +  N  balance  after  initiation  of  endurance  training

­ Trained  runners:

­ ­  N  balance  w/  0.9g/kg/d

­ +  N  balance  w/  1.5g/kg/d

­ General  recommendation:  1.2  ­  1.4  g/kg/d

­ Takes  into  account  of  SD

­ 15%  protein  diet  likely  sufficient

­ Protein  for  Strength  Athletes

­ Need  more  protein  coz  of  muscle  repair

­ No  further  increase  in  protein  synthesis  by  increasing  protein  intake  from  1.4  to 2.4g/kg/d

­ General  recommendation:  1.2  ­  1.7  g/kg/d

­ 15­20%  protein  diet  likely  sufficient

­ Safety  of  Elevated  Protein  Intake

­ Increased  protein  intake  →  increased  work  by  kidneys  to  clear  N  in  urine ­ Little  or  no  evidence  for  kidney  damage

­ Increased  fluid  need  to  avoid  dehydration

­ Safety  of  megadoses  of  amino  acids  is  unknown

Lecture 16 Fatigue

­ Fatigue  =  inability  to  maintain  a  given  exercise  intensity

­ Often  expressed  as  %  decline  in  force  or  power  output

­ Sites  of  fatigue:

­ Central  fatigue  ­  from  the  motor  cortex  to  the  neuromuscular  junction

­ Peripheral  fatigue  ­  after  the  neuromuscular  junction  into  the  muscle  n  tissues ­ Metabolite  Depletion  ­  The  Phosphagens

­ ATP  supports  muscle  contraction  +  most  cellular  processes  and  is  re­phosphorylated  by CP

­ ATP  is  little  affected  until  CP  is  significantly  depleted

­ CP  depletion  coincides  with  fatigue  during  isometric  exercise  and  supramaximal cycling

­ ATP  is  preserved  for  essential  function

­ Metabolite  Depletion  ­  Carbohydrate

­ Muscle  glycogen  depletion  during  prolonged  submaximal  exercise   highly  associated with  fatigue

­ Liver  glycogen  depletion  during  prolonged  submaximal  exercise  results  in hypoglycemia   without  exogenous  CHO  ingestion

­ Gluconeogenesis  is  inadequate  to  compensate

­ Especially  in  the  heat  when  blood  flow  to  liver  even  more  significantly  reduced ­ Metabolite  Depletion  ­  Acidosis

­ High  rates  of  glycolysis  is  responsible  for  decline  in  muscle  pH  with  intense  exercise ­ Hydrolysis  of  ATP  results  in  H +  production

­ Glycolysis  is  associated  with  the  net  production  of  H + 

­ Production  of  lactate  serves  multiple  functions:

­ Regeneration  of  NAD + 

­ Consumption  of  H +  _  (Buffers  H +)

­ Production  of  oxidizable  substrate

­ Means  of  transporting  reducing  equivalents  into  mitochondria

­ Production  of  GNG  precursor

­ Potential  negative  effects  of  H +  accumulation  (decrease  in  pH):

­ Inhibition  of  phosphorylase,  PFK,  PDH  (slows  down  metabolism)

­ Displace  Ca 2+  from  troponin

­ Inhibition  of  O 2  binding  to  Hb

­ Inhibition  of  hormone  sensitive  lipase  (inhibit  lipolysis)

­ Muscle  fiber  recruitment  in  increasing  intensities  of  exercise

­ Type  I  →  Type  IIa  →  Type  IIx

­ (most  to  least  oxidative  fiber  type)

­ Fatigue  is  more  closely  related  to  depletion  of  CP   than  decrease  in  pH

­ Increase  CP  availability  by:

­ Creatine  supplementation

­ Bicarbonate  loading  (HCO 3­  buffers/restores  CP)

­ Peripheral  Fatigue  ­  Calcium  Ion

­   Reduced  ability  of  sarcoplasmic  reticulum  to  release  Ca 2+ 

­ H +  interference  with  Ca 2+  binding  to  troponin  →  disruption  in  interaction  of  actin­myosin ­ Reduced  responsiveness  =  less  force  produced  for  any  given  concentration  of Ca 2+ 

­ Reduced  sensitivity  =  more  Ca 2+  release  needed  to  produce  the  same  amount  of force

­ Slowed  Ca 2+  reuptake  by  the  SR

­ Central  Fatigue

­ Originate  in  CNS  and  would  result  in:

­ Reduction  in  motor  units  activated

­ Reduction  in  motor  unit  firing  frequency

­ Difficult  to  study  CNS  function  during  exercise

­ Theory  that  supports  Central  Fatigue  →  Setchenov  phenomenon

­ Do  something  other  than  the  main  task  (mental  task,  cross  word  etc.,  diverts attention)  during  rest  →  increases  performance  in  the  consecutive  bouts

­ Opposition  →  Merton’s  experiments  on  the  adductor  pollicis  longus

­ Excessive  endurance  training  (over  training)

­ Reduce  performance  capacity,  prolonged  fatigue,  altered  mood  states,  sleep disturbance,  loss  of  appetite,  and  increased  anxiety

­ Possible  involvement  of  brain  neurotransmitter  serotonin

­ Large  %  of  troponin  is  bound  to  albumin,  and  small  %  is  free  troponin

­ Free  troponin  can  cross  BBB  via  receptors  that  also  transport  BCAAs

­ ^  Lipolysis  causes  more  FFA  to  bind  to  albumin  →  decreased  albumin  to  bind  to troponin  →  ^  free  troponin  in  the  blood  →  ^  serotonin  and  possible  fatigue  during prolonged  exercise

­ Technically  can  supplement  albumin  to  lower  free  troponin  level

­ “Central  Governor”  and  Fatigue

­ Chemoreceptors  (at  the  artoa)  senses  the  lack  of  oxygen  and  blood  flow  to  heart  & brain  →  limits  contraction  &  blood  flow  to  muscle

­ Healthy  humans  should  fatigue  before  ischemia

­ Summary

­ Fatigue  during  short,  high  intensity  exercise  is  most  likely  due  to  phosphagen  depletion and/or  metabolite  accumulation

­ Fatigue  during  long,  moderate  intensity  exercise  is  most  likely  due  to  CHO  depletion and/or  central  fatigue

KIN321  Class  Notes  Week  12  (11/07­11/11)

________________________________________________________________________________ From previous sections

­ Ergogenic Aids and Fatigue

________________________________________________________________________________ Lecture 17 The E┆�cacy of Exercise in the Prevention and Treatment of Type II Diabetes

­ The Scope of the Problem

­ 9% of population diagnosed with diabetes in 2011 (90­95% are Type II) ­ 34.9% of adults were classified obese in 2012

­ 65% are overweight or obese (BMI >25 = overweight, >30 = obese) ­ Likely underestimated because people tend to report taller and weigh less ­ Etiology of T2DM and Obesity

­ Genetic Disposition (Drifty Gene hypothesis)

­ The limit to energy storage is lifted off due to lack of predation

­ Energy Dense Environment

­ Easy access of calorie dense food

­ Behavioral Factors Favoring Positive Energy Balance

­ Excessive intake + lack of physical activity

­ Take Home #1

­ Physical inactivity represents the “most proximal behavioral cause of insulin resistance”

­ Exercise is an underutilized therapeutic modality in the prevention and treatment of T2DM

­ Evidence of the Efficacy of Exercise

­ Observational Evidence

­ Active men and women (~30 min/day of walking or cycling, 5 days/wk) had 25­56% lower incidence of diabetes than sedentary counterparts

­ Walking associated with similar risk reduction as vigorous exercise

(will work even if you just walk)

­ Intervention Evidence

­ 500­3200 men and women (45­55yrs) with Impaired Glucose Tolerance (at risk for T2DM)

­ Exercise and/or diet, metformin, and control interventions, 3­6yrs in duration

­ Reduction in risk of T2DM compared to control:

­ Diet: 31%

­ Exercise: 46%

­ Diet + Exercise: 42­58%

­ Metformin: 31%

­ Lowers hepatic (liver) glucose production → lowers blood


­ Exercise reduced risk even when weight loss goals of 5­7% were not met ­ Volume vs. Intensity Test

­ Intensity doesn’t matter

­ Overall volume is king

­ Take Home #2

­ Exercise is as or more effective than diet only and drugs in the prevention of T2DM

­ Low/moderate intensity is just as effective as high intensity exercise (overall volume is king)

­ Exercise still reduces risk of T2DM even if the subjects don’t lose weight ­ Etiology of T2DM Revisited

­ Obesity

­ Insulin Resistance

­ Progressive, hard to notice

­ Impaired Glucose Tolerance (IGT) ­ Pre­diabetic

­ Standard screening of blood glucose may not detect

­ But fasting blood insulin might be elevated

­ Highly reversible with exercise + diet

­ Early T2DM

­ Still hyperinsulinemia

­ Highly reversible with exercise + diet

­ Late T2DM

­ Hypo­insulinemia → pancreatic dysfunction

­ Improvable with exercise + diet to reduce severity

­ Insulin Resistance

­ Glucocentric, abnormality of glucose metabolism

­ Reduced number & function of insulin receptors

­ Reduction in insulin signal

­ Lower concentration of glut­4

­ Note: contraction­mediated glucose uptake is independent & additive to insulin

­ Adaptations to exercise (constant stress causing glycogen depletion, body needs to rebuild it):

­ Increased number & function of insulin receptors

­ Increase in insulin signal

­ Higher concentration of glut­4

­ Lipocentric, reduced ability to oxidize fat → causes insulin resistance ­ Genetics and sedentary lifestyle causes reduced ability to oxidize fat ­ Lower mitochondrial volume

­ Reduced ability to oxidize fat

­ Increased IMTG (fat storage in muscle) because FFA can’t go to


­ When IMTG storage limit is full, free flowing FFA in muscle blocks insulin signaling actions (to relocate glut­4)

­ Adaptations to ENDURANCE training ONLY:

­ Increased mitochondrial volume

­ ^ ability to oxidize fat

­ Lower IMTG, lower FFA in muscle

­ Take Home #3

­ Aerobic Exercise programs improve plasma glucose homeostasis in part through adaptations in muscle insulin signaling kinetics and fatty acid metabolism ­ Resistance Exercise programs induce adaptations in insulin signaling kinetics ­ Exercise recommendations for T2DM

­ Complete medical history and physical examination

­ Exercise ECG IF have one or more of following:

­ Known or suspected Coronary Arterial Disease (CAD)

­ T1DM >15yrs or T2DM >10yrs

­ Age >35

­ Other CAD risk factors (smoking, 1st relative, high BP, BMI, etc.) ­ Etc.

­ ACSM/CDC → >30min of accumulated moderate­intensity physical activity on most, and preferably all, days of the week (minimum needed to reduce risk of disease)

­ Minimum 10min bouts

­ Enough to achieve 700­200kcal /week energy expenditure

­ IOM → 60min of daily moderate­intensity or shorter periods of more vigorous exertion (jogging for 30min)

­ Enough to maintain normal BMI of 18.5­25 kg/m2 

­ As the patient progresses, we push the duration & frequency first, intensity last ­ Because intensity doesn’t matter that much

­ Low/moderate Intensity exercises are generally better as they provide no negative risks

­ Resistance Exercise:

­ Frequency of at least 2 days/wk with 48hrs between sessions

­ Muscle soreness = induced adaptations

­ Delayed → 24­48hr peak

­ 1­3 sets of 10­20 rep each

­ Conclusions

­ T2DM is largely a preventable and treatable disorder despite genetic disposition ­ Exercise helps T2DM because of the extensive molecular and metabolic adaptations that improve insulin sensitivity

­ As little as 30min of moderate­intensity exercise per day can reduce the incidence of T2DM

KIN321  Class  Notes  Week  13  (11/14­11/18)

________________________________________________________________________________ From previous sections

­ The E┆�cacy of Exercise in the Prevention and Treatment of Type II Diabetes ________________________________________________________________________________

Lecture 18 Special Populations

­ Childhood / Adolescence ­ Cardiorespiratory Function

­ Heart Rate

­ HR at rest decreases from childhood to adolescence

­ Due to the size of the heart getting bigger

­ ~85 bpm (age 5) to ~62 bpm (age 15)

­ Maximal HR changes very little before puberty, therefore (220­age) is NOT appropriate

­ Stroke Volume

­ SV increases from childhood to adolescence due to increase in LV size and NO change in contractility

­ Max SV ~25 ml/bt (age 5) to ~85 ml/bt (age 15)

­ Maximal CO increases due solely to increases in max SV

­ Maximal ventilation (VE) increases from childhood to adolescence → decrease in breathing frequency and increase in tidal volume ← bigger lung capacity ­ Absolute VO2max(L/min) increases gradually throughout childhood due to increase in SV

­ The increase is higher in boys > girls → mainly due to greater Q & muscle mass

­ Little change in relative VO2max(ml/kg/min) ← due to increase in BW ­ Children and adolescents have greater (a­v)O2 difference than adults → compensates for lower Cardiac Output

­ Children show limited improve in VO2max with training before puberty → limited size

­ Childhood / Adolescence ­ Thermoregulatory Function

­ Children have lower thermoregulatory capacity than adults due to:

­ Lower sweat rates

­ Higher sweating threshold → don’t start sweating until kinda high


­ Children at great risk than adults for heat injuries → importance of proper hydration

­ Childhood / Adolescence ­ Nutritional Recommendations

­ In general, active children doesn’t meet the RDA in total calories, iron, and calcium

­ Increased reliance on CHO & decreased reliance on lipids during exercise as children become adolescents

­ Recommended macronutrient intakes not different from adults

­ THOUGH protein intake is suggested to be ~ 1.0 g/kg/day (adult is 0.8) ­ Aging ­ Cardiorespiratory Function

­ Maximal HR decreases with aging due to: (inevitable)

­ Decrease in sympathetic response to exercise

­ Decrease in skeletal muscle mass

­ Submaximal and maximal SV and Q decrease with age due to:

­ Decrease in plasma volume, venous tone, and ventricular compliance (can’t stretch out as much) → dec. EDV (less filling)

­ Decrease in contractility due to reduction in ATPase activity of cardiac muscle fibers & increased TPR/high BP (afterload) → ^ ESV

­ Maximal (a­v)O2 difference decreases with aging due to:

­ Reduction in [Hb] → decreases (a)O2 

­ Reduction in capillary density → decreases (a)O2 

­ Reduction in mitochondrial volume → increases (v)O2 

­ VO2max decreases ~0.75 ­ 1.0% a year after the age of 30

­ VO2max of trained 70 year old is similar to sedentary 20 year old… ­ Aging decreases respiratory function:

­ Increase in size of alveoli and decrease in pulmonary capillary density → decrease in surface area for diffusion

­ Decrease in pulmonary elasticity

­ Weakening of respiratory muscles

­ Those greater than 75­80 years old have little to none cardiovascular improvements

­ Decrease ability to improve left ventricular size and function (very little) ­ The Female Athlete

­ No gender differences in macronutrient or fluid intake recommendations ­ Calcium intake may be of concern as women in general consume ~78% of RDA (800mg/d)

­ Adequate calcium intake important during first 2­3 decades of life to reach peak bone mass

­ Female athletes triad → disordered eating + amenorrhea + reduced bone density

­ Recommended calcium intake depends on:

­ Family history of osteoporosis

­ Training intensity and impact

­ Menstrual history and current status

­ Supplement / drug use

­ Iron deficiency also more common amongst active females than sedentary counterparts

­ Multivitamin may be needed for those with compromised diets

­ The Vegetarian Athlete

­ Nutrient of particular concern is protein

­ Likely adequate in lacto­ovo­ (consume milk & eggs) and ovo­vegetarians (consume eggs)

­ All plant proteins are incomplete → lack one or more essential amino acids ­ Variety of plant sources (protein sources) are critical to get a

complete amino acid profile

­ Grains ←→ Nuts and seeds

­ Milk products ←→ Legumes

­ Adequate total caloric intake is critical → sometimes difficult with bulk of food needed

­ Vitamin B12 found in animal protein

­ Likely adequate in lacto­ovo­ and ovo­

­ RDA is 2 ug/d & avg intake is 5­15

­ Essential to formation and function of RBCs

­ Vegans should consume fortified soy milk or vitamin B12 supplement ­ Alcohol and tobacco use → B12 malabsorption

­ Iron essential nutrient important for formation of hemoglobin, myoglobin, and cytochromes → transport and utilization of O2for energy production

­ Plants contain non­heme iron which is not absorbed as readily as heme iron found in red meat

­ Non­heme iron absorption improved by co­ingestion of foods high in Vit. C or by cooking in cast iron skillet

­ Non­heme iron absorption decreased by tea and coffee, high fiber foods, and excessive calcium intake

­ Plants with high iron content are: kidney beans, molasses, and spinach ­ Milk and dairy products are poor sources of iron → lacto­ovo­ and ovo­ are susceptible too

­ Vegetarians should focus on green leafy veges, legumes, and fortified grains

­ Calcium especially a problem for vegans

­ Either use calcium supplement or consume green leafy vegetables or calcium fortified soy products

­ The Type I Diabetic Athlete

­ Hypoglycemia is greatest risk due to:

­ Inadequate CHO intake

­ Too high insulin

­ Exacerbated by exercise → muscle contraction also induces glucose uptake

­ To avoid hypoglycemia during exercise:

­ Same pre­exercise meal recommendations (primarily CHO 1­4hrs before exercise) and reduce insulin dose by 30­50%

­ Take in CHO within 15min of the start of the exercise → insulin doesn’t have time to kick in

­ Perform short maximal sprint just prior to exercise or as warm up

­ Profile blood glucose response

­ Dont exercise if blood glucose is too low

­ Same CHO intake recommendations during exercise

­ Insulin injection likely needed after exercise to assure adequate muscle glycogen repletion

­ Beware of increased insulin sensitivity

­ Doesn’t need insulin that much during the rapid phase of glycogen repletion after exercise

­ But likely needs insulin during the slow phase of glycogen repletion ­ The Type II Diabetic “Athlete”

­ Exercise used as a form of therapy to improve insulin sensitivity and reduce body weight

­ Diet should focus on negative caloric intake and low fat

­ Avoid large meals → higher risk of hyperglycemia

­ Low risk of hypoglycemia

­ Exercise duration may not be long enough to require CHO supplementation before exercise

­ Impaired capability to exercise (<60min)

­ Trying to reach a negative caloric balance to lose weight

­ Impaired ability to synthesis muscle glycogen

­ Insulin resistant

­ Slower slow phase of glycogen repletion

Lecture 19 Eating Disorders

­ Anorexia  Nervosa

­ Refusal  to  maintain  normal  body  weight  (<85%  expected,  BMI<17.5)

­ Intense  fear  of  gaining  weight/becoming  fat,  even  though  underweight

­ Altered  sense  of  reality,  unaware  that  they  have  a  problem

­ May  only  seek  help  if  sports  performance  decreases  or  due  to  heavy  peer influence

­ Amenorrhea

­ Hypothermia  &  low  resting  HR

­ Lower  resting  metabolic  rate  coz  too  underweight

­ Bulimia  Nervosa

­ Recurrent  episodes  of  binge  eating

­ A  sense  of  lack  of  control  over  eating  during  the  episode

­ Recurrent  inappropriate  compensatory  behavior  after  binging  to  prevent  weight  gain ­ Self­induced  vomiting

­ Misuse  of  laxatives,  diuretics,  enemas,  etc.

­ Fasting  or  excessive  exercise

­ The  binge  eating  and  compensatory  behaviours  both  occur  at  least  twice  a  week  for  3 months

­ Eating  disorders  10x  more  prevalent  among  females  than  males

­ Anorexia  as  prevalent  in  female  athlete  as  general  female  (1.3%)

­ Bulimia  much  more  prevalent  in  female  athlete  (~8%)  than  general  female  population ­ Eating  disorders  most  prevalent  in  endurance,  aesthetic,  and  weight­dependent  sports ­ Causes  of  eating  disorders:

­ Largest  risk  factor  is  being  female

­ Heavy  training  loads  is  not   primary  cause  of  eating  disorders

­ Weight  gain  due  to  injury  or  offseason  may  lead  to  dieting  and  irrational  fear  of  weight gain  in  athletes

­ Low  self­esteem  and  overly  self­critical  +  impulsive

­ Addictiveness  scores  similar  to  drug  addicts

­ Overactivity  appears  to  be  a  consistent  symptom  of  eating  disorders  →  30­80%  of  those with  eating  disorders  are  compulsive  exercises

­ Deliberate  exercise

­ Involuntary  and  persistent  restlessness

­ Effects  of  Eating  Disorders:

­ Depression,  fatigue,  anxiety,  irritability

­ Prolonged  negative  energy  balance  →  decreased  FSH,  LH  from  anterior  pituitary  → decreased  estrogen,  progesterone  production  by  ovaries  →  amenorrhea

­ Due  more  to  low  energy  intake  than  low  BF%

­ Decreased  estrogen  causes  decreased  calcium  facilitated  into  bone  →  bone  loss and  risk  of  osteoporosis 

­ 95%  of  maximal  bone  density  reached  by  age  of  18

­ Likely  reversible  with  proper  lifestyle  change

­ Delayed  onset  of  puberty  →  poor  bone  development  and  susceptibility  to  fractures  later in  life

­ Female  athlete  triad  =  Disordered  eating  +  Amenorrhea  +  Osteoporosis ­ Most  at  risk  involved  in  sports  where  low  BF%  is  advantages  (endurance, gymnastics)  or  low  BW  required  (rowing,  martial  arts)

­ Death  rates  for  anorexia  in  general  population  is  6%  (may  be  as  high  as  18%) ­ excessive  fluid  and  electrolyte  imbalance  →  cardiac  arrest  is  primary  cause ­ Suicide  is  secondary  cause

­ Treatment  and  Prevention

­ Education  on  balanced  meal  and  regular  eating  pattern

­ Intervention  by  loved  ones:

­ Irrational  fear  of  admitting  problem

­ Early  diagnosis  is  essential

­ Manage  depression  first  →  most  life  threatening

­ Cognitive­behavioural  therapy

­ Antidepressant  medication

­ Maintain  moderate  supervised  exercise

­ Goal  of  maintaining  at  least  90%  of  ideal  BW  by  consuming  at  least  3  meals  a  day ­ Assess  bone  marrow  density  and  possible  hormone  replacement  therapy  to  prevent osteoporosis

­ Especially  in  amenorrhea  >  6  months

­ Coaches  play  a  key  role

­ Should  not  comment  on  athlete’s  body  weight,  size,  or  BF%

­ Team  approach  →  Physician,  dietician,  physiologist,  psychologist,  and  coaches ­ Early  intervention  is  KEY

KIN321  Class  Notes  Week  14  (11/28­12/02)

________________________________________________________________________________ From previous sections

­ Special Populations & Eating Disorders

________________________________________________________________________________ Lecture 20 Surgical and Pharmacological Approaches to Disease Management


­ Pacemakers

­ Ability to properly regulate HR especially important in maintaining adequate Q in those with cardiac disease due to lower than normal stroke volume → loss of muscle → lessened contractility

­ Consist of pulse generator (battery), leads, and contact electrodes

­ Most common indications for pacemakers

­ SA node dysfunction → symptomatic bradycardia (lower than normal HR), chronotropic incompetence (reduced ability to increase HR w/ exercise or stress

­ AV conduction system blockage → loss of AV synchrony

­ Always provides rhythm OR intermittently fires when SA node fails to provide appropriate rate → sensing capacity on a beat­by­beat basis

­ Two basic types of pacemakers:

­ Single­chamber → for SA node dysfunction only

­ Dual­chamber → for AV conduction blockage

­ Senses SA node and stimulates ventricles depending on level of AV blockage

­ Increases Q (primarily at rest) without increasing mVO2(myocardium O2 consumption) → increase risk of ischemia

­ Capable of shortening PR interval with increasing HR

­ Programmed to stimulate ventricular contraction at a set maximal

rate despite SA node activity

­ Important for atrial tachycardia (higher HR than normal)

­ Rate responsive pacing → capacity of pacemakers to increase HR when activity level is increased

­ Compensate for chronotropic incompetence

­ Sensor monitor changes in:

­ Body motion from an accelerometer

­ Ventilation from transthoracic impedance (lung action)

­ QT interval

­ Those with rate responsive pacemakers should undergo chronotropic assessment exercise protocol that mimics everyday activities to set:

­ Upper and lower HR limits

­ Angina threshold → at what HR would cause chest pain?

­ Sensitivity

­ Heart Transplantation

­ Accepted definitive treatment for end­stage chronic heart failure (weak enough heart that can’t support normal metabolism at rest, Q < 4­5 L/min), and may be considered for:

­ Cardiomyopathy

­ Congenital heart disease

­ Coronary artery disease

­ Heart valve disease

­ Orthotopic technique vs. Heterotrophic technique (Temporary and RARE, two hearts)

­ Abnormal HR regulation due to complete denervation → lack of parasympathetic and sympathetic inputs

­ Higher HR at rest

­ Lower HR during exercise

­ Higher HR during recovery

­ Primarily regulated by circulating CATS (norepinephrine & epinephrine) ­ Normal LV systolic function, but decreased LV diastolic function → reduced SV during exercise

­ SV still capable of increasing despite denervation due to Frank­Starling effect

­ HR responsiveness may improve over first months to years of recovery → partial reinnervation

­ Coronary Angioplasty

­ Percutaneous transluminal coronary angioplasty (PTCA)

­ 1. Guide wire passed from femoral, radial, or brachial artery to just beyond diseased portion

­ 2. Balloon catheter passed over guide wire to affected area

­ 3. Balloon inflated to compress plaque and stretch artery wall

­ 4. Wire mesh stent left in place

­ Quick recovery

­ Drug eluting stents → coated with drugs that help to prevent re­stenosis of artery by limiting growth of scar tissue

­ Coronary artery bypass graft surgery (CABG)

­ Grafting veins or arteries around narrowed coronary arteries

­ Unlike PTCA, CABG is an open heart procedure

­ Commonly used vessels include:

­ Left internal thoracic artery

­ Right internal thoracic artery

­ Great saphenous vein of the leg

­ Using artery is better:

­ Grafted only once (instead of 2 for veins)

­ Handle more pressure; more robust

­ More smooth muscle

­ Vein valves need to be removed

­ Saphenous vein is more available tho

­ Successful grafts may last 10­15 years with arterial grafts having longer latency than venous

Pharmacologic Approaches

­ Nitrates

­ Used in the treatment of angina (chest pain), acute MI, and heart failure ­ Vasodilation of systemic veins → ~45% reduction in preload

­ Vasodilation of systemic arteries → ~7% reduction in afterload

­ Quick medicine, can be carried around daily

­ ANS and Adrenergic Receptors

­ ANS:

­ Parasympathetic → control of resting function

­ Sympathetic → control of fight­or­flight response

­ Neurotransmitter of SNS is norepinephrine

­ Sympathetic stimulation of adrenal medulla → 4:1 release of epinephrine and norepinephrine

­ Norepinephrine → alpha receptors

­ Epinephrine → alpha and beta receptors

­ Fight­or­flight response:

­ Increased blood pressure

­ Increased blood flow to active muscle and decreased blood flow to GI tract, kidneys, etc.

­ Increased cellular metabolism including:

­ Increased lipolysis

­ Increased glycogenolysis in liver and muscle

­ Beta­1 → Cardiac function and lipolysis

­ Beta­2 → Tissue metabolism and vasodilation

­ Beta Blockers

­ Most common names end in “olol” → propranolol

­ Indications for use include:

­ Hypertension

­ Angina (chest pain related to ischemic heart disease)

­ Atrial and ventricular arrhythmias

­ If blocked Beta­1 receptors, which usually done by having cardioselectivity of the drug

­ Decreased HR

­ Decreased Contractility

­ Decreased Lipolysis

­ If blocked Beta­2 receptors, which might happen with high dose of beta blockers ­ Vasoconstriction

­ Bronchoconstriction

­ Decreased glycogenolysis (exacerbate hypoglycemia)


­ Some myocardial beta­2 blockers do exist, but rare

­ Beta Blockers differ in degree of intrinsic sympathomimetic activity (ISA) ­ ISA is the ability of beta blockers to weakly stimulate some beta receptors while inhibiting agonists such as CATS

­ Agents with high ISA may be beneficial for those with exertional angina ­ High ISA also reduces risk of bronchoconstriction and dyslipidemia with beta blockers use

­ High ISA → give patients normal HR at rest, but still protect them when under stress

­ Beta blockers, especially selective, reduce symptoms of angina by reducing myocardial O2 demand

­ Beta blockers lower blood pressure by:

­ Reducing cardiac output

­ Inhibition of renin release by kidneys → decrease in angiotensin

II­mediated vasoconstriction

­ Sub max test for someone w/ beta blockers to determine target HR ­ Calcium Channel Blockers

­ Coronary and peripheral vasodilation

­ Decreased HR and contractility → not to the same extent as beta blockers ­ Indications for use include:

­ Hypertension

­ Angina

­ By increasing myocardial O2 supply

­ By decreasing myocardial O2 demand → reduced afterload

­ ACE Inhibitors and Angiotensin II Receptor Blockers

­ X Angiotensin I → Angiotensin II (ACE inhibitor)

­ X Angiotensin II → Angiotensin II receptor

­ Used for the treatment of hypertension and heart failure

­ Most common side effect of ACE inhibitor is cough

­ ARB are as effective as ACE inhibitors and have fewer side effects ­ Hypolipidemic Agents

­ Statins → inhibit HMG CoA reductase (regulatory enzyme for cholesterol synthesis) involved in hepatic C synthesis → increase hepatic C need → increase LDL receptor activity and LDL clearance → 30­50% decrease LDL­C ­ Statins also lower risk of CAD by:

­ Improving endothelial function

­ Maintaining plaque stability

­ Prevent thrombus formation

­ Common Statins are Crestor, Lipitor, and Zocor

­ Ezetimibe lowers intestinal absorption of ingested Cholesterol

­ Commonly known as Zetia

­ Combined with (Zocor) to form Vytorin → dual therapy of reducing C absorption and increasing LDL­C clearance

­ Bile acid sequestrants → decrease bile reabsorption → increase hepatic C need → increase LDL receptor activity and LDL clearance → decrease in LDL­C ­ (Old drug, got replaced by Statin)

­ Nicotinic Acid (Niacin, Vitamin B3) → decrease adipose lipolysis → decrease available Actyl­CoA → decrease secretion of VLDL­C → decrease in LDL­C ­ (Minor)

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