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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?

Description

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 69 Views 3 Unlocks
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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?



If you want to learn more check out What were the arguments for and against unregulated capitalism?

- - [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

- 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 ] Don't forget about the age old question of What is tenebrism?

- Acute acclimatization = Hyperventilation = ↑PAO 2 → ↑SaO 2→ ↓PACO 2 (↑blood pH)

- We also discuss several other topics like What are the two models of the pace of speciation?

- 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 Don't forget about the age old question of Why did we have a civil war?

-

- Why VO2max stays the same at altitude? (stay depressed?) Don't forget about the age old question of What tables are to be interrogated by the search?

-

- Hormonal Acclimatization

- - Epinephrine → increase in glycolysis

- 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 Don't forget about the age old question of What are the aspects of athletic training?

- 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.

­ HIGH GLYCEMIC INDEX

­ 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?

*****NUMBERS

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

biopsy

­ 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

glucose

­ 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

mitochondria

­ 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

temperature

­ 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

Surgical:

­ 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)

­ (WE DONT WANT THIS)

­ 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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