Description
KIN321 Class Notes Week 10 (10/2410/28)
________________________________________________________________________________ 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 -
- - [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
- 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.
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)