Unit 2 Nutrition Notes PDF

**[Adaptations to Starvations:]** **[What is in the Body?]** - Body mostly made of water (\~60 -- 70% in children, \~50% in adults) - **Cells (lean tissue) are composed of about 20% protein ( true for almost all cells)** - 30 kg muscle x 20% = 6 kg protein x 4 kcal/kg = 2400 Kcal...

**[Adaptations to Starvations:]** **[What is in the Body?]** - Body mostly made of water (\~60 -- 70% in children, \~50% in adults) - **Cells (lean tissue) are composed of about 20% protein ( true for almost all cells)** - 30 kg muscle x 20% = 6 kg protein x 4 kcal/kg = 2400 Kcal - Maximum carbohydrate stores in body are miniscule: - Liver: \~5% x 1.5 kg = 75 g x 4 kcal/g = 300 kcal; Muscle: \ - Influence of nutrient intake/body comp affects gonadotropin secretion - Duration of unopposed estrogens/breast cancer - Loss of periods in women (body weight? Fat?). Anorexia nervosa; athletes, stress fractures - Adaptive explanation - Effects in men (e.g. cancer, HIV infection): therapeutic implications - Health implications in modern world (anorexia nervosa; fertility, bone health, cancer) - Thyroid axis (T4/T3/TSH); utility and downside in obesity - A major hormone influencing energy expenditure (if you lose weight, less active thyroid hormone) - Mechanisms: T3 is active hormone but T4 is secreted by thyroid gland; T4 to T3 conversion by peripheral tissues; influence of calorie intake/nutrient intake - Hypothalamic/pituitary also respond - Where is true control in this system? Liver - Utility and downside of adaptation in obesity - Insulin sensitivity: therapeutic uses - "Weight loss" often prescribed for treatment of T2DM - Whether weight loss effective apparent w/ first 5 lb of weight loss - Rapid effects of negative energy balance on liver glycogen stores reduces hepatic glucose production and fasting blood glucose concentrations w/I a few days - Starvation response and effect on insulin resistance has implications for how we think about weight loss - Leptin secretion: primary function (also it tells brain to make estrogen) - Primary function? "Adipostat" vs undernutrition defense in evolutionary history - Effects of acute starvation or carbohydrate deprivation compared to long-term weight loss on leptin levels and expression in adipose tissue - Effects of lower leptin vs higher leptin levels relative to normal levels - Therapeutic implications: weight loss treatment, infertility **[Starvation and Infection, Stunting/Calorie Restriction for Life-Span Extension:]** **[Classic Forms of Starvation: Adaptations Do Not Always Succeed]** - "**Marasmus**": Lose weight but look healthy, no swelling, usually do well - "**Kwashiorkor**": Appear sick/swollen belly; die often - One or other might occur due to food types and infection presence (theories) **[When the Starvation Response Fails: Interaction w/ infection:]** - Infection/Inflammation presence alters starvation response - Highly conserved biological program -- "acute-phase response" - Fever, low blood iron/anemia; sleep; fatigue; loss of appetite; poor grooming; high metabolic rate; blood protein change; blood lipid increase - Lose more nitrogen (muscle tissue) than in well adapted "simple" starvation; lower albumin (swelling); more infections; inability to gain lean tissue when nutrients are provided **[Examples of Starvation/Infection combination in humans:]** - **Tuberculosis**: Used to be called "consumption" - **Cancer**: Common look of cancer patients (cachexia); difficulty reversing feed wasting - **HIV/AIDS:** Common to have wasting early in HIV epidemic (slim disease in Africa) - Inability to reverse lean tissue losses by feeding strategies - Able to increase lean tissue only w/ targeted anabolic interventions **[Effects of Feeding in Infection/PCM:]** - Lean tissue wasting very common in HIV infection/cancer; correlates w/ and possibly causes death - Associated in men w/ low test - Gen no increase in lean body mass w/ nut interventions (gain only fat); parenteral nutrition, enteral supp, appetite stim - Alternative: Anabolic therapies (Growth hormone, androgens, resistance exercise +/- androgens) **[Conclusions:]** - Normal response to starvation is complex and highly effective; preserves lean tissue and allows longer survival - Imposition of infection changes everything: results in poorly adapted starvation & adverse outcomes **[Stunting:]** - 150 million infants/children suffer from Stunting (aka Environmental Enteric Dysfunction -- EED) - Characteristics: short stature, delayed development, impaired vaccine response, susceptibility to infections - Long-term/permanent conseq -- shorter stature and neuro-cognitive impairment (lower height/IQ than gene potential) - Multifactorial causes: GI/systemic infections, poor nutrition, bad water, chronic inflammation - One of most important problems that prevents people from reaching full potential **[Muscle mass is a marker of stunting:]** - Body weight not accurate enough; children can be normal weight but stunted (fat mass preserved) - Muscle largest reservoir of protein in body; responsive to chronic changes in nutritional status, inflammation/intercurrent ill - Skeletal muscle serves a \# of functions (in add. To locomotion) and not deposited in sick individuals - Muscle mass in children correlates w/ brain dev - As largest component of fat-free mass, muscle is the most accurate index of general nutritional status - Accordingly, measurement of muscle mass should be fundamental part of any stunting test - Couple of reliable ways to measure: MRI and biochemistry  **[Total-body skeletal muscle mass by D~3~-creatine dilution:]** - Single oral tracer dose of D~3~-creatine - Absorption/distribution/active uptake and dilution in skeletal muscle creatine pool - Conversion to creatinine (\~1.7% of total creatine per day; non-enzymatic reaction; irreversible in vivo) excreted in urine - Single urine sample at isotopic steady state )2-4 days in humans) - Dilution principle can then be applied - Analysis of D~3~-creatinine enrichment reveals total body creatine pool size, which reflects functional muscle mass (\ 95% of creatine is in skeletal muscle) **[Summary:]** - Enormous public health problem - Evaluating efficacy of interventions requires a reliable marker (test) - Muscle mass is an accurate metric of nutritional health, including brain growth - Next step will be to evaluate public health interventions in the field (e.g. sanitation/nutrition/water quality) for stunting **[Calorie Restriction ]** *Can we eat less and live longer?* **[Calorie Restriction (CR) Background]** - Calorie restriction: reducing caloric intake w/o malnutrition - Typically a (20-40%) less than ad-libitum fed controls - Achieved many different ways, all w/ same result - Increased lifespan - Decreased age-related diseases - Cancer, neurodegeneration, cardiovascular, immune dysfunction - CR extends healthspan/lifespan across variety of organisms (Worms/Flies/Rodent/Non-human primates) - 40% CR extends lifespan by \~20% in mice - Would be like people living to \> 120 years! **[Hormonal Consequences of Starvation or Semi-Starvation: Powerful effects on daily life:]** - Growth (growth factor, GH/IGF-1) axis: reproductive system (gonadotropins, gonadal function) - Thyroid axis (T4/T3/TSH) - Insulin sensitivity **[CR: Mechanisms unknown through many possibilities:]** - Scarcity adaptations, including turnover rates of cells and proteins globally - "Stress resistance" programs - Physiologic alterations due to hormonal/metabolic signals of calorie insufficiency - Less oxidative stress/free radicals - Slowing down of metabolic rates -- fewer mistakes, less damage and repair needed - None are proven, however ***How is CR in Mice different than in humans?*** **[Problems:]** 1. Are causes of death in small laboratory animals same as in humans? - Most mice in laboratories die of cancer - CR reduces cell division in many cell types - Cell division mechanistically linked to aging: - Increases promotional phase of carcinogenesis - Leads to senescence of cells and tissues - Many longevity models associated w/ decreased growth factors and cell division rates - Might CR not really extend maximal life-span but just prevent premature cancer deaths? - Extrapolation to humans would be limited, if this is explanation 2. Body size and metabolic rate 3. Difficulty in reducing daily calorie intake and bodyweight over a lifetime for most people 4. Length of studies required to test longevity effects (even in small animals) **[Simple Sugars, Surplus Carbohydrate Intake, Fatty Liver Disease and Metabolic Health:]** **[Hierarchy of Fuel Selection in humans:]** - Macronutrients compete for oxidation in tissues and in the whole body 1. When both CHO and fat are present: CHO wins = selected for oxidation - Why? CHO stimulates insulin -- combination inhibits oxidation of fatty acids by tissues (muscle/liver); increases CHO oxidation 2. Ethanol is converted to acetate, which is directly converted to acetyl-CoA and oxidized by mitochondria in tissues - Fuel oxidation hierarchy is as follows: Acetate (Ethanol) \> CHO \> Fats **[Conversion of CHO to fat:]** - All organisms can convert CHO to fat/make new fat from other sources - Process is called de novo lipogenesis (DNL) - Very active in some organisms - Grain-fed cows or pigs fatten; mice on high CHO diet; honeybees make wax (lipid) from honey - Plants and algae make TG from CO2/CHO (potential basis of biofuels!) - Occurs mostly in liver and fat cells (adipose) in mammals - Not very active in most human beings under most dietary circumstances, however. A diagram of a liver Description automatically generated **[What usually happens to surplus CHO:]** 1. Not primarily converted to fat (only a few grams) 2. But CHO gets burned instead of dietary fat, even after overnight fasting (CHO "spares" fat) 3. This occurs by the liver releasing more glucose into the bloodstream even while fasting 4. Net effect is that extra CHO will add to body fat, but not by being directly converted to body fat 5. Inhibitors of new fat synthesis (DNL) will therefore not be effective for preventing obesity: this is not the pathway traversed! **["Guru Walla" Tradition:]** - Coming of age tradition in Cameroon - Young male adolescents enter a tent; fed high-CHO sorghum food (7,000 kcal/d, \> 5,500 CHO/d) by young women - Leave after several months; gain \> 12 Kg fat - But total dietary fat intake \~ 4 kg - Conclusion: They must have converted CHO to body fat under these conditions. Important note: CHO intake in this case is much greater than total energy expenditure - Seems we force system (bodies) to convert CHI into fat -- by exceeding our capacity to burn the CHO! **[Are CHO and simple sugar calories therefore "free"?]** - No! - Macronutrients compete for oxidation in tissues and in the whole body - When both CHO and fat are present: CHO "wins" (selected for oxidation), which spares fat from being oxidized - Result is accrual of fat in the body - So the surplus CHO calories not free, although generally not directly converted to fat **[Dietary Fructose:]** - Fructose -- greatest change in US diet over past 40 years - Represents \~8% - 10% of calories in diet of young people (on average -- some people more) - Now about same average energy from fructose as saturated fat intake in American diet - Not from apples! From sweetened drinks (HFC syrup) and sweetened foods. Fructose sweeter than glucose - Sucrose -- equal parts glucose and fructose - HFCS = 55% fructose: 45% glucose - Intake of sugary soft drinks represent 20% or more of calories in certain groups A graph of different levels of glucose Description automatically generated A graph of blood sugar levels Description automatically generated with medium confidence **[Effects of Long-Term Fructose Intake on Metabolic Risk Factors in Humans:]** - Increased visceral fat - Increased post-prandial triglyceride levels (consistent w/ other studies) - Increased hepatic fat synthesis - Worse insulin sensitivity **[Dietary CHO and Blood TG:]** - CHO-induced hypertriglyceridemia (HPTG) real but complex - Timing of effect (initial; attenuation) - Dose-response w/ dietary CHO - Relationship to simple sugars - Modifying factors (weight loss, etc.) - Interaction w/ exercise - Greater effect on TG if sugars \>50% of Cho - Even 60/40% to 40/60% complex/simple sugar alter TGs; Fiber/whole food reduce - Fructose particularly causal **[Metabolic Dysfunction-Associated Fatty Liver Disease (MAFLD) and Steatohepatitis (NASH)]** - 3 causes of liver disease/cirrhosis: - Alcohol Intake - Viral hepatitis (A, B, C) - Gall bladder disease - 90 million Americans affected; 1/3 get NASH and ¼ of NASH get cirrhosis  **[Conclusion: Why is MAFLD so Common?]** - MAFLD seems to flow out of our body's program for differential sensitivity of some pathways compared to others to insulin - Obesity/sedentary lifestyle reduces insulin effectiveness on macronutrient metabolism in tissues (muscle, liver adipose) - = Insulin Resistance - Blood insulin concentrations increase as a compensation = Pancreatic beta cell secretion - High insulin and glucose levels around the clock stimulate liver lipogenesis (make/store more fat) -- liver lipogenesis is still sensitive to normal stimulatory effects of insulin - Liver sensitive to increased lipogenesis effects of insulin; resistant to inhibiting glucose production = differential insulin resistance for different pathways - As a result, elevated synthesis and storage of fat in liver common **[Effects of reduced sugar intake on liver fat content and metabolic outcomes:]** - Hepatic DNL was significantly decreased in the no-added sugar treatment group (from 34.6% to 24.1%) vs. controls (from 33.9% to 34.6%) - This was paralleled by greater decreases in hepatic fat (from 25.5% to 17.9% vs. 19.5% to 18.8%) - And fasting insulin (44.3 34,7 vs. 35.5 37.0 ulU/mL) - \% change in DNL during intervention correlated significantly w/ changes in free sugar intake **[Summary and Conclusions:]** - Intake of simple sugars has increased dramatically over the past generation, especially of fructose - Now represent about as many calories as saturated fat in the average US diet -- often liquid form - Adverse effects on metabolic health of excess simple sugars and fructose intake -- including fatty liver, resistance to insulin actions, altered fat distribution and HPTG - Restricting sugar intake reduces fatty liver, synthesis of fat in the liver and blood insulin levels in adolescents w/ fatty liver disease **[Natural History of Nutrition-Related Chronic Disease:]** **[What is Insulin Resistance?]** - Defined as a state (of a cell/tissue/system/body) in which greater-than-normal amounts of insulin are required to elicit a quantitatively normal response - Discovered by RIA high blood insulin levels in early type 2 diabetics w/ high blood glucose A diagram of a pancreas Description automatically generated **[Natural history of T2D:]** - Exact way that a chronic disease progresses is usually key to understanding what treatments work and when - Usually much easier to treat (or prevent) early than late in their natural history - Timing of progression and the underlying reasons (pathogenesis) tells us how nutritional/metabolic interventions work, and when they will or will not **[Progression from Obesity to T2D:]** - Does everyone w/ obesity have insulin resistance (IR)? - No but most do; 2/3 of obese individuals have insulin resistance; Non-IR obese people are called metabolically normal obese - Although T2D highly associated w/ obesity, complex relationship; some lean people are insulin resistant (\~20% of lean people may have IR, w/ other features of Metabolic Syndrome) - Only 25-30% of obese subjects develop T2D around the world, and for all causes of obesity/IR - Others can stay as compensated IR indefinitely. May have other problems (Metabolic Syndrome) but not T2D - Most people w/ obesity or IR will [not] develop T2D! Predicting who will progress to T2D is therefore very important  **[Everyone w/ hyperglycemia (T2D) must have beta cell failure, not just insulin resistance (IR)]** - There is a feedback connection b/t plasma glucose and insulin concentrations in vivo in healthy people or compensated IR Hyperglycemia only occurs if there is a problem w/ the beta cell and is unable to keep up **[Progression from Obesity to T2D to Severe T2D:]** - Hyperglycemia requires the beta cell to fail - What is basis for progressing from early T2D to more severe T2D? - The UKPDS showed that this is almost entirely due to worsening beta cell function (less insulin secretion), not worsening insulin resistance **[Implications of Beta Cell Exhaustion Model:]** - Can predict who progresses to T2D by identifying people w/ pre-diabetes (family history/personal gestational diabetes/borderline increase in blood glucose) - 50% of gestational DM progress to frank T2D w/I 5 years - If 2 parents have T2D, \~90% chance T2D (if obese) - Or by development of impaired glucose tolerance (IGT) = 2 hr post -- glucose load value of 140 -- 200 mg/dl (T2D value \> 200 mg/dl) - Or by development of impaired fasting glucose (IFG) = fasting value 100 -- 126 mg/dl (T2D \> 126 mg/dl) **[Why do Gestational DM, IFG or IGT Predict Progression to T2D so well?]** - Pregnancy is a stress test for the pancreas - There is IR in all pregnancies -- due to higher progesterone levels - Impaired Fasting Glucose (IFG) or Impaired Glucose Tolerance (IGT) mean that the pancreatic insulin response is starting to fail -- and inevitable will progress, w/o a therapeutic intervention - These conditions predict T2D so well that they are called prediabetes -- they predict the future - Once beta cells start to fail, it gets progressively worse on its own: - When the beta cell is asked to work too hard for a long time, in some people there is death of beta cells -- "Pancreatic Exhaustion" -- which is generally irreversible **[Importance of Beta Cell Exhaustion: Applications in Clinical Diabetes Care:]** - In brand new type 1 diabetics, there is often a "honeymoon period" - When insulin requirements fall to zero. Parents may think the child is cured, but in fact it is a brief respite due the beta cell being rested (by exogenous insulin). But the immunologic pancreatic destruction continues and soon diabetes re-emerges. - Treating early T2D through insulin sensitizing changes (weight loss, metformin, glitazones): Improves beta cell function (insulin secretion) - Treating early T2D patients w/ insulin: Improves beta cell function and insulin secretion (by resting the pancreas) - Treating pre-diabetics w/ metformin, glitazones, or exercise: Improves beta cell function and insulin secretion (by resting the pancreas) - Researchers have tired to delay destruction of the pancreas in Type 1 diabetes: by resting the pancreas and preventing exhaustion **[Therapeutic Implications of Natural History of T2DM Progression]** - Early intervention in T2D is more effective than late - Being aggressive early is contrary to our therapeutic impulses but makes more sense based on progression to insulin deficiency - Early is likely to be most responsive to interventions (exercise, diet, medications) that reduce IR, because beta cell is also helped - A patient is not the same in late T2D vs early (loss of beta cell reserve, which is generally irreversible) - Prevention of T2D is possible and may be more effective than treatment of established disease! - Several early interventions have been shown to delay the onset of T2D -- improving either IR or secretion improves the other! - Metformin, glitazones, working in the garden, taking walks -- all shown to prevent progression of prediabetes to diabetes for years **[Dietary treatment of T2D:]** - "Weight loss" often prescribed for treatment of T2D - Whether weight loss will be effective is usually apparent w/I 1^st^ 5 lb (2.3 kg) of weight loss (even in very overweight subjects) - Rapid effects of negative energy balance on liver glycogen stores reduces hepatic glucose production and fasting blood glucose concentrations w/I a few days - Reduced glucose release unburdens the beta cell and can allow it to recover -- often for weeks or longer! **[Genetics of T2D: "Missing Heritability"]** - T2D is strongly hereditary, based on family studies - If 2 parents have T2D and person gets obese, \~90% chance of developing T2D - But extensive (and expensive) genetic searches have identified discrete genes for \ 20 min sustained aerobic activity; \> 3 times/week - Intensity: high (e.g. 70%) vs lower (e.g. 40-50%) - Intermittent activity is not the same, e.g. "I walk at work" -- example of rats w/ running wheels vs treadmills) - Progressive increases in distance/speed required 3. Strength/resistance training - Scientific training regiments well established ("PRE") - E.g. 70% 1-rep max x 10 rep x 3 sets each muscle group; 3 times per week - Retest/modify for 1 rep max each month. Results in near maximal gains - Results in substantial gains in muscle mass/strength; variable among individuals (genetics; prior experience-muscle memory); influenced by dietary factors **[Strength/Power:]** - Factors that increase muscle **anabolism** 1. *Amino acids* -- Leucine/BCAA effects. KIC effects 2. *Carbohydrates* -- compete w/ AAs for oxidation 3. *Insulin* -- direct and indirect effects 4. *GH/IFG*-1 -- effects in adults; fuel selection; allows to get leaner/burn fat 5. *Testosterone* -- "long-linear dose-response curve: - 10 x increased dose doubles effect (implications for use and Rx) 6. *Muscle stretch/tension*: Resistance exercise 7. *Beta*-3 agonists -- e.g. clenbuterol 8. *Myostatin*? -- animal models, human data 9. *Genetics* -- some born lucky, some not - Strength, protein, hormones, genes - Factors that increase muscle **catabolism** 1. *Amino acid deficiency* -- Leucine/BCAA KIC 2. *CHO deficiency* -- less competition w/ AAs for oxidation 3. *Insulin deficiency* -- e.g. Type 1 Diabetes 4. *Bed rest, inactivity* -- e.g. post hip fx, space flight 5. *Cytokines* -- TNF, IL-1, IL-6, etc. (e.g. illness, cancer) 6. *Glucocorticoids* -- Protein breakdown 7. *Thyroid hormone* -- dual effects **[Aerobic Fitness:]** - Factors that increase **aerobic capacity** 1. Endurance exercise training -- high oxygen demand for prolonged periods 2. High altitude -- increases RBC 3. Increased hematocrit -- e.g. erythropoietin 4. ?PPAR delta agonists 5. Genetics - More oxygen delivery to exercising muscle (cardiac output; oxygen carrying capacity; capillaries in muscle); more capacity of exercising muscle to use oxygen (mitochondrial function) **[Athlete eating habits:]** 1. Aerobic activity depletes muscle (and liver) glycogen stores need to be filled by CHO (aerobic athletes crave) - CHO/glycogen loading for marathons -- theory of depletion and super-compensation (?effectiveness) 2. Protein intake increase accrual of muscle mass in setting of resistance exercise. Eating high protein diet w/o resistance exercise does not have significant impact on muscle mass - Body builders eat constantly; high protein supplements, high CHO meals (to stimulate insulin) 3. Lots of supplements used! Creatine; chromium; AA supplements; bee pollen; DHEA/Andro; energy bars and drinks; caffein; etc. **[Effectiveness of nutritional supplements for exercise performance:]** 1. Mostly cannot be shown to have any advantage, in proper controlled studies 2. Creatine supplementation may in fact improve certain power activities, based on reasonably good studies, w/ minimal adverse effects known 3. AA no more effective than protein 4. Energy bars/drinks hard to demonstrate advantages for (beyond std food/drink) 5. DHEA/Andro basically weak version of testosterone/anabolic steroids 6. Caffein may help some activities (stimulant effect; mobilize fatty acids/glycogen) and is limited **[Consequences of performance-enhancing drugs:]** 1. Androgens/anabolic steroids - For decades medical professionals denied effectiveness; in vain - Marked increase in muscle mass/strength when high doses of androgens + resistance exercise - Minimal gains in muscle mass/strength w/ use of androgenic/anabolic agens w/o resistance - Effects: - Very low HDLc; mood lability; acne; hair growth; breast shrinkage (women); liver tumors; loss of endogenous sex hormones; changes in libido; premature stop of bone growth; permanent changes in vocal chords (women) 2. Blood/doping/erythropoietin - Objective is to increase oxygen carrying capacity of blood to exercising muscles - Can be achieved legitimately by training at altitude - Storing of own blood for auto transfusion before races -- common in endurance athletes; difficult to detect and increases performance - Uses erythropoietin to stimulate production of endogenous RBCs; used medically for anemia - Consequences: - Blood sludging, strokes in young athletes Other performance-enhancing drugs: - Some power athletes use growth hormone, insulin injections/glucose (dangerous), beta 3 agonists - Physiologic effects to increase muscle mass; effects on power activity not established - Caffein and other stimulates not allowed (caffein found in urine rep \>200 mg intake =\> 3 cups coffee = not allowed) - Creatine supplementation is not outlawed by many organizations, thought it may improve some power-related activities Medical uses of exercise and performance-enhancing agents: - Key point for real world: therapeutic uses in medicine! - Aerobic exercise effective for conditions: - Prevention of diabetes (50-75% reduction); weight reduction/maintenance in obesity; raising HDLc in low HDL patients; lowering of BP (exercise prescription more effective than salt restriction) - Use of erythropoietin in conditions of anemia w/ reduced aerobic capacity is effective - Anabolic drugs useful in rehab and treatment of frailty in elderly patients, wasting due to bed-rest (after stroke, trauma, hip fracture, etc.), cancer, HIV infection, other catabolic illnesses - Based on principles and drugs to enhance exercise performance A table with numbers and text Description automatically generated **[Lipids:]** - Lipids are chemicals of biological origin, only marginally soluble in water - Fats and oils (TAG) are types of lipid - Fats are TAG that are solid at room temperature - Oils are TAG that are liquid at room temperature - Lipids contribute texture, flavor, and aroma to food - Fats and oils provide 9 kcal per gram - TAG are the major form of lipid in fat (food and body) - American diet contains 35% of its energy from TAG and other lipids **[Fasting/Feasting:]** - Feasting: When excess energy is consumed, stored as triglycerides in adipose tissue - Fasting: When no food has been eaten for a while, TG from adipose tissue are broken down, releasing fatty acids as an energy source. - TAG are stored as large lipid droplets in white adipocytes. A diagram of a fat cell Description automatically generated **[Fatty Acids:]** - Fatty acids can be: - Saturated = no double bonds - Saturated FA have carbons in a hydrocarbon chain bound to two hydrogens (all single bonds) - End or omega carbon has 3 H atoms - Most animal fats and tropical oils contain saturated fatty acids - Unsaturated: - Contain one or more carbons that are not saturated w/ H (contain double bonds) - Naturally occurring FA, double bonds are cis (H atoms are together facing each other) - Monounsaturated = one double bond (cis) - Have only one double bond - Polyunsaturated = more than one double bond (cis) - More than one double bond. Have cis double bonds - Last carbon of a FA is known as the omega carbon, regardless of \# of carbons in FA - Long chain = greater than 12 carbon atoms, usually solid at room temperature (beef fat) - Medium chain = 8 to 12 carbon atoms, solidify when chilled but are liquid at room temperature - Short chain = 4 to 7 carbon atoms, remain liquid at colder temperature (TAG in low-fat milk) - Cis double bonds = normal (two H atoms facing each other) - Trans double bonds = natural are minor, mostly introduced by human manipulation - Not found in nature in large amounts - Hydrogenation of oils creates trans fatty acids - Raise blood cholesterol levels and increase risk of heart disease - Found in margarine and peanut butter - Essential = required in the diet, essential for health - Polyunsaturated FA. Cannot be synthesized by mammals and must be obtained through diet (omega 3/6) - Contribute to growth, skin integrity, fertility, and the structure and functions of cell membranes - Symptoms of deficiency include: dry scaly rash, decreased growth, increased susceptibility to infection/poor wound healing - \# of double bonds also affect the melting point of the FA - Bottom line: both the \# of carbon atoms (more = higher mp) and \# of double bonds (more -- lower mp) in FA of TAG affect mp of Fat (TAG) A graph with red and black dots Description automatically generated **[Study Guide:]** - Lipids are not soluble in water - TG/TAG are the major form of fat in food and in your body - TG consist of 3 FA molecules covalently bound to a glycerol molecule - TG are stored in adipose tissue. While adipose (WAT) stores fat to undergo fatty acid oxidation (FAO) to supply energy - Visceral WAT is "bad" adipose. Surrounds organs and also localizes to mid-section - Sub-cutaneous WAT is good fat. Provides 50% of estrogen in non-pregnant females - Brown adipose (BAT) stores fat to burn to defend body temp - Fats and oils contain 9kcal/gram compared to carbohydrate and protein at 4 kcal/gram - Length of fatty aid chain in TAG contributes to melting point -- longer chains have higher melting points - Degree of unsaturation (double bonds) contributes to melting point -- double bonds decrease melting points - Double bonds in naturally occurring fatty acids have the cis configuration - EFA cannot be made by mammals and are essential for health - EFA occur as omega-6 or omega-3 - Omega 6 means last double bond occurs w/I terminal 6 carbon atoms - Omega-3 means last double bond occurs w/I terminal 3 carbon atoms - Linoleic (omega 6) and linolenic (omega 3) are two EFA - Omega-3 considered more anti-inflammatory than omega-6 - Optimum health requires balance b/t omega-6 and omega-3 - Many diseases associated with EFA deficiency - Hydrogenation of fats/oils creates trans fatty acids - Trans fatty acids raise blood cholesterol level and increase risk of heart disease - **[Nutrition and Exercise:]** **[Athletic Performance:]** - Aerobic, Endurance Exercise: Long distance running, cycling, cross country skiing - Anaerobic Exercise: sprinting (events lasting \< 30 seconds) - Strength and Power: weight lifting, shot-put, football (offensive and defensive line)tf A diagram of a structure Description automatically generated **[Substrate Utilization During Exercise:]** - Fuels for energy production: - Carbohydrate: Muscle glycogen. Blood glucose - Fat: Free fatty acids from fat stores, Triglycerides in muscle - Amino acids - Rate of glycogen utilization by muscle increases w/ exercise intensity - Muscle glycogen depletion results in fatigue - Conditioning increases reliance on fat and decreases the rate of glycogen use **[Aerobic/endurance exercise:]** - Causes of fatigue: - Dehydration: 1-2% reduces performance - Lactic acid accumulation: Muscle acidosis -- pH reduction **[Fueling Exercise by the Minute:]** - Instant energy: - During first few seconds, muscles get energy from stored ATP next 10 seconds, creatine phosphate stored in muscles broken down to form more ATP - Short-term energy: - Anaerobic metabolism of glucose; obtained from blood/muscle glycogen predominant source of ATP when creatine phosphate stores depleted; thirty seconds into activity pathways operating at full capacity - Long-term energy: - 2-3 minutes after, oxygen delivery to muscle increased enough to support aerobic metabolism, which uses fatty acids and glucose to produce ATP Fats used for low intensity work; Carbs used for high intensity - High conditioned athletes use more fats than low conditioned  In order to restore glycogen, need to eat a lot of carbohydrates. Effects of Pre-exercise CHO feeding on BG levels during exercise **[Caffeine:]** - Mobilizes ffa and decreases reliance on glycogen as a fuel - Demonstrated to improve exercise time to exhaustion by 22% to 23% compared w/ placebo - Decreases rated perceived exertion at same absolute exercise intensity - Enhances prolonged endurance performance and high-intensity short-duration exercise - Levels above 15 μg/ml considered Doping (enhanced performance) easily reached by 6-8 cups of coffee **[VO~2max~ = Cardiac Output \* A-V O~2~difference]** Cardiac Output = stroke volume (max amount of blood pumps per contraction) x Heart Rate A-V O~2~ difference = Muscle mass, conditioning - For most endurance athletes, cardiac output limits VO~2max~ - Ability to extract/use O~2~ exceeds ability to deliver it **[Blood doping:]** - B4 competition, RBCs taken out, and then re-infused to increase RBC count increases performance (more hemoglobin more oxygen delivered) **[Creatine:]** - ATP + Creatine Creatine phosphate + ADP - 90-95% in muscle - 1/3 as free creatine, 2/3 phosphocreatine - Active transport of creatine into muscle cells - CHO enhances creatine uptake -- 1 g glucose/kg 2 x day increased muscle creatine 9% vs creatine alone - Estimate of 80% of athletes in 1996 Olympics were using or had been using - When cooked, creatine becomes creatinine (useless); needs to be raw or supplemented - Dietary: - 5 g = 2.5 lbs of fresh uncooked steak; 20 g = 10 lbs of fresh uncooked steak - Supplementation: - Short term improvements: - Strength and power by 5-15% - Work performed during sets of maximal effort muscle contractions by 5-15% - Single effort sprint performance by 1-5% - Work performed during repetitive sprint performance by 5-15% - Long-term improvement - Greater gains in strength, sprint performance, and FFM (fat-free mass) during training - Side effect: Weight Gain Note: When creatine goes into muscles, water follows to maintain osmotic pressure (water weight = weight gain)