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THE BASAL METABOLIC RATE D. C. MIKULECKY PROFESSOR OF PHYSIOLOGY VIRGINIA COMMONWEALTH UNIVERSITY THE METABOLIC RATE METABOLIC RATE = ENERGY EXPENDITURE PER UNIT TIME (Calories/hour) FACTORS INFLUENCING METABOLIC RATE EXERCISE FOOD INTAKE SHIVERING ANXIETY BASAL METABOLIC RATE BODY’S “IDLING SPEED” (THE MINIMAL WAKING RATE OF INTERNAL ENERGY EXPENDITURE) DIRECT CALORIMETERY(MEASURE RATE OF HEAT PRODUCTION) INDIRECT CALORIMETERY (MEASURE OXYGEN CONSUMPTION) (SEE LAB NOTES FROM DEC.2) FACTORS WHICH INFLUENCE BMR FOOD INTAKE THYROID HOMONE EVEN LOWER LEVELS DURING SLEEP (10-15%) ENERGY THE CAPACITY TO DO WORK THE CALORIE IS THE AMMOUNT OF HEAT ENERGY NECESSARY TO RAISE THE TEMPERATURE OF 1 GRAM OF WATER 1 DEGREE CENTIGRADE THE NUTRITIONAL CALORIE IS 1000 CALORIES OR THE KILOCALORIE ENERGY BALANCE WITH RESPECT TO THE BODY INPUT - OUTPUT = STORAGE OR DEPLETION (CONTINUITY EQUATION ( E/t = 2E) ) OUTPUT = INTERNAL WORK + EXTERNAL WORK INTERNAL WORK ------> HEAT STORAGE AND/OR DEPLETION NEUTRAL ENERGY BALANCE OCCURS WHEN INPUT AND OUTPUT MATCH POSITIVE ENERGY BALANCE OCCURS WHEN INTAKE EXCEEDS OUTPUT ENERGY IS STORED AS GLYCOGEN OR FAT NEGATIVE ENERGY BALANCE OCCURS WHEN OUTPUT EXCEEDS INTAKE- ENERGY STORES ARE DEPLETED FOOD AS FUEL CARBOHYDRATE 4 CAL/G PROTEIN 4 CAL/G FAT 9 CAL/GRAM ETHANOL 7 CAL/G FOOD AS STORED FUEL 3500 CALORIES = 1 LB OF BODY MASS EFFICIENCY OF METABOLISM 50% GOES TO ATP 50% GOES TO HEAT FOOD INTAKE CONTROLED BY HYPOTHALAMUS FEEDING CENTERS SATIETY CENTERS CONTROL OF FUEL METABOLISM GLYCOGENESIS GLYCOGENOLYSIS GLUCONEOGENESIS PROTEIN SYNTHESIS PROTEIN DEGRADATION FAT SYNTHESIS FAT BREAKDOWN ANABOLISM VS CATABOLISM BUILD UP VS BREAKDOWN OF LARGE MOLECULES ANABOLISM REQUIRES ENERGY (ATP) CATABOLISM:ENERGY PRODUCTION BLOOD GLUCOSE ONE GRAM YIELDS ABOUT 4 CALORIES 70 KG PERSON 2,000 CALORIES/DAY NEED 500G GLUCOSE AS AN ISOTONIC SOLUTION THAT WOULD BE ABOUT 10L THE ACTUAL AMOUNT IS ABOUT 20G OR ENOUGH FOR 1 HOUR PANCREATIC HORMONES AND BLOOD GLUCOSE INSULIN GLUCAGON INSULIN: ACTION ON BLOOD SUGAR BETA CELLS IN ISLETS OF LANGERHANS: INSULIN FACILITIES GLUCOSE ENTRY INTO CELLS STIMULATES GLYCOGENESIS INHIBITS GLYCOGENOLYSIS INHIBITS GLUCONEOGENESIS INSULIN: ACTION ON FAT INCREASES TRANSPORT INTO ADIPOSE CELLS PROMTES TRIGLYCERIDE SYNTHESIS INHIBITS LIPOLYSIS INSULIN: ACTION ON PROTEIN PROMOTES UPTAKE OF AA BY MUSCLE AND OTHER TISSUE PROMOTES PROTEIN SYNTHESIS INHIBITS PROTEIN DEGRADATION CONTROL OF INSULIN SECRETION NEGATIVE FEEDBACK: BLOOD SUGAR BLOOD AA GI HORMONES PARASYMPATHETIC ACTIVITY TWO TYPES OF DIABETES MELLITUS TYPE I: AUTOIMMUNE DESTRUCTION OF BETA CELLS, LACK OF INSULIN SECRETION TYPE II: REDUCED SENSITIVITY OF INSULIN RECEPTORS ACUTE EFFECTS OF DIABETES MELLITUS EXTRACELLULAR GLUCOSE EXCESS GLUCOSE IN URINE EXCESS FLUID LOSS CIRCULATORY FAILURE RENAL FAILURE NERVOUS SYSTEM MALFUNCTION DUE TO DEHYDRATION EXCESSIVE FOOD INTAKE PROGRESSIVE WEIGHT LOSS MOBILIZTION OF FAT KETOSIS ACIDOSIS COMA AND DEATH GLUCAGON PANCREATIC ALPHA CELLS GENERALLY OPPOSES ACTIONS OF INSULIN DECREASE GLYCOGEN SYNTHESIS PROMOTE GLYCOGENOLYSIS STIMULATE GLUCONEOGENESIS PROMOTES FAT BREAKDOWN ONLY IN LIVER: PROTEIN CATABOLISM EPINEPHRINE, CORTISOL, AND GROWTH HORMONE ALL INCREASE BLOOD GLUCOSE AND FATTY ACIDS CORTISOL INCREASES BLOOD AA AND DECREASES MUSCLE PROTEIN GH DECREASES BLOOD AA AND INCREASES MUSCLE PROTEIN OVERALL REGULATION OF BLOOD GLUCOSE (+) RELEASE FROM LIVER - ( ) BLOOD GLUCOSE INSULIN (+) EPINEPHRINE AND NOREPINEPHRIN (+) GLUCAGON (+) GLUCOCORTICOIDS - ( ) - ( ) CONSUMPTION BY MUSCLE AND FAT CELLS GH