the basal metabolic rate d. c. mikulecky professor of physiology virginia commonwealth university
TRANSCRIPT
THE BASAL METABOLIC RATE
D. C. MIKULECKYPROFESSOR OF PHYSIOLOGYVIRGINIA 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 INTAKETHYROID HOMONEEVEN LOWER LEVELS DURING
SLEEP (10-15%)
ENERGY
THE CAPACITY TO DO WORKTHE 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
GLYCOGENESISGLYCOGENOLYSISGLUCONEOGENESISPROTEIN SYNTHESISPROTEIN DEGRADATIONFAT SYNTHESISFAT 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 CALORIES70 KG PERSON 2,000 CALORIES/DAYNEED 500G GLUCOSEAS AN ISOTONIC SOLUTION THAT
WOULD BE ABOUT 10LTHE 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 GLYCOGENESISINHIBITS GLYCOGENOLYSISINHIBITS 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 SYNTHESISINHIBITS PROTEIN DEGRADATION
CONTROL OF INSULIN SECRETION
NEGATIVE FEEDBACK: BLOOD SUGAR
BLOOD AAGI HORMONESPARASYMPATHETIC 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 CELLSGENERALLY OPPOSES ACTIONS OF
INSULINDECREASE GLYCOGEN SYNTHESISPROMOTE GLYCOGENOLYSISSTIMULATE GLUCONEOGENESISPROMOTES FAT BREAKDOWNONLY 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
BLOODGLUCOSE
RELEASE FROM LIVER
CONSUMPTIONBY
MUSCLE AND FAT CELLS
INSULIN
(-)
(+)
EPINEPHRINEAND
NOREPINEPHRIN
GLUCAGON
GLUCOCORTICOIDS
GH(-)
(-)
(+)
(+)
(+)