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(-)

(-)

(+)

(+)

(+)