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
(+)
EPINEPHRINE
FROM LIVER
-
( )
(+) AND
NOREPINEPHRIN
(+) GLUCAGON
BLOOD
INSULIN GLUCOSE GLUCOCORTICOIDS
-
( )
(+)
-
( ) GH
CONSUMPTION
BY
MUSCLE AND FAT CELLS