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

BODYS 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