Energy Cost Assessment in Humans

Heat generated by humans during rest and muscular activities can be measured by direct and indirect calorimetry.

Direct calorimetry: This is essentially an airtight, thermally insulated chamber where the subject is either resting or exercising. Humidified air providing O2 is constantly supplied while chemical absorbents remove CO2. The heat produced by the subject is picked up by a stream of cold water flowing at constant rate through coiled tubes. The difference in the temperature of water entering and leaving the chamber reflects the subject's heat production.

Indirect calorimetry: This is based on the fact that energy metabolism in the body ultimately depends on the utilization of oxygen. Therefore, oxygen consumption is measured and energy equivalent is determined. One liter of O2 consumption corresponds to 4.8 kcal. Closed circuit or open-circuit spirometer measures O2 consumption.

Relationship between work-output and O? consumption: If work-output can be measured, it can be converted into kcal equivalents. For example, on the bicycle ergometer with a fly wheel of 6 m and a pedaling rate of 50 RPM (300 m total distance per min) with 1 kg resistance, 300 kg.meter work are performed per min. Since 1 kg.meter corresponds to 0.00234 kcal, 300 kg.meter can be converted into 0.7 kcal of work-output. Assuming 25% efficiency, the total energy expenditure per minute is 4 x 0.7 = 2.8 kcal. Since 4.8 kcal corresponds to 1-liter O2 consumption, the 2.8 kcal is equivalent to 0.58-liter O2 consumption. (Note the following terms: work = force x distance; force = mass x acceleration; power = work per unit of time; energy = the capacity of performing work).

Many studies were carried out to relate different work-outputs under various conditions with oxygen consumption, in healthy individuals and in patients. Such studies are helping physicians to design programs for individuals to lose weight, improve athletic performance, or to rehabilitate following muscle injury or heart disease.

Oxygen debt: During an intense period of exercise, PCr level has decreased and much of the glycogen may have been converted to lactic acid. Oxygen debt has been created. Namely to restore the normal cellular metabolite levels, energy is needed and the muscle utilizes oxygen to provide energy for the cellular processes. The muscle continues to consume oxygen at a high rate after it has ceased to contract. Therefore, we breathe deeply and rapidly for a period of time, immediately following an intense period of exercise, repaying the oxygen debt.

Example for calculation of oxygen debt: After exercise, a total of 5.5 liters of O2 were consumed in recovery until the resting value of 0.31 liter/min was reached. The recovery time was 10 min.

Adaptation to exercise: It is customary to differentiate between high-intensity strength activities and low-intensity endurance exercises. The different types of exercises elicit different patterns of neural activity to muscle resulting in specific adaptation. High intensity strength activities, such as weight lifting and bodybuilding, induce hypertrophy of the muscle with an increase in strength. Endurance exercises, such as swimming and running, increase the capacity of muscle for aerobic metabolism with an increase in endurance.

Fatigue: Muscle fatigue is defined as a loss of work-output leading to a reduced performance of a given task. Fatigue may result from deleterious alterations in the muscle itself and/or from changes in the neural input to the muscle.

During prolonged endurance exercise, e.g. marathon-running, depletion of muscle glycogen, decrease in blood glucose, dehydration, or increase in body temperature contribute to fatigue. During intense muscular activity, e.g. short-distance running, lactic acid is formed via anaerobic glycolysis. The H+ ions dissociated from lactic acid decrease the pH of the muscle; this may inhibit metabolic processes, disturb excitation-contraction coupling, Ca2+ fluxes, actomyosin ATPase activity, and thereby decrease work output.


Cain, D.F. and Davies, R.E. (1962). Breakdown of adenosine triphosphate during contraction of working muscle. Biochem. Biophys. Res. Commun. 8, 361-366.

Carlson, F.D. and Wilkie, D.R. (1974). Muscle Physiology. Prentice-Hall, Inc. Needham, D. M. (1971). Machina Carnis. Cambridge University Press.

Paul, R. J., Ferguson, D.G., and Heiny, J. A. (1993). Muscle physiology: molecular mechanisms. In Physiology (N. Sperelakis and R.O. Banks, Eds.), pp.189-208. Little, Brown and Co.

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