The Role of Cortisol in Concurrent Training

by Robert A. Robergs, PhD and Len Kravitz, PhD on Oct 01, 2005

During exercise, regardless of whether it is strength or cardiorespiratory training, cortisol is released in proportion to the intensity of the effort.

Many exercise enthusiasts who are pressed for time may want to perform both strength and cardiorespiratory training in the same session or within a few hours of each other. But some studies have indicated that strength gains may be compromised when strength and cardiorespiratory training are performed concurrently. This has been referred to as the “interference phenomenon” (Doc-herty & Sporer 2000). Several hypotheses have been proposed to explain this phenomenon. One hypothesis suggests that increases in blood cortisol during endurance exercise increase protein catabolism, resulting in the breakdown of muscle. The topic of concurrent training as it relates to cortisol levels is regularly discussed and debated by fitness professionals at industry conferences.

This evidence-based concurrent training article will examine many of the confusing issues associated with cortisol and muscular growth by discussing how hormones work, the functions of cortisol, the association of cortisol with cardiorespiratory exercise, and the possible catabolic effect of cortisol on muscle mass and muscular strength.

How Do Hormones Work in the Body?

There are two main types of hormones: (1) amine and peptide, and (2) steroid. These hormone types differ in their chemical structure and cellular mechanism of action.

Amine and peptide hormones consist of one or more amino acids (the building blocks of protein). Since many amino acids have small electrical charges on some of their atoms, amino acid molecules interact well with the small charges found on water molecules, and hence can be dissolved in water. However, the amine and peptide hormones cannot cross cell membranes to get inside cells, since cell membranes are composed mainly of lipids, not water. Consequently, amine and peptide hormones bind to specialized protein receptors on the outside of cell membranes, causing changes in structure and/or charge distribution within the receptors and leading to the production of specific molecules that alter cell metabolism. For example, insulin, a polypeptide hormone released from the pancreas, binds to an insulin receptor on target cells and increases the movement of glucose transport proteins to the cell membrane, thereby increasing the cells’ glucose uptake.

Steroid hormones are derivatives of cholesterol that are soluble in lipids and repelled by water. To be transported in blood, which is largely water, they must be connected to proteins. However, on the cell membranes, steroid hormones do not need to bind to proteins to influence cell function. Rather, steroid hormones pass through cell membranes, and intracellular proteins aid in the hormones’ transport to the nucleus, where they exert their functions. Steroid hormone functions are often related to increasing or decreasing protein synthesis.

Few hormones do just one thing, and often there is a need for hormones to interact with other molecules to function. This is especially true for steroid hormones. Testosterone, for example, stimulates increased protein synthesis, but to do so, it requires the presence of molecules called “somatomedins” (a family of peptide hormones, also called “insulin-like growth factors”) produced in working skeletal muscle. This interdependence enhances muscle hypertrophy from strength training.

How Does Cortisol Function in the Body?

Cortisol is a steroid hormone that has multiple functions, one of which is to increase amino acid supply to the liver, thereby stimulating increased protein catabolism. However, the functions of cortisol are complex, and simple interpretations can be misleading. Like many steroid hormones, cortisol is released in a complex manner throughout the 24-hour daily cycle, with clear alterations in release caused by eating, sleeping and exercise (see “The Release Profile of Cortisol Across a 24-Hour Cycle,” left). Since the bulk of cortisol release and presence in the blood occurs during the sleeping hours, research into the hormone response to exercise is very difficult. The acute response of cortisol may be totally different from the overnight release profile—which could be when cortisol has its most marked impact on the balance between muscle protein synthesis and catabolism.

What Function Does Cortisol Play in Cardio-respiratory Exercise?

During exercise, regardless of whether it is strength or cardiorespiratory training, cortisol is released in proportion to the intensity of the effort. Thus even during strength training, cortisol is released—and in greater quantities than during cardiorespiratory exercise! With increases in exercise intensity, some hormones (e.g., cortisol, glucagon, adrenaline, noradrenaline and growth hormone) increase, and the concentration of other hormones in the blood (e.g., insulin) decreases. To accurately interpret the influence of hormones on body metabolism during and in response to exercise, you need to know how all hormones that influence a given metabolic function are responding. For some hormones, you may need to examine blood samples taken throughout the 24-hour cycle.

During prolonged cardiorespiratory exercise, cortisol clearly functions to preserve body carbohydrate stores. Cortisol increases alternate fuels for muscle, such as fatty acids and amino acids (from muscle amino acid stores and protein catabolism); impairs glucose entry into skeletal muscle; and supplies the fuels (amino acids) for the liver to increase glucose production (see “The Metabolic Actions of Cortisol on Different Tissues” on page 21). All these functions are increased when the body’s carbohydrate store is low, such as when blood glucose falls. Thus, during prolonged cardiorespiratory exercise, the muscle catabolic effects of cortisol can be diminished simply by maintaining blood glucose through the ingestion of carbohydrate. When cardiorespiratory exercise is performed for shorter durations that do not critically lower muscle or liver glycogen (less than 45 minutes), the exercise-induced cortisol release will most likely be irrelevant to muscle protein balance. Also, the theoretical metabolic effects of these increases in cortisol may be overcome by simultaneous increases in growth hormone, testosterone and muscle-specific somatomedins. The net result is the preservation of muscle mass.

Other Explanations for the Interference Phenomenon

What other than cortisol could explain the difficulty of increasing muscle mass during concurrent training? This is the crucial question. The explanations are twofold.

First, cardiorespiratory exercise adds a caloric expenditure to training that needs to be matched with proper fuel intake. If insufficient carbohydrate is being ingested—which may be the case with individuals who eat high-protein, low-carbohydrate diets—the situation is ripe for generating the low-carbohydrate conditions conducive to the action of cortisol as a carbohydrate-sparing, protein-catabolizing hormone. The problem is not the cardiorespiratory exercise, but inadequate carbohydrate nutrition!

The second explanation lies in the counterproductive effects of endurance training on the cell stimuli for muscle strength and hypertrophy. Although scientists do not yet know what these stimuli are, studies have shown that muscle strength (and hypertrophy) gains may be inhibited if strength training occurs too soon after cardiorespiratory exercise (e.g., the same day). However, this has nothing to do with a hormone response mechanism. Rather, researchers believe, the signals sent to working muscle that induce either strength or cardiorespiratory adaptations are diluted when combining the two types of training. The muscle is, in effect, getting mixed messages. On the one hand, during cardiorespiratory exercise, the body tells the muscle to build more protein for increasing mitochondrial mass (increasing the cell’s organelles involved in energy production); but during resistance exercise, the body tells the muscle not to focus on mitochondria, but to increase muscle contractile protein synthesis. No matter what the order of the training, both exercise conditions may have a somewhat lessened training response if care is not taken to properly sequence the exercises over the span of the week, with appropriate work and rest periods for each training regime.

Practical Applications

What are the take-home messages from this information regarding concurrent training and cortisol?

  • A single hormone response in the body should not be interpreted as the cause of a hormone-related effect. Body metabolism is a balanced re-gulation of multiple hormones in response to varying metabolic states.
  • For most exercisers, adding cardiorespiratory training to a workout routine will not appreciably affect muscle strength and/or hypertrophy as long as carbohydrate intake is adequate.
  • Competitive bodybuilders and athletes trying to maximize muscle growth should give careful thought to how much cardiorespiratory exercise they do—and should spread their workouts throughout the week.
  • For the many clients who wish to attain changes in body composition and body weight, cardiorespiratory exercise is an essential component of an exercise program, since it can help these clients reach their goals and at the same time experience the improved health benefits of a balanced fitness status.

20Cortisol (ug/ml)ExerciseControl15105 E M M 004812162024Hours

the metabolic actions of cortisol on different tissues

The following article may be helpful to fitness professionals seeking further information on concurrent training:

Leveritt, M., et al. 1999. Concurrent strength and endurance training: A review. Sports Medicine, 28 (6), 413–27.

Cardiorespiratory exercise adds a caloric expenditure to training that needs to be matched with proper fuel intake.


Docherty, D., & Sporer, B. 2000. A proposed model for examining the interference phenomenon between concurrent aerobic and strength training. Sports Medicine, 30 (6), 385–94.

Griffin, J.E., & Ojeda, S.R. 1988. Textbook of Endocrine Physiology. New York: Oxford University Press.

Robergs, R.A., & Roberts, S.O. 1997. Exercise Physiology: Exercise, Performance and Clinical Applications. St. Louis: Mosby.

IDEA Fitness Journal, Volume 2, Issue 9

© 2005 by IDEA Health & Fitness Inc. All rights reserved. Reproduction without permission is strictly prohibited.

About the Authors

Robert A. Robergs, PhD IDEA Author/Presenter

Robert A. Robergs, PhD, is a professor and the director of the exercise physiology laboratories at the University of New Mexico in Albuquerque. He has authored three textbooks on exercise physiology,...

Len Kravitz, PhD

Len Kravitz, PhD IDEA Author/Presenter

Len Kravitz, PhD, is the program coordinator of exercise science and a researcher at the University of New Mexico in Albuquerque, where he recently won the Outstanding Teacher of the Year award. Len w...