Post-exercise, oxygen consumption (VO2) will gradually return toward baseline levels in an exponential manner, demonstrating an initial rapid decrease followed by a slow, longer component. The overall VO2 that is consumed above resting values during this phase is referred to as the excess post-exercise oxygen consumption (or EPOC).
Worldwide, between 1980 and 2013, the proportion of overweight or obese adults increased from 28.8% to 36.9% among men and from 29.8% to 38.0% among women. Moreover, it has been reported that, over the last 50 years in the United States, daily occupation-related energy expenditure has decreased by approximately 140 calories, and this reduction in energy expenditure accounts for a significant portion of the increase in mean U.S. body weights for both women and men.
The number one goal for many individuals in initiating an exercise program is to lose weight. Given both the widespread prevalence of obesity and the fact that a progressive five-decade decrease in energy expenditure underpins the overall increase in mean U.S. body weight, weight loss is a commendable target. Scientific research has established a strong relationship between energy expenditure and multiple health outcomes, including various obesity indices, such as decreased fat mass and lower waist circumference. Traditionally, exercise programs designed to positively modify these obesity indices have focused exclusively on the energy expenditure of exercise itself. The reality is, however, that following exercise cessation, energy expenditure can remain significantly elevated for a prolonged period of time. An increase in post-exercise metabolism (EPOC) can contribute substantially to overall daily energy expenditure. Thus, EPOC may play an important long-term role in the prevention and treatment of obesity.
Archibald V. Hill and Hartley Lupton originally proposed in 1923 that the elevated VO2 post-exercise was an oxygen debt; this interpretation was based on the understanding that there would be an oxygen cost involved with replenishing creatine phosphate and also oxidation of lactate produced from glycolysis (i.e., the oxygen deficit). More recently it has been acknowledged that additional factors beyond those recognized by Hill and Lupton contribute to postexercise VO2. In reality, elevated post-exercise metabolism is a product of widespread disturbance of homeostatis, or the body's ability to maintain internal equilibrium, of which the settlement of the oxygen deficit is only a fractional contribution. Accordingly, in 1984, the term EPOC was coined to better represent the multiple factors that contribute to elevated postexercise metabolism.
The EPOC consists of a rapid phase and slow phase. The physiological mechanisms responsible for the rapid phase of EPOC include:
The slow phase of EPOC lasts considerably longer than the rapid phase of EPOC, and may persist for 12 to 48 hours depending on exercise type, intensity, duration, and environmental factors. The slow phase of EPOC, in particular, has the potential to make a significant impact on overall energy expenditure. The physiological mechanisms responsible for the slow phase of EPOC include:
Overall, it has been demonstrated that the EPOC generates approximately 10% of the total energy expenditure of exercise. Further, an increase in postexercise metabolism of 80–100 calories is generally considered to be a meaningful EPOC. It is important for individuals to appreciate the long-term benefits accrued from modest increases to overall exercise energy expenditure stemming from an elevated EPOC. For example, the cumulative effect of the EPOC over a one-year period may be the equivalent of 3–6 lbs. (1.4–2.7 kg) of adipose tissue.
Research has consistently demonstrated that duration of aerobic exercise has a strong influence on overall EPOC magnitude and duration; this is provided that the necessary threshold intensity has been satisfied. For instance, researchers have shown that in a group of men and women, EPOC increased more than five-fold (from 34 to 180 calories) when exercise time on a cycle ergometer was increased from 30 minutes to 60 minutes at an intensity of 70% VO2max. In a similar manner, another group of researchers found that EPOC was nearly doubled (43 calories vs. 76 calories) in a group of women who performed treadmill walking at 70% VO2max exercise when duration was increased from 20 minutes to 60 minutes. Prolonged exercise will lower muscle glycogen stores. It has been suggested that the post-exercise replenishment of muscle glycogen is one of the mechanisms responsible for the greater EPOC following longer duration exercise.
Research supports resistance training as an effective strategy for augmenting EPOC. The mechanisms responsible for greater EPOC values stemming from resistance training include increased protein turnover and tissue repair. Increased resistance-training volume and intensity are each linked with higher EPOC values; however, many protocols that previously had been studied would likely not be well-tolerated in the nonathletic population. In contrast, circuit-training routines consisting of more modest intensities/volumes coupled with shorter rest intervals appear to be a better alternative for the overweight or obese client. For instance, in a group of men, researchers showed a circuit routine (2 sets, 8 exercises, 20 repetitions, 75% of 20-RM, 20 seconds rest) elicited an EPOC of 50 calories. Additionally, in a group of nonstrength women, circuit training (3 sets, 7 exercises, 50%–55% of 1-RM) stimulated an EPOC equating to 35 calories.
A 2015 study demonstrated that systemic thermal therapy by regular administration of heat through a variety of methodologies (e.g., sauna and hot tub) affords a number of advantages to cardiovascular health. In fact, chronic exposure to heat stress (in the form of sauna bathing) has been associated with a reduced risk of cardiovascular disease and mortality from all causes. Additionally, it has also been reported that heat therapy reduces body weight and adiposity. Moreover, evidence indicates that exercise in conjunction with heat therapy provides cardiovascular health benefits. For instance, it has been demonstrated that three weeks of post-exercise sauna bathing elicits an improvement in cardiorespiratory fitness.
In 2016, researchers investigated the combined effects of exercise training with a sauna suit on exercise metabolism and EPOC. The researchers had 12 men complete four experimental trials: (1) 30 minutes of moderate-intensity exercise (55%–60% HRR) with a sauna suit, (2) 20 minutes of vigorous-intensity exercise (75%–80% HRR) with a sauna suit, (3) 30 minutes of moderate-intensity exercise (55%–60% HRR) without a sauna suit (i.e., control), and (4) 20 minutes of vigorous-intensity exercise (75%–80% HRR) without a sauna suit (i.e., control). The researchers reported a significant increase in post-exercise metabolism, as evidenced by a greater EPOC, when individuals exercised with the sauna suit as compared to the control groups. In the moderate-intensity exercise trial, a ~45% greater EPOC occurred with the sauna suit (70 calories) vs. the control condition (45 calories). Likewise, the vigorousintensity exercise trial group experienced a —20% greater EPOC with the sauna suit (72 calories) vs. the control group (88 calories).
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National Strength and Conditioning Association, 1885 Bob Johnson Dr., Colorado Springs, CO, 80906, (719) 632-6722, (800) 815-6826, Fax: (719) 632-6367, email@example.com, https://www.nsca.com/ .
Lance C. Dalleck, PhD