The effect of elevated excess post exercise oxygen consumption (EPOC) post high intensity exercise

EPOC occurs when VO2 remains above rest levels (Gaesser and Brooks 1984; Bell et al., 1997; Borsheim and Bahr 2003; LaForgia et al., 2006; Matsuo et al., 2012) and is indicative of increased energy utilisation to return the body to homeostasis (LaForgia et al.,

2006). Substrates are utilised during this time and as EPOC is an aerobic process, fat is the principal fuel source (Tremblay et al., 1990; Treuth 1996; Hunter et al., 1998; Balsom 1999; Al mulla et al., 2000; Yoshioka et al., 2001; Hall et al., 2002; Kuo et al., 2005; Benson et al.,

2007; Helge et al., 2007; Malatesta et al., 2009).

There is a defined short phase and a long phase of EPOC, encompassing the different metabolic mechanisms which are replenished, removed or returned to their pre-exercise values. During the short phase there is replenishment of myoglobin with oxygen in blood and muscle, resynthesis of ATP and CP, removal of lactate and increased body temperature, circulation and ventilation (Bell et al., 1997). The prolonged phase, which can last for hours

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(Iwayama and Tokuyama, 2012), is a little less understood and mechanisms more complex. There is glycogen resynthesis, protein breakdown and resynthesis (Borsheim and Bahr, 2003), increased sympathetic activity (Gladden et al., 1982; Gaesser and Brooks, 1984; Hermansen et al., 1984; Maehlum et al., 1986; Bahr et al., 1990; Sagnol et al., 1989; Campos et al., 2012) regulating triglyceride/fatty acid cycling (Yoshioka et al., 2001), this last process accounting for a significant portion of EPOC. The extent of EPOC is greatly attributed to the exercise intensity and duration (Iwayama and Tokyuama 2012).

2.9.2.3.1 The effect of exercise intensity and duration on EPOC

The magnitude and length of EPOC is significantly elevated as exercise duration is prolonged (Knuttgen, 1970; Bahr et al., 1987; Chad and Wenger 1988; Elliot et al., 1988; Sedlock et al., 1989; Gore and Withers 1990; Bahr et al., 1992; Sedlock, 1992; Neary et al.,

1993; Quinn et al., 1994; Sedlock et al., 1994; Imamura et al., 2004), see figure 2.11.Exercising at 70% VO2max for 20, 40 and 80 mins showed progressively increasing EPOC

as duration increased, from 11.1L, 14.7L and 31.9L, respectively (Bahr 1992).

Increasing exercise intensity also elevates EPOC exponentially (Knuttgen, 1962; Knuttgen, 1970; Haigberg et al., 1980; Sedlock et al., 1989; Bahr and Sejersted, 1991; Sedlock 1991; Elliot et al., 1992; Brockman et al., 1993; Dawson et al., 1996; LaForgia et al.,

1997; Phelian et al., 1997), see figure 2.11. A comprehensive study comparing submaximal and high intensities, exercising over 30, 50 and 70% VO2max and for 20, 50 and 80 mins

showed the combination to produce the greatest EPOC was exercising at 70% VO2max for 80

mins. EPOC was 7 hrs in length equating to approximately 297 kJ (Gore and Withers, 1990). It should be noted that one study produced results that contradict this trend, with the lower exercise intensity 50% compared to 70% VO2max, inducing greater EPOC. Reasons behind this

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conflicting result remain unclear and no method of analysis was discussed in the paper (Chad and Quigley 1991). An additional study observed no EPOC 35 mins post exercise after an exercise duration 20 mins at 80% VO2max (Hagberg et al., 1980). Given that intensity plays

a key part in EPOC, it is logical to assume that there would be even further elevations in EPOC after supra-maximal intensity exercise.

Figure 2.11: The effect of exercise intensity and exercise duration on EPOC (Taken from Borsheim and Bahr, 2003)

2.9.2.3.2 The effect of supra-maximal exercise intensity (>100% VO2max) on EPOC

EPOC is significantly elevated after supra-maximal intensity exercise compared to high intensity exercise (Bahr et al., 1992; Nummela and Rusko 1995), exercise intensities 105% VO2max and 70% VO2max respectively. There was a two-fold increase in EPOC with

magnitude of supramaximal intensity exercise 15L compared to 6.9L after high intensity exercise (Bahr et al., 1992).

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In treadmill sprinting and cycling, HIIE bouts significantly increased the magnitude of EPOC compared to CON exercise bouts (Devlin and Horton, 1985; Maehlum et al., 1986; Kaminsky et al., 1990; Brockman et al., 1993; Almuzaini et al., 1998; Scott; 1999; Tomlin and Wenger 2001; Lyons et al., 2005) although not all magnitudes and durations are significant enough to produce substantial changes to weight (LaForgia et al., 2006).

2.9.2.3.3 Limitations to EPOC

Measurements of EPOC can be limited by the practicality and accuracy of gas collection and measurement in experimental exercise trials. False VO2 measurements can

be obtained in the rest period prior to exercise due to increased sympathetic nervous stimulation caused by exercise anticipation (Borsheim and Bahr, 2003). Furthermore, the collection mask or mouth piece can be uncomfortable for participants. A canopy or hood may be a better method however the paramount method of collection is placing participants in a calorimetry chamber where they are not hooked up to any apparatus and permits hours of un-impinged measurement (Iwayama and Tokuyama 2012).

EPOC associated with high intensities only induce approximately 14-15% of the net total oxygen cost of the exercise (LaForgia et al., 2006). Daily accumulations of such small imbalances can contribute to inducing negative energy balance over time, but only contributes minimally (Scott, 2006). Over a twelve month period exercising at three days a week, the accumulated difference in energy balance may shift negative and may equate to a net loss of 1.5 kg of adipose tissue per year (LaForgia et al., 2006). Whereas, after 15 weeks of HIIT, Trapp et al. (2008), showed approximately a loss of 3 kg of fat mass (Trapp et al.,

2008). Since EPOC is probably only a minor contribution to overall increase energy expenditure post HIIE, another metabolic mechanism that is measured post exercise and

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may contribute to elevating energy expenditure is the ATP loss associated with purine base loss.

2.9.2.4 Increasing energy loss via purine nucleotide excretion post high