It’s been established that as the intensity of exercise increases, there is a shift in substrate mobilisation and utilisation (Romijn et al., 1993; Achten et al., 2002). Theoretically, plasma FFA and intramuscular triglycerides (IMTG) are the primary substrate
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sources while exercising at a low intensity (25-30% VO2max), while a moderate exercise
intensity (60-75% VO2max) utilises both fats and CHO sources (Romijn et al., 1993; van Loon et al., 2001). Thus, it is commonly thought that prolonged, continuous exercise at low to submaximal intensities results in higher aerobic capacity for fat oxidation (Talanian et al.,
2007).
A number of studies have demonstrated that maximum fat oxidation occurs between exercise intensities of 33-65% VO2max (Jones et al., 1980; Romijn et al., 1993;
Sidossis et al., 1997; Freidlander et al., 1998; Howlett 1998; Thompson 1998; Romijn et al.,
2000; Stisen et al., 2006; van Loon 2001 Venables and Jeukendrup, 2005). The significant variation (33-65% VO2max) may be due to sex, training status, tested protocol and diet
(Achten and Jeukendrup, 2004a). For instance, when employing hand bike cycling, 55% VO2max is when fat oxidation is at its peak, whilst its 75% VO2max for bike cycling (Knechtle et al., 2004). The intensity that elicits maximum fat oxidation also increased from 54%-65% VO2max in trained participants (Nordby et al., 2006). However, a study from 2002 using a
graded exercise test demonstrated the fatmax (maximal fat oxidation)zone and that 64 ± 4%
VO2max is the precise exercise intensity for maximal oxidation of fat (Achten et al., 2002).
2.8.1 Establishing Fatmax zone
Achten et al. (2002) used a graded exercise test to exhaustion to measure fat oxidation over a range of exercise intensities to exhaustion. Maximal fat oxidation occurred at 64 ± 4% VO2max, correlating to 74 ± 3% of maximum heart rate (Achten et al., 2002).
Utilising a similar protocol but with a trained cohort, fatmax was determined to be slightly
lower than the untrained cohort, 62.5 ± 9.8% VO2max, 73% maximum heart rate (Acheten
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maximise fat oxidation was also made clear, 55 ± 3% VO2max to 72 ± 4% VO2max. Exercising at
an intensity above this and fat oxidation begins to decline (Achten et al., 2002). This supported prior results from Romijn et al. (1993) who investigated substrate utilisation at three different intensities, low, moderate and high intensities (25% 65% and 85% of VO2max,
respectively). Participants cycled for 120 mins at intensities of 25% and 65% VO2max and 30
mins at 85% VO2max, finding that highest fat oxidation occurred at 65% VO2max, (see figure
2.8).
Figure 2.8: Substrate (glycogen, IMTG, plasmas FFA and plasma glucose) utilisation at 25%, 65% and 85% of VO2max when exercising continuously for 120 mins (Taken from Romijn et
al., 1993).
2.8.2 Fat oxidation is maximal whilst exercising at 65% VO2max
The percentage of CHO oxidation increases as exercise intensity increases, and total energy expenditure from lipid contribution decreases (Achten and Jeukendrup 2003; Achten
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and Jeukendrup 2004), demonstrated in figure 2.8. Whilst exercising at 85% VO2max,
lipolysis is similar to that of 65% VO2max however oxidation of fatty acids is decreased (see
figure 2.8) as they may be trapped in adipose tissue due to decreased blood flow (Romijn et al., 1993) or oxidation may be inhibited as detailed in section 2.7.2. Fatty acid oxidation is regulated by lipolysis, FFA delivery to muscle, transport across muscle and mitochondrial membranes and fatty (see section 2.2.1.1) and IMTG hydrolysis (Achten and Jeukendrup, 2004), therefore these pathways and mechanisms may be at optimal activity and not inhibited during exercise at 65% VO2max. Figure 2.8 shows the contribution of substrate to
exercise at three different exercise intensities and whilst exercising at 65% VO2max, a
significant portion of energy is produced from IMTG, with similar levels of plasma FFA contributing equally (Romijn et al., 1993). Significant oxidation of fatty acids derived from IMTG was also observed in trained individuals cycling at 60% VO2max (Watt et al., 2002) and
cycling between between 50-70% VO2max using magnetic resonance spectroscopy whilst
cycling (White et al., 2003).
Despite this significant evidence, individuals participating in high intensity physical activity(<80% VO2max) have less subcutaneous fat compared to those who participate in low
to moderate intensity physical activity (Tremblay et al., 1990; Hunter et al., 1998; Benson et al., 2008). More than 20yrs ago, 2623 (1366 women and 1257 men) participated in the 1981 Canada fitness survey and were measured for energy expenditure of leisure time activities, estimated maximal oxygen uptake (VO2max), subcutaneous fat and anthropometric
characteristics (Tremblay et al., 1990). Although using indirect methods, this study reported VO2max was greater in those undertaking moderate to high intensity physical activity when
compared to those not completing this level of physical activity. Participants that were characterised to be a part of the high intensity activity group had a reduced waist to hip
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ratio, most likely due to low waist circumferences. Moreover, women in the moderate to high intensity group and men in the high intensity activity group had lower amounts of subcutaneous fat. This may be unexpected given lower intensities of activity are associated with fat oxidation. Further when the energy cost of the physical activity was removed and not recognised as part of energy expenditure, a significant difference in subcutaneous fat was determined between participants undertaking vigorous activity and those not. Thus this shows that the effect of exercise intensity on body fat is not simply due to the energy cost of the physical activity, but to additional effects on other components of energy balance (Tremblay et al., 1990).
Additionally repeated bouts of high intensity exercise or high intensity intermittent training (HIIT) has been shown to be better than submaximal continuous exercise training (CONT) at inducing fat loss (Tremblay et al., 1994; Trapp et al., 2008; Macpherson et al.,
2011; Gremeaux et al., 2012). The scope of this thesis surrounds the metabolic shifts induced by HIIE which may induce energy loss, potentially contributing to heightening energy expenditure and reducing adiposity.