Fat utilisation during and post RSA and CCT exercise

It is unlikely that fat metabolism contributed significantly to energy supply during the CCT or RSA exercise trials or during the rest periods between sprints of the RSA trial. During exercise, there was an increase in plasma glycerol from rest (p<0.05) though no differences were detected between RSA and CCT trials (see figure 4.5; p<0.05). Elevated plasma glycerol is reflective of lipolysis; release of FFA for utilisation (McCartney et al., 1987; Coggan et al.,

2007; Trapp et al., 2007). However plasma FFA concentration significantly decreased from rest in both RSA and CCT trials (see figure 4.4; p<0.05). Collectively these results suggest that fat was not oxidised during either RSA or CCT exercise or during the RSA rest periods separating the five 6 s sprints. This is not consistent with fat utilisation associated with HIIE as per section 2.9.2.1 which due to the work and rest nature, the RSA exercise may have been expected to follow. It has been proposed that accelerated decreases in adiposity associated with HIIE are due to fat utilisation during this mode of exercise with heightened

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fat oxidation attributed to the work and rest nature of HIIE, particularly the rest periods between high intensity sprints (Tremblay et al., 1994). Perhaps the 24 s rest periods in the RSA exercise were too short a time for fat to be broken down and for FFA to be taken up by the mitochondria, and a longer duration of rest is needed for this to occur. It could be speculated that as plasma FFA concentration decreased below rest while plasma glycerol simultaneously increased, that FFA were utilised by the exercising skeletal muscle. Little research exists regarding lipid metabolism during all out, maximal effort exercise, however a study that employed isotopic palmitate tracers compared fat metabolism over three different exercise intensities; low (25% VO2max), moderate (65% VO2max) and high (85%

VO2max) and found significantly elevated plasma glycerol from rest during exercise, yet

depressed plasma FFA concentration, proposing fat oxidation is lowest during higher intensity exercise (Romijin et al., 1993). Furthermore, previous research suggests that elevated plasma glycerol concentrations are indicative of IMTG contribution to energy supplies of repeated wingate exercise (Greer et al., 1998) which is 30 s of maximal all out cycling, separated by a 4 min rest period. For that reason, while FFA may not have contributed to energy production during the RSA and CCT trials, IMTG may have been utilised as energy source.

FFA utilisation may have also declined during high intensity exercise due to significant muscle lactate production and subsequent increased H+ ion release, as per section 2.7.2. Upon exercise cessation, plasma lactate was significantly elevated from rest in both trials, peaking at approximately 14-15mmol/L at the end of the RSA and CCT bouts (p<0.05; see figure 4.6). FFA uptake into the mitochondria may be decreased due to CPT1 inhibition caused by a shift in pH, induced by lactate production, a validated metabolic

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response section 2.7.2. Although this study did not measure blood pH, a study employing males and similar RSA exercise demonstrated that blood lactate peaking at 9mmol/L caused muscle pH of 6.89 (Bishop et al., 2004); whereas in another study after exhaustive exercise muscle pH was 6.69 (Juel et al., 2003). If 9-10mmol/L equates to a muscle pH of 6.69-6.89, it may be assumed that 15mmol/L will correlate to a much lower muscle pH, hence inhibition of CPT1 may be the reason limiting fat utilisation in this study. These results and supportive evidence suggest that fat utilisation may have been depressed during exercise and not utilised.

Although lipid was not utilised during short duration, maximal effort all out exercise, a number of earlier studies suggests fat sources may be oxidised in the recovery periods once the high intensity sprint has ceased (Tremblay et al., 1990; Treuth et al., 1996; Hunter

et al., 1998; Balsom 1999; Al mulla et al., 2000; Yoshioka et al., 2001; van Hall et al., 2002; Benson et al., 2007; Helge et al., 2007) and in the EPOC period (Lyons, 2006). EPOC uses oxidative processes, characterised by elevated VO2 above rest, to replenish and restore

exercise-induced metabolic alterations, the primary substrate utilised being fat. Figure 4.1 shows a significant increase from rest in VO2 at the end of exercise (p<0.05), remaining

elevated until 10 min post exercise (p<0.05), yet no difference exists between RSA and CCT bouts. EPOC can last for several hours post vigorous exercise, established in section 2.9.2.3.4 and this duration was not a feasible measure for the current study. Additionally, due to short duration of gas exchange collection at rest in the current study, approximately 10 mins, the VO2 collected at rest may be falsely high, due to anticipation induced prior to

exercise (Borsheim and Bahr, 2003). As such EPOC may have extended further into the recovery period than is illustrated in figure 4.1.

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Nonetheless, after CCT and RSA exercise bouts, lipolysis may have increased as there was a progressive elevation in plasma glycerol concentrations until 30 mins of recovery. Upon termination of exercise, plasma FFA concentrations returned to rest, remaining consistent till the end of the 60 min recovery phase. During rest, a mixture of fat and CHO are oxidised with FFA dominant, and it is likely that fat oxidation increased post exercise as RER results were closer to 0.7 (see figure 4.2), reflective of lipid as the predominant utilised substrate. In all out exercise, RER is not entirely reflective of fat and CHO metabolism due to the influence of elevated H+ _{production (Bergman and Brooks, 1999) and the buffering by}

bicarbonate producing CO2 influencing the RER equation as per section 2.3.3.4 (Bergman

and Brooks, 1999). Nonetheless, RER supports plasma evidence of increased fat oxidation in the recovery period post exercise. Thus although not used to any great extent during high intensity exercise fat may be utilised post exercise, potentially contributing to decreasing adiposity associated with vigorous exercise.