ONDAS TROPOSFÉRICAS

Exercise metabolism between the genders varies significantly, specifically fibre type distribution, substrate utilisation and post exercise recovery mechanisms. A study employing three 30s all out sprints with 20 mins rest separating the sprints, showed an increased rate of recovery in females compared to males (Esbjornsson-Liljedahl et al., 2002). This was demonstrated by a decrease in high energy phosphates and accumulation of metabolic by products of ATP degradation in women compared to males (Esbjornsson-

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Liljedahl et al., 2002). Post exercise plasma concentrations of inosine, Hx, xanthine and uric acid increased, but the magnitude of accumulation was significantly lower in females compared to males. Furthermore, there were smaller exercise induced reductions of ATP, AMP, inosine and hypoxanthine in women compared to men in type II muscle fibres. The lower concentrations of inosine in females compared to male are reflective of faster reamination of IMP to ATP during the recovery periods between sprints and this may be due females containing smaller muscle mass and cross sectional area of muscle fibres; shorter diffusion distances may facilitate an easier recovery of IMP to ATP (Esbjornsson-Liljedahl et al., 2002). The implication of this study may be that females exhibit a reduced potential for purine loss via urinary excretion. Therefore excretion after two HIIE models will be investigated to see if a certain protocol will induce changes more suited to energy loss with female results are compared to the male counterparts.

Differences in lipid metabolism between males and females is contentious with a number of studies stating females derive a greater proportion of energy from lipid than men (Tarnopolsky et al., 1990; Phillips et al., 1993; Friedlander et al., 1998; Horton et al., 1998; Friedlander et al., 1999; Romijn et al., 2000; Blaak, 2001; Carter et al., 2001; Kanaley et al.,

2001; Henderson et al., 2007; Kang et al., 2007) whilst others contradict this and have demonstrated that females do not induce greater lipolysis (Burguera et al., 2000; Mittendorfer et al., 2002; Steffenson et al., 2002; Roepstorff et al., 2002; Riddell et al.,

2003). These discrepancies are most likely due to the differences in testing procedures such as analytical techniques as well as uncontrolled trial days where hormone levels are not accounted for. Oestrogen promotes lipolysis and elevates FFA availability as well as decreasing gluconeogenesis, sparing muscle and liver glycogen stores (Braun and Horton,

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2001; D’eon et al., 2002). Increased fat oxidation may transpire due to the oestrogenic effects on CPT1 which is up-regulated by oestrogen, increasing FFA uptake into the mitochondria for oxidation (D’eon et al., 2002) and citrate synthase, an enzyme involved in Krebs Cycle (Roepstorff et al., 2005). Hence providing physiological evidence that fat mobilisation and oxidation is greater in women (Henderson et al., 2007), yet conflicting evidence pertaining to IMTG utilisation remains (Mittendorfer et al., 2002; Roepstorff et al.,

2006).

Males on the other hand may derive usable fat from other sources such as IMTG (Mittendorfer et al., 2002) and have a greater total use of glycogen compared to females (Tarnopolsky et al. 1990; Esbjornsson-Liljedahl et al., 2002) and greater lactate production (Esbjornsson-Liljedahl et al., 2002) which may be due to skeletal muscle fibre type distribution. Females contain a higher percentage of type fibres 1 muscle fibres, hence more mitochondria thus opportunity for fat oxidation. This thesis will observe any differences between female and males in regards to the reliance on fat which has been shown with HIIE. A greater proportion of type I muscle fibres, implies females have lower amounts of type II glycolytic fibres hence lower glycolytic capacity compared to males. This is reflected in performance during repeat sprints when females show lower power outputs and fatigue at a faster rate. Interestingly the recovery between sprints is similar to that of males, accompanying faster resynthesis of ATP, and no differences between males and females in resting ATP and CP content (Esbjornsson-Liljedahl et al., 2002; Billaut et al., 2003).

The effects of hormonal elicit considerable differences between the genders, for instance catecholamine’s which stimulate lipolysis. Conflicting evidence exists pertaining to adrenaline and noradrenaline as increased adrenaline has been observed in men compared

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to women (Esbjornsson-Liljedahl et al., 2002; Roepstorff et al., 2006; Moro et al., 2007) while similar catecholamine responses in men and women were shown in another study (Mittendorfer et al., 2002).

The increased fat oxidation observed in females may be due to an increased

sensitivity to β-adrenergic stimulation in adipose tissue resulting in an increased FFA availability, possibly exacerbated as females contain greater adipose tissue depots. As mentioned earlier, exercise induced glycogen depletion is also smaller in women than men in type I muscle fibres which may also be partially due to β-adrenergic induced cAMP activation. Type I muscle fibres may have a greater adrenergic response as there is a greater abundance of receptors, three-fold difference between type II and type I muscle fibres (Esbjornsson-Liljedahl et al., 2002).

Irrespective of a greater fat oxidation capacity, women are not as successful at attaining decreases in adiposity in response to exercise training intervention (Ballot and Kersey 1991; Donnelly and Smith 2005, Henderson et al., 2007). It is possible that this may be due to post exercise differences in metabolism between the genders (Henderson et al.,

2007). As mentioned earlier, females ability to reaminate IMP to ATP more effectively than males will lead to a lower requirement of de novo synthesis of ATP (see section 2.3.5), hence energy expenditure will be significantly lower in females compared to males (Blaak, 2001; Roepstorff et al., 2006). This, along with ascertaining differences between substrate utilisation is a focus of this thesis.

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