Substrate oxidation and the influence of breakfast in normobaric hypoxia and normoxia

European Journal of Applied Physiology https://doi.org/10.1007/s00421-019-04179-6 ORIGINAL ARTICLE Substrate oxidation and the influence of breakfast in normobaric hypoxia and normoxia Alex Griffiths1 · Kevin Deighton1 · Oliver M. Shannon1,2 · Jamie Matu1 · Roderick King1 · John P. O’Hara1 Received: 2 April 2019 / Accepted: 17 June 2019 © The Author(s) 2019 Abstract Purpose Previous research has reported inconsistent effects of hypoxia on substrate oxidation, which may be due to differences in methodological design, such as pre-exercise nutritional status and exercise intensity. This study investigated the effect of breakfast consumption on substrate oxidation at varying exercise intensities in normobaric hypoxia compared with normoxia. Methods Twelve participants rested and exercised once after breakfast consumption and once after omission in normobaric hypoxia (4300 m: F iO2 ~ 11.7%) and normoxia. Exercise consisted of walking for 20 min at 40%, 50% and 60% of altitudespecific V̇ O2max at 10–15% gradient with a 10 kg backpack. Indirect calorimetry was used to calculate carbohydrate and fat oxidation. Results The relative contribution of carbohydrate oxidation to energy expenditure was significantly reduced in hypoxia compared with normoxia during exercise after breakfast omission at 40% (22.4 ± 17.5% vs. 38.5 ± 15.5%, p = 0.03) and 60% V̇ O2max (35.4 ± 12.4 vs. 50.1 ± 17.6%, p = 0.03), with a trend observed at 50% V̇ O2max (23.6 ± 17.9% vs. 38.1 ± 17.0%, p = 0.07). The relative contribution of carbohydrate oxidation to energy expenditure was not significantly different in hypoxia compared with normoxia during exercise after breakfast consumption at 40% (42.4 ± 15.7% vs. 48.5 ± 13.3%, p = 0.99), 50% (43.1 ± 11.7% vs. 47.1 ± 14.0%, p = 0.99) and 60% V̇ O2max (54.6 ± 17.8% vs. 55.1 ± 15.0%, p = 0.99). Conclusions Relative carbohydrate oxidation was significantly reduced in hypoxia compared with normoxia during exercise after breakfast omission but not during exercise after breakfast consumption. This response remained consistent with increasing exercise intensities. These findings may explain some of the disparity in the literature. Keywords Carbohydrate · Fat · Utilisation · Fasted · Fed · Altitude Abbreviations AUC Area under the curve FFA Free fatty acids FiO2 Fraction of inspired oxygen HIF-1α Hypoxia inducible factor 1 alpha PiO2 Partial pressure of inspired oxygen PPARα Peroxisome proliferator-activated receptor alpha RPE Rating of perceived exertion SD Standard deviation SE Standard error V̇ CO2 Carbon dioxide production Communicated by Susan Hopkins. * Alex Griffiths John P. O’Hara Kevin Deighton 1 Oliver M. Shannon Research Institute for Sport, Physical Activity and Leisure, Leeds Beckett University, Leeds LS6 3QS, UK 2 Human Nutrition Research Centre, Institute of Cellular Medicine, Newcastle University, Leech Building, Framlington Place, Newcastle Upon Tyne NE2 4HH, UK Jamie Matu Roderick King 13 Vol.:(0123456789) European Journal of Applied Physiology V̇ O2 Oxygen uptake V̇ O2max Maximal oxygen update Introduction Disparate metabolic responses have been observed during exercise matched for relative intensities in hypoxia compared with normoxia (Young et al. 1982; Braun et al. 2000; Beidleman et al. 2002; Lundby and Van Hall 2002; Friedmann et al. 2004; Péronnet et al. 2006; Katayama et al. 2010; Morishima et al. 2014; O’Hara et al. 2017; Matu et al. 2017). These contrasting findings within the literature appear to be due to differences in experimental design, specifically pre-exercise nutritional status and exercise intensity (Griffiths et al. 2019). Whilst the effect of pre-exercise breakfast consumption (Edinburgh et al. 2018) and exercise intensity (Van Loon et al. 2001) on metabolism are well documented in normoxic conditions, the metabolic response to these factors is yet to be quantified in hypoxia. In addition, due to the inconsistent use of pre-exercise breakfast consumption in the literature, a direct comparison of the two distinct states during exercise of varying intensities in normoxia and hypoxia may provide clarity on such equivocal findings. Further, whilst the use of studies utilising fasted participants to control for baseline metabolic status is warranted, knowledge of how this differs to fed participants is necessary to generate practical recommendations for relevant populations. It has been proposed that during exercise matched for relative intensities, the relative contribution of carbohydrate oxidation to energy expenditure is higher in hypoxia compared with normoxia when performed after breakfast consumption, but lower in hypoxia than normoxia when exercise was performed after breakfast omission (Griffiths et al. 2019). A potential explanation of findings observed after breakfast consumption is that greater oxidation and mobilisation of endogenous carbohydrate stores may be stimulated via the combined effect of hypoxia (Katayama et al. 2010) and feeding (Tentolouris et al. 2003) on the sympathetic nervous system. Additionally, a similar effect of hypoxia (Matu et al. 2018) and feeding (Blom et al. 2005) may increase circulating insulin concentration and subsequently inhibit lipolysis and free fatty acid (FFA) mobilisation (Coyle et al. 1997). It also seems plausible that greater fat oxidation may be observed in hypoxia, compared with normoxia after breakfast omission. Increased expression of the transcription factor hypoxia inducible factor 1 alpha (HIF-1α) may upregulate the fatty acid-activated transcription factor peroxisome proliferator-activated receptor alpha (PPARα) as per the metabolic response to hypoxia (Aragones et al. 2008). This response may be further stimulated by the fasted state (König et al. 1999), subsequently 13 inhibiting pyruvate dehydrogenase activity (Huang et al. 2002) and enabling greater mobilisation and oxidation of fat stores (Spriet and Watt 2003). Exercise intensity was also identified as a significant moderator of substrate oxidation during exercise matched to relative intensities in hypoxia (Griffiths et al. 2019). Specifically, the relative contribution of carbohydrate oxidation to energy expenditure was higher in hypoxia compared with normoxia during exercise performed at higher intensities. This was attributed to the hypoxic effect of both altitude and high intensity exercise, augmenting skeletal muscle hypoxia. The subsequent change in substrate oxidation could, therefore, be explained as per the normoxic response to increased exercise intensity (i.e., reduction in adipose tissue blood flow and lipolysis and/or downregulation of carnitine palmitoyltransferase-1) (Sahlin 1990; Romijn et al. 1993; Van Loon et al. 2001). Alternatively, sympathetic nervous system activity may be potentiated by hypoxia and greater exercise intensities, augmenting glycogenolysis and, therefore, carbohydrate oxidation (Watt et al. 2001). An investigation into the effects of pre-ex (...truncated)