Substrate utilization during prolonged exercise with ingestion of 13C-glucose in acute hypobaric hypoxia (4,300 m)

Abstract

Energy substrate oxidation was measured using indirect respiratory calorimetry combined with tracer technique in five healthy young male subjects, during a 80-min exercise period on ergocycle with ingestion of 140 g of (13)C-labelled glucose, in normoxia and acute hypobaric hypoxia (445 mmHg or 4,300 m), at the same relative [77% V(.-)((O)(2)(max))] and absolute workload (161+/-8 W, corresponding to 77 and 54% V(.-)((O)(2)(max)) in hypoxia and normoxia). The oxidation rate of exogenous glucose was not significantly different in the three experimental situations: 21.4+/-2.9, 20.2+/-1.2 and 17.2+/-0.6 g over the last 40 min of exercise at approximately 77 and approximately 54% V(.-)((O)(2)(max)) in normoxia and in hypoxia, respectively, providing 12.5+/-1.5, 16.8+/-1.1 and 14.9+/-1.1% of the energy yield, although ingestion of glucose during exercise resulted in a higher plasma glucose concentration in hypoxia than normoxia. The contribution of carbohydrate (CHO) oxidation to the energy yield was significantly higher in hypoxia (92.0+/-2.1%) than in normoxia for both a given absolute (75.3+/-5.2%) and relative workload (78.1+/-1.8%). This greater reliance on CHO oxidation in hypoxia was entirely due to the significantly larger contribution of endogenous glucose oxidation to the energy yield: 75.9+/-1.7% versus 66.6+/-3.3 and 55.2+/-3.7% in normoxia at the same relative and absolute workload.

Successive exposure to moderate hypoxia does not affect glucose metabolism and substrate oxidation in young healthy men

“…Several previous studies have indicated that hypoxia increases carbohydrate oxidation (Brooks et al 1991; Roberts et al 1996a, [b]). Enhanced reliance on plasma glucose oxidation for energy production under hypoxic conditions leads to the promotion of carbohydrate oxidation during rest or exercise (Brooks et al 1992; Peronnet et al 2006). Although the present results do not support this suggestion, previous studies have indicated enhancement of carbohydrate oxidation by hypoxia in elite endurance athletes, with marked differences between endurance athletes and sedentary individuals (Havel et al 1963, 1964; Hurley et al 1986; Bircher and Knechtle 2004).…”

“…Although the present results do not support this suggestion, previous studies have indicated enhancement of carbohydrate oxidation by hypoxia in elite endurance athletes, with marked differences between endurance athletes and sedentary individuals (Havel et al 1963, 1964; Hurley et al 1986; Bircher and Knechtle 2004). Furthermore, most previous studies (Brooks et al 1991, 1992; Roberts et al 1996a, [b]; Peronnet et al 2006) used severe hypoxia (altitude > 4000 m). Therefore, differences in the levels of hypoxia (i.e., altitude) between previous studies and the present study may explain the contradictory outcomes.…”

Acute Normobaric Hypoxia Increases Post-exercise Lipid Oxidation in Healthy Males

“…To maintain perfusion of O 2 during hypoxic exercise, breathing frequency (Bf), minute ventilation ($\dot{\text{V}}$E), and heart rate (HR) are all elevated above similar workloads performed at sea-level (Mazzeo, 2008). However, these physiological adjustments are limited as maximal oxygen uptake ($\dot{\text{V}}$O 2max ) decreases at a rate of approximately 7% for each 1,000-m increase in elevation above sea-level (Fulco et al, 1998; Peronnet et al, 2006; Mazzeo, 2008; Saunders et al, 2009). During constant-load exercise, both the absolute rate of carbohydrate oxidation (CHOox) and its relative contribution to the fuel mixture are elevated in hypoxia compared to normoxia (Wagner et al, 1986; Sutton et al, 1988; Lundby and Van Hall, 2002; Peronnet et al, 2006).…”

“…However, these physiological adjustments are limited as maximal oxygen uptake ($\dot{\text{V}}$O 2max ) decreases at a rate of approximately 7% for each 1,000-m increase in elevation above sea-level (Fulco et al, 1998; Peronnet et al, 2006; Mazzeo, 2008; Saunders et al, 2009). During constant-load exercise, both the absolute rate of carbohydrate oxidation (CHOox) and its relative contribution to the fuel mixture are elevated in hypoxia compared to normoxia (Wagner et al, 1986; Sutton et al, 1988; Lundby and Van Hall, 2002; Peronnet et al, 2006). Such a shift in substrate oxidation helps to maintain energy supply in reduced O 2 environments due to the greater energy yield per liter of O 2 consumed when glucose is completely oxidized compared to fatty acids and amino acids (Hochachka, 1988; Brooks et al, 1991b; Mazzeo, 2008).…”

Sélection des substrats lors de l’exercice prolongé avec ingestion de glucides : études par traçage au 13C

“…Il existe également peu de données systématiques sur l'effet du mode d'administration des glucides exogènes [bolus vs doses (Massicotte et al, 1996a) ; ingestion avant vs pendant l'exercice Caron et al, 2004;Krzentowski et al, 1984a) ; effet de la concentration de la solution ingérée (Jandrain et al, 1989;Jentjens et al, 2004bJentjens et al, , 2006Moodley et al, 1992)] sur leur oxydation. Un certain nombre d'études se sont penchées, par contre, sur l'effet de l'entraînement Jeukendrup et al, 1997;Krzentowski et al, 1984b;Péronnet et al, 2009;van Loon et al, 1999), de l'état nutritionnel (Ravussin et al, 1979), de certains facteurs environnementaux [froid (Galloway et al, 2001), chaud (Jentjens et al, 2006(Jentjens et al, , 2002, hypoxie (Péronnet et al, 2006)] et de certains nutriments ou agents pharmacologiques dont on sait qu'ils interfèrent ou pourraient interférer avec la digestion et l'absorption des glucides et la sélection des substrats [acarbose qui inhibe les glucosidases (Gerard et al, 1986), sodium (Massicotte et al, 1996b) qui pourrait faciliter l'absorption du glucose par le « sodium-glucose transporter 1 » (SLGT1) , métoclopramide qui accélère la vidange gastrique (Massicotte et al, 1996b), acipimox qui bloque la lipolyse (Gautier et al, 1994) ; caféine (Desbrow et al, 2009;Hulston et Jeukendrup, 2008;Yeo et al, 2005)]. …”