Energy intake at the buffet meals was reduced in hypoxia compared with normoxia (hypoxia 5291 ± 565 kJ [1265 ± 135 kcal], normoxia 7718 ± 675 kJ [1845 ± 161 kcal]; P = 0.001) but was similar between the control and exercise trials (6516 ± 612 kJ [1557 ± 146 kcal] and 6493 ± 586 kJ [1552 ± 140 kcal] respectively; P = 0.950, Figure 7.3).
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Figure 7.3 Total energy intake at the buffet meal (kJ). Values are means ± SEM, n = 10. *Hypoxic trials significantly different from normoxic trials (P < 0.001).
When expressed as a percentage of overall intake, macronutrient composition at the buffet meal differed between trials with a greater proportion of fat consumed during exercise compared with control (40 ± 2 % versus 38 ± 2 % respectively; P = 0.006) which appeared to be at the expense of protein where the proportion of protein was higher during the control trials compared with exercise (15 ± 1 % versus 13 ± 1 % respectively; P = 0.031). However, hypoxia did not influence macronutrient preference (Table 7.2).
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Table 7.2 Macronutrient intake at the buffet meal expressed as total intake (g) and percentage (%) of total caloric intake
Values are mean ± SEM, n = 10. NB: Mean percentage fat intake significantly higher during exercise versus control trials: 40 ± 2 % versus 38 ± 2 %; P = 0.006. Mean percentage protein intake significantly higher in control versus exercise trials: 15 ± 1 % versus 13 ± 1 %; P = 0.031. There are no significant differences in percentage intake of carbohydrate, fat or protein between hypoxic and normoxic trials.
7.3.4 Plasma acylated ghrelin
Fasting plasma acylated ghrelin concentration did not differ between trials at baseline (P = 0.219). There was a main effect of altitude (P = 0.005), exercise (P = 0.001) and time (P < 0.001) and an exercise x time interaction (P < 0.05) for plasma acylated ghrelin (Figure 7.4). Post hoc tests revealed mean plasma acylated ghrelin concentrations were suppressed in hypoxia compared with normoxia (82 ± 21 pg·mL-1 and 100 ± 22 pg·mL-1 respectively; P = 0.005) and lower during exercise trials than resting trials (86 ± 20 pg·mL-1 versus 97 ± 22 pg·mL-1 respectively; P = 0.001). Acylated ghrelin AUC values (Figure 7.5) were 18 % lower in hypoxia than normoxia (573 ± 153 pg·mL-1·7 h versus700 ± 146 pg·mL-1·7 h
Carbohydrate Fat Protein
Normoxic control g % 215 ± 26 47 ± 2 74 ± 7 37 ± 2 70 ± 5 16 ± 1 Normoxic exercise g % 207 ± 21 45 ± 2 90 ± 12 41 ± 2 66 ± 8 14 ± 1 Hypoxic control g % 151 ± 19 47 ± 2 59 ± 10 39 ± 2 48 ± 7 14 ± 1 Hypoxic exercise g % 144 ± 17 49 ± 2 55 ± 8 39 ± 2 39 ± 5 12 ± 1
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respectively; P < 0.05) and 10 % lower during exercise trials than control trials (602 ± 143 pg·mL-1·7 h versus 671 ± 154 pg·mL-1·7 h respectively; P = 0.001)
Figure 7.4 Plasma acylated ghrelin concentrations during the normoxic control trial (--○--) normoxic exercise trial (--●--), hypoxic control trial (―□―), and hypoxic exercise trial (―■―). Values are means ± SEM, n = 10. Some error bars have been omitted for clarity. Black rectangle indicates treadmill running, thin downward arrow ( ) indicates test meal consumption, bold downward arrow ( ) indicates buffet meal consumption. Repeated measures ANOVA revealed a main effect of altitude (P = 0.005), exercise (P = 0.001) and time (P < 0.001) and an exercise x time interaction (P < 0.05).
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Figure 7.5 Total area under the concentration versus time curve (AUC) for plasma acylated ghrelin. Values are means ± SEM, n = 10. *Hypoxic trials significantly different from normoxic trials (P < 0.05). aMean of exercise trials significantly lower than control trials (P = 0.001).
7.3.5 Peptide YY
Fasting plasma total PYY concentration did not differ at baseline between trials (P = 0.526). There was a main effect of exercise (P = 0.044), time (P < 0.001) and an altitude x time interaction (P = 0.016) for plasma total PYY (Figure 7.6). Post hoc tests showed that mean total PYY concentrations were higher in the exercise trials than the control trials (32.3 ± 3.2 pmol·L-1 versus 29.8 ± 2.7 pmol·L-1,; P = 0.044) and higher in normoxia (32.3 ± 2.8 pmol·L-1) than hypoxia (29.6 ± 3.1 pmol·L-1) although this latter difference did not quite reach significance (P = 0.059).
a
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Figure 7.6 Plasma total PYY concentrations during the normoxic control trial (--○--), normoxic exercise trial (--●--), hypoxic control trial (―□―), and hypoxic exercise trial (―■―). Values are means ± SEM, n = 10. Some error bars have been omitted for clarity. Black rectangle indicates treadmill running, thin downward arrow ( ) indicates test meal consumption, bold downward arrow ( ) indicates buffet meal consumption. Repeated measures ANOVA revealed a main effect of time (P < 0.001), a main effect of exercise (P < 0.05) and an altitude x time interaction (P = 0.016).
7.3.6 Leptin
Incomplete sets of data were obtained for serum leptin concentrations. In the present study fasting leptin concentration at baseline was determined for all participants during the hypoxic control trial. Serum leptin concentrations ranged from 1199 – 6295 pg·mL-1 with a mean of 2899 pg·mL-1. Where leptin concentration could not be determined, samples fell below the lowest standard of 15.6 pg·mL-1 when samples were diluted 100 fold. There was a trend for a positive correlation between fasting leptin concentrations at baseline and BMI (r = 0.607; P = 0.063) (Figure 7.7).
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Figure 7.7 Correlation between BMI and fasting leptin concentrations at baseline in the hypoxic control trial (n = 10).
7.3.7 Glucose and triacylglycerol
Fasting plasma glucose did not differ at baseline between the trials (P = 0.646). There was a main effect of time (P < 0.001), altitude (P = 0.048) and exercise (P = 0.008) for glucose. Plasma glucose was higher during the hypoxic trials (5.1 ± 0.2 mmol·L-1) than the normoxic trials (4.9 ± 0.1 mmol·L-1; P = 0.048). This finding was confirmed by analysis of AUC values for glucose for the entire 7 h trial duration (hypoxia 36.5 ± 1.2 mmol·L-1·7 h, normoxia 34.5 ± 0.6 mmol·L-1·7 h; P = 0.02). Plasma glucose was higher during the exercise trials than the control trials (5.2 ± 0.1 mmol·L-1 versus 4.9 ± 0.1 mmol·L-1 respectively; P = 0.008) and this was confirmed by analysis of AUC values (exercise 36.7 ± 1.0 mmol·L-1·7 h, control 34.4 ± 0.9 mmol·L-1·7 h; P = 0.015). Fasting plasma TAG concentrations were not significantly different between trials (P = 0.154). There was a significant effect of time (P < 0.001) but no other main effects (data not shown).
141 7.3.8 Oxygen saturation and AMS
There was a main effect of time (P < 0.001), altitude (P < 0.001), exercise (P < 0.05) and an altitude x time interaction (P < 0.001) for oxygen saturation. Post-hoc tests indicated oxygen saturation was significantly lower in hypoxia (82 ± 1 %) than normoxia (98 ± 0 %; P < 0.001) confirming the hypoxic nature of these trials. Mean capillary blood oxygen saturation was significantly lower in the exercise trials than the resting trials (89 ± 1 % versus 91 ± 1% respectively; P < 0.05). The decrease in capillary blood oxygen saturation during the hypoxic trials varied widely amongst participants, with the mean individual oxygen saturation across the trial duration ranging from 70 – 88 %. Exposure to hypoxia resulted in increases in Lake Louise Score with the participants reporting varying degrees of AMS. Symptoms across the trial duration ranged from 0 to 6 on the hypoxic control trial and 0 to 7 on the hypoxic exercise trial. On the normoxic control trial symptoms ranged from 0 to 2 and on the normoxic exercise trial symptoms ranged from 0 to 4. Symptoms of headache and AMS were prevalent in 6 out of 10 participants in the hypoxic control trial and 5 out of 10 participants during the hypoxic exercise trial on at least one occasion during the trials.