These values should be regarded as estimates because they are calculated indirectly from tracer and whole-body indirect calorimetry measurements.
Recovery of 13CO2 from oxidation will approach 100% after 60 min of exercise when the dilution in the bicarbonate pool becomes negligible (21,25). Furthermore, steady-state values for plasma glucose enrichment for all trials were only attained during 90-120 min of exercise. Therefore, to enable comparison between all trials, whole-body substrate oxidation and the oxidation of the respective CHO sources were averaged for the last 30 min of exercise.
All data are expressed as mean ± standard error of the mean (mean ± SE). One-way analysis of variance (ANOVA) for repeated measures was performed to study differences in exercise intensity (average over complete exercise bout) and substrate oxidation rates (average over the final 30 min) between trials. Significant effects were followed by pairwise comparisons using the false discovery rate procedure (9). Two-way ANOVA for repeated measures was performed to study differences over time between the trials for plasma metabolites and glucose enrichments. In this case, a Tukey post hoc test was applied where a significant interaction was detected. Analyses were adjusted using the Greenhouse-Geisser correction where necessary. For all statistical analyses, significance was accepted at P < 0.05.
Workload and exercise intensities.
The workload of 45% Wmax (129 ± 3 W) employed during the 2-h trials elicited at an average absolute V˙O2 of 1.96 ± 0.05, 1.96 ± 0.05, 1.92 ± 0.04, and 1.93 ± 0.05 L·min−1 for WAT, LOW, MOD, and HIGH respectively. Accordingly, the average relative exercise intensity and energy expended during exercise was similar between trials (59-60% V˙O2max and 40-41 kJ·min−1, respectively). Average heart rate during the 2-h exercise bouts were similar between WAT, LOW, and MOD (132 ± 5, 133 ± 5, and 133 ± 5 respectively) but was approximately 6 bpm higher during HIGH (139 ± 5, P < 0.05 vs other three trials). Average RPE (from 6 to 20) was 12 ± 0 for all trials.
RER, CHO, and fat oxidation.
As shown in Table 1, RER and CHO oxidation were lower and fat oxidation was higher when water was ingested compared with when CHO was ingested during exercise (main effect of trial, P < 0.05). Furthermore, RER and CHO oxidation was lower and fat oxidation was higher (P < 0.05) in LOW and MOD compared with HIGH; LOW and MOD did not differ significantly in these variables (Table 1). Compared with the first 30 min of exercise, total CHO oxidation had declined by 13 ± 4% by the last 30 min of exercise in the WAT trial (P < 0.05) but was not reduced significantly over time when CHO was ingested.
The relative contribution of substrates to energy is depicted in Figure 1. Total CHO oxidation contributed 42 ± 3, 48 ± 4, 51 ± 5, and 59 ± 4% for WAT, LOW, MOD, and HIGH, respectively. Compared with WAT, relative CHO oxidation was significantly higher when CHO was ingested during exercise (main effect of trial, P < 0.05). Relative CHO oxidation did not differ between LOW and MOD but was significantly higher in HIGH (P < 0.05 vs LOW and MOD) Conversely, fat contributed 58 ± 3, 52 ± 4, 49 ± 5, and 41 ± 4% for WAT, LOW, MOD, and HIGH, respectively.
Exogenous CHO and plasma glucose oxidation.
The average exogenous CHO oxidation over the last 30 min of exercise was significantly lower in LOW than MOD and HIGH, but no difference was observed between MOD and HIGH (Table 1). Peak oxidation rates achieved at the final collection point were 0.33 ± 0.02, 0.50 ± 0.03, and 0.48 ± 0.05 g·min−1 for LOW, MOD, and HIGH, respectively (P < 0.05 LOW vs MOD and HIGH). Exogenous CHO oxidation contributed significantly less to energy expenditure in LOW (13 ± 1%, P < 0.05 vs MOD and HIGH) compared with MOD and HIGH (19 ± 2 and 18 ± 2%, respectively) (Fig. 1).
As shown in Table 1, plasma glucose oxidation was significantly lower in the WAT trial compared with the CHO trials (main effect of trial, P < 0.05). Furthermore, plasma glucose oxidation was significantly lower in the LOW trial compared with MOD and HIGH (P < 0.05) but was similar in MOD and HIGH. This pattern held when plasma glucose oxidation was expressed as a function of total energy expenditure, contributing 16 ± 1, 24 ± 2, 30 ± 2, and 30 ± 2% in WAT, LOW, MOD, and HIGH, respectively.
Endogenous CHO oxidation.
Total endogenous CHO oxidation and the oxidation of the respective endogenous CHO sources during the last 30 min of exercise are shown in Table 1. Compared with WAT, endogenous CHO oxidation was significantly lower in LOW and MOD (P < 0.05) but not compared with HIGH. Endogenous CHO oxidation was lowest in MOD (P < 0.05 vs all other trials). Liver-derived glucose oxidation expressed as grams per minute (Table 1) or relative to energy expenditure (Fig. 1) was higher when WAT was ingested during exercise compared with CHO (main effect of trial, P < 0.05) but was not different between the CHO trials. Estimated muscle glycogen oxidation was not statistically different between trials when expressed as oxidation rates (Table 1) or as a relative contribution to energy expenditure (25 ± 4, 23 ± 3, 18 ± 3, and 27 ± 5% in WAT, LOW, MOD, and HIGH, respectively, Fig. 1). However, compared with the WAT trial, average muscle glycogen oxidation was 0.16 g·min−1 (~28%) lower in MOD. Furthermore, muscle glycogen use was significantly lower in MOD compared with HIGH (P < 0.05, Table 1).
Plasma metabolites and insulin.
Plasma glucose concentrations remained stable (between 4.0 and 4.3 mM) when water was ingested during the exercise period (Fig. 2A). In the WAT trial, glucose concentrations were significantly lower (P < 0.05) than those in the CHO trials from 15 min onwards. Also, glucose concentrations were significantly lower in LOW compared with MOD and HIGH toward the end of exercise (105- to 120-min period, P < 0.05) but not significantly different between MOD and HIGH. Plasma lactate concentrations increased significantly above resting values in all trials after 15 min of exercise (main effect of time, P < 0.05) and remained elevated for the duration of the exercise period (Fig. 2B). Plasma free fatty acid concentrations increased over time in the WAT, and this was statistically significant (from resting values) from 75 to 120 min (Fig. 2C). When CHO was ingested, plasma free fatty acid concentrations did not change significantly from resting values and were lower than those observed in WAT from approximately 30 to 45 min onwards (P < 0.05) but were not different between specific CHO trials.
Plasma insulin concentrations did not change significantly from baseline values over time in the WAT trial (Fig. 2D). Compared with WAT, the ingestion of CHO increased plasma insulin concentrations during exercise with significant differences observed with MOD and HIGH (P < 0.05, between 30-60 min and 30-90 min for MOD and HIGH, respectively, vs WAT). The total insulin area under the curve was 307 ± 39, 477 ± 69, 712 ± 100, and 774 ± 79 mU·mL−1 for WAT, LOW, MOD, and HIGH, respectively. This was lower when WAT was ingested compared with CHO (P < 0.05, WAT vs CHO) and also when LOW was ingested compared with MOD and HIGH (P < 0.05) but did not differ statistically between MOD and HIGH.
GI and related complaints are displayed in Table 2. These data will be discussed as descriptive data only; because of insufficient sample size, it is not possible to perform nonparametric statistical procedures on these nominal data. Participants reported fewer nonsevere GI complaints during WAT and LOW (12 and 10, respectively) compared with MOD and HIGH (23 and 22, respectively). In addition, participants reported more occurrences of severe GI complaints during HIGH (8) compared with the other three trials (~1-2).
In this study, the influence of the rate of CHO ingestion (0.5, 1.0, and 1.5 g·min−1) on carbohydrate use during exercise in endurance-trained women was investigated. The findings from this study demonstrate that 1) the highest rates of exogenous CHO oxidation were attained when the women ingested CHO at rates of 1.0 g·min−1 or above; 2) CHO ingestion during exercise reduced estimated liver-derived glucose oxidation; 3) endogenous CHO oxidation was lowest when CHO was ingested at 1.0 g·min−1, possibly as a result of muscle glycogen sparing; and 4) estimated muscle glycogen oxidation was significantly higher when CHO was ingested at 1.5 g·min−1 compared with 1.0 g·min−1. These findings are discussed sequentially.
Although well studied in investigations using only male participants (13), this is the first study to examine dose-response relationships between CHO intake and exogenous CHO oxidation during exercise in trained women. Increasing the CHO-ingestion rate from 0.5 to 1.0 g·min−1 (LOW and MOD respectively) increased exogenous CHO oxidation by approximately 42% (Table 1). However, exogenous CHO oxidation did not further increase when larger amounts of CHO (1.5 g·min−1, HIGH) were ingested during exercise. Additionally, the peak exogenous CHO oxidation rates observed in the present study (~0.5 g·min−1) are consistent with previous studies that have measured exogenous CHO oxidation during exercise in women (0.5-0.7 g·min−1) (18,24,29). These data complement the results from a similar previous study in trained men (28) and support previous conclusions that oxidation rates from ingested CHO during exercise do not increase once ingestion rates of 1.0-1.2 g·min−1 have been reached (13).
Although the peak oxidation rates observed for the women in the present study do seem to be slightly lower than the highest rates observed in studies performed on men (0.5 vs up to 1.1 g·min−1) (13), it is unlikely that this represents a true sex-related difference in peak exogenous CHO oxidation. In support of this, we recently reported similar peak oxidation rates (~0.7 g·min−1) in a well-matched group of men and women when 1.5 g·min−1 (HIGH) was ingested during prolonged cycling at approximately 67% V˙O2max (29). Rather, in the present study, the relatively low absolute workload (and thus the total requirement for CHO oxidation) may explain the lower oxidation rates observed (19).
Of note, the similar peak oxidation rates observed in MOD and HIGH were markedly lower than the rate of CHO ingestion (30-50% of the ingestion rate). This has been reported previously (28) and leads us to question both the fate of the nonoxidized ingested CHO and the limitation to the use of large amounts of ingested CHO as a source of blood glucose oxidation during exercise. Although it has not been directly determined, most evidence suggests that the limitation lies at the level of intestinal CHO absorption and/or CHO release from the splanchnic region (13). Glucose kinetics (rate of appearance of glucose from the gut and the liver) could not be determined from the methods used in the present study, and therefore, firm conclusions on this issue cannot be made. However, from the large number of gastrointestinal complaints reported in MOD (mainly nonsevere symptoms) and HIGH (nonsevere and severe symptoms) trials compared with LOW and WAT (Table 2), it could be speculated that a significant portion of the nonoxidized CHO is retained/accumulating in the gastrointestinal tract with the remainder directed towards other endogenous pools (such as the liver), as previously suggested (13,28).
CHO ingestion in the present study resulted in an approximately 30% reduction in estimated liver-derived glucose oxidation compared with when water was ingested (Table 1), indicating a sparing of this endogenous CHO source. A reduction in endogenous glucose production and/or oxidation has been reported in previous studies in men (3,16,20) and women (4,29) when CHO was fed during exercise. In men, it has been demonstrated that ingestion of small amounts of CHO during low-intensity exercise (35 g·h−1) can partially reduce hepatic glucose production (~65% reduction), whereas large amounts of CHO (175 g·h−1) can completely suppress hepatic glucose production (16). In contrast, the provision of small (30 g·h−1), moderate (60 g·h−1), or high (90 g·h−1) CHO doses in the present study exerted similar reductions in liver-derived glucose oxidation (Table 1). The present data are, however, not dissimilar (although slightly lower) to previous studies reporting that ingestion of CHO at moderate to large doses (50-100 g·h−1) reduced hepatic glucose production during moderate- to high-intensity exercise by 50-70% (3,4,20).
In the present study, the lowest rates of endogenous CHO oxidation were observed in MOD (Table 1). In addition to reduced liver-derived glucose oxidation with CHO feeding, compared with WAT, muscle glycogen use was approximately 28% lower in MOD (not statistically significant). Interestingly, this dose (~1 g·min−1) has previously been reported to spare muscle glycogen during exercise in trained women (4). However, CHO ingestion in general (6) or at a range of doses (14,16) does not affect muscle glycogen use during constant-load cycling exercise in men, suggesting that this response may be specific to women. The reason(s) for this apparent sparing of glycogen at this ingestion rate for the women studied presently cannot be determined from the present data. However, it could be that in these women, the elevated glucose and insulin concentrations in MOD, compared with WAT increased muscle glucose uptake to a magnitude sufficient to reduce muscle glycogenolysis. Such a mechanism has been proposed to explain the observation that CHO ingestion attenuates muscle glycogen use during constant-intensity running exercise (27). Verification of these observations with direct measurement of glycogen use in skeletal muscle could be of considerable practical importance for prescribing optimal CHO feeding strategies for women endurance athletes.
Interestingly, endogenous CHO and estimated muscle glycogen oxidation were not different between WAT and HIGH (Table 1). The latter confirms our previous report demonstrating that CHO ingestion at 90 g·h−1 does not affect muscle glycogen use in trained females (29). Therefore, unlike in MOD, the elevated glucose and insulin response in HIGH did not seem sufficient to attenuate estimated muscle glycogen use, and, in fact, glycogen use was significantly increased relative to MOD. The discrepancies between the observed muscle glycogen use in MOD and HIGH cannot be readily explained. However, heart rate was elevated in HIGH (by approximately 6 bpm), which may reflect a greater sympathetic nervous system response. Although catecholamine concentrations were not determined, an increased catecholamine response associated with increased sympathetic drive could explain the augmented muscle glycogenolysis (30). It might be speculated that the high incidence of severe gastrointestinal distress reported by participants in the HIGH trial (Table 2) contributed to the higher overall physiological stress in this condition. Alternatively, a reduction in the use of fat as a substrate in HIGH (Table 1) may actually have resulted in a compensatory augmentation of muscle glycogen use (2). Unfortunately, it is not possible to determine from the present data whether increased glycolytic flux (from increased muscle glycogen use) acted to suppress fat oxidation (7) or whether muscle glycogen oxidation was augmented secondary to action of insulin to reduce fat availability and oxidation during exercise (7,12).
In summary, the highest exogenous CHO oxidation rates and greatest sparing of endogenous CHO was observed when a moderate amount of CHO (1 g·min−1, 60 g·h−1) was ingested during exercise. These data extend previous recommendations based on studies using male participants to endurance-trained females. Thus, when a single CHO form is to be ingested, it seems that for men and women, optimal benefits in terms of exogenous energy delivery and endogenous CHO use are attained from ingesting approximately 60 g·h−1 (5,13). Future studies should be directed towards substantiating the effects of CHO feeding on muscle metabolism in endurance-trained women, and investigating if these optimal benefits in terms of whole-body carbohydrate metabolism translate into optimal endurance performance improvements.
This study was funded by a research grant from GlaxoSmithKline Consumer Healthcare (UK). The results of the present study do not constitute endorsement of the product by the authors or ACSM.
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Keywords:©2007The American College of Sports Medicine
SUBSTRATE OXIDATION; ENDURANCE EXERCISE; GLUCOSE INGESTION; STABLE ISOTOPES