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Isomaltulose Improves Postexercise Glycemia by Reducing CHO Oxidation in T1DM

WEST, DANIEL J.1,2; MORTON, RICHARD D.1,2; STEPHENS, JEFFREY W.2; BAIN, STEPHEN C.2; KILDUFF, LIAM P.1; LUZIO, STEVE3; STILL, RACHEL4; BRACKEN, RICHARD M.1,2

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Medicine & Science in Sports & Exercise: February 2011 - Volume 43 - Issue 2 - p 204-210
doi: 10.1249/MSS.0b013e3181eb6147
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Abstract

Physical exercise causes large reductions in blood glucose (BG) concentrations in individuals with type 1 diabetes mellitus (T1DM). Reductions to the preexercise insulin dose help preserve BG during and after exercise (7,23,29). Furthermore, current research advocates the consumption of CHO before exercise to prevent falls in glucose during and after a bout of exercise (7,15,22). However, specific factors related to the physical and chemical compositions of CHO, such as the glycemic index, have been under-researched.

The effects of changes in the type of CHO consumed by T1DM before performing exercise on BG responses after exercise have been under-researched. CHO with a low glycemic index (LGI) digest at slower rates than CHO with a high glycemic index (HGI) and are unable to cross the mucosal cell membrane within the small intestine and enter the bloodstream unless hydrolyzed into monosaccharides (35). Research has established the importance of including LGI CHO into the daily diets of T1DM, with observed benefits such as lower daily mean BG (26) and reduced incidence of hypoglycemia and reductions in HbA1c (11,36). Within the study of Nansel et al. (26), consumption of LGI foodstuffs, such as peaches, kidney beans, or brown rice, resulted in glucose concentrations (assessed using a continuous glucose monitor) being within a target range of 3.9-9.9 mmol·L−1 significantly more of the time than under the HGI trial (67% vs 47%). Moreover, the participants elicited a lower mean BG concentration (LGI 7.6 ± 2.0 vs HGI 10.1 ± 2.6 mmol·L−1) and required less bolus insulin per 10 g of CHO. There are limited data examining the postexercise metabolic responses of T1DM after ingestion of specific LGI CHO before exercise.

Isomaltulose is a disaccharide sucrose isomer with an α1,6 glycosidic bond between glucose and fructose, as opposed to an α1,2 glycosidic bond in sucrose, which slows the hydrosylation rate to 20%-25% of that of sucrose (14), giving it a GI value of 32. Research examining the metabolic effects of this CHO within obese nondiabetic individuals has demonstrated reduced postprandial glucose area under the curve, with concomitantly lower peaks in BG and insulin when compared with a sucrose-based meal (38). Furthermore, research has demonstrated smaller alterations in BG concentration during exercise in non-T1DM. Achten et al. (1) investigated plasma glucose responses to 150 min of cycling at ∼60% V˙O2max after ingesting isomaltulose or sucrose with little change in plasma glucose during the protocol after consumption of isomaltulose compared with a ∼1.2-mmol·L−1 greater plasma glucose concentration 15 min after sucrose consumption. Less fluctuation in BG responses during exercise would be beneficial for the exercising T1DM individual. However, an examination of the metabolic effects of preexercise isomaltulose ingestion on postexercise glycemia in T1DM warrants investigation.

Research demonstrates that consumption of isomaltulose alters exercising fuel metabolism in non-T1DM. CHO oxidation rates have been shown to decrease and lipid utilization increase during a bout of isoenergetic exercise in non-T1DM individuals after consumption of an LGI meal (1,34). Stevenson et al. (34) demonstrated a 31% lower CHO oxidation rate and a 56% greater lipid oxidation rate during a 1-h treadmill run at 65% V˙O2max 3 h after consumption of an LGI or an HGI meal in eight female participants. Similarly, ingestion of a 50-g bolus of isomaltulose reduced CHO oxidation rate by ∼0.2 g·min−1 and increased lipid oxidation more than sucrose during 150 min of cycling at 60% V˙O2max (1). This raises the possibility that consumption of isomaltulose may spare both endogenous and exogenous CHO use and increase fat oxidation in T1DM during exercise, resulting in better preservation of BG during the postexercise period.

Therefore, the aim of this study was to compare the effects of ingesting an HGI and LGI CHO, i.e., dextrose and isomaltulose, on metabolic and fuel oxidation responses before, during, and after running in T1DM individuals.

RESEARCH DESIGN AND METHODS

Subjects.

With local research ethics committee approval, eight participants with T1DM (seven males and one female; age = 35 ± 2 yr, body mass index = 26 ± 0.3 kg·m−2) with duration of diabetes of 14 ± 2 yr and HbA1c of 8.0% ± 0.2% volunteered to participate in this study. Patients were recruited from local clinics and through advertisements in the local press. After receiving a full explanation of the testing protocol, all participants provided informed consent and medical history forms before partaking in the study. All participants were currently regularly exercising, in moderate glycemic control, with no significant complications, except for mild background retinopathy, and were receiving no additional medication other than insulin.

Insulin regimen.

The insulin regimen of each participant was set according to specific algorithms formed as part of their treatment with their diabetes clinician. Participants were familiar with the CHO counting method and were administering 1.30 ± 0.06 U of insulin per 10 g of CHO. Basal insulin dose did not change during the study period and was administered at the same time of day (evening) and at the same anatomical region. All participants were using a basal-bolus regimen of once-daily insulin glargine (n = 5) or twice-daily insulin detemir (n = 3) and either insulin lispro (n = 2) or insulin aspart (n = 6) at meal times. The pharmacokinetics and dynamics of insulin aspart and insulin lispro are comparable (28), and their metabolic effects have been shown to be equivalent (16). Basal insulin glargine and detemir are promoted as equivalent in terms of a peakless 24-h profile (13).

Experimental protocol.

Participants initially attended the laboratory for a preliminary test to quantify peak rate of oxygen consumption (V˙O2peak) and peak HR (HRpeak). To obtain these variables, participants completed a continuous incremental treadmill assessment to volitional exhaustion. Beginning at a velocity of 8 km·h−1, on a level gradient, treadmill velocity was increased by 1 km·h−1 every 3 min until participants were unable to continue. The peak rates of V˙O2, HR, and RER were determined from the final minute of exercise.

After the preliminary visit, participants attended the exercise physiology laboratory on two occasions, at the same time (between 6 and 8 a.m.) and 7 d apart. Participants avoided strenuous activity for 48 h before arriving at the laboratory after an overnight fast, having consumed similar evening meals before each trial (assessed via dietary recording sheets). On arrival at the laboratory, participants were seated while a 20-gauge catheter (Venflon; Becton Dickinson, Stockholm, Sweden), with a three-way stop valve, was inserted into the antecubital vein of the nondominant arm, which was kept patent by regular infusion of saline. Fifteen minutes later, a resting blood sample (10 ± 1 mL) was obtained.

After this, participants were given, in a randomized and counterbalanced fashion, 75 g of either an HGI (dextrose (DEX); GI = 96) or LGI (isomaltulose (ISO); GI = 32) CHO, mixed with 750 mL of water (10% solution) (27). Immediately before ingestion, participants were instructed to administer their rapid-acting insulin, which had been reduced by 75% (2.1 ± 0.2 U) into the abdomen (29). Insulin aspart and insulin lispro were administered using Novopen3 (NovoNordisk, Crawley, UK) and Humapen Luxura (Eli Lilly, Basingstoke, UK), respectively. Once administered, participants consumed the test solution within 5 min and remained in a rested, seated position for the 120-min preexercise period, apart from when anthropometric measures were obtained. Blood samples were also obtained at 30, 60, 90, and 120 min after ingestion of the test drink. Sixty minutes after consumption of the drink, participants' stature (stadiometer; Holtain, Crymych, UK) and body mass (Seca Digital Scales; Seca Ltd., Birmingham, UK) were determined. At 105 min, resting measures of respiration (Metamax 3b; Cortex Biophysik, Leipzig, Germany) and HR were determined (RS-400; Polar, Kempele, Finland) with the participants lying in a supine position. Two hours after consumption of CHO and insulin administration, a preexercise blood sample was obtained, and participants subsequently performed 45 min of steady-state treadmill (Woodway, Weil am Rhein, Germany) running at a velocity equivalent to 80% ± 1% V˙O2peak. HR and breath-by-breath data were collected via radiotelemetry software (Metasoft; Cortex Biophysik, Germany) and analyzed for CHO and lipid oxidation rates using the equations of Frayn (9). On cessation of exercise, additional blood samples were obtained at 0, 5, 15, 30, 60, 120, and 180 min after exercise. Participants remained at rest for the entire 3-h postexercise period, drinking water ad libitum. Postexercise blood variables were corrected for changes in plasma volume via the method of Dill and Costill (8).

Blood samples.

An aliquot of blood was collected in a 4-mL Na+EDTA vacutainer and was analyzed for HbA1c by high performance liquid chromatography (HPLC) with cation exchange (G7; Tosoh, Theale, UK). A 1-mL sample of venous blood was obtained using a Ca2+-heparinized syringe, immediately capped, kept on ice, and then measured within 5 min for BG and lactate concentrations (GEM3000; Instrumentation Laboratories Ltd., Croft, UK). A 20-μL aliquot was also analyzed for blood hemoglobin (Hemocue AB, Angelholm, Sweden). Another blood sample was gathered and split equally into a 5-mL serum separation tube and a lithium-heparinized tube that contained 200 μL of 0.1 mol·L−1 of both ethylene glycol bis-(β-aminoethyl ether)-N′,N′,N′,N′-tetraacetic acid as anticoagulant and glutathione as antioxidant. The sample in the serum separation tube was left to clot for 30 min. Plasma and serum samples were centrifuged for 10 min at 3000 revolutions per minute with the resultant plasma and serum extracted and stored at −80°C for later analysis of nonesterified fatty acids (NEFA) and hormones (epinephrine, norepinephrine, cortisol, and glucagon). Plasma norepinephrine and epinephrine were measured using an ELISA kit (Cat-Combi, Kit No. RE59242; Immuno Diagnostic Systems Ltd., Crumlin, UK). Serum cortisol was measured via ELISA kit (Roche Modular System; Roche Diagnostics, Burgess Hill, UK). Serum NEFA values were measured by routine hospital analysis (Roche Modular System). Plasma was analyzed for glucagon via enzyme immunoassay (Alpco Diagnostics, Newmarket, UK). Because the glucagon response is typically attenuated or completely absent in T1DM individuals with a duration of diabetes >5 yr (25), measurements were taken at rest, immediately after exercise, and 3 h after exercise. Rapid-acting insulin was not measured because of assay cross-reactivity with insulin detemir.

Hypoglycemia was defined as BG concentration ≤3.5 mmol·L−1 (29). If participants experienced a hypoglycemic incident, a bolus of commercially available CHO drink (Lucozade; GlaxoSmithKline, Uxbridge, UK) that contained 20 g of CHO was administered. Hyperglycemia was defined as ≥12.4 mmol·L−1 (33).

Data analysis.

Statistical analysis was performed using SPSS software (version 16; SPSS, Inc., Chicago, IL), with significance set at P ≤ 0.05. Data were tested for normal distribution (Shapiro-Wilk test) and subsequently analyzed using repeated-measures ANOVA on two factors (treatment × time) with Bonferroni adjustment and dependent t-tests carried out where relevant. BG responses were calculated as a change from rest through the subtraction of resting concentrations from further glucose values within each condition. Moreover, BG area under the curve (BGAUC) was calculated using the method of Wolever and Jenkins (40) and time-averaged for the 3-h postexercise period. Data are presented as mean ± SEM.

RESULTS

Physiological responses.

The physiological responses to ISO and DEX are reported in Table 1. There were no differences in the resting rates of oxygen consumption or carbon dioxide production between ISO and DEX (P = 0.46). Participants exercised at a similar exercise intensity under both conditions (ISO 80.8% ± 0.9% vs DEX 78.2% ± 0.9% V˙O2peak, P = 0.12). However, there was a tendency for a greater rate of oxygen use during exercise under ISO (P = 0.05; Table 1). Resting and exercising HR values were similar between conditions (Table 1).

TABLE 1
TABLE 1:
Cardiorespiratory responses of participants at rest and during exercise after consumption of ISO and DEX.

BG responses.

Fasted BG concentrations were not different between conditions (ISO 7.6 ± 0.2 vs DEX 6.2 ± 0.3 mmol·L−1, P = 0.11). The absolute and relative BG responses to ISO or DEX ingestion are reported in Figure 1. There were no conditional differences when BG was examined in absolute concentrations (Fig. 1A); however, when expressed as change from baseline, significant conditional differences in BG responses were evident (Fig. 1B).

FIGURE 1
FIGURE 1:
A, BG responses to preexercise ingestion of ISO or DEX. There was a significant time effect (P = 0.001, ∂η 2 = 0.601) but no time × treatment interaction (P > 0.05). B, BG responses, relative to rest, after ingestion of ISO or DEX. There was a significant time (P = 0.001, ∂η 2 = 0.617) and treatment effect (P = 0.006, ∂η 2 = 0.686) and a significant time × treatment interaction (P = 0.04, ∂η 2 = 0.225). Data are presented as mean ± SEM (n = 8). Transparent sample points indicate significant difference from rest (P < 0.05). *Significant difference when compared with ISO (P < 0.05). Thatched area indicates exercise. Insulin and CHO solution was administered immediately after resting sample.

Peak BG under ISO (Δ+4.5 ± 0.4 mmol·L−1), occurred 120 min after ingestion and was less than DEX (Δ+9.1 ± 0.6 mmol·L−1, P < 0.01), which peaked at 90 min. The drop in BG with exercise was similar between conditions (ISO 4.4 ± 0.4 vs DEX 5.8 ± 0.3 mmol·L−1, P = 0.11). When examining individual responses, the drop in BG under ISO was not as great as that in DEX in six of eight participants. Immediately after exercise, BG concentrations under ISO were significantly lower than those under DEX and were not different from resting concentrations (Fig. 1B).

In the 3-h postexercise period, BG concentrations under ISO were lower than those under DEX at all time points (Fig. 1B). BG concentrations did not change from 0 to 180 min under either condition (ISO Δ+0.1 ± 0.3 vs DEX Δ+1.3 ± 0.3 mmol·L−1, P = 0.46). The ISO postexercise BGAUC and mean BG concentration, during the 180-min recovery period, was 21% ± 3% and 3.0 ± 0.4 mmol·L−1, lower in comparison to DEX, respectively (P < 0.05).

Hypoglycemia.

There were no incidences of hypoglycemia during the 2-h rest period or during treadmill running. In the postexercise period, there were two occasions where BG fell below 3.5 mmol·L−1 under both DEX (5 and 120 min after exercise) and ISO trials (30 and 180 min after exercise). One participant experienced a hypoglycemic encounter on both occasions (ISO 120 min and DEX 180 min after exercise).

Metabolic responses.

There were no conditional differences in resting rates of CHO (ISO 0.38 ± 0.02 vs DEX 0.34 ± 0.01 g·min−1, P = 0.36) or lipid oxidation (ISO 0.06 ± 0.01 vs DEX 0.08 ± 0.01 g·min−1, P = 0.34). The CHO and lipid oxidation rates during exercise are shown in Figure 2A. When expressing oxidation rates as changes from rest, there was a tendency for a lower CHO oxidation rate under ISO (ISO 2.52 ± 0.04 vs DEX 2.74 ± 0.05 g·min−1, P = 0.08) with a concomitant greater rate of lipid oxidation (ISO 0.23 ± 0.03 vs DEX 0.09 ± 0.02 g·min−1, P < 0.05). As exercise progressed, there was a lower CHO and greater lipid oxidation rate, such that by the last 10 min, CHO and lipid oxidation rates were significantly different under ISO compared with DEX, respectively (Fig. 2B).

FIGURE 2
FIGURE 2:
A, CHO and lipid oxidation rates during 45 min of exercise after preexercise ingestion of ISO or DEX. B, CHO and lipid oxidation rates during the final 10 min of exercise. Data are presented as mean ± SEM (n = 8). *Significant differences between ISO and DEX (P< 0.05).

The energy expended in both trials was similar (ISO 2.67 ± 0.04 vs DEX 2.63 ± 0.04 MJ, P = 0.41) with energy from CHO similar between the conditions (ISO 2.18 ± 0.04 vs DEX 2.32 ± 0.05 MJ, P = 0.13) and energy from lipids greater under ISO; however, this difference did not reach statistical significance (ISO 0.49 ± 0.05 vs DEX 0.31 ± 0.04 MJ, P = 0.06). Although not reaching statistical significance, there seemed to be a lower percentage contribution to total energy expenditure from CHO (ISO 83% ± 2 vs DEX 89% ± 2%, P = 0.07) and greater contribution from lipids (ISO 17% ± 2% vs DEX 11% ± 2%, P = 0.07) under ISO.

The serum NEFA responses at rest and after exercise are reported in Figure 3. Resting NEFA concentrations were similar (ISO 0.39 ± 0.03 vs DEX 0.36 ± 0.02 mmol·L−1, P = 0.71). After CHO consumption and insulin administration, there were no changes in circulating NEFA concentrations up to 120 min (ISO Δ−0.10 ± 0.03 vs DEX Δ−0.01 ± 0.02 mmol·L−1, P = 0.16). Moreover, serum NEFA concentrations did not increase when measured immediately after exercise; however, 5 min after the cessation of exercise, there was a twofold increase in NEFA concentrations under both conditions (P < 0.05; Fig. 3). NEFA concentrations peaked at 3 h after exercise (ISO 0.86 ± 0.04 vs DEX 0.92 ± 0.04 mmol·L−1, P = 0.22). There were no conditional differences in the serum NEFA concentrations.

FIGURE 3
FIGURE 3:
Serum NEFA responses to preexercise ingestion of ISO or DEX. There was a significant time effect (P < 0.01, ∂η 2 = 0.72); however, there were no treatment or treatment × time interactions (P > 0.05). Data are presented as mean ± SEM (n = 8). Transparent sample points indicate significant difference from rest (P < 0.05). #Significantly different from 0 min after exercise under both conditions (P < 0.05). Thatched area indicates exercise. Insulin and CHO solution was administered immediately after resting sample.

Two hours after consumption of the test meal, the blood lactate concentration under ISO was 0.5 ± 0.1 mmol·L−1 greater than DEX (Fig. 4). These differences disappeared with exercise as similar peak lactate concentrations were observed immediately after exercise (ISO 4.5 ± 0.4 vs DEX 4.4 ± 0.3 mmol·L−1, P = 0.31). There were no differences in blood lactate concentrations between conditions during the postexercise period (Fig. 4).

FIGURE 4
FIGURE 4:
Blood lactate responses to preexercise ingestion of ISO or DEX. There was a significant time (P = 0.01, ∂η 2 = 0.623) and treatment effect (P = 0.04, ∂η 2 = 0.366) and a significant time × treatment interaction (P = 0.04, ∂η 2 = 0.221). Data are presented as mean ± SEM (n = 8). Transparent sample points indicate significant difference from rest (P < 0.05). *Significant conditional difference (P < 0.05). Thatched area indicates exercise. Insulin and CHO solution was administered immediately after resting sample.

Hormonal responses.

There were no conditional effects on any of the counterregulatory hormonal responses to the trials (Table 2). Glucagon was unaltered from resting concentrations with exercise and remained unchanged at 180 min after exercise. Both epinephrine and norepinephrine increased with exercise peaking immediately after exercise and returned to resting concentrations by 180 min after exercise under both conditions (Table 2). Cortisol did not rise with exercise; however, concentrations began to increase significantly immediately after exercise, peaking at 15 min after exercise. Peak cortisol concentrations at 15 min (ISO 590 ± 16 vs DEX 595 ± 22 nmol·L−1, P = 0.46) were not different from rest or 0 min after exercise under either condition. At 180 min after exercise, serum cortisol concentrations were significantly lower than rest (ISO 276 ± 18 vs DEX 197 ± 6 nmol·L−1, P = 0.20) under both conditions (P < 0.05; Table 2).

TABLE 2
TABLE 2:
Counterregulatory hormonal responses of participants at rest and after exercise after consumption of ISO and DEX.

DISCUSSION

We compared the metabolic and fuel oxidation responses after ingestion of a 10% isomaltulose or dextrose solution before, during, and after running in T1DM. The results demonstrate that compared with dextrose ingestion, isomaltulose increased BG concentrations less before exercise and maintained BG better for 3 h after running. Furthermore, CHO oxidation was reduced and lipid oxidation increased after ISO ingestion, during the later stages of running.

There was a smaller increase in BG under ISO compared with DEX in the preexercise period. BG concentrations increased above resting values by 8.7 ± 0.5 mmol·L−1 under DEX, whereas BG increased to just half of this under ISO (4.5 ± 0.4 mmol·L−1). The hydrolyzation rate of isomaltulose is very slow and only 20%-25% of that of sucrose (14). Thus, the slow hydrolyzation of ISO, into glucose and fructose, and subsequent absorption at the brush border membrane within the gastrointestinal passage explains the later and lower peak in BG compared with DEX (21). DEX can quickly cross via the sodium glucose transporter 1 and can rapidly increase BG concentrations (Fig. 1). The reduced postprandial glucose excursions under ISO prevented BG reaching hyperglycemic concentrations, as opposed to DEX. This is an important finding because maintaining glycemia close to euglycemic concentrations is the fundamental component in the management of T1DM (6), especially when incorporating physical exercise into the lives of T1DM individuals.

There were greater lactate concentrations under ISO in the preexercise period (Fig. 3). Isomaltulose is digested via the same sucrase/isomaltase complex, within the gastrointestinal passage, as sucrose (12). During this process, within the cytosol of the small intestine, some fructose derived from ISO is converted to lactate; however, most is metabolized within the liver (2). As fructose bypasses the phosphofructokinase regulatory point in glycolysis, there is an increased flux through the glycolytic pathway, which results in an increased formation and subsequent release of lactate (19,32).

As exercise progressed, there was a significantly lower CHO oxidation rate evident under ISO compared with DEX. This reduced CHO oxidation rate under ISO may in part be due to differences in BG concentrations before and during exercise. Two hours after ingestion, BG concentrations under ISO were near hyperglycemic (12.2 ± 0.5 mmol·L−1), whereas those under DEX were ∼3 mmol·L−1 greater at the beginning of exercise. This may have limited substrate oxidation to predominantly CHO (17). Jenni et al. (17) demonstrated that when T1DM individuals perform prolonged exercise under BG concentrations clamped at 11 mmol·L−1, fuel metabolism was dominated by CHO oxidation with concomitantly lower rates of lipid oxidation, compared with a euglycemia condition; an effect due to the mass action of elevated BG concentrations (5). As BG dropped 4.4 ± 0.4 mmol·L−1 with exercise under ISO, the BG concentrations in the later stages of running returned to euglycemic conditions sooner when compared with DEX, suggesting a lesser effect of high BG concentrations in promoting CHO combustion and increasing the likelihood of observing differences in substrate oxidation in the later stages of exercise.

As exercise progressed, there was a greater lipid oxidation during exercise under ISO, in comparison with DEX, which became significantly greater during the final 10 min of exercise. Similar findings have been reported previously by Trenell et al. (37), who found that LGI, preexercise, CHO-based meals increased lipid oxidation by 10% during 90 min of cycling at 70% V˙O2max, in comparison with isoenergetic, HGI CHO meals. Within our study, the increase in the combustion of lipids, with time, is possibly due to an increased mobilization of intramuscular triglyceride stores because NEFA concentrations did not differ between conditions. A potential mechanism behind the differences in lipid oxidation demonstrated in the later stages of exercise may be related to differences in BG concentrations between the conditions (4,5). Coyle et al. (5) investigated lipid oxidation, during 40 min of cycling at 50% V˙O2peak in non-T1DM individuals, in a fasted state or having consumed 1.4 g·kg−1 body mass of glucose. An examination of substrate oxidation revealed that an increased glucose availability and an increased glycolytic flux, and ultimately CHO oxidation, directly suppress lipid metabolism. Moreover, the increased glucose availability induced a 27% reduction in the oxidation of NEFA concentrations derived from intramuscular triglycerides. Relating the findings of Coyle et al. to our study, the bolus of DEX ingested before exercise may have caused a similar suppression of lipid oxidation during exercise. Moreover, combining an increase in skeletal muscle hormone-sensitive lipase activity (39) and lower glucose availability under ISO may have provided a milieu where the oxidation of intramuscular NEFA concentrations was not as suppressed, compared with DEX, during exercise. Serum NEFA concentrations did not change with exercise; an effect likely the result of a reduction in adipose tissue blood flow, with exercise intensities >70% V˙O2max, reducing the removal of NEFA (18,30,31). A redistribution of blood flow to adipose tissue is also the likely mechanism behind the rapid rise in NEFA concentrations after the cessation of exercise (31).

Postexercise glycemia was lower under ISO, compared with DEX, with BGAUC and mean BG being 21% ± 3% and 3.0 ± 0.4 mmol·L−1 lower, respectively, during the 3-h recovery period. There were similar changes in BG within each condition. The preservation of BG might potentially be due to exercise-induced increases in skeletal lipoprotein lipase activity (20), increasing TG breakdown and NEFA availability. Furthermore, the similar concentrations of counterregulatory hormones may help explain the similar preservation of BG with time, across conditions. From a T1DM individual's perspective, this is important because avoiding high BG concentrations after exercise is not only beneficial for improved glycemic control but also may help avoid the occurrence of hypoglycemia, as individuals are less likely to have to administer corrective insulin units, which, in a postexercise insulin-sensitized state, could cause unexpected falls in BG. Both types of CHO were equally effective at preventing hypoglycemia during the 3-h recovery period, with two episodes under each condition. Despite the increased appearance of lactate under ISO during the preexercise period, the conditional differences in this metabolite were not evident after running was completed. Potentially, greater lactate concentrations under ISO resulted in lactate being channeled into oxidative pathways within the heart (10) and the active musculature (24) and/or into hepatic gluconeogenesis (3).

In conclusion, this study examined the effects of consuming isomaltulose and dextrose on metabolic and fuel oxidation responses before, during, and after running in T1DM individuals. These data demonstrate that consuming isomaltulose improves BG responses during and after exercise through reduced CHO and increased lipid oxidation during exercise. Regularly using this strategy could be beneficial for long-term glycemic control within exercising T1DM individuals.

This project was funded by the Welsh Office of Research and Development.

The authors thank Gareth Dunseath and the staff at the Clinical Biochemistry laboratories (ABMU Trust) for their contributions to the analysis of blood parameters.

The results of the present study do not constitute endorsement by the American College of Sports Medicine.

REFERENCES

1. Achten J, Jentjens RL, Brouns F, Jeukendrup AE. Exogenous oxidation of isomaltulose is lower than that of sucrose during exercise in men. J Nutr. 2007;137:1143-8.
2. Ahlborg G, Björkman O. Splanchnic and muscle fructose metabolism during and after exercise. J Appl Physiol. 1990;69(4):1244-51.
3. Ahlborg G, Felig P. Lactate and glucose exchange across the forearm, legs and splanchnic bed during and after prolonged exercise. J Clin Invest. 1982;69(1):45-53.
4. Coyle EF, Hamilton MT, Gonzalez Alonso J, Montain SJ, Ivy JL. Carbohydrate metabolism during intense exercise when hyperglycaemic. J Appl Physiol. 1991;70(2):834-40.
5. Coyle EF, Jeukendrup AE, Wagenmakers AJM, Saris WHM. Fatty acid oxidation is directly regulated by carbohydrate metabolism during exercise. Am J Physiol Endocrinol Metab. 1997;273:E268-75.
6. Cryer PE, Davis SN, Shamoon H. Hypoglycemia in diabetes. Diabetes Care. 2003;26(6):1902-12.
7. De Feo P, Di Loreto C, Ranchelli A, et al. Exercise and diabetes. Acta Biomed. 2006;77(1):14-7.
8. Dill DB, Costill DL. Calculation of percentage changes in volumes of blood, plasma, and red cells in dehydration. J Appl Physiol. 1974;37(2):247-8.
9. Frayn KN. Calculation of substrate oxidation rates in vivo from gaseous exchange. J Appl Physiol. 1983;55(2):628-34.
10. Gertz EW, Wisneski JA, Stanley WC, Neese RA. Myocardial substrate utilization during exercise in humans. Dual carbon-labelled carbohydrate isotope experiments. J Clin Invest. 1988;82:2017-25.
11. Gilbertson HR, Brand-Miller JC, Thorburn AW, Evans S, Chondros P, Wether GA. The effect of flexible low glycemic index dietary advise versus measured carbohydrate diets on glycemic control in children with type 1 diabetes. Diabetes Care. 2001;34(7):1137-43.
12. Goda T, Hosoya N. Hydrolysis of palatinose by rat intestinal sucrase-isomaltase complex. Nihon Eiyo Shokuryo Gakkai Shi. 1983;36:169-73.
13. Gulve EA. Exercise and glycemic control in diabetes: benefits, challenges, and adjustments to pharmacotherapy. Phys Ther. 2008;88(11):1297-321.
14. Gunther S, Heymann H. Di- and oligosaccharide substrate specificities and subsite binding energies of pig intestinal glucoamylase-maltase. Arch Biochem Biophys. 1998;354:111-6.
15. Hibbert-Jones E, Regan G. Diet and nutritional strategies during sport and exercise in type 1 diabetes. In: Nagi D, editor. Exercise and Sport in Diabetes. 2nd ed. Hoboken (NJ): Wiley; 2005. p. 45-66.
16. Homko C, Deluzio A, Jimenez C, Kolaczynski JW, Boden G. Comparison of insulin aspart and lispro: pharmacokinetic and metabolic effects. Diabetes Care. 2003;26(7):2027-31.
17. Jenni S, Oetliker S, Allemann M. Fuel metabolism during exercise in euglycaemia and hyperglycaemia in patients with type 1 diabetes mellitus-a prospective single-blinded randomised crossover trial. Diabetologia. 2008;51:1457-65.
18. Jones NL, Heigenhauser JF, Kuksis A, Matsos CG, Sutton JR, Toews CJ. Fat metabolism in heavy exercise. Clin Sci. 1980;59(6):469-78.
19. Kaye R, Williams ML, Barbero G. Comparative study of glucose and fructose metabolism in infants with reference to utilization and to the accumulation of glycolytic intermediates. J Clin Invest. 1958;37(5):752-62.
20. Kiens B, Lithell H, Mikines KJ, Richter EA. Effects of insulin and exercise on muscle lipoprotein lipase activity in man and its relation to insulin action. J Clin Invest. 1989;84(4):1124-9.
21. Lina BAR, Jonker D, Kozianowski G. Isomaltulose (Palatinose®): a review of biological and toxicological studies. Food Chem Toxicol. 2002;40(10):1375-81.
22. Maahs D, Taplin CE, Fiall-Scharer R. Type 1 diabetes mellitus and exercise. In: Regensteiner JG, Reusch JEB, Stewart KJ, Veves A, editors. Diabetes and Exercise. Totowa (NJ): Humana Press; 2009. p. 293-9.
23. Mauvais-Jarivs F, Sobngwi E, Porcher R, et al. Glucose response to intense aerobic exercise in type 1 diabetes. Diabetes Care. 2003;26(4):1316-7.
24. Mazzeo RS, Brooks GA, Schoeller DA, Budinger TA. Disposal of [1-13C]-lactate during rest and exercise. J Appl Physiol. 1986;60:232-41.
25. Mokan M, Mitrakou A, Veneman T, Ryan C, Korytkowski M, Cryer P. Hypoglycemia unawareness in IDDM. Diabetes Care. 1994;17(12):1397-1403.
26. Nansel TR, Gellar L, McGill A. Effect of varying glycemic index meals on blood glucose control assessed with continuous glucose monitoring in youth with type 1 diabetes on basal-bolus insulin regimens. Diabetes Care. 2008;31(4):695-7.
27. Perrone C, Laitano O, Mayer F. Effect of carbohydrate ingestion on the glycemic response to type 1 diabetic adolescents during exercise. Diabetes Care. 2005;28(10):2537-8.
28. Plank J, Wutte A, Brunner G, et al. A direct comparison of insulin aspart and insulin lispro in patients with type 1 diabetes. Diabetes Care. 2002;25(11):2053-7.
29. Rabasa-Lhoret R, Bourque J, Ducros F, Chiasson, J. Guidelines for premeal insulin dose reduction for postprandial exercise of difference intensities and durations in type 1 diabetic subjects treated intensively with a basal-bolus insulin regimen (Ultralente-Lispro). Diabetes Care. 2001;24(4):625-30.
30. Romjin JA, Coyle EF, Sidossis L, et al. Regulation of endogenous fat and carbohydrate metabolism in relation to exercise intensity and duration. Am J Physiol. 1993;265(3 Pt 1):E380-91.
31. Romjin JA, Coyle EF, Zhang X-J, Sidossis LS, Wolfe RR. Fat oxidation is impaired somewhat during high intensity exercise by limited plasma FFA mobilization. J Appl Physiol. 1995;79:1939-45.
32. Sahebjami H, Scalettar R. Effects of fructose infusion on lactate and uric acid metabolism. Lancet. 1971;297(7695):366-9.
33. Stettler C, Jenni S, Allemann S, et al. Exercise capacity in subjects with type 1 diabetes mellitus and eu- and hyperglycemia. Diabetes Metab Res Rev. 2006;22:300-6.
34. Stevenson EJ, Williams C, Mash LE, Phillips B, Nute ML. Influence of high-carbohydrate mixed meals with different glycemic indexes on substrate utilisation during subsequent exercise in women. Am J Clin Nutr. 2006;84(2):354-60.
35. Southgate DAT. Digestion and metabolism of sugars. Am J Clin Nutr. 1995;62(suppl):203s-11s.
36. Thomas DE, Elliott EJ, Baur L. Low glycemic index or low glycemic load diets for overweight and obesity. Cochrane Databse Syst Rev. 2007;18(2):1-38.
37. Trenell MI, Stevenson E, Stockmann K, Brand-Miler J. Effect of high and low glycaemic index recovery diets on intramuscular lipid oxidation during aerobic exercise. Br J Nutr. 2008;99:326-32.
38. Van Can JG, Ljzerman TH, Van Loon LJ, Brouns F, Blaak EE. Reduced glycaemic and insulinaemic responses following isomaltulose ingestion: implications for post-prandial substrate use. Br J Nutr. 2009;11:1-6.
39. Watt MJ, Heigenhauser GJF, Spriet LL. Effects of dynamic exercise intensity on activation of hormone sensitive lipase in human skeletal muscle. J Physiol. 2003;547:301-8.
40. Wolever TMS, Jenkins DJA. The use of glycemic index in predicting the blood glucose response to mixed meals. Am J Clin Nutr. 1988;43:167-72.
Keywords:

BLOOD GLUCOSE; TYPE 1 DIABETES MELLITUS; LIPID OXIDATION; DEXTROSE; GLYCEMIC INDEX

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