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Postexercise Fructose–Maltodextrin Ingestion Enhances Subsequent Endurance Capacity


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Medicine & Science in Sports & Exercise: May 2018 - Volume 50 - Issue 5 - p 1039–1045
doi: 10.1249/MSS.0000000000001516


Humans have the capacity to store finite amounts of carbohydrate energy as glycogen, predominantly in the skeletal muscle (1) and liver (2). Carbohydrates provide quantitatively the most important metabolic substrate for fuel metabolism during exercise of moderate-to-high intensities (3). Most research has focused on the role of muscle glycogen, and it has long been known that exercise of sufficient length and intensity will eventually deplete these stores to very low concentrations (1), implicating endogenous carbohydrate availability as a limiting factor during prolonged, thermoneutral exercise. This hypothesis is supported by recent suggestions that preferential, accelerated depletion of glycogen stored in the intramyofibrillar compartment has deleterious effects on muscle function and therefore elicits fatigue (4).

Maximizing recovery of muscle glycogen content in the postexercise period is pertinent to athletes seeking to optimize performance in repeated bouts of prolonged exercise with limited recovery time. Indeed, recent evidence suggests that the muscle glycogen-mediated limitation to prolonged exercise capacity holds true for repeated bouts (5). Current guidelines recommend ingestion of moderate-to-high glycemic index carbohydrates such as glucose-based sources at rates of 1–1.2 g·kg−1·h−1, beginning as soon as logistically possible after exercise, when recovery duration is short (<4 h) (6). This nutritional strategy should facilitate rapid and sufficient substrate availability to maximize insulin-dependent muscle glycogen synthesis (7) and take advantage of the insulin-independent contraction-mediated muscle glucose uptake and glycogen synthesis that occurs in the initial postexercise period (8).

The liver functions as a carbohydrate reservoir for release into the circulation and resultant oxidation by working skeletal muscle, as well as in the maintenance of euglycemia (9). Although glucose is the primary carbohydrate substrate for muscle glycogen synthesis (10), fructose exerts a superior effect on hepatic glycogen synthesis (11). Indeed, some studies have now observed superior hepatic and equal muscle glycogen synthesis with coingestion of large amounts of fructose–glucose carbohydrate sources during acute recovery from prolonged exercise compared with isocaloric glucose ingestion (12–14). This may have implications for subsequent exercise capacity through increased whole-body carbohydrate availability.

To date, no study has investigated if the apparent metabolic advantage ascertained through coingestion of fructose–glucose carbohydrate sources during short-term recovery from prolonged exhaustive exercise translates into a discernible effect on subsequent exercise performance or capacity. The aims of the present investigation were to elucidate if such an effect exists and to determine how any differences manifest metabolically and perceptually. It was hypothesized that fructose–maltodextrin coingestion during short-term recovery from prolonged exhaustive exercise would result in superior subsequent exercise capacity compared with isocaloric glucose–maltodextrin ingestion.



Eight (six males and two females) healthy, trained endurance runners and triathletes participated in the present investigation (age, 31 ± 6 yr; height, 176 ± 6 cm; mass, 68.4 ± 5.6 kg; V˙O2max, 3.76 ± 0.47 L·min−1). The sample size was chosen based on pragmatic reasons, balancing logistical, financial, and recruitment-related considerations for such an arduous experimental protocol, as well as reflecting the number of participants used in previous similar studies (15,16). All participants were engaging in training for endurance running events, habitually covering a self-reported 63 ± 19 km·wk−1. Experimental procedures were approved by the University of Birmingham (United Kingdom) Ethics Committee, and all participants provided written informed consent.

Study design

The present investigation adopted a single-blinded, randomized, and counterbalanced crossover design involving four laboratory visits. In the first laboratory visit, a maximal treadmill test (preliminary test) was performed to determine maximum oxygen uptake (V˙O2max). The second visit consisted of full familiarization to procedures performed in the subsequent experimental trials, without venous cannulation and blood collection. Thereafter, two experimental trials were conducted 4–16 d apart in a random, counterbalanced order ( Participants were blinded to trial order. Experimental trials consisted of treadmill running to exhaustion at 70% V˙O2max, a 4-h recovery with 90 g·h−1 maltodextrin and glucose (MAL + GLU) or maltodextrin and fructose (MAL + FRU) ingestion (1.5:1 ratio), and a second bout of treadmill running to exhaustion at 70% V˙O2max.

Preliminary test

To determine V˙O2max, an incremental step test to volitional exhaustion was performed on a motorized treadmill (quasar; h/p cosmos, Germany) during the first laboratory visit (18°C ± 1°C, 48% ± 14% rH). Height (Model 220; Seca, Germany) and body mass (Champ II, OHAUS, Switzerland) of each participant were measured before the test. Participants then completed 4-min stages at 7, 9, 11, and 13 km·h−1 against a 1% gradient to simulate the energetic cost of level-gradient outdoor running (17). HR (Polar Electro, Kempele, Finland) and RPE according to Borg’s 6–20 scale (18) were recorded in the final 60 s of each stage. Oxygen uptake (V˙O2) was measured continuously using an automated analyzer (JAEGER® Vyntus CPX, CareFusion, Germany) and calculated at each velocity as the average value during the final 30 s. After completion of the 13-km·h−1 stage, treadmill velocity was reduced to 11 km·h−1 and subsequently increased by 0.5 km·h−1 every 30 s until attainment of volitional exhaustion. Maximum oxygen uptake (V˙O2max) was accepted as the highest V˙O2 15-breath rolling average if two of the following three criteria were met: respiratory exchange ratio ≥1.10, HR ± 10 bpm of age-predicted maximum (205.8 − 0.685[age (yr)]) (19), and attainment of volitional exhaustion. Simple regression equations were used to estimate the speed required to elicit 70% V˙O2max for use in the subsequent trials.

Experimental trials

At least 5 d after the familiarization trial, participants reported to the laboratory at ∼08:00 h having fasted overnight and refrained from caffeine, alcohol, and vigorous exercise for 24 h and having completed a 3-d pretrial diet diary to be repeated in the run-up to the final experimental trial. Participants were fitted with an antecubital venous cannula (BD VenflonTM, Helsingborg, Sweden), and a 5-mL baseline venous blood sample was drawn. A treadmill run to volitional exhaustion at 70% V˙O2max then commenced (quasar, h/p cosmos), with venous blood samples obtained after 30 min, 60 min, and at exhaustion from an extension line to minimize the effect on running gait and technique. Expired gas samples were collected every 15 min and at exhaustion and analyzed for V˙O2 and V˙CO2 using an automated analyzer (JAEGER® Vyntus CPX, CareFusion). Water was consumed ad libitum. On attainment of volitional exhaustion, treadmill speed was reduced to 4.4 km·h−1 for 2 min. Treadmill speed was then restored to that eliciting 70% V˙O2max, and the participant was again asked to run to volitional exhaustion. This process was repeated, so only at the third attainment of volitional exhaustion was the test terminated. This protocol has lower coefficient of variation for exercise capacity compared with traditional single-exhaustion protocols (5.4%, 95% confidence interval = 1.4–9.6) (20).

Participants then passively rested for 4 h, during which sedentary activities such as reading and use of laptops were permitted. Participants immediately ingested a 300-mL beverage containing 18 g glucose (GLU + MAL) or fructose (FRU + MAL) with 27 g maltodextrin and, therefore, in a 1:1.5 ratio. Carbohydrates ingested during recovery were of high 13C natural abundance (−11.36 and −11.39 δ13CV-PDB ‰; The Hut Group, Cheshire, UK; Sports Supplements Ltd., Essex, UK). Identical beverages were ingested every 30 min throughout recovery ending 30 min before the end of the recovery period, such that 2.4 L of fluid and 90 g·h−1 of carbohydrate was ingested over the 4-h period. Venous blood samples and scales for gastrointestinal comfort (GC) (21) were obtained every hour during recovery. The GC scales assessed nausea, stomach fullness, and abdominal cramping using a 10-point Likert scale.

After the 4-h recovery period, participants commenced a second treadmill run to volitional exhaustion at 70% V˙O2max as before. Venous blood samples, GC scales, RPE, and a scale for lower-limb muscle soreness (22) were obtained every 15 min and at exhaustion. Expired gas samples were also obtained for 4 min every 15 min and at exhaustion and analyzed for V˙O2 and V˙CO2 using an automated analyzer (JAEGER® Vyntus CPX, CareFusion). The exhaustion time point expired gas sample was collected during a period of running between the first and the final claim of volitional exhaustion. At these time points, and also immediately after the first exercise bout, breath samples were collected into 10-mL evacuated tubes (Exetainer® Breath Vial, Labco Ltd., UK).

Blood analyses

Venous blood samples were aliquoted into ∼5 mL prechilled ethylenediaminetetraacetic acid tubes, centrifuged for 10 min at 4°C and 3500 rpm, and stored at −25°C. Plasma glucose, nonesterified fatty acid, and lactate concentrations were later determined through duplicate colorimetric assays using a semiautomatic analyzer (ILab 650; Instrumentation Laboratory, Bedford, MA) and commercially available kits (Randox Laboratories Ltd., County Antrim, UK).

Gas analyses

V˙O2 and V˙CO2 were calculated using an automated analyzer (JAEGER® Vyntus CPX, CareFusion). This allowed for the calculation of whole-body rates of fat and carbohydrate (CHOtot) oxidation at each time point during the first and the second bouts of the experimental trials using the following equations, which assume a negligible contribution of protein oxidation to metabolism (equations 1 and 2) (23):

In addition, nonlinear modeling software was used (Microsoft Excel 2011, Redmond, WA) such that CHOtot could be compared between trials at the point of exhaustion in the second bout of the shorter duration trial (equation 3). For example, if exhaustion occurred for one individual at 55 min in the second bout of the GLU + MAL trial, and 70 min in the FRU + MAL trial, the curve for CHOtot versus time in the FRU + MAL trial was nonlinearly modeled such that CHOtot could be estimated at 55 min:

where t is the time point (min) and a, b, and c are solved such that the modeled equation produced the lowest cumulative deviation from known values in each individual.

The isotopic enrichment of breath samples collected into 10-mL evacuated tubes (Exetainer® Breath Vial, Labco Ltd.) at each time point was determined by gas chromatography isotope ratio mass spectrometry (IsoAnalytical Ltd., Crewe, UK) using the following equation (24) (equation 4):

where isotopic enrichment was expressed as δ per milliliter and related to an international standard (Pee Dee Belemnite (PDB)).

Subsequently, the oxidation rate of carbohydrate ingested during recovery (CHOing) at each time point during the second bout could then be calculated according to the following equation (equation 5):

where δExp = 13C enrichment of expired gas sample, δIng = 13C enrichment of ingested carbohydrate, Expbkg = 13C enrichment of expired gas sampled after the first exercise bout, and 0.7467 = V˙CO2 of 1 g glucose oxidation.

A consideration when attempting to measure specific oxidation of ingested high natural abundance 13C carbohydrates in expired breath is temporary retention of the 13C label in the body’s endogenous bicarbonate pool as 13CO2 during the initial 60 min of moderate-intensity exercise, resulting in the underestimation of calculated ingested carbohydrate oxidation rates (25). As this underestimation is likely to be systematic between trials, no arbitrary correction factor was deemed necessary given the crossover design of the present investigation. Nonetheless, the ingested carbohydrate oxidation rates presented here should be considered minimal estimates.

Statistical analyses

Data were analyzed using commercially available software (SPSS Statistics, v22, SPSS Inc., Chicago, IL). Data collected in the first exercise bout, recovery period, and second exercise bout were considered separately. Sample distribution data are expressed as mean ± SD. Statistical significance was inferred when P ≤ 0.05.

Between- and within-trial time point–specific substrate oxidation rate comparisons (CHOtot, CHOing, and fat oxidation), as well as those for plasma glucose, nonesterified fatty acid, and lactate concentrations, and psychometric scales were made using a two-way repeated-measures ANOVA. Nonspherical data were corrected using the Greenhouse–Geisser (epsilon < 0.75) or the Huynh–Feldt (epsilon > 0.75) adjustment. Where a significant effect was indicated for these variables, the Holm–Bonferroni stepwise correction was made for location of variance post hoc, and these P values are reported.

Total substrate oxidation, i.e., CHOtot, CHOing, and fat oxidation in grams, was estimated for the second exercise bout in each trial through manually calculated area under the curve (grams per minute vs time). These variables, and exercise capacity, were compared between trials using paired t-tests or Wilcoxon signed rank tests, dependent on normality. The magnitude of statistically significant effects in these variables was determined through within-subject Cohen’s d effect sizes (ES) computed using a purpose-built spreadsheet (26). ES, presented as ±90% confidence limit, was interpreted according to Cohen’s criteria: small, 0.2–0.5; moderate, 0.5–0.8; and large, >0.8 (27). Where appropriate, percent changes are presented as ±confidence limit, and post hoc calculation of achieved power was made using the ES, sample size, and P value (G*Power 3.1, Universität Düsseldorf, Germany).


Exercise capacity

Exercise intensity was matched between trials in bout 1 (69.4% ± 2.5% vs 69.3% ± 2.4% V˙O2max in GLU + MAL and FRU + MAL, respectively, P = 0.91) and bout 2 (69.6% ± 1.3% vs 69.3% ± 1.9% V˙O2max in GLU + MAL and FRU + MAL, respectively, P = 0.64). Bout 1 exercise capacity was not significantly different between trials (131.3 ± 36.1 vs 134.6 ± 34.6 min in GLU + MAL and FRU + MAL, respectively, P = 0.38). The within-subject SD for bout 1 exercise capacity was 6.4 ± 3.4 min, with a coefficient of variation of 5.5% ± 3.2%. No order effect was observed (P = 0.41).

Second bout exercise capacity was significantly greater in the FRU + MAL trial (81.4 ± 22.3 vs 61.4 ± 9.6 min, P = 0.02; Fig. 1), a large magnitude effect (ES = 1.84 ± 1.12, 32.4% ± 19.9%). This effect was observed in seven of the eight participants. Post hoc analysis revealed the study had 95% statistical power to reveal an enhanced exercise capacity based on the sample size used and ES observed. No order effect was observed (P = 0.69).

Mean responses for second bout exercise capacity (min) in the GLU + MAL and FRU + MAL trials (N = 8). *P = 0.02 between trials.

Substrate metabolism

CHOtot oxidation rates were not significantly different between trials during bout 1 (P = 0.96). CHOtot oxidation rates at 15 min, 30 min, and exhaustion in bout 2 were not significantly different between trials (P = 0.171; Table 1) but were significantly reduced at exhaustion versus 15 and 30 min (P < 0.005). The modeled CHOtot oxidation rate in bout 2 of the trial with superior exercise capacity at the point of exhaustion in the trial with inferior exercise capacity was significantly greater than the CHOtot oxidation rate at the point of exhaustion in the trial with inferior exercise capacity (2.74 ± 0.52 vs 1.88 ± 0.52 g·min−1, P = 0.002). This effect was consistent in all eight participants and was of large magnitude (ES = 1.46 ± 0.89, 58% ± 28%). In the seven participants who had greater second bout exercise capacity with FRU + MAL, the modeled CHOtot oxidation rate in the FRU + MAL trial at the point of exhaustion in the GLU + MAL trial was significantly greater than the CHOtot oxidation rate at exhaustion in the GLU + MAL trial (2.71 ± 0.55 vs 1.84 ± 0.55 g·min−1, P = 0.03). This effect was consistent in all seven participants and was of large magnitude (ES = 1.36 ± 0.97, 60% ± 34%). The absolute amount of CHOtot oxidized during bout 2 was significantly greater with FRU + MAL, a large magnitude effect (Table 1).

Whole-body total (CHOtot) and ingested (CHOing) carbohydrate oxidation in bout 2 of the GLU + MAL and FRU + MAL trials (N = 8).

CHOing oxidation rates were significantly greater after 15 and 30 min in the FRU + MAL versus GLU + MAL trial (P < 0.002; Table 1). CHOing oxidation rate at exhaustion was significantly decreased versus 15 and 30 min in both trials (P < 0.005). In the GLU + MAL trial, CHOing was also significantly lower at 30 versus 15 min (P = 0.002). The absolute amount of CHOing oxidized during bout 2 was significantly greater with FRU + MAL, a large magnitude effect (Table 1).

Plasma variables

Because of clotting, blood data sets in bout 2 are available for six participants (bout 1 and recovery, N = 8). Plasma variables were not significantly different between trials, except plasma glucose concentration at the point of exhaustion in bout 2 (6.3 ± 1.0 vs 5.3 ± 0.7 mmol·L−1, in GLU + MAL and FRU + MAL, respectively, P = 0.003) and plasma lactate concentrations after 60, 120, and 180 min of recovery (FRU + MAL > GLU + MAL, P < 0.02; see Figure, Supplemental Digital Content, Plasma metabolite responses to the experimental protocols,

Perceptual responses

Bout 2 RPE was significantly lower with FRU + MAL versus GLU + MAL after 30 min (13 ± 1 vs 14 ± 2 AU, P = 0.02). Muscle soreness in bout 2 was not significantly different between trials (P = 0.31) but was significantly elevated in bout 2 at exhaustion versus all other time points in both trials (P < 0.05).

Nausea, stomach fullness, and abdominal cramping were not significantly different between trials during recovery (P > 0.27). Between-trial differences in nausea (P = 0.04) and stomach fullness (P = 0.03) during bout 2 were not significant at any time point after post hoc analysis (P > 0.10). Stomach fullness was significantly lower at each time point versus all previous time points during bout 2 with FRU + MAL (P = 0.05; Fig. 2).

Self-reported nausea (A), stomach fullness (B), and abdominal cramping (C) (1–10, AU) during recovery and bout 2 of the GLU + MAL and FRU + MAL trials (N = 8).


The aim of the present investigation was to determine whether the previously observed metabolic advantages ascertained through coingestion of fructose–glucose carbohydrate sources during short-term recovery from prolonged exercise translate into a discernible effect on subsequent exercise capacity. The main finding was that short-term recovery of endurance exercise capacity was significantly augmented with coingestion of fructose and maltodextrin during recovery compared with isocaloric glucose and maltodextrin ingestion by 32.4% ± 19.9%. Using a conversion described previously (28), it can be estimated that this equates to an ∼5.9% improvement in time trial performance. This novel finding provides functional relevance to previous metabolic investigations demonstrating enhanced hepatic and equivalent effects on skeletal muscle glycogen storage during acute recovery from prolonged exhaustive exercise with such nutritional regimens (12–14,29–32).

In the present investigation, improved recovery of exercise capacity was observed with FRU + MAL in seven of eight participants. This contradicts a previous study adopting a similar experimental design (12). Casey et al. (12) had participants ingest a single 1-g·kg−1 glucose or sucrose bolus at the start of a 4-h recovery period. This amounted to ∼19 g·h−1 of carbohydrate on average compared with 90 g·h−1 throughout recovery in the present investigation. The dosing provided by Casey et al. (12) was substantially lower than those demonstrating enhanced hepatic, with similar muscle, glycogen synthesis during short-term recovery from prolonged exercise with fructose–glucose carbohydrate sources (∼69–116 g·h−1) (13,14,31). Indeed, Casey and colleagues observed no significant differences in muscle or hepatic glycogen synthesis between the sucrose and the glucose trials. Therefore, although no measure of glycogen synthesis was made presently, it is possible that the failure to observe an effect on subsequent exercise capacity by Casey et al. (12) occurred due to the lower carbohydrate doses and similar metabolic recovery provided between conditions. The use of exercise capacity protocols has been questioned regarding issues of reliability (33), but a strong coefficient of variation for bout 1 exercise capacity was observed presently, replicating recent work (20). The larger carbohydrate doses used in the present investigation may have facilitated a metabolic advantage with FRU + MAL, and this may be required to ascertain the observed large beneficial effect on subsequent exercise capacity.

In the present investigation, there is some indication second bout exercise capacity was limited by carbohydrate availability for oxidation, presumably in skeletal muscle, as the CHOtot oxidation rate significantly declined at exhaustion in both trials. This reduction in carbohydrate oxidation rate is in line with some (5,15,34,35), but not all (16,36,37), previous investigations adopting similar repeated exercise capacity protocols. Although speculative, carbohydrate oxidation rates during the second bout in the present study may have become unsustainable to fuel the exercise intensity. It is possible that the enhanced second bout exercise capacity observed with FRU + MAL is attributable to an ability to maintain whole-body carbohydrate oxidation rates for longer before the reduction seemingly associated with fatigue. Accordingly, the absolute CHOtot oxidized in bout 2 was significantly greater with FRU + MAL (Table 1), although this could be an artifact of the enhanced bout 2 exercise duration. The existence of this effect is supported by the modeled relationship between CHOtot oxidation rate and time with FRU + MAL. That is, CHOtot in FRU + MAL was estimated to be significantly greater at the point of exhaustion in GLU + MAL in the seven participants who performed better in the FRU + MAL trial. This suggests that the augmented bout 2 exercise capacity seen with FRU + MAL might be attributed to enhanced ability to sustain whole-body carbohydrate oxidation at the rate required to support the exercise intensity. In further support of a metabolic explanation for the observed effect is that the one participant who demonstrated reduced bout 2 exercise capacity with FRU + MAL exhibited poorer maintenance of carbohydrate oxidation rate in that trial.

As compared with GLU + MAL, greater CHOing oxidation rates were observed at 15 and 30 min with FRU + MAL, alongside similar declines at exhaustion. This supports the suggestion that enhanced carbohydrate availability facilitated the greater second bout exercise capacity with FRU + MAL. Greater CHOing oxidation rates may reflect augmented hepatic, and similar muscle, glycogen synthesis with FRU + MAL, an effect observed previously with similar dosing regimens (13,14,31). Greater whole-body glycogen synthesis, derived from the ingested carbohydrate, may therefore facilitate greater carbohydrate availability for oxidation by working skeletal muscle during bout 2. It must also be acknowledged that the source of the additional oxidized ingested carbohydrates cannot be discerned in the present investigation. That is, it is not possible to determine what proportion of the oxidized ingested carbohydrate was first stored in muscle, in liver, or oxidized directly after absorption. There is a wealth of literature describing the more rapid intestinal absorption and oxidation of glucose–fructose carbohydrate sources ingested during exercise compared with glucose alone (10), which could plausibly contribute to the observed effect on CHOing oxidation rates if participants began bout 2 with any unabsorbed carbohydrate residing in the gut. Furthermore, greater plasma lactate concentrations were observed during the recovery period with FRU + MAL, a finding in line with previous investigations (14,30–32). This likely reflects augmented hepatic lactate production derived from ingested fructose (10). Lactate is a glycogenic precursor (10) and carbohydrate substrate that can be oxidized directly (38). The observed greater plasma lactate concentrations during recovery with FRU + MAL may therefore be derived from ingested fructose-derived hepatic lactate production and provide substrate for whole-body glycogen synthesis or direct oxidation in the early stages of bout 2, thereby supporting the greater CHOing oxidation rates with FRU + MAL. Further mechanistic work is required to establish the metabolic route by which carbohydrate ingested during recovery is oxidized during bout 2.

Similar to previous investigations adopting similar repeated exercise capacity protocols (5,15,16,34–37), it does not appear that hypoglycemia limited exercise in the present investigation, as evidenced by the absence of low plasma glucose concentrations at exhaustion in both trials (Supplementary Fig. 1). However, there is now acknowledgment that differences in gut comfort can affect prolonged exercise performance (39). In the present investigation, no clear significant differences between trials were observed for gut comfort during recovery, which is in contradiction to previous investigations reporting greater self-reported symptoms of gastrointestinal distress with glucose ingestion alone, although the severity of these symptoms was unclear, and a second bout of exercise was not performed (14,31). Any differences during bout 2 were of small numeric magnitude (Fig. 2). The mean value for nausea in the GLU + MAL trial at exhaustion (3.1 ± 2.2 AU) reflects symptoms between “slight” and “moderate.” Interestingly, during bout 2, stomach fullness progressively, and significantly, declined with FRU + MAL, but this was not observed with GLU + MAL. Greater stomach fullness with MAL + GLU might be explained by accumulation of carbohydrate in the gut, given the more rapid intestinal absorption of fructose–glucose sources (40). Again, stomach fullness at exhaustion with GLU + MAL was less than “moderate” (3.8 ± 2.4 AU). However, although these values appear of small magnitude, it is not possible to discern the threshold nausea and stomach fullness values likely to affect exercise cessation, and so between-trial differences in GC cannot be dismissed as an explanation for the observed effect on exercise capacity.

In conclusion, the present investigation has for the first time demonstrated that maltodextrin–fructose coingestion enhances short-term recovery of endurance exercise capacity. Second, accompanying data suggest that some of the effect may be explained by increased carbohydrate availability, although a contribution from improved GC cannot be dismissed. If verified in future work, these results have implications for endurance athletes aiming to optimize performance in repeated bouts of prolonged exhaustive exercise with limited recovery duration.

The authors thank all participants for their time and effort. T. P. was funded by a Public Scholarship, Development, Disability, and Maintenance Fund of the Republic of Slovenia. No other sources of funding were used.

The authors declare no conflicts of interest. The results of the present study are presented clearly, honestly, and without fabrication, falsification, or inappropriate data manipulation and do not constitute endorsement by the American College of Sports Medicine.


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