![[Feedback]](/icons/banner/feedbackACT.gif){kind=icon}
![[For Subscribers]](/icons/banner/subscriberACT.gif){kind=icon}
![[Archive]](/icons/banner/archiveACT.gif){kind=icon}
![[Search]](/icons/banner/searchACT.gif){kind=icon}
![[Contents]](/icons/banner/tocACT.gif){kind=icon}
|
|
|
|
|
||
*
Kentucky Equine Research, Inc., Versailles, Kentucky 40383 and
Equine Studies Group, WALTHAM Centre for Pet Nutrition, Waltham-on-the-Wolds, Leicestershire, LE14 5RT, UK.
2To whom correspondence should be addressed.
 |
ABSTRACT |
|---|
 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
KEY WORDS: • horse • carbohydrate • fructose • glucose • endurance exercise
|
INTRODUCTION |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
). The slow twitch fibers
of the middle gluteal muscle (7 to 38% of the total fiber population)
may become totally glycogen-depleted during an 80-km endurance ride
(Snow et al. 1981
). Furthermore, an intravenous glucose
infusion has been shown to delay the development of fatigue in horses
during submaximal treadmill exercise (Farris et al. 1995
). To increase carbohydrate availability, competitive
endurance horses are often fed at rest stops during races. These meals
are usually high in starch (grain) and, when hydrolyzed in the small
intestine, such feeds provide a large amount of glucose. In horses fed
grain, marked increases in plasma glucose and insulin concentrations
occur within 1 h of ingestion (Pagan and Harris 1999
). When ~1 kg corn is given 1 h before exercise,
there is a rapid decrease in plasma glucose at the onset of exercise,
and free fatty acid concentrations are suppressed compared to unfed
horses (Lawrence et al. 1995
, Stull and Rodiek 1995
). Moreover, consumption of grain 1 h before exercise
has been shown to accelerate glycogen utilization (Lawrence et al. 1995
).
Fructose, an isomer of glucose, may be a useful alternative source of
supplemental carbohydrate. In resting humans, the increases in blood
glucose and insulin after fructose ingestion are only 10 to 20% of
those measured after an equivalent amount of glucose (Crapo et al. 1980
). Ingestion of fructose 30 to 60 min before exercise
results in a lower insulin peak and less marked fluctuations in blood
glucose concentrations during exercise, in comparison to glucose
(Guezennec et al. 1989
, Ventura et al. 1994
).
In humans, a potential drawback with the use of fructose, as a
carbohydrate supplement, is the risk of development of gastrointestinal
distress. Abdominal discomfort and diarrhea are frequently experienced
when ~1 g/kg body weight fructose is ingested before or during
exercise (Erickson et al. 1987
, Murray et al. 1989
). These effects are caused by the limited capacity for
fructose absorption (Ravich et al. 1983
). Fructose that
is not absorbed in the small intestine passes into the large intestine
and undergoes fermentation. The products of fermentation result in
excess gas formation and development of osmotic diarrhea. In humans,
co-ingestion of glucose with fructose facilitates fructose
absorption (Shi et al. 1997
). Therefore, compared to
fructose alone, a mixture of fructose and glucose may be preferable as
a carbohydrate supplement for human athletes.
Anecdotally, honey is sometimes fed to endurance horses before and
during competitions. Honey contains, on average, 38% fructose and 31%
glucose (Berlitz and Grosch 1987
). Horses can consume 1
g/kg body weight of a 50% glucose/50% fructose mixture, as a 200 g/L
solution, without adverse effects (Roberts 1975
).
However, to the authors’ knowledge, there has been no research into
the effects of feeding fructose without glucose to the exercising
horse. The high incidence of gastrointestinal disturbances in humans
following ingestion of fructose raises concern of similar problems in
horses after consumption of meals high in fructose. In horses,
fermentation of soluble carbohydrate in the large intestine can result
in lactic acidosis and diarrhea (Garner et al. 1977
,
Roberts 1975
).
The overall aim of the present study was to evaluate the suitability of fructose as a carbohydrate supplement for horses. Specifically, we determined the glycemic response following oral administration of fructose, glucose and a 50% glucose/50% fructose mixture, both at rest and during an endurance exercise protocol.
|
MATERIALS AND METHODS |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
. Three Arabian geldings (ages: 7, 9 and 10 y; bodyweights: 395, 442 and 478 kg) were used. Horses were housed in
3 m x 3 m box stalls during the night and at pasture during
the day (0830 to 1600 h). While at pasture, horses were muzzled to
prevent grazing. Horses had access to water at all times and to a salt
block while housed in stalls. Horses were exercised between 0830 and
1600 h. For the 5-mo period before the study, the horses were
exercised 3 d/wk on a treadmill at 0° incline (Stratton Equine
Enterprises Inc., Lexington, KY). On all other days, the horses were
walked for 1 h on a mechanical exerciser. Treadmill exercise was
gradually increased in intensity until the horses could complete 1 h of trotting at 3.6 m/s without difficulty. The horses consumed a constant basal diet throughout the study. Daily, each horse was fed 6.8 kg mixed grass/alfalfa hay (divided and fed at 0700, 1600 and 2200 h) [As fed (g/kg): 153 crude protein, 346 acid detergent fiber, 511 neutral detergent fiber, 26 crude fat, 149 nonstructural carbohydrate, 9.3 calcium, 3.4 phosphorus, 1.7 magnesium, 22.9 potassium, 0.09 sodium, 0.127 iron, 0.022 zinc, 0.008 copper, 0.063 manganese, 0.001 molybdenum.] and 2 kg of an unfortified grain mix (450 g/kg whole oats, 450 g/kg cracked corn, 100 g/kg molasses), divided into two feedings (0700 and 1600 h). [As fed (g/kg): 91 crude protein, 63 acid detergent fiber, 141 neutral detergent fiber, 46 crude fat, 585 nonstructural carbohydrate, 1.4 calcium, 3.2 phosphorus, 1.5 magnesium, 7.9 potassium, 0.58 sodium, 0.103 iron, 0.024 zinc, 0.024 manganese, 0.0019 molybdenum.]. In addition, each horse was fed 84 g of a pelleted mineral and vitamin supplement (Microphase; Kentucky Equine Research, Inc., Lexington, KY) [As fed (g/kg): 133 protein, 27 calcium, 13 phosphorus, 0.88 copper, 2.5 zinc, 0.009 selenium, 0.21 vitamin A, 0.0009 vitamin D, 2.2 vitamin E, 0.21 thiamin, 5.8 choline, 0.11 folic acid, 1.06 niacin, 0.44 pantothenic acid, 0.35 riboflavin, 0.001 vitamin B-12.].
Experimental protocol.
Three treatments were used: D-fructose (F),
D-glucose (G) and 50% fructose/50% glucose (GF). The
study was divided into three periods of 10 d each, with no
interval between periods. In period 1, one horse was allocated to each
treatment. In periods 2 and 3, the treatments were rotated between
horses using an unreplicated 3 x 3 Latin square design.
Fig. 1
summarizes the timetable for each period. On d 1 of each period, no
treatment was given. On d 2–6, the assigned treatment was administered
in the grain fed at 0700 h. The amount of carbohydrate used was
gradually increased (25 g on d 2, then 50 g, 100 g, 200 g and 300 g on d 3–6, respectively). On d 4 and 5 an incremental
exercise test (HR3.6 Test) was performed for determination
of heart rate at a running speed of 3.6 m/s (see below). On d 7, the
Resting Test was conducted (see below). On d 8, no treatment was given.
On d 9 and 10, the Exercise Test was conducted (see below). On days
when the horses were not tested, they were walked for 1 h on a
mechanical exerciser. Three tests were used.
|
(ii) Resting test: On the day before the resting test, the horses were fed 3.4 kg hay and 84 g vitamin and mineral supplement at 2200 h. No feed was provided the following morning. At 0700 h, 300 g of the assigned treatment (dissolved in 1.5 L water; 200 g/L) was administered by stomach tube. Before treatment, two venous blood samples were collected from the jugular vein via a catheter (Abocath, 14 g, 13 cm; Abbott Laboratories, Abbott Park, IL). Following treatment, samples were collected at 30-min intervals over an 8-h period. The plasma was harvested and stored at -18°C. Throughout the study, water was provided in 18-L buckets. Before and 10 and 24 h after treatment, the water buckets were weighed to the nearest 1 g (Ohaus I-10; Ohaus Corporation, Florham Park, NJ) for determination of water consumption. Feces were collected using a commercially available equine harness (Equisan PTY Ltd., Melbourne, Australia). The harness was emptied at 7, 15 and 24 h post-treatment and the feces were weighed. For each collection period, a 400-g sample of feces was taken and frozen at -18°C.
(iii) Exercise test: In each period, horse 1 was tested on the morning of d 9, horse 2 on the afternoon of d 9 and horse 3 on the morning of d 10. Grain was withheld for at least 15 h before each exercise test. A normal allotment of hay was fed 5 h before the protocol. Horses completed two bouts of exercise with the treadmill set at a 0° incline. The total distance was 36,840 m, at a mean speed of 2.9 m/s. The first exercise period (Bout 1) comprised a 5-min walk (1.3 m/s), 60-min trot (3.6 m/s) and 5-min walk (1.3 m/s) on the treadmill, followed by a 20-min walk on a mechanical exerciser (~1.2 m/s). Bout 2 comprised a 5-min walk (1.3 m/s), 90-min trot (3.6 m/s) and 5-min walk (1.3 m/s) on the treadmill, followed by a 20-min walk on the exerciser (~1.2 m/s). Water was offered when the horses were transferred from the treadmill to the exerciser. Between exercise bouts, horses were returned to their stalls and allowed access to water. After completion of Bout 1 (~10 min), 300 g of the assigned treatment (dissolved in 1.5 L water) was administered by stomach tube. Bout 2 commenced 45 min after treatment. Venous blood samples were collected from the jugular vein via a catheter. Samples were obtained: before Bout 1 (Pre-ex 1), after 30 and 60 min of the first trot (Trot 1), before carbohydrate treatment, 30 min after treatment, before Bout 2 (Pre-ex 2), after 15, 30, 45, 60, 75 and 90 min of the second trot (Trot 2), and 30 min after completion of Trot 2 (Post 30). Plasma was harvested and stored at -18°C. HR was recorded at 15-s intervals from 20 min before exercise until 5 min after Bout 2, using a HR monitor (Vantage XL; Polar, Woodbury, NY). Water consumption was measured from the end of Trot 1 until 1 h after Trot 2. Four analyses were performed.
(i) Fecal analysis: To determine fecal water content, three samples of ~50 g were taken from each 400-g sample. These samples were weighed on an analytical balance (Ohaus Corporation, Florham Park, NJ) while still frozen, dried overnight (12 h) at ~100°C and then weighed at 1-h intervals until a constant weight (to the nearest 0.1 g) was achieved. Percentage water content was calculated and the results for the three samples averaged.
(ii) Plasma analysis: Plasma concentrations of L-lactate
and glucose were measured by use of an automated analyzer (2300 STAT;
YSI, Yellow Springs, OH). All samples were analyzed in duplicate; the
reported values represent the average of the two measurements. Total
protein concentration was determined by refractometry (Rood and Riddle
Equine Hospital, Lexington, KY). All samples from the Exercise Test,
except those obtained at 15, 30, 60 and 75 min of Trot 2, were analyzed
for total plasma protein. From the data for total plasma protein, the
percentage change in plasma volume was calculated using the method of
van Beaumont et al. (1972)
.
Plasma insulin concentration was determined by radioimmunoassay (BET Labs, Lexington, KY). In the Resting Test, plasma insulin was measured in samples collected before treatment and in samples that correspond to peak plasma glucose and 30 min after peak glucose. The highest insulin concentration in these latter two samples was taken as peak insulin concentration. In the Exercise Test, insulin was determined in samples collected before and 45 min after carbohydrate administration (Pre-ex 2). Free fatty acid concentration was determined in samples obtained at Pre-ex 1, 60 min of Trot 1, Pre-treatment, Pre-ex 2, 45 and 90 min of Trot 2 and Post 30, by use of an enzymatic colorimetric assay (NEFA C Kit, Wako Chemicals, Richmond, VA).
(iii) HR analysis: The effect of study period on HR and HR3.6 was used to detect changes in fitness during the study. Linear regression analysis was used to detect changes in HR over each bout of trotting (excluding the first 20 min). A significant, positive regression was taken to indicate cardiovascular drift.
(iv) Calculations and statistical analysis: The plasma glucose and lactate data from the Resting Test were used to calculate a number of parameters: (i) the area enclosed between the glucose or lactate vs. time curve and the time axis (AUC5 );(ii) peak plasma glucose or lactate concentration during the 8-h measurement period; and (iii) time elapsed between carbohydrate administration and the occurrence of the peak glucose and lactate concentrations. The average of the two samples obtained before treatment was taken as the baseline value.
Treatment effects were detected using the general linear model for
ANOVA (Minitab version 12.22; Minitab Inc., State College, PA), with
horse, period and treatment as model terms and horse as a random
factor. When the F ratio indicated a significant treatment effect,
planned pair-wise comparisons for treatment were made using
Tukey’s procedure. Homogeneity of variance was tested separately
within each factor using Bartlett’s test. Where variances differed
significantly, natural logs were taken before analyzing the results as
above. Where a skewed distribution was suspected, because of a large
standard deviation in relation to the mean, ranks were taken before
analyzing the results as above. All results are given as mean ± SEM. The null hypothesis was rejected at 
= 0.05.
In the Exercise Test, the pretreatment blood sample for horse 3 in the
fructose treatment was not obtained and is treated as a missing value
throughout.
|
RESULTS |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
The treatments were delivered without complications over an ~1-min period. None of the horses showed signs of gastrointestinal discomfort (colic) or diarrhea.
Fecal weight and water content (overall mean: 76.92 ± 0.46%) were not affected by treatment and were not different for the three fecal collection periods (0 to 7 h post-treatment, 7 to 15 h post-treatment and 15 to 24 h post-treatment).
Water intake between 0700 and 1700 h was not significantly affected by treatment (F: 9.91 ± 1.35; G: 9.18 ± 0.31; GF: 8.91 ± 0.66 kg). However, water intake between 1700 and 0700 h the next day was greater (P = 0.01) after the F treatment (11.42 ± 1.27 kg) than after the G (9.03 ± 1.48 kg) and GF (8.01 ± 0.57 kg) treatments.
With the exception of 300-min post-treatment, when plasma glucose
was lower after the G treatment than after the F or GF treatments
(P = 0.01), the magnitude and time course of the plasma
glucose response did not differ among treatments (Fig. 2A
). Treatment had no effect on peak glucose concentration, time of peak
glucose concentration or AUC (F: 180.5 ± 26.3; G: 162.4 ± 44.9; GF: 179.6 ± 26.0 mmol · min/L).
|
) for plasma lactate
concentration to be higher with the F and GF treatments, compared to
the G treatment. Peak lactate followed the same pattern (P
= 0.08). There was also a trend (P = 0.09) for
lactate to be higher after the F treatment compared with after the G
treatment, 150 min after treatment. Treatment had no effect on time of
peak lactate concentration or AUC (F: 62.0 ± 20.8; G: 16.7
± 12.5; GF: 48.7 ± 11.3 mmol · min/L).
The plasma insulin response was not affected by treatment (Fig. 2C)
.
Exercise test.
All horses completed the exercise test. Variation occurred in the time necessary for administration of the carbohydrate treatments. Hence, the length of the rest period between exercise bouts varied slightly (range 56 to 67 min). However, Bout 2 always commenced 45 min post-treatment. Ambient temperature ranged between 3.3 and 16.1°C and did not differ significantly with treatment (F: 11.90 ± 1.43; G: 8.82 ± 2.60; GF: 12.18 ± 1.26°C) or horse, but was higher (P = 0.007) for period 1 compared to 3.
HR3.6 did not change by period (period 1: 90.6 ± 1.9;
2: 94.0 ± 3.2; 3: 89.90 ± 2.8 beats per min). HR response
to the exercise test was not affected by treatment or period. This
suggests that fitness did not change over time. Mean HR responses for
the combined treatments are presented in Fig. 3
. Cardiovascular drift (0.17 ± 0.02 beats/min2;
P < 0.001) occurred during all bouts of trotting
except period 1, Bout 1 for all horses, and period 3, Bout 1 for horse
3. The gradient of the regression of HR against time was not related to
treatment.
|
The change in plasma volume (as calculated from measurements of total plasma protein) during exercise varied between -9.1 and +6.1%. There was no consistent pattern over the exercise test and no effect of treatment was detected.
In all treatments, plasma glucose concentration increased (P
< 0.001) following carbohydrate administration (Fig. 4A
). At30 min post-treatment, plasma glucose concentration was greater
(P = 0.01) after the GF treatments than after the G
treatments, and greater (P = 0.005) after the G
treatments than after the F treatments. Similarly, at Pre-ex 2,
plasma glucose was greater (P = 0.02) after the GF and
G treatments than after the F treatments. In all trials, plasma glucose
concentration decreased (P < 0.001) during the first
30 min of exercise. However, plasma glucose subsequently increased and,
in each treatment, mean concentrations were relatively stable at ~4.5
to 5.0 mmol/L for the remainder of exercise. During exercise, there
were no differences between treatments for plasma glucose
concentration.
|
Plasma lactate concentration was below baseline during both exercise
bouts, but increased during the interval between exercise bouts (Fig. 4B)
. There was a nonsignificant trend (P = 0.1) for
plasma lactate to be higher after the GF treatments than after the G
treatments at Pre-ex 2 and at 60 min of Trot 2. At 30-min
post-exercise, plasma lactate was higher (P = 0.02)
after the F and GF treatments, than after the G treatments.
Plasma free fatty acid concentration decreased (P = 0.004) following carbohydrate administration and increased
(P < 0.001) with exercise (Fig. 4C)
. At 45 min of Trot
2, there was a nonsignificant trend (P = 0.1) for a
lower free fatty acid concentration after the GF treatments, compared
to the F treatments.
Plasma insulin concentration increased (P < 0.001)
following carbohydrate administration. At Pre-ex 2, plasma insulin
concentration was higher (P = 0.03) after the GF
treatments than after the F treatments (Fig. 4D)
. There was also a
nonsignificant trend (P = 0.06) for higher insulin
after the G treatments, compared to the F treatments, at Pre-ex 2.
|
DISCUSSION |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
Oral administration of 300 g fructose in 1.5 L water (200 g/L)
appears to be safe in horses, as indicated by the absence of adverse
effects or alterations in fecal weight or water content. The plasma
glucose concentration vs. time curves were similar for all treatments.
These results suggest that fructose is well-absorbed by horses and
is rapidly converted to glucose. In agreement with the current study,
Roberts (1975)
found that the glycemic response to a
50% glucose/50% fructose mixture was very similar to the response to
an equivalent dose of glucose. In contrast, fructose administration (50
g) in humans produces only 10 to 20% of the increase in plasma glucose
concentration observed after an equivalent glucose load (Crapo et al. 1980
). This difference suggests that fructose is better
absorbed in horses than in humans, or that horses convert a greater
proportion of absorbed fructose to glucose.
Water consumption between 10 and 24 h after carbohydrate treatment was significantly greater after the F treatments than after the G or GF treatments. The mechanism for this increase in water consumption is not readily apparent. Fructose ingestion did not increase fecal water loss. It is possible that the osmotic effects of unabsorbed fructose could draw water into the intestine, causing a compensatory increase in water consumption. However, it is unlikely that this would occur more than 10 h after fructose administration.
There was a nonsignificant trend for higher peak lactate concentration
after the F and GF treatments, compared with the G after treatments
(Fig. 4B)
. There are three possible reasons for the increase in plasma
lactate concentration. Fructose may be converted to lactate in the
liver and kidney, as has been described in humans (Atwell and Waterhouse 1971
; Björkman and Felig 1982
).
Lactate-producing bacteria in the stomach and small intestine
(Kern et al. 1974
) may metabolize fructose.
Lactate-producing bacteria in the large intestine also may
contribute, as nutrients delivered by stomach tube can reach the cecum
in as little as 60 min (Cuddeford 1999
). In the bovine
rumen, which has a similar microbial population to the equine cecum
(Kern et al. 1974
), both D- and
L-lactate are produced by the fermentation of soluble
carbohydrate (Slyter and Rumsey 1991
). Because only
L-lactate was measured in the current study, the amount of
fructose that underwent microbial fermentation may have been
underestimated. However, the similarity of the glycemic responses to
each treatment suggests that only a small proportion of ingested
fructose was converted to lactate. Further investigation is needed to
determine whether ingested fructose is converted to lactate by horses
and, if so, by what mechanism.
Exercise test.
Plasma insulin concentration at Pre-ex 2 was lower when horses were
given fructose, compared to a 50:50 mixture of fructose and glucose.
There was also a nonsignificant trend for a lower insulin concentration
following fructose administration, compared to glucose. In humans,
commencement of exercise with elevated plasma insulin inhibits
lipolysis and fat oxidation and increases reliance on carbohydrate
oxidation (Costill et al. 1977
). This is disadvantageous
because it increases the rate at which carbohydrate stores are
depleted. While the supply of fat in the body is almost unlimited, the
supply of carbohydrate is not. Depletion of muscle glycogen stores may
cause fatigue during endurance exercise. However, despite the lower
pre-exercise insulin concentration after fructose administration,
free fatty acid concentrations during exercise were similar for all
treatment groups. Further research is needed to determine whether the
lower plasma insulin concentrations in horses after fructose
administration would influence substrate utilization during exercise.
Plasma free fatty acid concentration decreased following carbohydrate administration. However, it recovered rapidly at the onset of exercise and continued to increase throughout exercise. These results suggest that 300 g glucose or fructose could be administered to horses at rest stops during endurance rides, without adversely inhibiting lipolysis.
Pre-exercise elevation in plasma insulin following carbohydrate
consumption can result in a sharp decrease in plasma glucose
concentration early during exercise. This response has been attributed
to an insulin-mediated increase in the rate of glucose uptake by
the peripheral tissues (Horowitz et al. 1997
). However,
despite the lower plasma insulin concentration following fructose
administration, plasma glucose concentrations during the subsequent
bout of exercise were similar for all treatments (Fig. 4A)
. In humans,
pre-exercise (1 h before) fructose ingestion also results in a
smaller increase in plasma insulin concentration compared to an
equivalent dose of glucose. Furthermore, the increase in whole-body
glucose disposal and decrease in plasma glucose concentration during
the first 20 min of low-intensity exercise are attenuated after
fructose ingestion compared to glucose ingestion (Horowitz et al. 1997
). Further study using isotopic tracer methods is
required to determine the effects of these two carbohydrate treatments
on glucose flux in horses during exercise.
Post treatment (30 min), plasma glucose concentration was significantly higher after the GF treatments, than after the G treatments. It is not possible to determine the reason for this from the current study.
It is important to note that the exercise test used in the current study involved only low-intensity exercise. A different response may have been observed for higher intensity exercise. In addition, the use of a small sample size limits the statistical power of the study, so that some treatment effects may not have been detected. For this reason, the authors recommend that further work, utilizing a larger sample size, would be beneficial.
In resting horses, administration of fructose, or a 50% glucose/50% fructose mixture, results in a glycemic response similar to that measured after an equivalent glucose load. These findings indicate that fructose is well-absorbed and rapidly converted to glucose. Furthermore, fructose appears to be well-tolerated by horses, at least at the dose used in this study (~0.7 g/kg body weight). Pre-exercise plasma insulin concentration was lower following fructose administration, than in the other two treatments. The authors suggest fructose may be useful as a carbohydrate supplement for horses before and/or during endurance exercise. However, further research with a larger sample size and use of isotopic tracer methods is needed to assess the effect of fructose supplementation on exercise metabolism and performance.
|
ACKNOWLEDGMENTS |
|---|
|
FOOTNOTES |
|---|
5 Abbreviations used: AUC, the area enclosed between the glucose or lactate vs. time curve and the time axis; F, fructose; G, glucose; GF, 50% glucose/50% fructose; HR, heart rate; HR3.6, heart rate at 3.6 m/s as calculated by linear regression.
Manuscript received November 15, 1999. Initial review completed January 7, 2000. Revision accepted March 23, 2000.
|
REFERENCES |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
1. Atwell M. E., Waterhouse C. Glucose production from fructose. Diabetes 1971;20:193-199[Medline]
2. Berlitz H. D., Grosch W. Sugars, sugar alcohols and honey. Food Chemistry 1987:638 Springer Verlag Berlin
3. Björkman O., Felig P. Role of the kidney in the metabolism of fructose in 60-hour fasted humans. Diabetes 1982;31:516-520[Abstract]
4.
Costill D. L., Coyle E., Dalsky G., Evans W., Fink W., Hoopes D. Effects of elevated plasma FFA and insulin on muscle glycogen usage during exercise. J. Appl. Physiol. 1977;43:695-699
5. Crapo P. A., Kolterman O. G., Olefsky J. M. Effects of oral fructose in normal, diabetic and impaired glucose tolerance subjects. Diabetes Care 1980;3:575-581[Abstract]
6. Cuddeford D. Starch digestion in the horse. Proceedings KER Equine Nutrition Conference 1999:129-139 Lexington, KY.
7. Erickson M. A., Schwarzkopf R. J., McKenzie R. D. Effects of caffeine, fructose and glucose ingestion on muscle glycogen utilization during exercise. Med. Sci. Sports Exerc. 1987;19:579-583[Medline]
8. Farris J. W., Hinchcliff K. W., McKeever K. H., Lamb D. R. Glucose infusion increases duration of prolonged treadmill exercise in Standardbred horses. Equine Vet. J. Suppl. 1995;18:357-361
9. Garner H. E., Hutcheson D. P., Coffman J. R., Hahn A. W., Salem C. Lactic acidosis: A factor associated with equine laminitis. J. Anim. Sci. 1977;45:1037-1041
10. Guezennec C. Y., Satabin P., Duforez F., Merino D., Peronnet F., Koziet J. Oxidation of corn starch, glucose and fructose ingested before exercise. Med. Sci. Sports Exerc. 1989;21:45-50[Medline]
11. Guide for the Care and Use of Agricultural Animals in Agricultural Research and Teaching (1988) Consortium for Developing a Guide for the Use of Agricultural Animals in Agricultural Research and Teaching, Champaign, IL.
12. Horowitz J. F., Mora-Rodriguez R., Byerley L. O., Coyle E. F. Lipolytic suppression following carbohydrate ingestion limits fat oxidation during exercise. Am. J. Physiol. (Endocrinol. Metab. 36) 1997;:E768-E775
13. Kern D. L., Slyter L. L., Leffel E. C., Weaver J. M., Oltjen R. R. Ponies vs. steers: Microbial and chemical characteristics of intestinal ingesta. J. Anim. Sci. 1974;38:559-564
14. Lawrence L. M., Hintz H. F., Soderholm L. V., Williams J., Roberts A. M. Effect of time of feeding on metabolic response to exercise. Equine Vet. J. Suppl. 1995;18:392-395
15. Lindholm A., Bjerneld H., Saltin B. Glycogen depletion pattern in muscle fibres of trotting horses. Acta Physiol. Scand. 1974;90:475-484[Medline]
16. Murray R., Paul G. L., Seifert J. G., Eddy D. E., Halaby G. A. The effects of glucose, fructose and sucrose ingestion during exercise. Med. Sci. Sports Exerc. 1989;21:275-282[Medline]
17. Pagan J. D., Harris P. A. The effects of timing and amount of forage and grain on exercise response in thoroughbred horses. Equine Vet. J. Suppl. 1999;30:451-457[Medline]
18. Ravich W. J., Bayless T. M., Thomas M. Fructose: incomplete intestinal absorption in humans. Gastroenterology 1983;84:26-29[Medline]
19. Roberts M. C. Carbohydrate digestion and absorption studies in the horse. Res. Vet. Sci. 1975;18:64-69[Medline]
20. Shi X., Schedl H. P., Summers R. M., Lambert G. P., Chang R., Xia T., Gisolfi C. Fructose transport mechanisms in humans. Gastroenterology 1997;113:1171-1179[Medline]
21. Slyter L. L., Rumsey T. S. Effect of coliform bacteria, feed deprivation and pH on ruminal D-lactic acid production by steer or continuous-culture microbial populations changed from forage to concentrates. J. Anim. Sci. 1991;69:3055-3066[Abstract]
22. Snow D. H., Baxter P., Rose R. J. Muscle fibre composition and glycogen depletion in horses competing in an endurance ride. Vet. Rec. 1981;108:374-378[Abstract]
23. Stull C., Rodiek A. Effects of post prandial interval and feed type on substrate availability during exercise. Equine Vet. J. Suppl. 1995;18:362-366
24.
van Beaumont W., Greenleaf J. E., Juhos L. Disproportional changes in hematocrit, plasma volume and proteins during exercise and bed rest. J. Appl. Physiol. 1972;33:55-61
25. Ventura J. L., Estruch A., Rodas G., Segura R. Effect of prior ingestion of glucose or fructose on the performance of exercise of intermediate duration. Eur. J. Appl. Physiol. 1994;68:345-349
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
0.05): a = F
and G different; b = G and GF different.
