Influence of Exercise Mode and Carbohydrate on the Immune Response to Prolonged Exercise

1999 ◽  
Vol 9 (2) ◽  
pp. 213-228 ◽  
Author(s):  
Dru A. Henson ◽  
David C. Nieman ◽  
Andy D. Blodgett ◽  
Diane E. Butterworth ◽  
Alan Utter ◽  
...  

The influence of exercise mode and 6% carbohydrate (C) versus placebo (P) beverage ingestion on lymphocyte proliferation, natural killer cell cytotoxicily (NKCA), Interleukin (IL)-1ß production, and hormonal responses to 2.5 hr of intense running and cycling (~75% ) was measured in 10 triathletes serving as their own controls. The C versus P condition (but not exercise mode) resulted in higher plasma glucose concentrations, lower plasma cortisol concentrations, reduced poslexercise lymphocytosis and NKCA, and a lessened T-cell reduction during recovery. No condition or mode effects were observed for concanavalin A and phytohemagglutinin-induced lymphocyte proliferation. Significant mode (but not condition) effects were observed for lipopolysaccharide-induced IL-1ß production over time. However, when expressed per monocyte, the mode effect was abolished and a sustained suppression in IL-1 ß/monocyte was observed in all sessions throughout recovery. These data indicate that carbohydrate ingestion significantly affects plasma glucose and cortisol concentrations, blood lymphocyte counts, and NKCA, whereas exercise mode has no effect on these parameters.

2003 ◽  
Vol 15 (3) ◽  
pp. 266-276 ◽  
Author(s):  
Jean-Marc Foricher ◽  
Nathalie Boisseau ◽  
Nathalie S. Ville ◽  
Phanélie M. Berthon ◽  
Dominique Bentué-Ferrer ◽  
...  

To examine hormonal and metabolic effects of an oral challenge in glucose (≈ 16 g), 15 prepubertal girls performed a 30-min ergocycle test at 60% of Wmax. Among them, 8 ingested an oral glucose challenge between 2 and 3 min after the beginning of the exercise whereas the other 7 girls received no fluid intake. Plasma glucose is influenced by the oral challenge, as the values obtained at the 15th and 30th min are higher than those of the control group. Plasma FFA, catecholamines, and insulin are not significantly modified by the oral challenge. Therefore, it seems that a challenge in glucose at the beginning of a prolonged exercise could avoid a fall in plasma glucose.


2001 ◽  
Vol 11 (2) ◽  
pp. 149-161 ◽  
Author(s):  
Alexander J. Koch ◽  
Jeffrey A. Potteiger ◽  
Marcia A. Chan ◽  
Stephen H. Benedict ◽  
Bruce B. Frey

The effect of carbohydrate supplementation (CHO) on the lymphocyte response to acute resistance exercise was examined in 10 resistance-trained males. Subjects completed a randomized double-blind protocol with sessions separated by 14 days. The exercise session consisted of a high intensity, short rest interval squat workout. Subjects consumed 1.0 g · kg body mass−1 CHO or an equal volume of placebo (PLC) 10 min prior to and 10 min following exercise. Blood was collected at rest (REST), immediately post exercise (POST), and at 1.5 hours and 4.0 hours of recovery, and analyzed for plasma glucose, serum cortisol, leukocyte subsets, and phytohemagglutinin (PHA)-stimulated lymphocyte proliferation. A significant Treatment × Time effect was observed for lymphocyte proliferation between CHO and PLC, but post hoc analyses revealed no between-treatment differences at any post-exercise time point. Lymphocyte proliferation was significantly depressed below REST at POST (−39.2% for PLC, −25.7% for CHO). Significant fluctuations in leukocyte subset trafficking were observed for both treatments at POST, 1.5 hours, and 4.0 hours. Plasma glucose was significantly increased POST in CHO compared to PLC. Cortisol was significantly increased from REST to POST in both treatments. These data support a minimal effect of carbohydrate ingestion on the lymphocyte response to high-intensity resistance exercise.


1985 ◽  
Vol 58 (3) ◽  
pp. 731-737 ◽  
Author(s):  
V. A. Koivisto ◽  
M. Harkonen ◽  
S. L. Karonen ◽  
P. H. Groop ◽  
R. Elovainio ◽  
...  

We examined the influence of various carbohydrates of fuel homeostasis and glycogen utilization during prolonged exercise. Seventy-five grams of glucose, fructose, or placebo were given orally to eight healthy males 45 min before ergometer exercise performed for 2 h at 55% of maximal aerobic power (VO2max). After glucose ingestion, the rises in plasma glucose (P less than 0.01) and insulin (P less than 0.001) were 2.4- and 5.8-fold greater than when fructose was consumed. After 30 min of exercise following glucose ingestion, the plasma glucose concentration had declined to a nadir of 3.9 +/- 0.3 mmol/l, and plasma insulin had returned to basal levels. The fall in plasma glucose was closely related to the preexercise glucose (r = 0.98, P less than 0.001) and insulin (r = 0.66, P less than 0.05) levels. The rate of endogenous glucose production and utilization rose similarly by 2.8-fold during exercise in fructose group and were 10–15% higher than in placebo group (P less than 0.05). Serum free fatty acid levels were 1.5- to 2-fold higher (P less than 0.01) after placebo than carbohydrate ingestion. Muscle glycogen concentration in the quadriceps femoris fell in all three groups by 60–65% (P less than 0.001) during exercise. These data indicate that fructose ingestion, though causing smaller perturbations in plasma glucose, insulin, and gastrointestinal polypeptide (GIP) levels than glucose ingestion, was no more effective than glucose or placebo in sparing glycogen during a long-term exercise.


1987 ◽  
Vol 63 (6) ◽  
pp. 2388-2395 ◽  
Author(s):  
A. R. Coggan ◽  
E. F. Coyle

Seven cyclists exercised at 70% of maximal O2 uptake (VO2max) until fatigue (170 +/- 9 min) on three occasions, 1 wk apart. During these trials, plasma glucose declined from 5.0 +/- 0.1 to 3.1 +/- 0.1 mM (P less than 0.001) and respiratory exchange ratio (R) fell from 0.87 +/- 0.01 to 0.81 +/- 0.01 (P less than 0.001). After resting 20 min the subjects attempted to continue exercise either 1) after ingesting a placebo, 2) after ingesting glucose polymers (3 g/kg), or 3) when glucose was infused intravenously (“euglycemic clamp“). Placebo ingestion did not restore euglycemia or R. Plasma glucose increased (P less than 0.001) initially to approximately 5 mM and R rose (P less than 0.001) to approximately 0.83 with glucose infusion or carbohydrate ingestion. Plasma glucose and R then fell gradually to 3.9 +/- 0.3 mM and 0.81 +/- 0.01, respectively, after carbohydrate ingestion but were maintained at 5.1 +/- 0.1 mM and 0.83 +/- 0.01, respectively, by glucose infusion. Time to fatigue during this second exercise bout was significantly longer during the carbohydrate ingestion (26 +/- 4 min; P less than 0.05) or glucose infusion (43 +/- 5 min; P less than 0.01) trials compared with the placebo trial (10 +/- 1 min). Plasma insulin (approximately 10 microU/ml) and vastus lateralis muscle glycogen (approximately 40 mmol glucosyl U/kg) did not change during glucose infusion, with three-fourths of total carbohydrate oxidation during the second exercise bout accounted for by the euglycemic glucose infusion rate (1.13 +/- 0.08 g/min).(ABSTRACT TRUNCATED AT 250 WORDS)


2001 ◽  
Vol 91 (1) ◽  
pp. 109-114 ◽  
Author(s):  
David C. Nieman ◽  
Dru A. Henson ◽  
Lucille L. Smith ◽  
Alan C. Utter ◽  
Debra M. Vinci ◽  
...  

The influence of carbohydrate (1 l/h of a 6% carbohydrate beverage), gender, and age on pro- and anti-inflammatory plasma cytokine and hormone changes was studied in 98 runners for 1.5 h after two competitive marathon races. The marathoner runners were randomly assigned to carbohydrate (C, n = 48) and placebo (P, n = 50) groups, with beverages administered during the races in a double-blind fashion using color codes. Plasma glucose was higher and cortisol was lower in the C than in the P group after the race ( P < 0.001). For all subjects combined, plasma levels of interleukin (IL)-10, IL-1 receptor antagonist (IL-1ra), IL-6, and IL-8 rose significantly immediately after the race and remained above prerace levels 1.5 h later. The pattern of change in all cytokines did not differ significantly between the 12 women and 86 men in the study and the 23 subjects ≥50 yr of age and the 75 subjects <50 yr of age. The pattern of change in IL-10, IL-1ra, and IL-8, but not IL-6, differed significantly between the C and the P group, with higher postrace values measured for IL-10 (109% higher) and IL-1ra (212%) in the P group and for IL-8 (42%) in the C group. In conclusion, plasma levels of IL-10, IL-1ra, IL-6, and IL-8 rose strongly in runners after a competitive marathon, and this was not influenced by age or gender. Carbohydrate ingestion, however, had a major effect in attenuating increases in cortisol and two anti-inflammatory cytokines, IL-10 and IL-1ra.


1981 ◽  
Vol 51 (4) ◽  
pp. 783-787 ◽  
Author(s):  
V. A. Koivisto ◽  
S. L. Karonen ◽  
E. A. Nikkila

To examine the effect of various carbohydrates on the metabolic and hormonal response to exercise, 75 g glucose, fructose, or placebo were given to nine well-trained males (VO2 max 60 +/- 1 ml . kg-1 . min-1) 45 min before cycle ergometer exercise performed at 75% VO2 max for 30 min. After glucose ingestion, the rise in plasma glucose was 3-fold (P less than 0.005) in plasma insulin 2.5-fold (P less than 0.01) greater than after fructose. During exercise, after glucose administration plasma glucose fell from 5.3 +/- 0.3 to 2.5 +/- 0.2 mmol/l (P less than 0.001) and after fructose from 4.5 +/- 0.1 to 3.9 +/- 0.3 mmol/l (P less than 0.05). The fall in plasma glucose was closely related to the preexercise levels of plasma insulin (r = 0.82, P less than 0.001) and glucose (r = 0.81, P less than 0.001). Both glucose and fructose ingestion decreased the FFA levels by 40–50% (P less than 0.005) and during exercise they remained 30–40% lower after carbohydrate than placebo administration (P less than 0.02). This study suggests that glucose ingestion prior to exercise results in hypoglycemia during vigorous exercise, this rapid fall in plasma glucose is mediated, at least in part, by hyperinsulinemia, and fructose ingestion is associated with a modest rise in plasma insulin and does not result in hypoglycemia during exercise.


1996 ◽  
Vol 271 (1) ◽  
pp. R191-R199 ◽  
Author(s):  
M. Kjaer ◽  
S. F. Pollack ◽  
T. Mohr ◽  
H. Weiss ◽  
G. W. Gleim ◽  
...  

To examine the importance of blood-borne vs. neural mechanisms for hormonal responses and substrate mobilization during exercise, six spinal cord-injured tetraplegic (C5-T1) males (mean age: 35 yr, range: 24-55 yr) were recruited to perform involuntary, electrically induced cycling [functional electrical stimulation (FES)] to fatigue for 24.6 +/- 2.3 min (mean and SE), and heart rate rose from 67 +/- 7 (rest) to 107 +/- 5 (exercise) beats/min. Voluntary arm cranking in tetraplegics (ARM) and voluntary leg cycling in six matched, long-term immobilized (2-12 mo) males (Vol) served as control experiments. In FES, peripheral glucose uptake increased [12.4 +/- 1.1 (rest) to 19.5 +/- 4.3 (exercise) mumol.min-1.kg-1; P < 0.05], whereas hepatic glucose production did not change from basal values [12.4 +/- 1.4 (rest) vs. 13.0 +/- 3.4 (exercise) mumol.min-1.kg-1]. Accordingly, plasma glucose decreased [from 5.4 +/- 0.3 (rest) to 4.7 +/- 0.3 (exercise) mmol/l; P < 0.05]. Plasma glucose did not change in response to ARM or Vol. Plasma free fatty acids and beta-hydroxybutyrate decreased only in FES experiments (P < 0.05). During FES, increases in growth hormone (GH) and epinephrine and decreases in insulin concentrations were abolished. Although subnormal throughout the exercise period, norepinephrine concentrations increased during FES, and responses of heart rate, adrenocorticotropic hormone, beta-endorphin, renin, lactate, and potassium were marked. In conclusion, during exercise, activity in motor centers and afferent muscle nerves is important for normal responses of GH, catecholamines, insulin, glucose production, and lipolysis. Humoral feedback and spinal or simple autonomic nervous reflex mechanisms are not sufficient. However, such mechanisms are involved in redundant control of heart rate and neuroendocrine activity in exercise.


2006 ◽  
Vol 291 (3) ◽  
pp. E566-E573 ◽  
Author(s):  
Robert S. Lee-Young ◽  
Matthew J. Palmer ◽  
Kelly C. Linden ◽  
Kieran LePlastrier ◽  
Benedict J. Canny ◽  
...  

There is evidence that increasing carbohydrate (CHO) availability during exercise by raising preexercise muscle glycogen levels attenuates the activation of AMPKα2 during exercise in humans. Similarly, increasing glucose levels decreases AMPKα2 activity in rat skeletal muscle in vitro. We examined the effect of CHO ingestion on skeletal muscle AMPK signaling during exercise in nine active male subjects who completed two 120-min bouts of cycling exercise at 65 ± 1% V̇o2 peak. In a randomized, counterbalanced order, subjects ingested either an 8% CHO solution or a placebo solution during exercise. Compared with the placebo trial, CHO ingestion significantly ( P < 0.05) increased plasma glucose levels and tracer-determined glucose disappearance. Exercise-induced increases in muscle-calculated free AMP (17.7- vs. 11.8-fold), muscle lactate (3.3- vs. 1.8-fold), and plasma epinephrine were reduced by CHO ingestion. However, the exercise-induced increases in skeletal muscle AMPKα2 activity, AMPKα2 Thr172 phosphorylation and acetyl-CoA Ser222 phosphorylation, were essentially identical in the two trials. These findings indicate that AMPK activation in skeletal muscle during exercise in humans is not sensitive to changes in plasma glucose levels in the normal range. Furthermore, the rise in plasma epinephrine levels in response to exercise was greatly suppressed by CHO ingestion without altering AMPK signaling, raising the possibility that epinephrine does not directly control AMPK activity during muscle contraction under these conditions in vivo.


1998 ◽  
Vol 275 (4) ◽  
pp. R1227-R1231
Author(s):  
H. B. Nielsen ◽  
N. H. Secher ◽  
M. Kappel ◽  
B. K. Pedersen

This study evaluated whether N-acetylcysteine (NAC) attenuates the reduced lymphocyte proliferation and natural killer (NK) cell activity responses to exercise in humans. Fourteen oarsmen were double-blind randomized to either NAC (6 g daily for 3 days) or placebo groups. During 6-min “all-out” ergometer rowing, the concentration of lymphocytes in the peripheral blood increased, with no significant difference between NAC and placebo as reflected in lymphocyte subsets: CD4+, CD8+, CD16+, and CD19+ cells. The phytohemagglutinin-stimulated lymphocyte proliferation decreased from 9,112 ± 2,865 to 5,851 ± 1,588 cpm ( P < 0.05), but it was not affected by NAC. During exercise, the NK cell activity was elevated from 17 ± 3 to 38 ± 4% and it decreased to 7 ± 1% below the resting value 2 h into recovery. Yet, when evaluated as lytic units per CD16+ cell, the NK cell activity decreased during and after exercise without a significant effect of NAC. We conclude that NAC does not attenuate the reduction in lymphocyte proliferation and NK cell activity associated with intense exercise.


2002 ◽  
Vol 12 (4) ◽  
pp. 398-413 ◽  
Author(s):  
Roy L.P.G. Jentjens ◽  
Asker E. Jeukendrup

Pre-exercise carbohydrate feeding may result in rebound hypoglycemia in some but not all athletes. The aim of the present study was to examine whether insulin sensitivity in athletes who develop rebound hypoglycemia is higher compared with those who do not show rebound hypoglycemia. Twenty trained athletes (V̇O2max of 61.8 ± 1.4 ml · kg−1 · min−1) performed an exercise trial on a cycle ergometer. Forty-five minutes before the start of exercise, subjects consumed 500 ml of a beverage containing 75 g of glucose. The exercise trial consisted of · 20 min of submaximal exercise at 74 ± 1% V̇O2max immediately followed by a time trial. Based upon the plasma glucose nadir reached during submaximal exercise, subjects were assigned to a Hypo group (<3.5 mmol/L) and a Non-hypo group (≥3.5 mmol/L). An oral glucose tolerance test was performed to obtain an index of insulin sensitivity (ISI). The plasma glucose nadir during submaximal exercise was significantly lower (p < .01) in the Hypo-group (n = 10) compared with the Non-hypo group (n = 10) (2.7 ± 0.1 vs. 4.1 ± 0.2 mmol/L, respectively). No difference was found in ISI between the Hypo and the Non-hypo group (3.7 ± 0.4 vs. 3.8 ± 0.5, respectively). The present results suggest that insulin sensitivity does not play an important role in the occurrence of rebound hypoglycemia.


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