Exercise In CON Research Articles

Two Short, Daily Activity Bouts vs. One Long Bout: Are Health and Fitness Improvements Similar Over Twelve and Twenty-Four Weeks?

This study sought to determine whether a 12-week intermittent (INT; 2 x 15 min.d(-1)) exercise program yielded similar improvements in cardiovascular health and fitness, compared with a traditional 12-week, 30-minute continuous (CON; 1 x 30 min.d(-1)) exercise program. A second purpose was to determine the effects of switching exercise programs and continuing training for an additional 12 weeks. Twenty women and 17 men, (age 48.8 +/- 9.0 years) were divided randomly into 2 groups: INT (n = 20) and CON (n = 17). Aerobic exercise was performed 4 d.wk(-1) for 12 weeks. Subjects then crossed over to the opposite training program for an additional 12 weeks of training. Subjects exercised incrementally for weeks 1-4 and training was conducted at 70-80% heart rate reserve for weeks 5-24. Both groups showed comparable exercise adherence, completing 96.6 +/- 12.2% (CON) and 96.3% +/- 17.7% (INT) of the prescribed exercise time. The INT walked at a lower percentage of Vo(2)max, maximum heart rate, systolic blood pressure, and diastolic blood pressure (p < 0.05). Maximal oxygen consumption increased by 4.5% in CON and by 8.7% in INT. Following the second 12 weeks, Vo(2)max increased by 3.6 and 7.7% in CON and INT, respectively. Treadmill test time increased by 41 seconds in CON (p < 0.05) and 71 seconds in INT (p < 0.05) after 12 weeks of training. High-density lipoproteins significantly increased in the INT group following the first 12 weeks of training. This study suggests that an INT exercise program, which is incremental in nature, provides comparable, and in some cases greater, health and fitness benefits than those expected following traditional CON exercise training.

Impact of glutamine supplementation on glucose homeostasis during and after exercise

The interaction of glutamine availability and glucose homeostasis during and after exercise was investigated, measuring whole body glucose kinetics with [3-3H]glucose and net organ balances of glucose and amino acids (AA) during basal, exercise, and postexercise hyperinsulinemic-euglycemic clamp periods in six multicatheterized dogs. Dogs were studied twice in random treatment order: once with glutamine (12 micromol.kg(-1).min(-1); Gln) and once with saline (Con) infused intravenously during and after exercise. Plasma glucose fell by 7 mg/dl with exercise in Con (P < 0.05), but it did not fall with Gln. Gln further stimulated whole body glucose production and utilization an additional 24% above a normal exercise response (P < 0.05). Net hepatic uptake of glutamine and alanine was greater with Gln than Con during exercise (P < 0.05). Net hepatic glucose output was increased sevenfold during exercise with Gln (P < 0.05) but not with Con. Net hindlimb glucose uptake was increased similarly during exercise in both groups (P < 0.05). During the postexercise hyperinsulinemic-euglycemic period, glucose production decreased to near zero with Con, but it did not decrease below basal levels with Gln. Gln increased glucose utilization by 16% compared with Con after exercise (P < 0.05). Furthermore, net hindlimb glucose uptake in the postexercise period was increased approximately twofold vs. basal with Gln (P < 0.05) but not with Con. Net hepatic uptake of glutamine during the postexercise period was threefold greater for Gln than Con (P < 0.05). In conclusion, glutamine availability modulates glucose homeostasis during and after exercise, which may have implications for postexercise recovery.

Heat stress, cytokines, and the immune response to exercise

To examine the effect of exercise and heat stress on cytokine production, seven males (77 ± 2 kg; VO 2peak = 4.7 ± 0.4 L min −1) completed two (15 °C; CON or 35 °C; HEAT) 90 min cycling trials at 70% VO 2peak. Blood samples were collected throughout and analysed for spontaneous, and LPS-stimulated intracellular monocyte cytokine production, plasma cytokine levels, and circulating stress hormone concentration. Plasma epinephrine, norepinephrine, and cortisol concentration were elevated ( P < .05) as a result of exercise in CON. HEAT increased ( P < .05) epinephrine and norepinephrine levels, however, cortisol concentration was not different between the two trials. Exercise had no effect on the concentration of circulating monocytes spontaneously producing IL-6, TNF-α or IL-1α, however, there was a decrease in the amount of TNF-α per cell post-compared with pre-exercise. HEAT had no effect on spontaneous intracellular cytokine production. Circulating levels of both IL-6 and TNF-α were elevated in HEAT, but not in CON. Upon stimulation with LPS, the concentration of monocytes positive for IL-6, TNF-α, and IL-1α production was elevated ( P < .01) post- and 2 h post-compared with pre-exercise. Stimulated cells, however, produced less ( P < .05) TNF-α post-exercise and less ( P < .05) TNF-α and IL-6 2 h post-exercise. HEAT resulted in an increase ( P < .05) in the concentration of stimulated cells positive for TNF-α and IL-1α, however, did not affect the amount of cytokine produced by stimulated monocytes. These results demonstrate that exercise decreases the amount of cytokine produced by LPS-stimulated monocytes, possibly due to elevated levels of circulating stress hormones. Heat stress did not, however, augment the suppression in the amount of cytokine produced by circulating monocytes upon stimulation, despite elevated catecholamines.

Suppression of plasma free fatty acids upregulates peroxisome proliferator-activated receptor (PPAR) α and δ and PPAR coactivator 1α in human skeletal muscle, but not lipid regulatory genes

Fatty acids are an important ligand for peroxisome proliferator-activated receptor (PPAR) activation and transcriptional regulation of metabolic genes. To examine whether reduced plasma free fatty acid (FFA) availability affects the mRNA content of proteins involved in fuel metabolism in vivo, the skeletal muscle mRNA content of various transcription factors, transcriptional coactivators and genes encoding for lipid regulatory proteins were examined before and after 3 h of cycle exercise with (NA) and without (CON) pre-exercise ingestion of nicotinic acid (NA). NA resulted in a marked (3- to 6-fold) increase (P<0.05) in PPARalpha, PPARdelta and PPAR coactivator 1alpha (PGC1alpha) mRNA, but was without effect on nuclear respiratory factor-1 and Forkhead transcription factor, fatty acid transcolase/CD36, carnitine palmitoyl transferase 1, hormone sensitive lipase (HSL) and pyruvate dehydrogenase kinase 4. Exercise in CON was associated with increased (P<0.05) PPARalpha, PPARdelta and PGC1alpha mRNA, which was similar in magnitude to levels observed with NA at rest. Exercise was generally without effect on the mRNA content of lipid regulatory proteins in CON and did not affect the mRNA content of the measured subset of transcription factors, transcriptional co-activators and lipid regulatory proteins during NA. To determine the possible mechanisms by which NA might affect PGC1alpha expression, we measured p38 MAP kinase (MAPK) and plasma epinephrine. Phosphorylation of p38 MAPK was increased (P<0.05) by NA treatment at rest, and this correlated (r2=0.84, P<0.01) with increased PGC1alpha. Despite this close relationship, increasing p38 MAPK in human primary myotubes was without effect on PGC1alpha mRNA content. Plasma epinephrine was elevated (P<0.05) by NA at rest (CON: 0.27+/-0.06, NA: 0.72+/-0.11 nM) and throughout exercise. Incubating human primary myotubes with epinephrine increased PGC1alpha independently of changes in p38 MAPK phosphorylation. Hence, despite the fact that NA ingestion decreased FFA availability, it promoted the induction of PPARalpha/delta and PGC1alpha gene expression to a similar degree as prolonged exercise. We suggest that the increase in PGC1alpha may be due to the elevated plasma epinephrine levels. Despite these changes in transcription factors/coactivators, the mRNA content of lipid regulatory proteins was generally unaffected by plasma FFA availability.

Hyperthermia Increases Exercise-induced Oxidative Stress

The purpose of this investigation was to examine oxidative markers after exercise in a hyperthermic environment (35 degrees C, 70 % RH) (Hot) versus a neutral environment (25 degrees C, 40 % RH) (Con). Hyperthermia may exacerbate oxidative stress by uncoupling the mitochondrial respiratory chain or by inhibiting antioxidant defense mechanisms, but this has not been assessed in vivo. Six male subjects performed low-intensity exercise (50 % VO(2max)) on a treadmill in Hot until a core temperature of 39.5 degrees C was reached, and for an equivalent time in Con. Blood samples were drawn before and immediately after exercise and at 8 min and 15 min following exercise. Samples were analyzed for F2 isoprostanes (FIP), lipid hydroperoxides (LPO), and lactate. A 2 x 4 repeated measures ANOVA was used to test for treatment, time, and interaction effects for FIP, LPO, and lactate. Differences in VO(2) were tested with Student's t-test. Significance was set at p < 0.05. Oxygen consumption was not significantly different between Hot and Con. The pattern of change of FIP and lactate in Hot was significant versus exercise in Con. LPO was significantly elevated over time in both Hot and Con, but the pattern of change was not significantly different. Ending core temperatures and heart rates were significantly elevated in Hot versus Con. These data indicate that hyperthermia increases oxidative stress and selectively affects specific lipid markers, independent of oxygen consumption.

Glucose ingestion attenuates the exercise-induced increase in circulating heat shock protein 72 and heat shock protein 60 in humans

Heat shock protein (Hsp) 72 is a cytosolic stress protein that is highly inducible by several factors including exercise. Hsp60 is primarily mitochondrial in cellular location, plays a key role in the intracellular protein translocation and cytoprotection, is increased in skeletal muscle by exercise, and is found in the peripheral circulation of healthy humans. Glucose deprivation increases Hsp72 in cultured cells, whereas reduced glycogen availability elevates Hsp72 in contracting human skeletal muscle. To determine whether maintained blood glucose during exercise attenuates the exercise-induced increase in intramuscular and circulating Hsp72 and Hsp60, 6 males performed 120 minutes of semirecumbent cycling at approximately 65% maximal oxygen uptake on 2 occasions while ingesting either a 6.4% glucose (GLU) or sweet placebo (CON) beverage throughout exercise. Muscle biopsies, obtained before and immediately after exercise, were analyzed for Hsp72 and Hsp60 protein expression. Blood samples were simultaneously obtained from a brachial artery, a femoral vein, and the hepatic vein before and during exercise for the analysis of serum Hsp72 and Hsp60. Leg and hepatosplanchnic blood flow were measured to determine Hsp72-Hsp60 flux across these tissue beds. Neither exercise nor glucose ingestion affected the Hsp72 or Hsp60 protein expression in, or their release from, contracting skeletal muscle. Arterial serum Hsp72 increased (P < 0.05) throughout exercise in both trials but was attenuated (P < 0.05) in GLU. This may have been in part because of the increased (P < 0.05) hepatosplanchnic Hsp72 release in CON, being totally abolished (P < 0.05) in GLU. Serum Hsp60 increased (P < 0.05) after 60 minutes of exercise in CON before returning to resting levels at 120 minutes. In contrast, no exercise-induced increase in serum Hsp60 was observed in GLU. We detected neither hepatosplanchnic nor contracting limb Hsp60 release in either trial. In conclusion, maintaining glucose availability during exercise attenuates the circulating Hsp response in healthy humans.

Regulation of glucose kinetics during intense exercise in humans: effects of α- and β-adrenergic blockade

This study examined the effect of combined α- and β-adrenergic blockade on glucose kinetics during intense exercise. Six endurance-trained men exercised for 20 minutes at approximately 78% of their peak oxygen consumption (V o 2) following ingestion of a placebo (CON) or combined α- (prazosin hydrochloride) and β- (timolol maleate) adrenoceptor antagonists (BLK). Plasma glucose increased during exercise in CON (0 minutes: 5.5 ± 0.1; 20 minutes: 6.5 ± 0.3 mmol · L −1, P < .05). In BLK, the exercise-induced increase in plasma glucose was abolished (0 minutes: 5.7 ± 0.3; 20 minutes: 5.7 ± 0.1 mmol · L −1). Glucose kinetics were measured using a primed, continuous infusion of [6,6- 2H] glucose. Glucose production was not different between trials; on average these values were 25.3 ± 3.9 and 30.9 ± 4.4 μmol · kg −1 · min −1 in CON and BLK, respectively. Glucose uptake during exercise was greater ( P < .05) in BLK (30.6 ± 4.6 μmol · kg −1 · min −1) compared with CON (18.4 ± 2.5 μmol · kg −1 · min −1). In BLK, plasma insulin and catecholamines were higher ( P < .05), while plasma glucagon was unchanged from CON. Free fatty acids (FFA) and glycerol were lower ( P < .05) in BLK. These findings demonstrate that adrenergic blockade during intense exercise results in a blunted plasma glucose response that is due to enhanced glucose uptake, with no significant change in glucose production.

Effects of plasma adrenaline on hormone-sensitive lipase at rest and during moderate exercise in human skeletal muscle.

We investigated the effect of increased plasma adrenaline on hormone-sensitive lipase (HSL) activity and extracellular regulated kinase (ERK) 1/2 phosphorylation during exercise. Seven untrained men rested for 20 min and exercised for 10 min at 60 % peak pulmonary oxygen uptake on three occasions: with adrenaline infusion throughout rest and exercise (ADR), with no adrenaline infusion (CON) and with adrenaline infusion commencing after 3 min of exercise (EX+ADR). Muscle samples were obtained at rest before (Pre, -20 min) and after (0 min) infusion, and at 3 and 10 min of cycling. Exogenous adrenaline infusion increased (P < 0.05) plasma adrenaline at rest during ADR, which resulted in greater HSL activity (Pre, 2.14 +/- 0.10 mmol min-1 (kg dry matter (dm))-1; 0 min, 2.74 +/- 0.20 mmol min-1 (kg dm)-1). Subsequent exercise had no effect on HSL activity. During exercise in CON, HSL activity was increased (P < 0.05) above rest at 3 min but was not increased further by 10 min. The infusion of exogenous adrenaline at 3 min of exercise in EX+ADR resulted in a marked elevation in plasma adrenaline levels (3 min, 0.57 +/- 0.12 nM; 10 min, 10.08 +/- 0.84 nM) and increased HSL activity by 25 %. HSL activity at 10 min was greater (P < 0.05) in EX+ADR compared with CON. There were no changes between trials in the plasma concentrations of insulin and free fatty acids (FFA) and the muscle contents of free AMP, all putative regulators of HSL activity. ERK1/2 phosphorylation increased at 3 min in CON and EX+ADR. Because HSL activity did not increase during exercise when adrenaline was infused prior to exercise (ADR) and because HSL activity increased when adrenaline was infused during exercise (EX+ADR), we conclude that (1) high adrenaline levels can stimulate HSL activity regardless of the metabolic milieu and (2) large increases in adrenaline during exercise, independent of changes in other putative regulators, are able to further stimulate the contraction-induced increase in HSL activity. The results also demonstrate that increased ERK 1/2 phosphorylation coincides with elevated HSL activity, indicating that ERK 1/2 may mediate the contraction-induced increase in HSL activity early in exercise.

GLUCOSE INGESTION ATTENUATES THE EXERCISE-INDUCED INCREASE IN PDK4 mRNA IN HUMAN SKELETAL MUSCLE

Recent studies have demonstrated that a single exercise bout increases the transcription rates and mRNA levels of certain metabolic genes, such as PDK4, UCP-3, hexokinase II and LPL, in human skeletal muscle. Furthermore, reduced pre-exercise muscle glycogen potentiated the effect of exercise, suggesting that substrate availability may modulate exercise effects on gene expression. PURPOSE To examine whether increased glucose availability attenuated exercise-induced increases in PDK4 mRNA in human skeletal muscle. METHODS Six male subjects (28±7 yrs; 83±3 kg; VO2peak = 47±6 ml.kg−1 ml·kg−1.min−1) performed 60 min of cycling at 74±2% of VO2peak on two separate occasions, at least one week apart. On one occasion, subjects ingested a 6% CHO-electrolyte drink (GLU), while on the other an equal volume of a sweet placebo (CON) was ingested. A total of 118±17g of CHO was ingested during exercise and recovery in GLU. Muscle samples were obtained from vastus lateralis before and immediately after exercise and after 3 hr of passive recovery. PDK4 mRNA was measured using real time RT-PCR and expressed relative to the housekeeping gene cyclophilin, the expression of which was unaltered by exercise. Plasma samples were measured for glucose, insulin and FFA. RESULTS Exercise in CON resulted in a 20-fold increase (p < 0.05) in PDK4 mRNA, measured 3 hr post-exercise. In contrast, there was no change in PDK4 mRNA in GLU. Plasma insulin levels were higher (p < 0.05) during exercise and recovery in GLU compared with CON, while plasma FFA were lower (0.25±0.02 vs. 0.75±0.06 mmol.l−1, P > 0.05). CONCLUSION Glucose ingestion attenuates the exercise-induced increase in PDK4 mRNA in human skeletal muscle, possibly due to reduced plasma FFA and/or increased plasma insulin.

Exercise with low muscle glycogen augments TCA cycle anaplerosis but impairs oxidative energy provision in humans.

We tested the hypotheses that: (i) exercise with low muscle glycogen would reduce pyruvate flux through the alanine aminotransferase (AAT) reaction and attenuate the increase in tricarboxylic acid (TCA) cycle intermediates, and (ii) attenuation of tricarboxylic acid cycle intermediate (TCAI) pool expansion would limit TCA cycle flux, thereby accelerating phosphocreatine (PCr) degradation. Eight men cycled for 10 min at 70 % of their (VO(2,max) on two occasions: (i) following their normal diet (CON) and (ii) after cycling to exhaustion and consuming a low carbohydrate diet for approximately 2 days (LG). Biopsies (m. vastus lateralis) confirmed that [glycogen] was lower in LG vs. CON at rest (257 +/- 18 vs. 611 +/- 54 mmol (kg dry mass)(-1); P 0.05); however, net glycogenolysis was not different after 1 or 10 min of exercise. PCr degradation from rest to 1 min was approximately 26 % higher in LG vs. CON (38 +/- 4 vs. 28 +/- 4 mmol (kg dry mass)(-1); P< or =0.05). The sum of five measured TCAIs (approximately 90 % of total pool) was not different between trials at rest and after 1 min, but was higher after 10 min in LG vs. CON (5.51 +/- 0.43 vs. 4.45 +/- 0.49 mmol (kg dry mass)(-1); P 0.05). Pyruvate dehydrogenase complex (PDC) activity was lower during exercise in LG vs. CON (2.2 +/- 0.2 vs. 1.4 +/- 0.2 mmol min(-1) (kg wet weight)(-1) after 10 min; P< or =0.05), and acetylcarnitine was approximately threefold less, implying increased pyruvate availability for flux through AAT. Resting muscle [glutamate] was higher in LG vs. CON (16.1 +/- 0.8 vs. 11.8 +/- 0.4 mmol (kg dry mass)(-1); P< or =0.05) and the net decrease in [glutamate] during exercise was approximately 30 % greater in LG vs. CON. These findings suggest that: (i) contrary to our hypotheses, LG increased anaplerosis by decreasing PDC flux and/or increasing the conversion of glutamate carbon to TCAIs, and (ii) accelerating the rate of muscle TCAI expansion did not affect oxidative energy provision during the initial phase of contraction, since changes in [TCAI] were not temporally related to PCr degradation.

Human neuromuscular fatigue is associated with altered Na+-K+-ATPase activity following isometric exercise.

The purpose of this study was to investigate the hypothesis that reductions in Na+-K+- ATPase activity are associated with neuromuscular fatigue following isometric exercise. In control (Con) and exercised (Ex) legs, force and electromyogram were measured in 14 volunteers [age, 23.4 +/- 0.7 (SE) yr] before and immediately after (PST0), 1 h after (PST1), and 4 h after (PST4) isometric, single-leg extension exercise at ~60% of maximal voluntary contraction for 30 min using a 0.5 duty cycle (5-s contraction, 5-s rest). Tissue was obtained from vastus lateralis muscle before exercise in Con and after exercise in both the Con (PST0) and Ex legs (PST0, PST1, PST4), for the measurements of Na+-K+-ATPase activity, as determined by the 3-O-methylfluorescein phosphatase (3-O-MFPase) assay. Voluntary (maximal voluntary contraction) and elicited (10, 20, 50, 100 Hz) force was reduced 30-55% (P < 0.05) at PST0 and did not recover by PST4. Muscle action potential (M-wave) amplitude and area (measured in the vastus medialis) and 3-O-MFPase activity at PST0-Ex were less than that at PST0-Con (P < 0.05) by 37, 25, and 38%, respectively. M-wave area at PST1-Ex was also less than that at PST1-Con (P < 0.05). Changes in 3-O-MFPase activity correlated to changes in M-wave area across all time points (r = 0.38, P < 0.05, n = 45). These results demonstrate that Na+-K+- ATPase activity is reduced by sustained isometric exercise in humans from that in a matched Con leg and that this reduction in Na+-K+-ATPase activity is associated with loss of excitability as indicated by M-wave alterations.

Enhanced pyruvate dehydrogenase activity does not affect muscle O2 uptake at onset of intense exercise in humans.

It has been proposed that the activation state of pyruvate dehydrogenase (PDH) may influence the rate of skeletal muscle O2 uptake during the initial phase of exercise; however, this has not been directly tested in humans. To remedy this, we used dichloroacetate (DCA) infusion to increase the active form of PDH (PDH(a)) and, subsequently, measured leg O2 uptake and markers of anaerobic ATP provision during conditions of intense dynamic exercise, when the rate of muscle O2 uptake would be very high. Six subjects performed brief bouts of one-legged knee-extensor exercise at approximately 110% of thigh peak O2 uptake (65.3 +/- 3.7 W) on several occasions: under noninfused control (Con) and DCA-supplemented conditions. Needle biopsy samples from the vastus lateralis muscle were obtained at rest and after 5 s, 15 s, and 3 min of exercise during both experimental conditions. In addition, thigh blood flow and femoral arteriovenous differences for O2 and lactate were measured repeatedly during the 3-min work bouts (Con and DCA) to calculate thigh O2 uptake and lactate release. After DCA administration, PDH(a) was four- to eightfold higher (P < 0.05) than Con at rest, and PDH(a) remained approximately 130% and 100% higher (P < 0.05) after 5 and 15 s of exercise, respectively. There was no difference between trials after 3 min. Despite the marked difference in PDH(a) between trials at rest and during the initial phase of exercise, thigh O2 uptake was the same. In addition, muscle phosphocreatine utilization and lactate production were similar after 5 s, 15 s, and 3 min of exercise in DCA and Con. The present findings demonstrate that increasing PDH(a) does not alter muscle O2 uptake and anaerobic ATP provision during the initial phase of intense dynamic knee-extensor exercise in humans.

Adrenaline and glycogenolysis in skeletal muscle during exercise: a study in adrenalectomised humans.

The role of adrenaline in regulating muscle glycogenolysis and hormone-sensitive lipase (HSL) activity during exercise was examined in six adrenaline-deficient bilaterally adrenalectomised, adrenocortico-hormonal-substituted humans (Adr) and in six healthy control individuals (Con). Subjects cycled for 45 min at approximately 70% maximal pulmonary O2 uptake (VO2,max) followed by 15 min at approximately 86% VO2,max either without (-Adr and Con) or with (+Adr) adrenaline infusion that elevated plasma adrenaline levels (45 min, 4.49+/-0.69 nmol l(-1); 60 min, 12.41+/-1.80 nmol l(-1)). Muscle samples were obtained at 0, 45 and 60 min of exercise. In -Adr and Con, muscle glycogen was similar at rest (-Adr, 409+/-19 mmol (kg dry wt)(-1); Con, 453+/-24 mmol (kg dry wt)(-1)) and following exercise (-Adr, 237+/-52 mmol (kg dry wt)(-1); Con, 227+/-50 mmol (kg dry wt)(-1)). Muscle lactate, glucose-6-phosphate and glucose were similar in -Adr and Con, whereas glycogen phosphorylase (a/a + b x 100 %) and HSL (% phosphorylated) activities increased during exercise in Con only. Adrenaline infusion increased activities of phosphorylase and HSL as well as blood lactate concentrations compared with those in -Adr, but did not enhance glycogen breakdown (+Adr, glycogen following exercise: 274+/-55 mmol (kg dry wt)(-1)) in contracting muscle. The present findings demonstrate that during exercise muscle glycogenolysis can occur in the absence of adrenaline, and that adrenaline does not enhance muscle glycogenolysis in exercising adrenalectomised subjects. Although adrenaline increases the glycogen phosphorylase activity it is not essential for glycogen breakdown in contracting muscle. Finally, a novel finding is that the activity of HSL in human muscle is increased in exercising man and this is due, at least partly, to stimulation by adrenaline.

Glucose production during strenuous exercise in humans: role of epinephrine.

The increase in hepatic glucose production (HGP) that occurs during intense exercise is accompanied by a simultaneous increase in epinephrine, which suggests that epinephrine may be important in regulating HGP. To further investigate this, six trained men were studied twice. The first trial [control (Con)] consisted of 20 min of cycling at 40 +/- 1% peak oxygen uptake (VO2 peak) followed by 20 min at 80 +/- 2% VO2 peak. During the second trial [epinephrine (Epi)], subjects exercised for 40 min at 41 +/- 2% VO2 peak. Epinephrine was infused during the latter 20 min of exercise and resulted in plasma levels similar to those measured during intense exercise in Con. Glucose kinetics were measured using a primed, continuous infusion of [3-3H]glucose. HGP was similar at rest (Con, 11.0 +/- 0.5 and Epi, 11.1 +/- 0.5 micromol. kg-1. min-1). In Con, HGP increased (P < 0.05) during exercise to 41.0 +/- 5.2 micromol. kg-1. min-1 at 40 min. In Epi, HGP was similar to Con during the first 20 min of exercise. Epinephrine infusion increased (P < 0.05) HGP to 24.0 +/- 2.5 micromol. kg-1. min-1 at 40 min, although this was less (P < 0.05) than the value in Con. The results suggest that epinephrine can increase HGP during exercise in trained men; however, epinephrine during intense exercise cannot fully account for the rise in HGP. Other glucoregulatory factors must contribute to the increase in HGP during intense exercise.

Oral glucose ingestion increases endurance capacity in normal and diabetic (type I) humans.

The effects of an oral glucose administration (1 g/kg) 30 min before exercise on endurance capacity and metabolic responses were studied in 21 type I diabetic patients [insulin-dependent diabetes mellitus (IDDM)] and 23 normal controls (Con). Cycle ergometer exercise (55-60% of maximal O2 uptake) was performed until exhaustion. Glucose administration significantly increased endurance capacity in Con (112 +/- 7 vs. 125 +/- 6 min, P < 0.05) but only in IDDM patients whose blood glucose decreased during exercise (70.8 +/- 8.2 vs. 82.8 +/- 9.4 min, P < 0.05). Hyperglycemia was normalized at 15 min of exercise in Con (7.4 +/- 0.2 vs. 4.8 +/- 0.2 mM) but not in IDDM patients (12.4 +/- 0.7 vs. 15.6 +/- 0.9 mM). In Con, insulin and C-peptide levels were normalized during exercise. Glucose administration decreased growth hormone levels in both groups. In conclusion, oral glucose ingestion 30 min before exercise increases endurance capacity in Con and in some IDDM patients. In IDDM patients, in contrast with Con, exercise to exhaustion attenuates hyperglycemia but does not bring blood glucose levels to preglucose levels.

No effect of carbohydrate feeding on glycogen synthase in human muscle during exercise.

The effect of carbohydrate (CHO) feedings on exercise-mediated changes in glycogen synthase fractional (GSF) activity has been investigated. Subjects cycled at approximately 70% of maximal oxygen uptake on two occasions: the first to fatigue (135 +/- 17 min; mean +/- SE) (control, CON), and the second at the same workload and duration as the first, but with the addition of frequent ingestion of CHO during exercise (0.27 g kg-1 body weight every 15 min). Biopsies were taken from the quadriceps femoris muscle before and immediately after exercise. Plasma glucose and insulin decreased during CON exercise, but remained elevated throughout CHO exercise (end of exercise: glucose = 4.4 +/- 0.2 mM CON vs. 5.8 +/- 0.2 CHO, P < 0.01; insulin = 9 +/- 1 uU ml-1 CON vs. 19 +/- 3 CHO, P < 0.05). Glycogen decreased to approximately 10% of the basal value during CON and to approximately 20% during CHO, and there was no significant difference in net glycogenolysis between treatments. GSF activity averaged 0.25 +/- 0.03 and 0.22 +/- 0.05 at rest, and increased to 0.51 +/- 0.08 and 0.48 +/- 0.09 after exercise in CON and CHO, respectively (P > 0.05 between treatments). It is concluded that under the present conditions CHO feedings do not alter the exercise-mediated changes in GSF activity. The increase in GSF during exercise is attributed at least in part to the decrease in muscle glycogen (which increases the suitability of GS as substrate for GS phosphatase).

Blood glutathione status during exercise: effect of carbohydrate supplementation.

Blood glutathione status and activities of antioxidant enzymes have been investigated during prolonged exercise with or without carbohydrate (CHO) supplementation. Eight subjects cycled at approximately 70% of maximal oxygen uptake to fatigue [134 +/- 19 (SE) min] on the first occasion (control, CON) and at the same work load and duration on the second occasion but with CHO ingestion during exercise. Blood reduced glutathione (GSH) concentration increased from 0.55 +/- 0.05 mM at rest to 0.77 +/- 0.09 mM after 120 min of exercise during CON (P < 0.01) but remained constant during CHO exercise. Blood glutathione disulfide (GSSG) levels were unchanged during CON and CHO exercise. Blood GSH + GSSG content and GSH/GSSG ratio were also significantly (P < 0.05) elevated during CON but not during CHO exercise. The increases in GSH and GSH + GSSG in CON were associated with decreases in plasma glucose and insulin levels. Activities of blood GSH peroxidase, GSSG reductase, and glucose-6-phosphate dehydrogenase were significantly increased during the CHO exercise, whereas only GSSG reductase activity was elevated during the CON ride. It is concluded that blood GSH increases during prolonged exercise and that CHO supplementation may prevent blood GSH increase possibly because of its inhibitory effects on hepatic hormonal releases, which stimulate GSH output.