Pro- and macroglycogenolysis: relationship with exercise intensity and duration.

We examined the net catabolism of two pools of glycogen, proglycogen (PG) and macroglycogen (MG), in human skeletal muscle during exercise. Male subjects (n = 21) were assigned to one of three groups. Group 1 exercised 45 min at 70% maximal O(2) uptake (VO(2 max)) and had muscle biopsies at rest, 15 min, and 45 min. Group 2 exercised at 85% VO(2 max) to exhaustion (45.4 +/- 3.4 min) and had biopsies at rest, 10 min, and exhaustion. Group 3 performed three 3-min bouts of exercise at 100% VO(2 max) separated by 6 min of rest. Biopsies were taken at rest and after each bout. Group 1 had small MG and PG net glycogenolysis rates (ranging from 3.8 +/- 1.0 to 2.4 +/- 0.6 mmol glucosyl units. kg(-1). min(-1)) that did not change over time. In group 2, the MG glycogenolysis rate remained low and unchanged over time, whereas the PG rate was initially elevated (11.3 +/- 2.3 mmol glucosyl units. kg(-1). min(-1)) and declined (P < or = 0.05) with time. During the first 10 min, PG concentration ([PG]) declined (P < or = 0.05), whereas MG concentration ([MG]) did not. Similarly, in group 3, in both the first and the second bouts of exercise [PG] declined (P < or = 0.05) and [MG] did not, although by the end of the second exercise period the [MG] was lower (P < or = 0.05) than the rest level. The net catabolic rates for PG in the first two exercises were 22.6 +/- 6.8 and 21.8 +/- 8.2 mmol glucosyl units. kg(-1). min(-1), whereas the corresponding values for MG were 17.6 +/- 6.0 and 10.8 +/- 5.6. The MG pool appeared to be more resistant to mobilization, and, when activated, its catabolism was inhibited more rapidly than that of PG. This suggests that the metabolic regulation of the two pools must be different.     

Glycogenin activity in human skeletal muscle is proportional to muscle glycogen concentration

The de novo biosynthesis of glycogen is catalyzed by glycogenin, a self-glucosylating protein primer. To date, the role of glycogenin in regulating glycogen metabolism and the attainment of maximal glycogen levels in skeletal muscle are unknown. We measured glycogenin activity after enzymatic removal of glucose by alpha-amylase, an indirect measure of glycogenin amount. Seven male subjects performed an exercise and dietary protocol that resulted in one high-carbohydrate leg (HL) and one low-carbohydrate leg (LL) before testing. Resting muscle biopsies were obtained and analyzed for total glycogen, proglycogen (PG), macroglycogen (MG), and glycogenin activity. Results showed differences (P < 0.05) between HL and LL for total glycogen (438.0 +/- 69.5 vs. 305.7 +/- 57.4 mmol glucosyl units/kg dry wt) and PG (311.4 +/- 38.1 vs. 227.3 +/- 33.1 mmol glucosyl units/kg dry wt). A positive correlation between total muscle glycogen content and glycogenin activity (r = 0.84, P < 0.001) was observed. Similar positive correlations (P < 0.05) were also evident between both PG and MG concentration and glycogenin activity (PG, r = 0.82; MG, r = 0.84). It can be concluded that glycogenin does display activity in human skeletal muscle and is proportional to glycogen concentration. Thus it must be considered as a potential regulator of glycogen synthesis in human skeletal muscle.     

Muscle glycogenolysis and H+ concentration during maximal intermittent cycling

The relationships between muscle glycogenolysis, glycolysis, and H+ concentration were examined in eight subjects performing three 30-s bouts of maximal isokinetic cycling at 100 rpm. Bouts were separated by 4 min of rest, and muscle biopsies were obtained before and after bouts 2 and 3. Total work decreased from 20.5 +/- 0.7 kJ in bout 1 to 16.1 +/- 0.7 and 13.2 +/- 0.6 kJ in bouts 2 and 3. Glycogenolysis was 47.2 and 15.1 mmol glucosyl U/kg dry muscle during bouts 2 and 3, respectively. Lower accumulations of pathway intermediates in bout 3 confirmed a reduced glycolytic flux. In bout 3, the work done represented 82% of the work in bout 2, whereas glycogenolysis was only 32% of that in bout 2. Decreases in ATP and phosphocreatine contents were similar in the two bouts. Muscle [H+] increased from 195 +/- 12 to 274 +/- 19 nmol/l during bout 2, recovered to 226 +/- 8 nmol/l before bout 3, and increased to 315 +/- 24 nmol/l during bout 3. Muscle [H+] could not be predicted from lactate content, suggesting that ion fluxes are important in [H+] regulation in this exercise model. Low glycogenolysis in bout 3 may be due to an inhibitory effect of increased [H+] on glycogen phosphorylase activity. Alternately, reduced Ca2+ activation of fast-twitch fibers (including a possible H+ effect) may contribute to the low overall glycogenolysis. Total work in bout 3 is maintained by a greater reliance on slow-twitch fibers and oxidative metabolism.     

Regulation of fuel metabolism by preexercise muscle glycogen content and exercise intensity.

To date, the results of studies that have examined the effects of altering preexercise muscle glycogen content and exercise intensity on endogenous carbohydrate oxidation are equivocal. Differences in the training status of subjects between investigations may, in part, explain these inconsistent findings. Accordingly, we determined the relative effects of exercise intensity and carbohydrate availability on patterns of fuel utilization in the same subjects who performed a random order of four 60-min rides, two at 45% and two at 70% of peak O(2) uptake (Vo(2 peak)), after exercise-diet intervention to manipulate muscle glycogen content. Preexercise muscle glycogen content was 596 +/- 43 and 202 +/- 21 mmol/kg dry mass (P < 0.001) for high-glycogen (HG) and low-glycogen (LG) conditions, respectively. Respiratory exchange ratio was higher for HG than LG during exercise at both 45% (0.85 +/- 0.01 vs. 0.74 +/- 0.01; P < 0.001) and 70% (0.90 +/- 0.01 vs. 0.79 +/- 0.01; P < 0.001) of Vo(2 peak). The contribution of whole body muscle glycogen oxidation to energy expenditure differed between LG and HG for exercise at both 45% (5 +/- 2 vs. 45 +/- 5%; P < 0.001) and 70% (25 +/- 3 vs. 60 +/- 3%; P < 0.001) of Vo(2 peak). Yet, despite marked differences in preexercise muscle glycogen content and its subsequent utilization, rates of plasma glucose disappearance were similar under all conditions. We conclude that, in moderately trained individuals, muscle glycogen availability (low vs. high) does not influence rates of plasma glucose disposal during either low- or moderate-intensity exercise.     

Short-term training attenuates muscle TCA cycle expansion during exercise in women.

Muscle glycogenolytic flux and lactate accumulation during exercise are lower after 3-7 days of "short-term" aerobic training (STT) in men (e.g., Green HJ, Helyar R, Ball-Burnett M, Kowalchuk N, Symon S, and Farrance B. J Appl Physiol 72: 484-491, 1992). We hypothesized that 5 days of STT would attenuate pyruvate production and the increase in muscle tricarboxylic acid cycle intermediates (TCAI) during exercise, because of reduced flux through the reaction catalyzed by alanine aminotransferase (AAT; pyruvate + glutamate <--> 2-oxoglutarate + alanine). Eight women [22 +/- 1 yr, peak oxygen uptake (Vo2 peak) = 40.3 +/- 4.6 ml. kg-1. min-1] performed seven 45-min bouts of cycle exercise at 70% Vo2 peak over 9 days (1 bout/day; rest only on days 2 and 8). During the first and last bouts, biopsies (vastus lateralis) were obtained at rest and after 5 and 45 min of exercise. Muscle glycogen concentration was approximately 50% higher at rest after STT (493 +/- 38 vs. 330 +/- 20 mmol/kg dry wt; P 相似文献   

Substrate usage during prolonged exercise following a preexercise meal

The effect of a high-carbohydrate meal 4 h before 105 min of exercise at 70% of maximal O2 uptake was determined in seven endurance-trained cyclists and compared with exercise following a 16-h fast. The preexercise meal produced a transient elevation of plasma insulin and blood glucose, which returned to fasting basal levels prior to the initiation of exercise. The meal also resulted in a 42% elevation (P less than 0.05) of glycogen within the vastus lateralis at the beginning of exercise. The 1st h of exercise when subjects were fed was characterized by a 13-25% decline (P less than 0.05) in blood glucose concentration, a suppression of the normal increase in plasma free fatty acids and blood glycerol, and a 45% (P less than 0.05) greater rate of carbohydrate oxidation compared with exercise when subjects were fasted. After 105 min of exercise, there were no significant differences when subjects were fed or fasted regarding blood glucose levels, rate of carbohydrate oxidation, or muscle glycogen concentration. The greater muscle glycogen utilization (97 +/- 18 vs. 64 +/- 8 mmol glucosyl units X kg-1; P less than 0.05) and carbohydrate oxidation when subjects were fed appeared to be derived from the glycogen synthesized following the meal. These results indicate that preexercise feedings alter substrate availability despite a return of plasma insulin to fasting levels prior to exercise and that these effects persist until the 2nd h of exercise.     

Glycogenin activity and mRNA expression in response to volitional exhaustion in human skeletal muscle.

Glycogenolysis results in the selective catabolism of individual glycogen granules by glycogen phosphorylase. However, once the carbohydrate portion of the granule is metabolized, the fate of glycogenin, the protein primer of granule formation, is not known. To examine this, male subjects (n = 6) exercised to volitional exhaustion (Exh) on a cycle ergometer at 75% maximal O2 uptake. Muscle biopsies were obtained at rest, 30 min, and Exh (99 +/- 10 min). At rest, total glycogen concentration was 497 +/- 41 and declined to 378 +/- 51 mmol glucosyl units/kg dry wt following 30 min of exercise (P < 0.05). There were no significant changes in proglycogen, macroglycogen, glycogenin activity, or mRNA in this period (P > or = 0.05). Exh resulted in decreases in total glycogen, proglycogen, and macroglycogen as well as glycogenin activity (P < 0.05). These decrements were associated with a 1.9 +/- 0.4-fold increase in glycogenin mRNA over resting values (P < 0.05). Glycogenolysis in the initial exercise period (0-30 min) was not adequate to induce changes in glycogenin; however, later in exercise when concentration and granule number decreased further, decrements in glycogenin activity and increases in glycogenin mRNA were demonstrated. Results show that glycogenin becomes inactivated with glycogen catabolism and that this event coincides with an increase in glycogenin gene expression as exercise and glycogenolysis progress.     

Acute exercise and GLUT4 expression in human skeletal muscle: influence of exercise intensity.

To examine the influence of exercise intensity on the increases in vastus lateralis GLUT4 mRNA and protein after exercise, six untrained men exercised for 60 min at 39 +/- 3% peak oxygen consumption (V(O2 peak)) (Lo) or 27 +/- 2 min at 83 +/- 2% V(O2 peak) (Hi) in counterbalanced order. Preexercise muscle glycogen levels were not different between trials (Lo: 408 +/- 35 mmol/kg dry mass; Hi: 420 +/- 43 mmol/kg dry mass); however, postexercise levels were lower (P < 0.05) in Hi (169 +/- 18 mmol/kg dry mass) compared with Lo (262 +/- 35 mmol/kg dry mass). Thus calculated muscle glycogen utilization was greater (P < 0.05) in Hi (251 +/- 24 mmol/kg) than in Lo (146 +/- 34). Exercise resulted in similar increases in GLUT4 gene expression in both trials. GLUT4 mRNA was increased immediately at the end of exercise (approximately 2-fold; P < 0.05) and remained elevated after 3 h of postexercise recovery. When measured 3 h after exercise, total crude membrane GLUT4 protein levels were 106% higher in Lo (3.3 +/- 0.7 vs. 1.6 +/- 0.3 arbitrary units) and 61% higher in Hi (2.9 +/- 0.5 vs. 1.8 +/- 0.5 arbitrary units) relative to preexercise levels. A main effect for exercise was observed, with no significant differences between trials. In conclusion, exercise at approximately 40 and approximately 80% V(O2 peak), with total work equal, increased GLUT4 mRNA and GLUT4 protein in human skeletal muscle to a similar extent, despite differences in exercise intensity and duration.     

Preexercise metabolic alkalosis induced via bicarbonate ingestion accelerates Vo2 kinetics at the onset of a high-power-output exercise in humans.

The present study investigated the effect of preexercise metabolic alkalosis on the primary component of oxygen uptake (Vo(2)) kinetics, characterized by tau(1). Seven healthy physically active nonsmoking men, aged 22.4 +/- 1.8 (mean +/- SD) yr, maximum Vo(2) (Vo(2 max)) 50.4 +/- 4 ml.min(-1).kg(-1), performed two bouts of cycling, corresponding to 40 and 87% of Vo(2 max), lasting 6 min each, separated by a 20-min pause, once as a control study and a few days later at approximately 90 min after ingestion of 3 mmol/kg body wt of NaHCO(3). Blood samples for measurements of bicarbonate concentration and hydrogen ion concentration were taken from antecubital vein via catheter. Pulmonary Vo(2) was measured continuously breath by breath. The values of tau(1) were calculated by using six various approaches published in the literature. Preexercise level of bicarbonate concentration after ingestion of NaHCO(3) was significantly elevated (P < 0.01) compared with the control study (28.96 +/- 2.11 vs. 24.84 +/- 1.18 mmol/l; P < 0.01), and [H(+)] was significantly (P < 0.01) reduced (42.79 +/- 3.38 nmol/l vs. 46.44 +/- 3.51 nmol/l). This shift (P < 0.01) was also present during both bouts of exercise. During cycling at 40% of Vo(2 max), no significant effect of the preexercise alkalosis on the magnitude of tau(1) was found. However, during cycling at 87% of Vo(2 max), the tau(1) calculated by all six approaches was significantly (P < 0.05) reduced, compared with the control study. The tau(1) calculated as in Borrani et al. (Borrani F, Candau R, Millet GY, Perrey S, Fuchsloscher J, and Rouillon JD. J Appl Physiol 90: 2212-2220, 2001) was reduced on average by 7.9 +/- 2.6 s, which was significantly different from zero with both the Student's t-test (P = 0.011) and the Wilcoxon's signed-ranks test (P = 0.014).     

Time course of insulin sensitivity and skeletal muscle glycogen synthase activity after a single bout of exercise in horses.

The time course of insulin sensitivity, skeletal muscle glycogen and GLUT4 content, and glycogen synthase (GS) activity after a single bout of intense exercise was examined in eight horses. On separate days, a euglycemic-hyperinsulinemic clamp (EHC) was undertaken at 0.5, 4, or 24 h after exercise or after 48 h of rest [control (Con)]. There was no increase in mean glucose infusion rate (GIR) with exercise (0.5-, 4-, and 24-h trials), and GIR was significantly decreased at 0.5 h postexercise (GIR: 8.6 +/- 2.7, 6.7 +/- 2.0, 9.0 +/- 2.0, and 10.6 +/- 2.2 mg.kg(-1).min(-1) for Con and at 0.5, 4, and 24 h, respectively). Before each EHC, muscle glycogen content (mmol glucosyl units/kg dry muscle) was higher (P < 0.05) for Con (565 +/- 102) than for other treatments (317 +/- 84, 362 +/- 79, and 382 +/- 74 for 0.5, 4, and 24 h, respectively) and muscle GLUT4 content was unchanged. Pre-EHC active-to-total GS activity ratio was higher (P < 0.05) at 0.5, 4, and 24 h after exercise than in Con. Post-EHC active GS and GS activity ratio were higher (P < 0.05) in Con and at 24 h. There was a significant inverse correlation (r = -0.43, P = 0.02) between glycogen content and GS activity ratio but no relationship between GS activity and GIR. The lack of increase in insulin sensitivity, determined by EHC, after exercise that resulted in a significant reduction in muscle glycogen content is consistent with the slow rate of muscle glycogen resynthesis observed in equine studies.     

Preexercise medium-chain triglyceride ingestion does not alter muscle glycogen use during exercise.

This investigation determined whether ingestion of a tolerable amount of medium-chain triglycerides (MCT; approximately 25 g) reduces the rate of muscle glycogen use during high-intensity exercise. On two occasions, seven well-trained men cycled for 30 min at 84% maximal O(2) uptake. Exactly 1 h before exercise, they ingested either 1) carbohydrate (CHO; 0.72 g sucrose/kg) or 2) MCT+CHO [0.36 g tricaprin (C10:0)/kg plus 0.72 g sucrose/kg]. The change in glycogen concentration was measured in biopsies taken from the vastus lateralis before and after exercise. Additionally, glycogen oxidation was calculated as the difference between total carbohydrate oxidation and the rate of glucose disappearance from plasma (R(d) glucose), as measured by stable isotope dilution techniques. The change in muscle glycogen concentration was not different during MCT+CHO and CHO (42.0 +/- 4.6 vs. 38.8 +/- 4.0 micromol glucosyl units/g wet wt). Furthermore, calculated glycogen oxidation was also similar (331 +/- 18 vs. 329 +/- 15 micromol. kg(-1). min(-1)). The coingestion of MCT+CHO did increase (P < 0.05) R(d) glucose at rest compared with CHO (26.9 +/- 1.5 vs. 20.7 +/- 0. 7 micromol.kg(-1). min(-1)), yet during exercise R(d) glucose was not different during the two trials. Therefore, the addition of a small amount of MCT to a preexercise CHO meal did not reduce muscle glycogen oxidation during high-intensity exercise, but it did increase glucose uptake at rest.     

Effects of feeding on muscle blood flow during prolonged exercise in miniature swine

Eight exercise-trained miniature swine were studied during prolonged treadmill runs (100 min) under fasting and preexercise feeding conditions. Each animal ran at identical external work loads that corresponded to 65% of the heart rate reserve (210-220 beats/min) for the two exercise bouts. Cardiac outputs and stroke volumes were higher and heart rates lower for fed than for fasting runs (P less than 0.05). Preexercise feeding did not alter oxygen consumption, core temperature, mean arterial pressure, and arterial-mixed venous oxygen difference during prolonged exercise; however, mixed venous lactate concentration was lower at end exercise than during fasting conditions (1.2 vs. 2.6 mM, P less than 0.05). Microsphere measurements of regional blood flow revealed significantly higher total gastrointestinal flow (23%) for fed than for fasting conditions. Throughout the exercise bout, blood flow to the biceps femoris, semitendinosus, and tibialis anterior muscles was lower in fed than in fasted animals (P less than 0.05). Combined hindlimb muscle blood flow averaged 15 ml.min-1.100 g-1 (18%, P less than 0.05) lower under feeding than fasting run conditions. These findings provide further evidence that cardiovascular reflexes originate in the gut after feeding to increase cardiac output and redistribute a portion of the blood flow away from active muscle to the gastrointestinal tract during prolonged exercise.     

Effects of age and resistance exercise on skeletal muscle interstitial prostaglandin F(2alpha)

Prostaglandin (PG) F2alpha has been shown to contribute to the anabolic events in skeletal muscle. We measured the skeletal muscle interstitial concentration of PGF2alpha at rest and following a standard bout of resistance exercise in eight young (27+/-2 year) and eight old (75+/-4 year) men. Interstitial PGF2alpha concentration was determined from microdialysate samples obtained from two microdialysis probes placed in the vastus lateralis. Microdialysates were collected 1h pre- and 5-6, 8-9, and 24-25 h postexercise. The exercise bout consisted of 4 exercises (3 sets of 8 replications at 80% 1 RM per exercise) emphasizing the quadriceps. Interstitial PGF2alpha levels were not different (P>0.05) between young and old at rest (1.50+/-0.35 vs. 1.52+/-0.30 ng ml-1) or at any time point following the resistance exercise bout. For the young and old combined there was a change (P<0.05) in PGF2alpha levels at 5-6 h (93%) and 8-9 h (95%), which had returned to preexercise levels by 24-25 h. These results show that PGF2alpha is increased in skeletal muscle following a standard bout of resistance exercise and aging does not alter interstitial levels of this PG at rest or after exercise. These data, coupled with previous findings, suggest that the anabolic factor PGF2alpha should be considered when discussing the complex processes that regulate muscle mass in young and old individuals.     

Fiber type-specific muscle glycogen sparing due to carbohydrate intake before and during exercise.

The effect of carbohydrate intake before and during exercise on muscle glycogen content was investigated. According to a randomized crossover study design, eight young healthy volunteers (n = 8) participated in two experimental sessions with an interval of 3 wk. In each session subjects performed 2 h of constant-load bicycle exercise ( approximately 75% maximal oxygen uptake). On one occasion (CHO), they received carbohydrates before ( approximately 150 g) and during (1 g.kg body weight(-1).h(-1)) exercise. On the other occasion they exercised after an overnight fast (F). Fiber type-specific relative glycogen content was determined by periodic acid Schiff staining combined with immunofluorescence in needle biopsies from the vastus lateralis muscle before and immediately after exercise. Preexercise glycogen content was higher in type IIa fibers [9.1 +/- 1 x 10(-2) optical density (OD)/microm(2)] than in type I fibers (8.0 +/- 1 x 10(-2) OD/microm(2); P < 0.0001). Type IIa fiber glycogen content decreased during F from 9.6 +/- 1 x 10(-2) OD/microm(2) to 4.5 +/- 1 x 10(-2) OD/microm(2) (P = 0.001), but it did not significantly change during CHO (P = 0.29). Conversely, in type I fibers during CHO and F the exercise bout decreased glycogen content to the same degree. We conclude that the combination of carbohydrate intake both before and during moderate- to high-intensity endurance exercise results in glycogen sparing in type IIa muscle fibers.     

MR measurements of muscle damage and adaptation after eccentric exercise.

The purposes of this study were, first, to clarify the long-term pattern of T2 relaxation times and muscle volume changes in human skeletal muscle after intense eccentric exercise and, second, to determine whether the T2 response exhibits an adaptation to repeated bouts. Six young adult men performed two bouts of eccentric biceps curls (5 sets of 10 at 110% of the 1-repetition concentric maximum) separated by 8 wk. Blood samples, soreness ratings, and T2-weighted axial fast spin-echo magnetic resonance images of the upper arm were obtained immediately before and after each bout; at 1, 2, 4, 7, 14, 21, and 56 days after bout 1; and at 2, 4, 7 and 14 days after bout 2. Resting muscle T2 [27.6 +/- 0.2 (SE) ms] increased immediately postexercise by 8 +/- 1 ms after both bouts. T2 peaked 7 days after bout 1 at 47 +/- 4 ms and remained elevated by 2.5 ms at 56 days. T2 peaked lower (37 +/- 4 ms) and earlier (2-4 days) after bout 2, suggesting an adaptation of the T2 response. Peak serum creatine kinase values, pain ratings, and flexor muscle swelling were also significantly lower after the second bout (P < 0.05). Total volume of the imaged arm region increased transiently after bout 1 but returned to preexercise values within 2 wk. The exercised flexor compartment swelled by over 40%, but after 2 wk it reverted to a volume 10% smaller than that before exercise and maintained this volume loss through 8 wk, consistent with partial or total destruction of a small subpopulation of muscle fibers.     

Electron spin resonance spectroscopy, exercise, and oxidative stress: an ascorbic acid intervention study.

Oxygen free radicals are highly reactive species that are produced in increased quantities during strenuous exercise and can damage critical biological targets such as membrane phospholipids. The present study examined the effect of acute ascorbic acid supplementation on exercise-induced free radical production in healthy subjects. Results demonstrate increases in the intensity of the alpha-phenyl-tert-butylnitrone adduct (0.05 +/- 0.02 preexercise vs. 0.19 +/- 0.03 postexercise, P = 0.002, arbitrary units) together with increased lipid hydroperoxides (1.14 +/- 0.06 micromol/l preexercise vs. 1.62 +/- 0.19 micromol/l postexercise, P = 0.005) and malondialdehyde (0.70 +/- 0.04 micromol/l preexercise vs. 0.80 +/- 0.04 micromol/l postexercise, P = 0.0152) in the control phase. After supplementation with ascorbic acid, there was no significant increase in the electron spin resonance signal intensity (0.02 +/- 0. 01 preexercise vs. 0.04 +/- 0.02 postexercise, arbitrary units), lipid hydroperoxides (1.12 +/- 0.21 micromol/l preexercise vs. 1.12 +/- 0.08 micromol/l postexercise), or malondialdehyde (0.63 +/- 0.07 micromol/l preexercise vs. 0.68 +/- 0.05 micromol/l postexercise). The results indicate that acute ascorbic acid supplementation prevented exercise-induced oxidative stress in these subjects.     

Caffeine ingestion does not impede the resynthesis of proglycogen and macroglycogen after prolonged exercise and carbohydrate supplementation in humans.

The purpose of this study was to examine the effects of caffeine (Caf) ingestion on pro- (PG) and macroglycogen (MG) resynthesis in 10 healthy men. Subjects completed two trials, consisting of a glycogen-depleting exercise, while ingesting either Caf or placebo capsules. Throughout recovery, biopsies were taken at 0 (exhaustion), 30, 120, and 300 min, and 75 g of carbohydrate were ingested at 0, 60, 120, 180, and 240 min. Whereas Caf ingestion resulted in a higher blood glucose concentration and decreased glycogen synthase fractional velocity (P 相似文献   

Effects of "priming" exercise on pulmonary O2 uptake and muscle deoxygenation kinetics during heavy-intensity cycle exercise in the supine and upright positions.

We hypothesized that the performance of prior heavy exercise would speed the phase 2 oxygen consumption (VO2) kinetics during subsequent heavy exercise in the supine position (where perfusion pressure might limit muscle O2 supply) but not in the upright position. Eight healthy men (mean +/- SD age 24 +/- 7 yr; body mass 75.0 +/- 5.8 kg) completed a double-step test protocol involving two bouts of 6 min of heavy cycle exercise, separated by a 10-min recovery period, on two occasions in each of the upright and supine positions. Pulmonary O2 uptake was measured breath by breath and muscle oxygenation was assessed using near-infrared spectroscopy (NIRS). The NIRS data indicated that the performance of prior exercise resulted in hyperemia in both body positions. In the upright position, prior exercise had no significant effect on the time constant tau of the VO2 response in phase 2 (bout 1: 29 +/- 10 vs. bout 2: 28 +/- 4 s; P = 0.91) but reduced the amplitude of the VO2 slow component (bout 1: 0.45 +/- 0.16 vs. bout 2: 0.22 +/- 0.14 l/min; P = 0.006) during subsequent heavy exercise. In contrast, in the supine position, prior exercise resulted in a significant reduction in the phase 2 tau (bout 1: 38 +/- 18 vs. bout 2: 24 +/- 9 s; P = 0.03) but did not alter the amplitude of the VO2 slow component (bout 1: 0.40 +/- 0.29 vs. bout 2: 0.41 +/- 0.20 l/min; P = 0.86). These results suggest that the performance of prior heavy exercise enables a speeding of phase 2 VO2 kinetics during heavy exercise in the supine position, presumably by negating an O2 delivery limitation that was extant in the control condition, but not during upright exercise, where muscle O2 supply was probably not limiting.     

Regional hemodynamics during postexercise hypotension. II. Cutaneous circulation.

After an acute bout of exercise, there is an unexplained elevation in systemic vascular conductance that is not completely offset by an increase in cardiac output, resulting in a postexercise hypotension. The contributions of the splanchnic and renal circulations are examined in a companion paper (Pricher MP, Holowatz LA, Williams JT, Lockwood JM, and Halliwill JR. J Appl Physiol 97: 2065-2070, 2004). The purpose of this study was to determine the contribution of the cutaneous circulation in postexercise hypotension under thermoneutral conditions (approximately 23 degrees C). Arterial blood pressure was measured via an automated sphygmomanometer, internal temperature was measured via an ingestible pill, and skin temperature was measured with eight thermocouples. Red blood cell flux (laser-Doppler flowmetry) was monitored at four skin sites (chest, forearm, thigh, and leg), and cutaneous vascular conductance (CVC) was calculated (red blood cell flux/mean arterial pressure) and scaled as percent maximal CVC (local heating to 43 degrees C). Ten subjects [6 men and 4 women; age 23 +/- 1 yr; peak O(2) uptake (Vo(2 peak)) 45.8 +/- 2.0 ml.kg(-1).min(-1)] volunteered for this study. After supine rest (30 min), subjects exercised on a bicycle ergometer for 1 h at 60% of their Vo(2 peak) and were then positioned supine for 90 min. Exercise elicited a postexercise hypotension reaching a nadir at 46.0 +/- 4.5 min postexercise (77 +/- 1 vs. 82 +/- 2 mmHg preexercise; P < 0.05). Internal temperature increased (38.0 +/- 0.1 vs. 36.7 +/- 0.1 degrees C preexercise; P < 0.05), remaining elevated at 90 min postexercise (36.9 +/- 0.1 degrees C vs. preexercise; P < 0.05). CVC at all four skin sites was elevated by the exercise bout (P < 0.05), returning to preexercise values within 50 min postexercise (P > 0.05). Therefore, although transient changes in CVC occur postexercise, they do not appear to play an obligatory role in mediating postexercise hypotension under thermoneutral conditions.