Caffeine, performance, and metabolism during repeated Wingate exercise tests

1998 ◽  
Vol 85 (4) ◽  
pp. 1502-1508 ◽  
Author(s):  
F. Greer ◽  
C. McLean ◽  
T. E. Graham

Investigations examining the ergogenic and metabolic influence of caffeine during short-term high-intensity exercise are few in number and have produced inconsistent results. This study examined the effects of caffeine on repeated bouts of high-intensity exercise in recreationally active men. Subjects ( n = 9) completed four 30-s Wingate (WG) sprints with 4 min of rest between each exercise bout on two separate occasions. One hour before exercise, either placebo (Pl; dextrose) or caffeine (Caf; 6 mg/kg) capsules were ingested. Caf ingestion did not have any effect on power output (peak or average) in the first two WG tests and had a negative effect in the latter two exercise bouts. Plasma epinephrine concentration was significantly increased 60 min after Caf ingestion compared with Pl; however, this treatment effect disappeared once exercise began. Caf ingestion had no significant effect on blood lactate, O2 consumption, or aerobic contribution at any time during the protocol. After the second Wingate test, plasma NH3concentration increased significantly from the previous WG test and was significantly higher in the Caf trial compared with Pl. These data demonstrate no ergogenic effect of caffeine on power output during repeated bouts of short-term, intense exercise. Furthermore, there was no indication of increased anaerobic metabolism after Caf ingestion with the exception of an increase in NH3 concentration.

1999 ◽  
Vol 9 (2) ◽  
pp. 229-239 ◽  
Author(s):  
Elizabeth Applegate

Athletes use a variety of nutritional ergogenic aids to enhance performance. Most nutritional aids can be categorized as a potential energy source, an anabolic enhancer, a cellular component, or a recovery aid. Studies have consistently shown that carbohydrates consumed immediately before or after exercise enhance performance by increasing glycogen stores and delaying fatigue. Protein and amino acid supplementation may serve an anabolic role by optimizing body composition crucial in strength-related sports. Dietary antioxidants, such as vitamins C and E and carotenes, may prevent oxidative stress that occurs with intense exercise. Performance during high-intensity exercise, such as sprinting, may be improved with short-term creatine loading, and high-effort exercise lasting 1-7 min may be improved through bicarbonate loading immediately prior to activity. Caffeine dosing before exercise delays fatigue and may enhance performance of high-intensity exercise.


2019 ◽  
Vol 14 (8) ◽  
pp. 1117-1123
Author(s):  
Dennis van Erck ◽  
Eric J. Wenker ◽  
Koen Levels ◽  
Carl Foster ◽  
Jos J. de Koning ◽  
...  

Background: Although cyclists often compete at altitude, the effect of altitude on gross efficiency (GE) remains inconclusive. Purpose: To investigate the effect of altitude on GE at the same relative exercise intensity and at the same absolute power output (PO) and to determine the effect of altitude on the change in GE during high-intensity exercise. Methods: Twenty-one trained men performed 3 maximal incremental tests and 5 GE tests at sea level, 1500 m, and 2500 m of acute simulated altitude. The GE tests at altitude were performed once at the same relative exercise intensity and once at the same absolute PO as at sea level. Results: Altitude resulted in an unclear effect at 1500 m (−3.8%; ±3.3% [90% confidence limit]) and most likely negative effect at 2500 m (−6.3%; ±1.7%) on pre-GE, when determined at the same relative exercise intensity. When pre-GE was determined at the same absolute PO, unclear differences in GE were found (−1.5%; ±2.6% at 1500 m; −1.7%; ±2.4% at 2500 m). The effect of altitude on the decrease in GE during high-intensity exercise was unclear when determined at the same relative exercise intensity (−0.4%; ±2.8% at 1500 m; −0.7%; ±1.9% at 2500 m). When GE was determined at the same absolute PO, altitude resulted in a substantially smaller decrease in GE (2.8%; ±2.4% at 1500 m; 5.5%; ±2.9% at 2500 m). Conclusion: The lower GE found at altitude when exercise is performed at the same relative exercise intensity is mainly caused by the lower PO at which cyclists exercise.


2010 ◽  
Vol 108 (6) ◽  
pp. 1472-1478 ◽  
Author(s):  
Patrice Brassard ◽  
Thomas Seifert ◽  
Mads Wissenberg ◽  
Peter M. Jensen ◽  
Christian K. Hansen ◽  
...  

Whether sympathetic activity influences cerebral blood flow (CBF) and oxygenation remains controversial. The influence of sympathetic activity on CBF and oxygenation was evaluated by the effect of phenylephrine on middle cerebral artery (MCA) mean flow velocity ( Vmean) and the near-infrared spectroscopy-derived frontal lobe oxygenation (ScO2) at rest and during exercise. At rest, nine healthy male subjects received bolus injections of phenylephrine (0.1, 0.25, and 0.4 mg), and changes in mean arterial pressure (MAP), MCA Vmean, internal jugular venous O2 saturation (SjvO2), ScO2, and arterial Pco2 (PaCO2) were measured and the cerebral metabolic rate for O2 (CMRO2) was calculated. In randomized order, a bolus of saline or 0.3 mg of phenylephrine was then injected during semisupine cycling, eliciting a low (∼110 beats/min) or a high (∼150 beats/min) heart rate. At rest, MAP and MCA Vmean increased ∼20% ( P < 0.001) and ∼10% ( P < 0.001 for 0.25 mg of phenylephrine and P < 0.05 for 0.4 mg of phenylephrine), respectively. ScO2 then decreased ∼7% ( P < 0.001). Phenylephrine had no effect on SjvO2, PaCO2, or CMRO2. MAP increased after the administration of phenylephrine during low-intensity exercise (∼15%), but this was attenuated (∼10%) during high-intensity exercise ( P < 0.001). The reduction in ScO2 after administration of phenylephrine was attenuated during low-intensity exercise (−5%, P < 0.001) and abolished during high-intensity exercise (−3%, P = not significant), where PaCO2 decreased 7% ( P < 0.05) and CMRO2 increased 17% ( P < 0.05). These results suggest that the administration of phenylephrine reduced ScO2 but that the increased cerebral metabolism needed for moderately intense exercise eliminated that effect.


2007 ◽  
Vol 293 (1) ◽  
pp. R392-R401 ◽  
Author(s):  
Andrew M. Jones ◽  
Daryl P. Wilkerson ◽  
Nicolas J. Berger ◽  
Jonathan Fulford

We hypothesized that a period of endurance training would result in a speeding of muscle phosphocreatine concentration ([PCr]) kinetics over the fundamental phase of the response and a reduction in the amplitude of the [PCr] slow component during high-intensity exercise. Six male subjects (age 26 ± 5 yr) completed 5 wk of single-legged knee-extension exercise training with the alternate leg serving as a control. Before and after the intervention period, the subjects completed incremental and high-intensity step exercise tests of 6-min duration with both legs separately inside the bore of a whole-body magnetic resonance spectrometer. The time-to-exhaustion during incremental exercise was not changed in the control leg [preintervention group (PRE): 19.4 ± 2.3 min vs. postintervention group (POST): 19.4 ± 1.9 min] but was significantly increased in the trained leg (PRE: 19.6 ± 1.6 min vs. POST: 22.0 ± 2.2 min; P < 0.05). During step exercise, there were no significant changes in the control leg, but end-exercise pH and [PCr] were higher after vs. before training. The time constant for the [PCr] kinetics over the fundamental exponential region of the response was not significantly altered in either the control leg (PRE: 40 ± 13 s vs. POST: 43 ± 10 s) or the trained leg (PRE: 38 ± 8 s vs. POST: 40 ± 12 s). However, the amplitude of the [PCr] slow component was significantly reduced in the trained leg (PRE: 15 ± 7 vs. POST: 7 ± 7% change in [PCr]; P < 0.05) with there being no change in the control leg (PRE: 13 ± 8 vs. POST: 12 ± 10% change in [PCr]). The attenuation of the [PCr] slow component might be mechanistically linked with enhanced exercise tolerance following endurance training.


2003 ◽  
Vol 94 (6) ◽  
pp. 2135-2144 ◽  
Author(s):  
Murli Manohar ◽  
Thomas E. Goetz ◽  
Aslam S. Hassan

It is reported that preexercise hyperhydration caused arterial O2 tension of horses performing submaximal exercise to decrease further by 15 Torr (Sosa-Leon L, Hodgson DR, Evans DL, Ray SP, Carlson GP, and Rose RJ. Equine Vet J Suppl 34: 425–429, 2002). Because hydration status is important to optimal athletic performance and thermoregulation during exercise, the present study examined whether preexercise induction of hypervolemia would similarly accentuate the arterial hypoxemia in Thoroughbreds performing short-term high-intensity exercise. Two sets of experiments (namely, control and hypervolemia studies) were carried out on seven healthy, exercise-trained Thoroughbred horses in random order, 7 days apart. In resting horses, an 18.0 ± 1.8% increase in plasma volume was induced with NaCl (0.30–0.45 g/kg dissolved in 1,500 ml H2O) administered via a nasogastric tube, 285–290 min preexercise. Blood-gas and pH measurements as well as concentrations of plasma protein, hemoglobin, and blood lactate were determined at rest and during incremental exercise leading to maximal exertion (14 m/s on a 3.5% uphill grade) that induced pulmonary hemorrhage in all horses in both treatments. In both treatments, significant arterial hypoxemia, desaturation of hemoglobin, hypercapnia, acidosis, and hyperthermia developed during maximal exercise, but statistically significant differences between treatments were not found. Thus preexercise 18% expansion of plasma volume failed to significantly affect the development and/or severity of arterial hypoxemia in Thoroughbreds performing maximal exercise. Although blood lactate concentration and arterial pH were unaffected, hemodilution caused in this manner resulted in a significant ( P < 0.01) attenuation of the exercise-induced expansion of the arterial-to-mixed venous blood O2 content gradient.


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