Rowlands DS, Thorburn MS, Thorp RM, Broadbent S, Shi X. Effect of graded fructose coingestion with maltodextrin on exogenous 14 C-fructose and 13 C-glucose oxidation efficiency and high-intensity cycling performance. J Appl Physiol 104: 1709-1719, 2008. First published March 27, 2008 doi:10.1152/japplphysiol.00878.2007.-The ingestion of solutions containing carbohydrates with different intestinal transport mechanisms (e.g., fructose and glucose) produce greater carbohydrate and water absorption compared with singlecarbohydrate solutions. However, the fructose-ingestion rate that results in the most efficient use of exogenous carbohydrate when glucose is ingested below absorption-oxidation saturation rates is unknown. Ten cyclists rode 2 h at 50% of peak power then performed 10 maximal sprints while ingesting solutions containing 13 C-maltodextrin at 0.6 g/min combined with 14 C-fructose at 0.0 (No-Fructose), 0.3 (Low-Fructose), 0.5 (Medium-Fructose), or 0.7 (High-Fructose) g/min, giving fructose:maltodextrin ratios of 0.5, 0. 8, and 1.2. Mean (percent coefficient of variation) exogenous-fructose oxidation rates during the 2-h rides were 0.18 (19), 0.27 (27), 0.36 (27) g/min in Low-Fructose, Medium-Fructose, and High-Fructose, respectively, with oxidation efficiencies (ϭoxidation/ingestion rate) of 62-52%. Exogenous-glucose oxidation was highest in Medium-Fructose at 0.57 (28) g/min (98% efficiency) compared with 0.54 (28), 0.48 (29), and 0.49 (19) in Low-Fructose, High-Fructose, No-Fructose, respectively; relative to No-Fructose, only the substantial 16% increase (95% confidence limits Ϯ16%) in Medium-Fructose was clear. Total exogenous-carbohydrate oxidation was highest in Medium-Fructose at 0.84 (26) g/min. Although the effect of fructose quantity on overall sprint power was unclear, the metabolic responses were associated with lower perceptions of muscle tiredness and physical exertion, and attenuated fatigue (power slope) in the Medium-Fructose and HighFructose conditions. With the present solutions, low-medium fructose-ingestion rates produced the most efficient use of exogenous carbohydrate, but fatigue and the perception of exercise stress and nausea are reduced with moderate-high fructose doses. dose response; dual-tracer method; substrate metabolism; gastrointestinal distress; fatigue IT IS NOW WIDELY ACCEPTED that ingestion of carbohydrate solutions can delay fatigue and improve endurance performance during high-intensity exercise of ϳ60 min or longer (reviewed in Ref. 25). The proposed mechanisms for performance enhancement are related to the prevention of hypoglycemia and the maintenance of high carbohydrate-oxidation rates during the later stages of exercise, when endogenous muscle and liver carbohydrate stores may become depleted (8). For these reasons and for reasons relating to hydration, there is interest from industry, scientists, and athletes in finding the formulation that will best optimize performance.During exercise, ingested glucose is rapidly absorbed into the circulation and oxidized b...
lands. Attenuated gastric distress but no benefit to performance with adaptation to octanoate-rich esterified oils in well-trained male cyclists. J Appl Physiol 101: [1733][1734][1735][1736][1737][1738][1739][1740][1741][1742][1743] 2006. First published July 13, 2006; doi:10.1152/japplphysiol.00393.2006.-We investigated the effects of modifying a normal dietary fatty acid composition and ingestion of high-fat exercise supplements on gastrointestinal distress, substrate oxidation, and endurance cycling performance. Nine welltrained male cyclists completed a randomized triple-crossover comprising a 2-wk diet high in octanoate-rich esterified oil (MCFA) or twice long-chain fatty acids (LCFA). Following the diets, participants performed 3-h of cycling at 50% of peak power followed by 10 maximal sprints while ingesting either 1) a carbohydrate (CHO)ϩMCFA-rich oil emulsion after the 2-wk MCFA-rich dietary condition (MC-MC, Intervention) and 2) after one of the LCFA-rich dietary conditions (LC-MC, Placebo) or 3) CHO only following a LCFA-rich diet (LC-CHO, Control). During the 3-h ride MCFAadaptation decreased octanoic-acid oxidation by 24% (90% confidence interval: 14 -34%). The CHOϩMCFA-rich oil emulsion reduced endogenous fat oxidation by 61% (33-89%) and 110% (89 -131%) in the MC-MC and LC-MC conditions, respectively, and MCFA-adaptation reduced endogenous-carbohydrate oxidation by 10% (Ϫ3-23%). MCFA-adaptation attenuated gastrointestinal distress and nausea during the sprints, but the effect of the oil emulsion was to lower sprint power by 10.9% (7.7-14.1%) in the LC-MC condition and by 7.1% (5.7-8.5%) in the MC-MC condition, relative to the LC-CHO control; every one unit increase in nausea decreased mean power by 6.0 W (3.2-8.8 W). We conclude that despite some attenuation of endogenous-carbohydrate oxidation and gastric distress following adaptation to a MCFA-rich diet, repeat sprint performance was substantially impaired in response to the ingestion of a CHOϩMCFA-rich oil emulsion. medium-chain fatty acids; structured triacylglycerols; dietary adaptation; supplementation THE FINITE AVAILABILITY of endogenous glycogen as an energy substrate contributes to the development of fatigue and is therefore a limiting factor in athletic performance during prolonged strenuous exercise (23). An increase in plasma free fatty acid (FFA) and fat oxidation has been shown to spare endogenous glycogen, most reliably via fat infusion studies (38). However, fat infusion during racing conditions is not feasible, and long-chain triglyceride ingestion before or during exercise has not been shown to enhance performance (14,32,40). More recently, interest has focused on the ingestion of medium-chain triglycerides (MCTs). Unlike long-chain fatty acids, medium-chain fatty acids (MCFA) can be absorbed more rapidly and directly from the intestinal lumen (5, 13), and their entry into mitochondria does not appear to be rate limited by the acyl-carnitine transfer system to the extent of long chain fatty acids during high-intensity exercise ...
Exercise increases mean body temperature ( Tbody) and cytokine concentrations in plasma. Cytokines facilitate PG production via cyclooxygenase (COX) enzymes, and PGE2 can mediate fever. Therefore, we used a COX-2 inhibitor to test the hypothesis that PG-mediated pyrogenicity may contribute to the raised T body in exercising humans. In a double-blind, cross-over design, 10 males [age: 23 yr (SD 5), V O2 max: 53 ml⅐ kg Ϫ1 ⅐ min Ϫ1 (SD 5)] consumed rofecoxib (50 mg/day; NSAID) or placebo (PLAC) for 6 days, 2 wk apart. Exercising thermoregulation was measured on day 6 during 45-min running (ϳ75% V O2 max) followed by 45-min cycling and 60-min seated recovery (28°C, 50% relative humidity). Plasma cytokine (TNF-␣, IL-10) concentrations were measured at rest and 30-min recovery. T body was similar at rest in PLAC (35.59°C) and NSAID (35.53°C) and increased similarly during running, but became 0.33°C (SD 0.26) lower in NSAID during cycling (37.39°C vs. 37.07°C; P ϭ 0.03), and remained lower throughout recovery. Sweating was initiated at T body of ϳ35.6°C in both conditions but ceased at higher T body in PLAC than NSAID during recovery [36.66°C (SD 0.36) vs. 36.39°C (SD 0.27); P ϭ 0.03]. Cardiac frequency averaged 6 ⅐ min Ϫ1 higher in PLAC (P Ͻ 0.01), whereas exercising metabolic rate was similar (505 vs. 507 W ⅐ m Ϫ2 ; P ϭ 0.56). A modest increase in both cytokines across exercise was similar between conditions. COX-2 specific NSAID lowered exercising heat and cardiovascular strain and the sweating (offset) threshold, independently of heat production, indicating that PGE-mediated inflammatory processes may contribute to exercising heat strain during endurance exercise in humans.
The caudal zona incerta target within the posterior subthalamic area is an investigational site for deep brain stimulation (DBS) in Parkinson disease (PD) and tremor. The authors report on a patient with tremor-predominant PD who, despite excellent tremor control and an otherwise normal neurological examination, exhibited profound difficulty swimming during stimulation. Over the last 20 years, anecdotal reports have been received of 3 other patients with PD who underwent thalamic or pallidal lesioning or DBS surgery performed at the authors' center and subsequently drowned. It may be that DBS puts patients at risk for drowning by specifically impairing their ability to swim. Until this finding can be further examined in larger cohorts, patients should be warned to swim under close supervision soon after DBS surgery.
OBJECTIVEPosterior subthalamic area (PSA) deep brain stimulation (DBS) targeting the zona incerta (ZI) is an emerging treatment for tremor syndromes, including Parkinson’s disease (PD) and essential tremor (ET). Evidence from animal studies has indicated that the ZI may play a role in saccadic eye movements via pathways between the ZI and superior colliculus (incerto-collicular pathways). PSA DBS permitted testing this hypothesis in humans.METHODSSixteen patients (12 with PD and 4 with ET) underwent DBS using the MRI-directed implantable guide tube technique. Active electrode positions were confirmed at the caudal ZI. Eye movements were tested using direct current electrooculography (EOG) in the medicated state pre- and postoperatively on a horizontal predictive task subtending 30°. Postoperative assessments consisted of stimulation-off, constituting a microlesion (ML) condition, and high-frequency stimulation (HFS; frequency = 130 Hz) up to 3 V.RESULTSWith PSA HFS, the first saccade amplitude was significantly reduced by 10.4% (95% CI 8.68%–12.2%) and 12.6% (95% CI 10.0%–15.9%) in the PD and ET groups, respectively. With HFS, peak velocity was reduced by 14.7% (95% CI 11.7%–17.6%) in the PD group and 27.7% (95% CI 23.7%–31.7%) in the ET group. HFS led to PD patients performing 21% (95% CI 16%–26%) and ET patients 31% (95% CI 19%–38%) more saccadic steps to reach the target.CONCLUSIONSPSA DBS in patients with PD and ET leads to hypometric, slowed saccades with an increase in the number of steps taken to reach the target. These effects contrast with the saccadometric findings observed with subthalamic nucleus DBS. Given the location of the active contacts, incerto-collicular pathways are likely responsible. Whether the acute finding of saccadic impairment persists with chronic PSA stimulation is unknown.
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