The effects of carbohydrate supplementation during the second of two prolonged cycling bouts on immunoendocrine responses

The purpose of this study was to examine the effect of carbohydrate (CHO) feeding during the second of two 90-min cycling bouts (EX1 started at 09:00 and EX2 started at 13:30) at 60% on leucocyte redistribution, neutrophil degranulation and oxidative burst and plasma IL-6 and stress hormone responses. This study consisted of two trials, which were completed in a counterbalanced order and separated by at least 4 days. Subjects (n=9) consumed a lemon flavoured 10% w/v CHO (glucose) or placebo (PLA) beverage during EX2: 500 ml just before exercise and 250 ml every 20 min during exercise. Venous blood samples were taken 5 min before exercise, immediately post-exercise, and 18-h post-EX2 for both trials. The main findings of this study were that ingestion of CHO compared with PLA during EX2 better maintained plasma glucose concentration, blunted the responses of plasma adrenaline, ACTH, cortisol, GH and IL-6, and attenuated the leukocytosis and monocytosis, but had no effect on neutrophil degranulation and oxidative burst activity. Furthermore, the immunoendocrine disturbances induced by two bouts of prolonged exercise returned to resting values within 18 h. These findings suggest that ingestion of CHO compared with PLA during the second of two bouts of 90-min cycling at 60% better maintains plasma glucose, blunts hypothalamic–pituitary–adrenal activation, and attenuates leucocyte trafficking, but does not affect neutrophil function. Furthermore, the disturbances of immunoendocrine responses induced by two bouts of prolonged exercise on the same day recover within 18 h.     

The effect of 2 weeks vitamin C supplementation on immunoendocrine responses to 2.5 h cycling exercise in man

An increased systemic concentration of stress hormones (of the hypothalamic-pituitary adrenal axis) and some cytokines may contribute to the depression of immune cell function typically observed after prolonged exercise. The aim of the present study was to determine the effect of 2 weeks of supplementation with vitamin C (VC) on cortisol, adrenocorticotrophic hormone, interleukin-6, oxidative stress and neutrophil responses to a single bout of endurance exercise. Nine healthy endurance-trained males exercised for 2.5 h at 60% after 2 weeks of placebo (PLA) or VC (1,000 mg day⁻¹) supplementation. All participants completed both trials utilising a randomised crossover design with a minimum 14 day washout period between trials. There was a significant trial × time interaction effect for plasma cortisol concentration (P = 0.039) which tended to be lower in the VC trial but post hoc analysis found no specific between trial differences. There was a significantly lower post-exercise neutrophilia (P < 0.014) in the VC trial, compared with the PLA trial. There was no trial × time interaction for measures of neutrophil function (bacteria-stimulated elastase release, fMLP or PMA-stimulated oxidative burst). However, there was a trend for higher fMLP-stimulated neutrophil oxidative burst in the VC compared with PLA trial (trial × time interaction, P = 0.075). These results suggest that supplementation with VC for a period of up to 2 weeks provides little to no protection against the depression of neutrophil function which typically occurs after endurance exercise.     

Mobilization and oxidative burst of neutrophils are influenced by carbohydrate supplementation during prolonged cycling in humans

Prolonged, strenuous exercise may lead to suppressive effects on the immune system, which might be responsible for a greater susceptibility to opportunistic infections. The aim of this study was to examine the influence of carbohydrate substitution (CHS) during prolonged, strenuous exercise on neutrophil granulocytes and their oxidative burst (intracellular oxidation of dihydrorhodamine₁₂₃ to rhodamine₁₂₃ after induction by formylized 1-methionyl-1-leucyl-1-phenylalanin) using flow cytometry. In three trials different concentrations of CHS (placebo compared to 6% and 12% CHS; 50 ml·kg^–1) were given randomly to 14 endurance trained cyclists [mean (SD) age 25 (5) years, maximal oxygen uptake 67 (6) ml·min^–1·kg^–1] cycling for 4 h in a steady state at 70% of their individual anaerobic threshold. Blood samples were taken before, immediately after cessation, 1 h and 19 h after exercise. A significant rise in neutrophil counts was observed immediately after cessation and 1 h after exercise with a return to normal rest values 19 h after exercise for all three conditions (P<0.001). The relative proportions of rhodamine₁₂₃+ neutrophils were significantly diminished in all three conditions 1 h after exercise (P<0.01), while the mean fluorescence intensity was lowest in the placebo trial and differed significantly to the 12% CHS trial (P=0.024) and almost significantly to the 6% CHS trial (P=0.052). In conclusion, these data suggest a beneficial effect of CHS on the neutrophil oxidative burst and a possible attenuation of the susceptibility to infections, presumably due to the reduction of metabolic stress in prolonged, strenuous exercise. Electronic Publication     

Is the magnitude of acute post-exercise hypotension mediated by exercise intensity or total work done?

The purpose of this study was to investigate the effects of exercise intensity on the magnitude of acute post-exercise hypotension while controlling for total work done over the exercise bout. Seven normotensive physically active males aged 28 ± 6 years (mean ± SD) completed four experimental trials, a no exercise control, 30 min of semi-recumbent cycling at 70% (INT), cycling for 30 min at 40% (SMOD) and cycling at 40% for a time which corresponded to the same total work done as in the intense trial (LMOD). Blood pressure (BP), heart rate, stroke volume, cardiac output, total peripheral resistance, core body temperature and forearm skin and limb blood flow were measured prior to and for 20 min following the exercise bout. Post-exercise summary statistics were compared between trials with a one-factor general linear model. The change in systolic BP, averaged over the 20-min post-exercise period was significantly lower only following the INT (−5 ± 3 mm Hg) and LMOD exercise (−1 ± 7 mm Hg) compared to values in control (P < 0.04). The changes in systolic BP and MAP following INT and LMOD were not significantly different from each other (P > 0.05). Similar results were obtained when the minimum values of these variables recorded during the post-exercise period were compared. Mean changes in cardiac output (1.9 ± 0.3 l min⁻¹) and total peripheral resistance (−3 ± 1 mm Hg l⁻¹ min⁻¹) after INT exercise were also different from those in CON (P < 0.0005). The acute post-exercise reduction in BP was clinically similar following high intensity short duration exercise and moderate intensity longer duration exercise that was matched for total work done.     

The effect of acute aerobic exercise on pulse wave velocity and oxidative stress following postprandial hypertriglyceridemia in healthy men

Oxidative stress is postulated to be responsible for the postprandial impairments in vascular function. The purpose of this study was to measure pulse wave velocity (PWV) and markers of postprandial oxidative stress before and after an acute bout of moderate exercise. Ten trained male subjects (age 21.5 ± 2.5 years, VO₂ max 58.5 ± 7.1 ml kg⁻¹ min⁻¹) participated in a randomised crossover design: (1) high-fat meal alone (2) high-fat meal followed 2 h later by a bout of 1 h moderate (60% max HR) exercise. PWV was examined at baseline, 1, 2, 3, and 4 h postprandially. Blood Lipid hydroperoxides (LOOHs), Superoxide dismutase (SOD) and other biochemical markers were measured. PWV increased at 1 h (6.49 ± 2.1 m s⁻¹), 2 h (6.94 ± 2.4 m s⁻¹), 3 h (7.25 ± 2.1 m s⁻¹) and 4 h (7.41 ± 2.5 m s⁻¹) respectively, in the control trial (P < 0.05). There was no change in PWV at 3 h (5.36 ± 1.1 m s⁻¹) or 4 h (5.95 ± 2.3 m s⁻¹) post ingestion in the exercise trial (P > 0.05). LOOH levels decreased at 3 h post ingestion in the exercise trial compared to levels at 3 h (P < 0.05) in the control trial. SOD levels were lower at 3 h post ingestion in the control trial compared to 3 h in the exercise trial (0.52 ± 0.05 vs. 0.41 ± 0.1 units μl⁻¹; P < 0.05). These findings suggest that a single session of aerobic exercise can ameliorate the postprandial impairments in arterial function by possibly reducing oxidative stress levels.     

Post-exercise protein synthesis rates are only marginally higher in type I compared with type II muscle fibres following resistance-type exercise

We examined the effect of an acute bout of resistance exercise on fractional muscle protein synthesis rates in human type I and type II muscle fibres. After a standardised breakfast (31 ± 1 kJ kg⁻¹ body weight, consisting of 52 Energy% (En%) carbohydrate, 34 En% protein and 14 En% fat), 9 untrained men completed a lower-limb resistance exercise bout (8 sets of 10 repetitions leg press and leg extension at 70% 1RM). A primed, continuous infusion of l-[ring-¹³C₆]phenylalanine was combined with muscle biopsies collected from both legs immediately after exercise and after 6 h of post-exercise recovery. Single muscle fibres were dissected from freeze-dried biopsies and stained for ATPase activity with pre-incubation at a pH of 4.3. Type I and II fibres were separated under a light microscope and analysed for protein-bound l-[ring-¹³C₆]phenylalanine labelling. Baseline (post-exercise) l-[ring-¹³C₆]phenylalanine muscle tissue labelling, expressed as (∂¹³C/¹²C), averaged −32.09 ± 0.28, −32.53 ± 0.10 and −32.02 ± 0.16 in the type I and II muscle fibres and mixed muscle, respectively (P = 0.14). During post-exercise recovery, muscle protein synthesis rates were marginally (8 ± 2%) higher in the type I than type II muscle fibres, at 0.100 ± 0.005 versus 0.094 ± 0.005%/h, respectively (P < 0.05), whereby rates of mixed muscle protein were 0.091 ± 0.005%/h. Muscle protein synthesis rates following resistance-type exercise are only marginally higher in type I compared with type II muscle fibres.     

Effect of β-adrenoceptor stimulation on oxygen consumption and triglyceride/fatty acid cycling after exercise

The purpose of this study was to characterize the effects of prolonged β-adrenoceptor stimulation on O₂ uptake and triglyceride/fatty acid (TG/FA) cycling during rest with and without previous exercise. Eight men performed two exercise (90 min cycling at 56 ± 3 (SD)% of maximal O₂ uptake, followed by 4.5 h bed rest) and two rest-control experiments. In one rest and one exercise experiment a bolus dose (5 μg) of the β-adrenoceptor agonist isoprenaline was given immediately after exercise, followed by a continuous infusion (20 ng kg^–1 min^–1), and at the corresponding time in the rest experiment. In the other experiments saline was given instead. The O₂ uptake increased in the post-exercise period both with and without β-stimulation. The total excess post-exercise oxygen consumption (EPOC) was not different between saline (8.1 ± 1.8 (SE) L) and isoprenaline administration (10.8 ± 1.8 L, P = 0.40). Also, the total accumulated increase in O₂ uptake for the 4.5 h period after isoprenaline infusion was not different between the rest (12.5 ± 2.0 L) and the exercise experiments (15.2 ± 1.7 L, P = 0.40). The rate of TG/FA cycling increased after both exercise and isoprenaline treatment, but no interaction effect was found. In conclusion, the increases observed in O₂ uptake and the rate of TG/FA cycling during β-adrenoceptor stimulation were not increased by a previous exercise bout.     

Effect of post-exercise protein–leucine feeding on neutrophil function, immunomodulatory plasma metabolites and cortisol during a 6-day block of intense cycling

Whey protein and leucine ingestion following exercise increases muscle protein synthesis and could influence neutrophil function during recovery from prolonged intense exercise. We examined the effects of whey protein and leucine ingestion post-exercise on neutrophil function and immunomodulators during a period of intense cycling. In a randomized double-blind crossover, 12 male cyclists ingested protein/leucine/carbohydrate/fat (LEUPRO 20/7.5/89/22 g h^?1, respectively) or isocaloric carbohydrate/fat control (CON 119/22 g h^?1) beverages for 1–3 h post-exercise during 6 days of high-intensity training. Blood was taken pre- and post-exercise on days 1, 2, 4 and 6 for phorbol myristate acetate (PMA)-stimulated neutrophil superoxide (O₂ ^?) production, immune cell counts, amino acid and lipid metabolism via metabolomics, hormones (cortisol, testosterone) and cytokines (interleukin-6, interleukin-10). During recovery on day 1, LEUPRO ingestion increased mean concentrations of plasma amino acids (glycine, arginine, glutamine, leucine) and myristic acid metabolites (acylcarnitines C14, myristoylcarnitine; and C14:1-OH, hydroxymyristoleylcarnitine) with neutrophil priming capacity, and reduced neutrophil O₂ production (15–17 mmol O₂ ^? cell^?1 ± 90 % confidence limits 20 mmol O₂ ^? cell^?1). On day 2, LEUPRO increased pre-exercise plasma volume (6.6 ± 3.8 %) but haematological effects were trivial. LEUPRO supplementation did not substantially alter neutrophil elastase, testosterone, or cytokine concentrations. By day 6, however, LEUPRO reduced pre-exercise cortisol 21 % (±15 %) and acylcarnitine C16 (palmitoylcarnitine) during exercise, and increased post-exercise neutrophil O₂ ^? (33 ± 20 mmol O₂ ^? cell^?1), relative to control. Altered plasma amino acid and acylcarnitine concentrations with protein–leucine feeding might partly explain the acute post-exercise reduction in neutrophil function and increased exercise-stimulated neutrophil oxidative burst on day 6, which could impact neutrophil-dependent processes during recovery from intense training.     

Temporal association of elevations in serum cardiac troponin T and myocardial oxidative stress after prolonged exercise in rats

The objective of this study was to determine if prolonged exercise resulted in the appearance of cardiac troponin T (cTnT) in serum and whether this was associated with elevated levels of myocardial oxidative stress. Forty-five male Sprague–Dawley rats were randomized into four groups and killed before (PRE-EX), immediately (0HR), 2 (2HR) and 24 h (24HR) after a 3-h bout of swimming with 5% body weight attached to their tail. In all animals serum cTnT was assayed using 3rd generation electrochemiluminescence. In homogenized heart tissue myocardial malondialdehyde (MDA), a marker of lipid peroxidation, glutathione (GSH), and a non-enzymatic estimate of total antioxidant capacity (T-AOC) were assessed spectrophotometrically. At PRE-EX cTnT was undetectable in all animals. At 0HR (median, range: 0.055, 0.020–0.100) and 2HR post-exercise (0.036, 0.016–2.110) cTnT was detectable in all animals (P < 0.05). At 24HR post-exercise cTnT was undetectable in all animals. An elevation in MDA was observed 0HR (mean ± SD: 1.7 ± 0.2 nmol mgpro⁻¹) and 2HR (1.6 ± 0.3 nmol mgpro⁻¹) post-exercise compared with PRE-EX (1.3 ± 0.2 nmol mgpro⁻¹; P < 0.05). The antioxidant response to this challenge was a significant (P < 0.05) decrease in GSH 2HR and 24HR post-exercise. Despite this T-AOC did not alter across the trial (P > 0.05). The results indicated that prolonged and strenuous exercise in rats resulted in an elevation in cTnT, a biomarker of cardiomyocyte damage, in all animals 0HR and 2HR after exercise completion. The time course of cTnT elevation was temporally associated with evidence of increased lipid peroxidation in the rat heart.     

Influence of muscle mass and work on post-exercise glucose and insulin responses in young untrained subjects

The 18 h post-exercise glucose and insulin responses of six male and six female subjects were measured following one- or two-leg cycling to determine the influence of muscle mass involvement and work. Each subject performed three exercise trials on a Cybex Met 100 cycle ergometer: (1) two-leg exercise for 30 min at 60% of the two-leg VO _{2 max}; (2) one-leg exercise for 30 min at 60% of one-leg VO _{2 max}; and (3) one-leg exercise (one-legTW) at 60% of the one-leg VO _{2 max} with the total work performed equal to that of the two-leg trial (duration ≈50 min). These trials were preceded by 2 days of inactivity and followed by an 18 h post-exercise 75 g oral glucose tolerance test (OGTT). The glucose response during the baseline OGTT demonstrated that the subjects had normal glucose tolerance with fasting serum glucose levels of 5.1 mM , and 1 and 2 h serum glucose less than 7.8 mM , respectively. The 18 h post-exercise glucose responses were significantly lower following the two-leg trial (P < 0.05), with the area under the curve values being 129.9 mM h^?1 less than the resting control level. The 18 h post-exercise insulin AUC response of the two-leg trial was significantly lower than either of the one-leg responses (14.7 pM below the one-leg and 5.0 pM below the one-leg TW) but was not associated with a change in C-peptide. The 18 h post-exercise insulin levels of the one-leg and one-legTW trials were above or near the resting control values, but were not accompanied by a significant change in C-peptide. In conclusion, the data presented here show that the amount of muscle tissue utilized during an exercise bout can influence both the glucose and insulin responses, whereas the amount of total work employed during the exercise had no effect on either of these parameters.     

Syncope is unrelated to supine and postural hypotension following prolonged exercise

Syncope is widely reported following prolonged exercise. It is often assumed that the magnitude of exercise-induced hypotension (post-exercise hypotension; PEH), and the hypotensive response to postural change (initial orthostatic hypotension; IOH) are predictors of syncope post-exercise. The aim of this study was to determine the relationship between PEH, IOH, the residual IOH and syncope following prolonged exercise. Blood pressure (BP; Finometer) was measured continuously in 19 athletes (47 ± 20 years; BMI: 23.2 ± 2.2 kg m²; [(V)\dot] \dot{V} O₂ max: 51.3 ± 10.8 mL kg⁻¹ min⁻¹) whilst supine and during head-up tilt (HUT) to 60° for 15 min (or to syncope), prior to and following 4 h of running at 70–80% maximal heart rate. Syncope developed in 15 of 19 athletes post-exercise [HUT-time completed, Pre: 14:39 (min:s) ± 0:55; Post: 5:59 ± 4:53; P < 0.01]. PEH was apparent (−7 ± 7 mmHg; −8 ± 8%), but was unrelated to HUT-time completed (r ² = 0.09; P > 0.05). Although the magnitude of IOH was similar to post-exercise [−28 ± 12 vs. −20 ± 14% (pre-exercise); P > 0.05], the BP recovery following IOH was incomplete [−9 ± 9 vs. −1 ± 11 (pre-exercise); P < 0.05]; however, neither showed a relation to HUT-time completed (r ² = 0.18, r ² = 0.01; P > 0.05, respectively). Although an inability to maintain BP is a common feature of syncope post-exercise, the magnitude of PEH, IOH and residual IOH do not predict time to syncope. Practically, endurance athletes who present with greater hypotension are not necessarily at a greater risk of syncope than those who present with lesser reductions in BP.     

Carbohydrate supplementation during prolonged cycling exercise spares muscle glycogen but does not affect intramyocellular lipid use

Using contemporary stable-isotope methodology and fluorescence microscopy, we assessed the impact of carbohydrate supplementation on whole-body and fiber-type-specific intramyocellular triacylglycerol (IMTG) and glycogen use during prolonged endurance exercise. Ten endurance-trained male subjects were studied twice during 3 h of cycling at 63 ± 4% of maximal O₂ uptake with either glucose ingestion (CHO trial; 0.7 g CHO kg⁻¹ h⁻¹) or without (CON placebo trial; water only). Continuous infusions with [U-¹³C] palmitate and [6,6-²H₂] glucose were applied to quantify plasma free fatty acids (FFA) and glucose oxidation rates and to estimate intramyocellular lipid and glycogen use. Before and after exercise, muscle biopsy samples were taken to quantify fiber-type-specific IMTG and glycogen content. Plasma glucose rate of appearance (R _a) and carbohydrate oxidation rates were substantially greater in the CHO vs CON trial. Carbohydrate supplementation resulted in a lower muscle glycogen use during the first hour of exercise in the CHO vs CON trial, resulting in a 38 ± 19 and 57 ± 22% decreased utilization in type I and II muscle-fiber glycogen content, respectively. In the CHO trial, both plasma FFA R _a and subsequent plasma FFA concentrations were lower, resulting in a 34 ± 12% reduction in plasma FFA oxidation rates during exercise (P < 0.05). Carbohydrate intake did not augment IMTG utilization, as fluorescence microscopy revealed a 76 ± 21 and 78 ± 22% reduction in type I muscle-fiber lipid content in the CHO and CON trial, respectively. We conclude that carbohydrate supplementation during prolonged cycling exercise does not modulate IMTG use but spares muscle glycogen use during the initial stages of exercise in endurance-trained men.     

Carbohydrate feeding and exercise: effect of beverage carbohydrate content

Summary The purpose of this study was to determine the effect of ingesting fluids of varying carbohydrate content upon sensory response, physiologic function, and exercise performance during 1.25 h of intermittent cycling in a warm environment (T _db=33.4°C). Twelve subjects (7 male, 5 female) completed four separate exercise sessions; each session consisted of three 20 min bouts of cycling at 65% , with each bout followed by 5 min rest. A timed cycling task (1200 pedal revolutions) completed each exercise session. Immediately prior to the first 20 min cycling bout and during each rest period, subjects consumed 2.5 ml·kg BW⁻¹ of water placebo (WP), or solutions of 6%, 8%, or 10% sucrose with electrolytes (20 mmol·l⁻¹ Na⁺, 3.2 mmol·l⁻¹ K⁺). Beverages were administered in double blind, counterbalanced order. Mean (±SE) times for the 1200 cycling task differed significantly: WP=13.62±0.33 min, *6%=13.03±0.24 min, 8%=13.30±0.25 min, 10%=13.57±0.22 min (*=different from WP and 10%,P<0.05). Compared to WP, ingestion of the CHO beverages resulted in higher plasma glucose and insulin concentrations, and higher RER values during the final 20 min of exercise (P<0.05). Markers of physiologic function and sensory perception changed similarly throughout exercise; no differences were observed among subjects in response to beverage treatments for changes in plasma concentrations of lactate, sodium, potassium, for changes in plasma volume, plasma osmolality, rectal temperature, heart rate, oxygen uptake, rating of perceived exertion, or for indices of gastrointestinal distress, perceived thirst, and overall beverage acceptance. Compared to ingestion of a water placebo, consumption of beverages containing 6% to 10% sucrose resulted in similar physiologic and sensory response, while ingestion of the 6% sucrose beverage resulted in significantly improved end-exercise performance following only 60 min of intermittent cycling exercise.     

Post-exercise ketosis and the glycogen content of liver and muscle in rats on a high carbohydrate diet

Summary Post-exercise ketosis is known to be suppressed by physical training and by a high carbohydrate diet. As a result it has often been presumed, but not proven, that the development of post-exercise ketosis is closely related to the glycogen content of the liver. We therefore studied the effect of 1 h of treadmill running on the blood 3-hydroxybutyrate and liver and muscle glycogen concentrations of carbohydrate-loaded trained (n=72) and untrained rats (n=72). Resting liver and muscle glycogen levels were 25%–30% higher in the trained than in the untrained animals. The resting 3-hydroxybutyrate concentrations of both groups of rats were very low: <0.08 mmol·1⁻¹. Exercise did not significantly influence the blood 3-hydroxybutyrate concentrations of trained rats, but caused a marked post-exercise ketosis (1.40±0.40 mmol·1⁻¹ 1 h after exercise) in the untrained animals, the time-course of which was the approximate inverse of the changes in liver glycogen concentration. Interpreting the results in the light of similar data obtained after a normal and low carbohydrate diet it has been concluded that trained animals probably owe their relative resistance to post-exercise ketosis to their higher liver glycogen concentrations as well as to greater peripheral stores of mobilizable carbohydrate.     

White blood cell response to uphill walking and downhill jogging at similar metabolic loads

Summary The object of this study was to determine whether leukocytosis would occur in response to eccentric exercise, to concentric exercise, and/or to possible increases in serum corticol levels. Eight men performed 2 bouts of exercise at 46% for 40 min. Subjects initially walked up a 10% grade (UW); 2 weeks later they jogged down a 10% grade (DJ), a form of eccentric exercise known to induce delayed onset muscle soreness (DOMS). Venous blood samples were drawn before and after each exercise bout (0, 0.5, 1, 1.5, 2, 2.5, 3, 3.5, 4, and 5 h). Total and differential WBCc and serum cortisol levels were assessed. Results were analyzed using repeated measures ANOVA (2 × 11). Subjects experienced severe DOMS after DJ. There was a significant difference in TWBCc (p<0.0001) between UW and DJ. Post-hoc testing revealed no significant increase over baseline values for UW; after DJ there was a 46% increase over baseline values (p<0.05) initially seen at 1.0 h. These increases in TWBCc were predominantly a reflection of increases in neutrophils which were significant (p<0.0001) when compared to baseline values at 1.0, 1.5 and 2.0 h (∼60%). No significant neutrophil increases were seen after UW. Cortisol levels were similar for both groups pre-exercise (UW=367.1±38.6, DJ=320.2±44.16 mnol · L⁻¹ x±SE) and decreased similarly for both groups after exercise, and thus were not related to the post-exercise neutrophilia. In conclusion, the neutrophilia seen after the DJ appeared to be a response to differences in the exercise, not plasma cortisol levels. Thus a bout of eccentric exercise appears to induce a significant post-exercise increase in neutrophils seen between 1.0 and 2.0 h after the termination of exercise.     

Performance following prolonged sub-maximal cycling at optimal versus freely chosen pedal rate

It was tested whether cyclists perform better during all-out cycling following prolonged cycling at the pedal rate resulting in minimum oxygen uptake (VO₂), i.e. the energetically optimal pedal rate (OPR) rather than at the freely chosen pedal rate (FCPR). Nine trained cyclists cycled at 180 W to determine individual OPR and FCPR. Baseline performance was determined by measuring mean power output (W_5min) and peak VO₂ during 5-min all-out cycling at FCPR. Subsequently, on two separate days, the cyclists cycled 2.5 h at 180 W at OPR and FCPR, with each bout followed by a 5-min all-out trial. FCPR was higher (P < 0.05) than OPR at 180 W (95 ± 7 and 73 ± 11 rpm, respectively). During the prolonged cycling, VO₂, heart rate (HR), and rate of perceived exertion (RPE) were 7–9% higher (P < 0.05) at FCPR than at OPR and increased (P < 0.05) 2–21% over time. During all-out cycling following prolonged cycling at OPR and FCPR, W_5min was 8 and 10% lower (P < 0.05) than at baseline, respectively. Peak VO₂ was lower (P < 0.05) than at baseline only after FCPR. The all-out trial power output was reduced following 2.5 h of cycling at 180 W at both OPR and FCPR. However, this aspect of performance was similar between the two pedal rates, despite a higher physiological load (i.e. VO₂, HR, and RPE) at FCPR during prolonged cycling. Still, a reduced peak VO₂ only occurred after cycling at FCPR. Therefore, during prolonged sub-maximal cycling, OPR is at least as advantageous as FCPR for performance optimization in subsequent all-out cycling.     

Resting plasma and salivary IL-6 concentrations are not correlated in distance runners

Measurement of IL-6 has been widely undertaken to examine inflammatory and immune responses to exercise. Use of salivary IL-6 offers an alternative to the invasive collection procedures required for IL-6 measurement in plasma samples. Rarely, however, has the degree of association between plasma and salivary IL-6 been reported. The aim of the current study was to investigate the relationship between resting salivary and plasma IL-6 concentrations in 45 trained distance runners (36 males, 9 females; age: 35.1 ± 8.0 y, mean ± SD). Plasma and saliva samples were collected from athletes under resting conditions. Plasma IL-6 concentrations were determined using a Bioplex suspension array system and commercially available reagents. Salivary IL-6 concentrations were determined using a commercially available high-sensitivity ELISA kit. At rest, the mean (± SD) plasma IL-6 concentration was 3.43 ± 3.75 pg mL⁻¹ compared to a mean salivary IL-6 concentration of 1.80 ± 4.25 pg mL⁻¹. IL-6 concentrations in plasma and saliva samples were not correlated (r = −0.031, p = 0.85). At rest, salivary IL-6 concentrations do not reflect plasma IL-6 concentrations. The potential for salivary IL-6 to act as a surrogate marker for plasma IL-6 responses when examining inflammatory and immune responses to exercise, therefore, appears unlikely.     

The effect of severe eccentric exercise-induced muscle damage on plasma elastase, glutamine and zinc concentrations

The aim of this study was to determine if severe exercise-induced muscle damage alters the plasma concentrations of glutamine and zinc. Changes in plasma concentrations of glutamine, zinc and polymorphonuclear elastase (an index of phagocytic cell activation) were examined for up to 10 days following eccentric exercise of the knee extensors of one leg in eight untrained subjects. The exercise bout consisted of 20 repetitions of electrically stimulated eccentric muscle actions on an isokinetic dynamometer. Subjects experienced severe muscle soreness and large increases in plasma creatine kinase activity indicative of muscle fibre damage. Peak soreness occurred at 2 days post-exercise and peak creatine kinase activity [21714 (6416) U · l⁻¹, mean (SEM)] occurred at 3 days post-exercise (P < 0.01 compared with pre-exercise). Plasma elastase concentration was increased at 3 days post-exercise compared with pre-exercise (P < 0.05), and is presumably indicative of ongoing phagocytic leucocyte infiltration and activation in the damaged muscles. There were no significant changes in plasma zinc and glutamine concentrations in the days following eccentric exercise. We conclude that exercise-induced muscle damage does not produce changes in plasma glutamine or zinc concentrations despite evidence of phagocytic neutrophil activation. Accepted: 3 November 1997     

The effect of sodium bicarbonate and sodium citrate ingestion on anaerobic power during intermittent exercise

Summary The effect of sodium bicarbonate and sodium citrate ingestion on cycling performance in three 30 s Wingate Anaerobic Tests separated by 6 min recovery periods has been studied using 6 male subjects. Subjects ingested either sodium bicarbonate (B), sodium bicarbonate plus sodium citrate (BC), sodium citrate (C) or sodium chloride (P) 2.5 h prior to exercise in a dose of 0.3 g kg⁻¹ body weight. Pre-exercise blood pH was 7.44±0.06, 7.42±0.05, 7.41±0.05 and 7.38±0.04 in the C, BC, B and P conditions respectively. Mean and peak power output were significantly reduced by successive Wingate tests but not significantly affected by the treatments. Performance in the second and third tests was highest following C, BC and B ingestion. The total work done in the 3 tests was 103%, 102% and 101% of that achieved in the P condition after C, BC and B ingestion respectively. The increased alkali reserve recorded subsequent to bicarbonate and citrate treatment reduced mean post-exercise acidosis, although pH was significantly higher only in the C condition (p<0.05) compared to P after each exercise bout. No significant differences in plasma lactate concentration were recorded at any time. Citrate ingestion appears to be most effective in elevating blood pH and [HCO₃ ⁻], and in enhancing performance in short-term intermittent exercise. This study demonstrates that alkali ingestion results in significant shifts in the acid-base balance of the blood and has a small, but non-significant, effect on anaerobic power and capacity as measured in a series of 3 Wingate Anaerobic Tests.     

The impact of exercise intensity on the release of cardiac biomarkers in marathon runners

We sought to determine the influence of exercise intensity on the release of cardiac troponin I (cTnI) and N-terminal pro-brain natriuretic peptide (NT-proBNP) in amateur marathon runners. Fourteen runners completed three exercise trials of the same duration but at exercise intensities corresponding to: (a) a competitive marathon [mean ± SD: heart rate 159 ± 7 beat min⁻¹, finish time 202 ± 14 min]; (b) 95% of individual anaerobic threshold [heart rate 144 ± 6 beat min⁻¹] and; (c) 85% of individual anaerobic threshold [heart rate 129 ± 5 beat min⁻¹]. cTnI and NT-proBNP were assayed from blood samples collected before, 30 min and 3 h post-exercise for each trial. cTnI and NT-proBNP were not different at baseline before each trial. After exercise at 85% of individual anaerobic threshold cTnI was not significantly elevated. Conversely, cTnI was elevated after exercise at 95% of individual anaerobic threshold (0.016 μg L⁻¹) and to an even greater extent after exercise at competition intensity (0.054 μg L⁻¹). Peak post-exercise values of NT-proBNP were elevated to a similar extent after all exercise trials (P < 0.05). The upper reference limit for cTnI (0.04 μg L⁻¹) was exceeded in six subjects at competition intensity. No data for NT-proBNP surpassed its upper reference limit. Peak post-exercise values for cTnI and NT-proBNP were correlated with their respective baseline values. These data suggest exercise intensity influences the release of cTnI, but not NT-proBNP, and that competitive marathon running intensity is required for cTnI to be elevated over its upper reference limit.