The effect of exercise training on sleep quality in heart failure

Background: Heart failure is a serious condition estimated to affect 1.5-2.0% of the Australian population with a point prevalence of approximately 1% in people aged 50-59 years, 10% in people aged 65 years or more and over 50% in people aged 85 years or over (National Heart Foundation of Australian and the Cardiac Society of Australia and New Zealand, 2006). Sleep disturbances are a common complaint of persons with heart failure. Disturbances of sleep can worsen heart failure symptoms, impair independence, reduce quality of life and lead to increased health care utilisation in patients with heart failure. Previous studies have identified exercise as a possible treatment for poor sleep in patients without cardiac disease however there is limited evidence of the effect of this form of treatment in heart failure. Aim: The primary objective of this study was to examine the effect of a supervised, hospital-based exercise training programme on subjective sleep quality in heart failure patients. Secondary objectives were to examine the association between changes in sleep quality and changes in depression, exercise performance and body mass index. Methods: The sample for the study was recruited from metropolitan and regional heart failure services across Brisbane, Queensland. Patients with a recent heart failure related hospital admission who met study inclusion criteria were recruited. Participants were screened by specialist heart failure exercise staff at each site to ensure exercise safety prior to study enrolment. Demographic data, medical history, medications, Pittsburgh Sleep Quality Index score, Geriatric Depression Score, exercise performance (six minute walk test), weight and height were collected at Baseline. Pittsburgh Sleep Quality Index score, Geriatric Depression Score, exercise performance and weight were repeated at 3 months. One hundred and six patients admitted to hospital with heart failure were randomly allocated to a 3-month disease-based management programme of education and self-management support including standard exercise advice (Control) or to the same disease management programme as the Control group with the addition of a tailored physical activity program (Intervention). The intervention consisted of 1 hour of aerobic and resistance exercise twice a week. Programs were designed and supervised by an exercise specialist. The main outcome measure was achievement of a clinically significant change (.3 points) in global Pittsburgh Sleep Quality score. Results: Intervention group participants reported significantly greater clinical improvement in global sleep quality than Control (p=0.016). These patients also exhibited significant improvements in component sleep disturbance (p=0.004), component sleep quality (p=0.015) and global sleep quality (p=0.032) after 3 months of supervised exercise intervention. Improvements in sleep quality correlated with improvements in depression (p<0.001) and six minute walk distance (p=0.04). When study results were examined categorically, with subjects classified as either "poor" or "good" sleepers, subjects in the Control group were significantly more likely to report "poor" sleep at 3 months (p=0.039) while Intervention participants were likely to report "good" sleep at this time (p=0.08). Conclusion: Three months of supervised, hospital based, aerobic and resistance exercise training improved subjective sleep quality in patients with heart failure. This is the first randomised controlled trial to examine the role of aerobic and resistance exercise training in the improvement of sleep quality for patients with this disease. While this study establishes exercise as a therapy for poor sleep quality, further research is needed to investigate the effect of exercise training on objective parameters of sleep in this population.

Is recovery driven by central or peripheral factors? A role for the brain in recovery following intermittent-sprint exercise

Prolonged intermittent-sprint exercise (i.e., team sports) induce disturbances in skeletal muscle structure and function that are associated with reduced contractile function, a cascade of inflammatory responses, perceptual soreness, and a delayed return to optimal physical performance. In this context, recovery from exercise-induced fatigue is traditionally treated from a peripheral viewpoint, with the regeneration of muscle physiology and other peripheral factors the target of recovery strategies. The direction of this research narrative on post-exercise recovery differs to the increasing emphasis on the complex interaction between both central and peripheral factors regulating exercise intensity during exercise performance. Given the role of the central nervous system (CNS) in motor-unit recruitment during exercise, it too may have an integral role in post-exercise recovery. Indeed, this hypothesis is indirectly supported by an apparent disconnect in time-course changes in physiological and biochemical markers resultant from exercise and the ensuing recovery of exercise performance. Equally, improvements in perceptual recovery, even withstanding the physiological state of recovery, may interact with both feed-forward/feed-back mechanisms to influence subsequent efforts. Considering the research interest afforded to recovery methodologies designed to hasten the return of homeostasis within the muscle, the limited focus on contributors to post-exercise recovery from CNS origins is somewhat surprising. Based on this context, the current review aims to outline the potential contributions of the brain to performance recovery after strenuous exercise.

Rodent models for resolving extremes of exercise and health

The extremes of exercise capacity and health are considered a complex interplay between genes and the environment. In general, the study of animal models has proven critical for deep mechanistic exploration that provides guidance for focused and hypothesis driven discovery in humans. Hypotheses underlying molecular mechanisms of disease, and gene/tissue function can be tested in rodents in order to generate sufficient evidence to resolve and progress our understanding of human biology. Here we provide examples of three alternative uses of rodent models that have been applied successfully to advance knowledge that bridges our understanding of the connection between exercise capacity and health status. Firstly we review the strong association between exercise capacity and all-cause morbidity and mortality in humans through artificial selection on low and high exercise performance in the rat and the consequent generation of the "energy transfer hypothesis". Secondly we review specific transgenic and knock-out mouse models that replicate the human disease condition and performance. This includes human glycogen storage diseases (McArdle and Pompe) and α-actinin-3 deficiency. Together these rodent models provide an overview of the advancements of molecular knowledge required for clinical translation. Continued study of these models in conjunction with human association studies will be critical to resolving the complex gene-environment interplay linking exercise capacity, health, and disease.

Effect of caffeine ingestion during prolonged exhaustive exercise on salivary immunoglobulin A, alpha-amylase and cortisol

Exercise can have deleterious effects on the secretion of salivary immunoglobulin A (s-IgA), which appears to be related to perturbations in sympatheticoadrenal activation (Teeuw et al., 2004). Caffeine, commonly used for its ergogenic properties is associated with increased sympathetic nervous system activity, and it has been previously shown that caffeine ingestion before intensive cycling enhances s-IgA responses during exercise (Bishop et al., 2006). Therefore, the aim of the present study was to examine the effect of a performance cereal bar, containing caffeine, before and during prolonged exhaustive cycling on exercise performance and the salivary secretion of IgA, alpha-amylase activity and cortisol. Using a randomised cross-over design and following a 10 – 12 hour overnight fast, 12 trained cyclists, mean (SEM) age: 21(1) yr; height: 179(2) cm; body mass: 73.6(2.5) kg; maximal oxygen uptake, VO2max: 57.9(1.2) completed 2.5 h of cycling at 60%VO2max (with regular water ingestion) on a stationary ergometer, which was followed by a ride to exhaustion at 75% VO2max. Immediately before exercise, and after 55 min and 115 min of exercise participants ingested a 0.9 MJ cereal bar containing 45 g carbohydrate, 5 g protein, 3 g fat and 100 mg of caffeine (CAF) or an isocaloric noncaffeine bar (PLA). Unstimulated timed saliva samples were collected immediately before exercise, after 70 min and 130 min of exercise, and immediately after the exhaustive exercise bout. Saliva was analysed for s-IgA, alpha-amylase activity and cortisol concentration. Saliva flow rates were determined to calculate the s-IgA secretion rate. Data were analysed using a 2-way repeated measures ANOVA and post-hoc t-tests with Holm Bonferroni adjustments applied where appropriate. Time to exhaustion was 35% longer in CAF compared with PLA ((2177 (0.2) vs 1615 (0.16) s; P < 0.05)). Saliva flow rate did not change significantly during the exercise protocol. Exercise was associated with elevations in s-IgA concentration (9% increase), s-IgA secretion rate (24% increase) and alpha-amylase activity (224% increase) post-exhaustion (P < 0.01), but there was no effect of CAF on these responses. Salivary cortisol concentration increased by 64% post-exhaustion in the CAF trial only (P < 0.05), indicating an increase in adrenal activity following caffeine ingestion. Values were 35.7 (5.5) and 19.6 (3.4) nmol/L post-exhaustion for CAF and PLA, respectively. These findings show that ingestion of a caffeine containing cereal bar during prolonged exhaustive cycling enhances endurance performance, increases salivary cortisol secretion post-exhaustion, but does not affect the exercise-induced increases in s-IgA or alpha-amylase activity.

Systemic oxidative-nitrosative-inflammatory stress during acute exercise in hypoxia; implications for microvascular oxygenation and aerobic capacity

New Findings

What is the central question of this study?Exercise performance is limited during hypoxia by a critical reduction in cerebral and skeletal tissue oxygenation. To what extent an elevation in systemic free radical accumulation contributes to microvascular deoxygenation and the corresponding reduction in maximal aerobic capacity remains unknown.What is the main finding and its importance?We show that altered free radical metabolism is not a limiting factor for exercise performance in hypoxia, providing important insight into the fundamental mechanisms involved in the control of vascular oxygen transport.

Exercise performance in hypoxia may be limited by a critical reduction in cerebral and skeletal tissue oxygenation, although the underlying mechanisms remain unclear. We examined whether increased systemic free radical accumulation during hypoxia would be associated with elevated microvascular deoxygenation and reduced maximal aerobic capacity (). Eleven healthy men were randomly assigned single-blind to an incremental semi-recumbent cycling test to determine  in both normoxia (21% O_{2) and hypoxia (12% O2) separated by a week. Continuous-wave near-infrared spectroscopy was employed to monitor concentration changes in oxy- and deoxyhaemoglobin in the left vastus lateralis muscle and frontal cerebral cortex. Antecubital venous blood samples were obtained at rest and at  to determine oxidative (ascorbate radical by electron paramagnetic resonance spectroscopy), nitrosative (nitric oxide metabolites by ozone-based chemiluminescence and 3-nitrotyrosine by enzyme-linked immunosorbent assay) and inflammatory stress biomarkers (soluble intercellular/vascular cell adhesion 1 molecules by enzyme-linked immunosorbent assay). Hypoxia was associated with increased cerebral and muscle tissue deoxygenation and lower  (P < 0.05 versus normoxia). Despite an exercise-induced increase in oxidative–nitrosative–inflammatory stress, hypoxia per se did not have an additive effect (P > 0.05 versus normoxia). Consequently, we failed to observe correlations between any metabolic, haemodynamic and cardiorespiratory parameters (P > 0.05). Collectively, these findings suggest that altered free radical metabolism cannot explain the elevated microvascular deoxygenation and corresponding lower  in hypoxia. Further research is required to determine whether free radicals when present in excess do indeed contribute to the premature termination of exercise in hypoxia.}

The effect of carbohydrate mouth rinse on a 30-minute arm cranking performance

The aim of this study was to examine the effect of carbohydrate mouth rinse on 30-min arm cranking performance. Twelve healthy, active males (age 21.6, standard deviation (SD)=3.1 years; mass 76.2, SD=12.2 kg) volunteered in a single-blind, randomised crossover design. Firstly they completed an incremental exercise test to exhaustion (VO2max test) on an arm crank (50W for 2 min, increasing by 10W every min). During visit 2 and 3 they arm cranked for maximal distance over 30 min at a resistance equivalent to 50% of their peak power, mouth rinsing for 5 s with either 25 ml of a tasteless 6.4% maltodextrin solution (CHO) or 25 ml of water (placebo) every 6 min. A letter cancellation test was performed pre and post exercise to measure cognitive function. The result showed that cognitive function was not significantly different between trials (P=0.874). There was no significant difference in distance arm cranked between trials (P=0.164) even though 9 out of 12 participants had improved performance on the CHO trial. In conclusion, further research is needed to determine the ergogenic effect of CHO mouth rinsing on upper body exercise performance.

The effects of upper extremity functional electrically stimulated (FES) exercise training on upper limb function in individuals with tetraplegia

Functional Electrically Stimulated (FES) ami cycle ergometry is a relatively new technique for exercise in individuals with impairments of the upper limbs. The purpose of this study was to determine the effects of 12 weeks of FES arm cycle ergometry on upper limb function and cardiovascular fitness in individuals with tetraplegia. F!ve subjects (4M/1F; mean age 43.8 ± 15.4 years) with a spinal cord injury of the cervical spine (C3- C7; ASIA B-D) participated in 12 weeks of3 times per week FES arm cycle ergometry training. Exercise performance measures (time to fatigue, distance to fatigue, work rate) were taken at baseline, 6 weeks, and following 12 weeks of training. Cardiovascular measures (MAP, resting HR, average and peak HR during exercise, cardiovascular efficiency) and self reported upper limb function (as determined by the CUE, sf-QIF, SCI-SET questionnaires) were taken at baseline and following 12 weeks of training. Increases were found in time to fatigue (84.4%), distance to fatigue (111.7%), and work rate (51.3%). These changes were non-significant. There was a significant decrease in MAP (91.1 ± 13.9 vs. 87.7 ± 14.7 mmHg) following 12 weeks ofFES arm cycle ergometry. There was no significant change in resting HR or average and peak HR during exercise. Cardiovascular efficiency showed an increase following the 12 weeks ofFES training (142.9%), which was non-significant. There were no significant changes in the measures of upper limb function and spasticity. Overall, FES arm cycle ergometry is an effective method of cardiovascular exercise for individuals with tetraplegia, as evidenced by a significant decrease in MAP, however it is unclear whether 12 weeks of thrice weekly FES arm cycle ergometry may effectively improve upper limb function in all individuals with a cervical SCI.

Effect of glycerol-induced hyperhydration on thermoregulation and metabolism during exercise in the heat

This study examined the effect of glycerol ingestion on fluid homeostasis, thermoregulation, and metabolism during rest and exercise. Six endurance-trained men ingested either 1 g glycerol in 20 ml H₂O.kg^-1 body weight (bw) (GLY) or 20 ml H₂O.kg^-1bw (CON) in a randomized double-blind fashion, 120 min prior to undertaking 90 min of steady state cycle exercise (SS) at 98 % of lactate threshold in dry heat (35 degrees C, 30 % RH), with ingestion of CHO-electrolyte beverage (6 % CHO) at 15-min intervals. A 15-min cycle, where performance was quantified in kJ, followed (PC). Pre-exercise urine volume was lower in GLY than CON (1119 ± 97 vs. 1503 ± 146 ml· 120 min^-1; p < .05). Heart rate was lower (p < .05) throughout SS in GLY, while forearm blood flow was higher (17.1 ± 1.5 vs. 13.7 ± 3.0 ml.100 g tissue·min^-1; p < .05) and rectal  temperature lower (38.7 ± 0.1 vs. 39.1 ± 0.1 ° C; p < .05) in GLY late in SS. Despite these changes, skin and muscle temperatures and circulating catecholamines were not different between trials. Accordingly, no differences were observed in muscle glycogenolysis, lactate accumulation, adenine nucleotide, and phosphocreatine degradation or inosine 5'-monophosphate accumulation when comparing GLY with CON. Of note, the work performed during PC was 5 % greater in GLY (252 ± 10 vs. 240 ± 9 kJ; p < .05). These results demonstrate that glycerol, when ingested with a bolus of water 2 hours prior to exercise, results in fluid retention, which is capable of reducing cardiovascular strain and enhancing thermoregulation. Furthermore, this practice increases exercise performance in the heat by mechanisms other than alterations in muscle metabolism.

Plasma glucose kinetics during prolonged exercise in trained humans when fed carbohydrate

Nine endurance-trained men exercised on a cycle ergometer at ~68% peak O₂ uptake to the point of volitional fatigue [232 ± 14 (SE) min] while ingesting an 8% carbohydrate solution to determine how high glucose disposal could increase under physiological conditions. Plasma glucose kinetics were measured using a primed, continuous infusion of [6,6-²H]glucose and the appearance of ingested glucose, assessed from [3-³H]glucose that had been added to the carbohydrate drink. Plasma glucose was increased (P < 0.05) after 30 min of exercise but thereafter remained at the preexercise level. Glucose appearance rate (Ra) increased throughout exercise, reaching its peak value of 118 ± 7 µmol · kg^-1 · min^-1 at fatigue, whereas gut R_a increased continuously during exercise, peaking at 105 ± 10 µmol · kg^-1 · min^-1 at the point of fatigue. In contrast, liver glucose output never rose above resting levels at any time during exercise. Glucose disposal (R_d) increased throughout exercise, reaching a peak value of 118 ± 7 µmol · kg^-1 · min^-1 at fatigue. If we assume 95% oxidation of glucose R_d, estimated exogenous glucose oxidation at fatigue was 1.36 ± 0.08 g/min. The results of this study demonstrate that glucose uptake increases continuously during prolonged, strenuous exercise when carbohydrate is ingested and does not appear to limit exercise performance.

The effect of acute fenitrotion exposure on a variety of physiological indices, including avian aerobic metabolism during exercise and cold exposure

The effect of fenitrothion exposure on birds was examined by measuring aerobic metabolism, blood hemoglobin content, plasma cholinesterases, and body weight for up to 21 d postdose. Peak metabolic rate was measured in a flight chamber in three-dose groups of house sparrows (Passer domesticus; 100 mg/kg = high, 60 mg/kg = medium, 30 mg/kg = low) and one-dose groups of zebra finches (Taeniopygia guttata; 3 mg/kg) and king quails (Coturnix chinensis; 26 mg/kg). Aerobic metabolism was measured during 1 h of exposure to subfreezing thermal conditions in low-dose house sparrows and king quails (26 mg/kg). Fenitrothion had no effect on metabolic rate during cold exposure or on blood hemoglobin at any time. By contrast, aerobic performance during exercise in sparrows was reduced by 58% (high), 18% (medium), and 20% (low), respectively, 2 d postdose. House sparrows (high) had the longest recovery period for peak metabolic rate (21 d) and plasma cholinesterase activity (14 d). House sparrows (high) and treated king quails had significantly lower myoglobin at 48 h postdose, whereas myoglobin was invariant in zebra finches and house sparrows (medium and low). Cholinesterase was maximally inhibited at 6 h postdose, and had recovered within 24 h, in house sparrows (low), king quails, and zebra finches. Exercise peak metabolic rate in zebra finches and king quails was reduced by 23% at 2 d and 3 d, respectively, despite these birds being asymptomatic in both behavior and plasma cholinesterase activities.

L-Arginine infusion increases glucose clearance during prolonged exercise in humans

Nitric oxide synthase (NOS) inhibition has been shown in humans to attenuate exercise-induced increases in muscle glucose uptake. We examined the effect of infusing the NO precursor L-arginine (L-Arg) on glucose kinetics during exercise in humans. Nine endurance-trained males cycled for 120 min at 72 ± 1% VO2 peak followed immediately by a 15-min "all-out" cycling performance bout. A [6,6-2H]glucose tracer was infused throughout exercise, and either saline alone (Control, CON) or saline containing L-Arg HCl (L-Arg, 30 g at 0.5 g/min) was coinfused in a double-blind, randomized order during the last 60 min of exercise. L-Arg augmented the increases in glucose rate of appearance, glucose rate of disappearance, and glucose clearance rate (L-Arg: 16.1 ± 1.8 ml·min–1·kg–1; CON: 11.9 ± 0.7 ml·min–1·kg–1 at 120 min, P < 0.05) during exercise, with a net effect of reducing plasma glucose concentration during exercise. L-Arg infusion had no significant effect on plasma insulin concentration but attenuated the increase in nonesterified fatty acid and glycerol concentrations during exercise. L-Arg infusion had no effect on cycling exercise performance. In conclusion, L-Arg infusion during exercise significantly increases skeletal muscle glucose clearance in humans. Because plasma insulin concentration was unaffected by L-Arg infusion, greater NO production may have been responsible for this effect.

Impaired K+ regulation contributes to exercise limitation in end-stage renal failure

Background

Patients with end-stage renal failure (ESRF) exhibit grossly impaired maximal exercise performance. This study investigated whether K+ regulation during exercise is impaired in ESRF and whether this is related to reduced exercise performance.

Methods

Nine stable hemodialysis patients and eight controls (CON) performed incremental cycling exercise to volitional fatigue, with measurement of peak oxygen consumption (VdotO2 peak). Arterial blood was sampled during and following exercise and analyzed for plasma [K+] (PK).

Results

The VdotO2 peak was approximately 44% less in ESRF than in CON (P < 0.001), whereas peak exercise PK was greater (7.23 plusminus 0.38 vs. 6.23 plusminus 0.14 mmol dot L-1, respectively, P < 0.001). In ESRF, the rate of rise in PK during exercise was twofold greater (0.43 plusminus 0.05 vs. 0.23 plusminus 0.03 mmol dot L-1dotmin-1, P < 0.005) and the ratio of rise in PK relative to work performed was 3.7-fold higher (90.1 plusminus 13.5 vs. 24.7 plusminus 3.3 nmol dot L-1dot J-1, P < 0.001). A strong inverse relationship was found between VdotO2 peak and the DeltaPKdot work-1 ratio (r = -0.80, N = 17, P < 0.001).

Conclusions

Patients with ESRF exhibit grossly impaired extrarenal K+ regulation during exercise, demonstrated by an excessive rise in PK relative to work performed. We further show that K+ regulation during exercise was correlated with aerobic exercise performance. These results suggest that disturbed K+ regulation in ESRF contributes to early muscle fatigue during exercise, thus causing reduced exercise performance.

Alkalosis increases muscle K+ release, but lowers plasma [K+] and delays fatigue during dynamic forearm exercise

Alkalosis enhances human exercise performance, and reduces K⁺ loss in contracting rat muscle. We investigated alkalosis effects on K⁺ regulation, ionic regulation and fatigue during intense exercise in nine untrained volunteers. Concentric finger flexions were conducted at 75% peak work rate (-3 W) until fatigue, under alkalosis (Alk, NaHCO₃, 0.3 g kg⁻¹) and control (Con, CaCO₃) conditions, 1 month apart in a randomised, double-blind, crossover design. Deep antecubital venous (v) and radial arterial (a) blood was drawn at rest, during exercise and recovery, to determine arterio-venous differences for electrolytes, fluid shifts, acid–base and gas exchange. Finger flexion exercise barely perturbed arterial plasma ions and acid–base status, but induced marked arterio-venous changes. Alk elevated [HCO₃⁻] and P^CO2, and lowered [H+] (P < 0.05). Time to fatigue increased substantially during Alk (25 ± 8%, P < 0.05), whilst both [K⁺]_a and [K⁺]_v were reduced (P < 0.01) and [K⁺]_a-v during exercise tended to be greater (P= 0.056, n= 8). Muscle K⁺ efflux at fatigue was greater in Alk (21.2 ± 7.6 µmol min⁻¹, 32 ± 7%, P < 0.05, n= 6), but peak K⁺ uptake rate was elevated during recovery (15 ± 7%, P < 0.05) suggesting increased muscle Na⁺,K^+-ATPase activity. Alk induced greater [Na⁺]_a, [Cl⁻]_v, muscle Cl⁻ influx and muscle lactate concentration ([Lac⁻]) efflux during exercise and recovery (P < 0.05). The lower circulating [K⁺] and greater muscle K⁺ uptake, Na⁺ delivery and Cl⁻ uptake with Alk, are all consistent with preservation of membrane excitability during exercise. This suggests that lesser exercise-induced membrane depolarization may be an important mechanism underlying enhanced exercise performance with Alk. Thus Alk was associated with improved regulation of K⁺, Na⁺, Cl⁻ and Lac⁻.

Interaction of hypercaloric diet and physical exercise on lipid profile, oxidative stress and antioxidant defenses

The present study examined the interaction of hypercaloric diet (HD) and physical exercise on lipid profile and oxidative stress in serum and liver of rats. Male Wistar rats (60-days-old) were fed with a control (C) and hypercaloric diet (H). Each of the two dietary groups (C and H) was divided into three subgroups (n = 8), sedentary (CS and HS), exercised 2 days a week (CE2 and HE2) and exercised 5 days a week (CE5 and HE5). The swimming was selected as a model for exercise performance. After 8-weeks exercised rats showed decreased lactate dehydrogenase serum activities, demonstrating the effectiveness of the swimming as an aerobic-training protocol. Exercise 5-days a week reduced the body weight gain. Triacylglycerol (TG) and very low-density lipoprotein (VLDL-C) were increased in HD-fed rats. HE5 and CE5 rats had decreased TG, VLDL-C and cholesterol. HE2 rats had enhanced high-density lipoprotein (HDL-C) in serum. No alterations were observed in lipid hydroperoxide (LH), while total antioxidant substances (TAS) were increased in serum of exercised rats. HD-fed rats had hepatic TG accumulation. Superoxide dismutase activities were increased and catalase was decreased in liver of exercised rats. The interaction of HD and physical exercise reduced TAS and enhanced LH levels in hepatic tissue. In conclusion, this study confirmed the beneficial effect of physical exercise as a dyslipidemic-lowering component. Interaction of HD and physical exercise had discrepant effects on serum and liver oxidative stress. The interaction of HID and physical exercise reduced the oxidative stress in serum. HD and physical exercise interaction had pro-oxidant effect on hepatic tissue, suggesting that more studies should be done before using physical exercise as an adjunct therapy to reduce the adverse effects of HD. (c) 2006 Elsevier Ltd. All rights reserved.

Effects of caffeine on time to exhaustion in exercise performed below and above the anaerobic threshold

Controversy still exists concerning the potential ergogenic benefit of caffeine (CAF) for exercise performance. The purpose of this study was to compare the effects of CAF ingestion on endurance performance during exercise on a bicycle ergometer at two different intensities, i.e., approximately 10% below and 10% above the anaerobic threshold (AT). Eight untrained males, non-regular consumers of CAF, participated in this study. AT, defined as the intensity (watts) corresponding to a lactate concentration of 4 mM, was determined during an incremental exercise test from rest to exhaustion on an electrically braked cycle ergometer. on the basis of these measurements, the subjects were asked to cycle until exhaustion at two different intensities, i.e., approximately 10% below and 10% above AT. Each intensity was performed twice in a double-blind randomized order by ingesting either CAF (5 mg/kg) or a placebo (PLA) 60 min prior to the test. Venous blood was analyzed for free fatty acid, glucose, and lactate, before, during, and immediately after exercise. Rating of perceived exertion and time to exhaustion were also measured during each trial. There were no differences in free fatty acids or lactate levels between CAF and PLA during and immediately after exercise for either intensity. Immediately after exercise glucose increased in the CAF trial at both intensities. Rating of perceived exertion was significantly lower (CAF = 14.1 ± 2.5 vs PLA = 16.6 ± 2.4) and time to exhaustion was significantly higher (CAF = 46.54 ± 8.05 min vs PLA = 32.42 ± 14.81 min) during exercise below AT with CAF. However, there was no effect of CAF treatment on rating of perceived exertion (CAF = 18.0 ± 2.7 vs PLA = 17.6 ± 2.3) and time to exhaustion (CAF = 18.45 ± 7.28 min vs PLA = 19.17 ± 4.37 min) during exercise above AT. We conclude that in untrained subjects caffeine can improve endurance performance during prolonged exercise performed below AT and that the decrease of perceived exertion can be involved in this process