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Showing papers on "Exercise physiology published in 1994"


Journal ArticleDOI
TL;DR: The results indicate that T30 is mediated primarily by vagal reactivation, independent of sympathetic withdrawal, and is significantly smaller in athletes and significantly larger in patients with chronic heart failure than that in respective age-matched normal control subjects.

932 citations


Journal ArticleDOI
TL;DR: There is an age-associated decline in heart rate, ejection fraction, and cardiac output responses to supine exercise in healthy men and both the young and old increased peak exercise cardiac output by use of the Frank-Starling mechanism (ie, cardiac dilatation) as well as an increase in ejectedion fraction.
Abstract: BACKGROUND Cardiac aging alters many of the acute responses to exercise stress, but the extent to which chronic exercise (ie, training) can alter or improve the effects of aging in humans is largely unknown. METHODS AND RESULTS Cardiovascular responses to graded supine exercise stress (beginning at 200 kpm and increasing by 200 kpm every 3 minutes till exhaustion) were assessed using radionuclide ventriculography in 13 older (age, 60 to 82 years) and 11 young (age, 24 to 32 years) rigorously screened healthy men before and after 6 months of endurance training. Repeated-measures ANOVA was used to test significance. During exercise, the old group had a lesser increase in heart rate (+105% old versus +166% young), a greater increase in mean blood pressure (+35% old versus +22% young), lesser increases in ejection fraction (+3 ejection fraction units old versus +11 units young) and peak ejection rate (+62% old versus +119% young), a greater increase in end-diastolic volume index (+8% old versus -10% young), a lesser fall in end-systolic volume index (-0% old versus -32% young), and a lesser increase in cardiac index (+135% old versus +189% young) (all P < .01 young/old versus exercise stage). Stroke volume index response to exercise was not different with aging (+14% old versus +6% young, P = NS). Exercise training increased maximal oxygen intake by 21% in the older group (28.9 +/- 4.6 to 35.1 +/- 3.8 mL.kg-1.min-1, P < .001) and by 17% in the young (44.5 +/- 5.1 to 52.1 +/- 6.3 mL.kg-1.min-1, P < .001) and increased peak workload by 24% in the old and 28% in the young. Exercise training had no differential effects on old versus young men. Among all subjects, training significantly reduced the resting heart rate by 12% (-8 beats per minute) and increased resting end-diastolic volume index by 13% (+9 mL/M2) and resting stroke volume index by 18% (+7 mL/M2) (all P < .01). At peak exercise, cardiac index increased by 16% (+1.07 L.M-2.min-1) compared with before training, which was the result of an increase in stroke volume of 18% (+7 mL/M2) (P < .001); peak heart rate was unchanged. The increase in stroke volume index at peak exercise was the result of both a 12% increase in end-diastolic volume index (+8 mL/M2) (P < .01) and an increase in ejection fraction (+3 ejection fraction units) (P < .05) at peak exercise. The increased ejection fraction at peak exercise occurred despite a 9% increase in systolic blood pressure (+18 mm Hg) (P < .01), suggesting an increase in contractility. Thus, both the young and old increased peak exercise cardiac output by use of the Frank-Starling mechanism (ie, cardiac dilatation) as well as an increase in ejection fraction. CONCLUSIONS We conclude that there is an age-associated decline in heart rate, ejection fraction, and cardiac output responses to supine exercise in healthy men. Although the stroke volume responses of the young and old are similar, the old tend to augment stroke volume during exercise more through cardiac dilatation, with an increase in end-diastolic volume (+8%) but without much change in ejection fraction (+3 ejection fraction units), whereas the young rely more on an increase in the ejection fraction (+11 ejection fraction units) with no cardiac dilatation (-10%). Despite the significant cardiovascular changes that occur in the response to a single bout of exercise with aging, adaptations to chronic exercise training were not different with aging and included improvements in maximal workload and increases in ejection fraction, stroke volume index, and cardiac index at peak exercise.

412 citations


Journal ArticleDOI
TL;DR: Data at this time support a "J" curve relationship between risk of URTI and increasing exercise workloads, and changes in the immune system that might explain the altered risk of infection.
Abstract: In this article, emphasis was placed on the relationship between exercise and upper respiratory tract infection (URTI) in humans, experimentally induced infections in animals subjected to varying levels of exertion, and potential changes in the immune system that might explain the altered risk of infection. With regard to induced infections in animals, the influence of any exercise intervention appears to be pathogen specific, and dependent on the species, age, and sex of the animals selected for study, and the type of exercise paradigm. In general, although further research with larger subject pools and improved study designs is needed, published data at this time support a "J" curve relationship between risk of URTI and increasing exercise workloads. For example, individuals exercising moderately may lower their risk of URTI while those undergoing heavy exercise regimens may have higher than normal risk. Although researchers have investigated changes in immune function that might provide a biological rationale for the "J" curve model of infection and exercise, the wide variety of research designs, exercise protocols, subject characteristics, and methodologies combined with the innate complexity of the immune system have made interpretation of published findings equivocal. T and NK cell function, for example, is often reported to be decreased during recovery from high-intensity exercise. However, when adjustments are made for exercise-induced perturbations in blood lymphocyte subsets, any link to decreased host protection is unlikely.

409 citations


Journal ArticleDOI
TL;DR: It appears that boys experience an adolescent growth spurt in peak VO2, which reaches a maximum gain near the time of PHV, but data are insufficient to offer any generalization for girls, and scaling for differences in body size may provide further clarification.
Abstract: Our understanding of the development of children and adolescents' aerobic fitness is limited by ethical considerations and methodological constraints. Protocols, apparatus, and criteria of maximal effort used with adults are often unsuitable for use with children. In normal children and adolescents, peak VO2 increases with growth and maturation, although there are indications that girls' peak VO2 may level off around 14 years of age. Males exhibit higher values of peak VO2 than females, and the sex difference increases as they progress through adolescence. The difference between males and females has been attributed to the boys' greater muscle mass and hemoglobin concentration. It appears that boys experience an adolescent growth spurt in peak VO2, which reaches a maximum gain near the time of PHV, but data are insufficient to offer any generalization for girls. Peak VO2 has usually been expressed in relation to body mass, and with this convention it appears that boys' values are consistent throughout the developmental period, whereas girls' values decrease as they get older. This type of analysis may, however, have clouded our understanding of growth and maturational changes in peak VO2, and scaling for differences in body size may provide further clarification. If differences are shown where none were previously thought to exist, then physiological explanations must be sought. Methodological issues have also hindered the understanding of how children's blood lactate responses to exercise develop. The actual lactate level recorded during an exercise test is influenced by the site of sampling and the blood handling and assay techniques. Valid interstudy comparisons can only be made where similar procedures have been employed. In general, children demonstrate lower blood lactate levels at peak VO2 than adults, although individual variation is wide. Therefore the use of blood lactate measures to confirm the attainment of peak VO2 cannot be supported. Exercise at the same relative submaximal intensity elicits a lower blood lactate in children than in adults, but interpretation and identification of developmental and maturational patterns of response are limited by the use of different testing conditions and reference points (e.g., lactate threshold and fixed level reference points). There is growing evidence that the 2.5 mM reference level should be used in preference to the 4.0 mM level, as the adult criterion occurs close to maximal exercise in many children and adolescents. Explanations for child-adult differences in blood lactate responses to exercise are difficult to elucidate.(ABSTRACT TRUNCATED AT 400 WORDS)

385 citations


Journal ArticleDOI
TL;DR: It is shown that both Crf and Crphos levels in skeletal muscle can be increased, and performance of high intensity intermittent exercise enhanced, following a period of creatine supplementation, however, neither endurance exercise performance nor maximal oxygen uptake appears to be enhanced.
Abstract: Since the discovery of creatine in 1832, it has fascinated scientists with its central role in skeletal muscle metabolism. In humans, over 95% of the total creatine (Crtot) content is located in skeletal muscle, of which approximately a third is in its free (Crf) form. The remainder is present in a phosphorylated (Crphos) form. Crf and Crphos levels in skeletal muscle are subject to individual variations and are influenced by factors such as muscle fibre type, age and disease, but not apparently by training or gender. Daily turnover of creatine to creatinine for a 70kg male has been estimated to be around 2g. Part of this turnover can be replaced through exogenous sources of creatine in foods, especially meat and fish. The remainder is derived via endogenous synthesis from the precursors arginine, glycine and methionine. A century ago, studies with creatine feeding concluded that some of the ingested creatine was retained in the body. Subsequent studies have shown that both Crf and Crphos levels in skeletal muscle can be increased, and performance of high intensity intermittent exercise enhanced, following a period of creatine supplementation. However, neither endurance exercise performance nor maximal oxygen uptake appears to be enhanced. No adverse effects have been identified with short term creatine feeding. Creatine supplementation has been used in the treatment of diseases where creatine synthesis is inhibited.

376 citations


Journal Article
TL;DR: It is indicated that exercise-induced anorexia can be characterized by a brief suppression of hunger, accompanied by a delay to the onset of eating, which may best be measured by the resistance to begin eating rather than the amount of food consumed.
Abstract: OBJECTIVE To examine the effects of exercise on short term energy intake and to investigate the existence of exercise-induced anorexia. DESIGN Two studies were conducted, both with three treatment conditions and employing a repeated measures design. SETTING The Human Appetite Research Unit at Leeds University Psychology department. SUBJECTS Twenty three healthy, lean male subjects (n = 11 and n = 12 respectively) were recruited from the student/staff population of Leeds University. INTERVENTIONS Subjects were randomly assigned to a control, low intensity and high intensity exercise treatment in the first study and to a control, short duration and long duration exercise treatment (high intensity) in the second. Motivation to eat was measured by visual analogue rating scales and by the length of the time between the end of exercise and the volitional onset of eating. Energy and macronutrient intakes were measured by means of a free-selection test meal and by recorded intakes for the next 2 days. RESULTS Subjective feelings of hunger were significantly suppressed during and after intense exercise sessions (P 0.01), but the suppression was short-lived. Exercise sessions had no significant effect on the total amount of food consumed in the test meal but intense exercise delayed the start of eating (P < 0.05). When energy intake was assessed relative to the energy expended during the exercise or control periods, only the long duration, high intensity session created a significant short-term negative energy balance (P < 0.001). CONCLUSIONS These studies indicate that exercise-induced anorexia can be characterized by a brief suppression of hunger, accompanied by a delay to the onset of eating. The temporal aspects of exercise-induced anorexia may best be measured by the resistance to begin eating rather than the amount of food consumed.

361 citations


Journal ArticleDOI
TL;DR: A proposed model stretching regime is presented based on the literature reviewed and implications of stretching on muscle/tendon flexibility, minimizing injury, enhancing athletic performance, and generally preparing the athlete for exercise are discussed.
Abstract: Stretching exercises are either performed alone or with other exercises as part of the athlete's warm-up. The warm-up is designed to increased muscle/tendon suppleness, stimulate blood flow to the periphery, increase body temperature, and enhance free, coordinated movement. The purpose of this paper is to review the literature regarding stretching, with the aim of defining its role during the warm-up. Implications of stretching on muscle/tendon flexibility, minimizing injury, enhancing athletic performance, and generally preparing the athlete for exercise are discussed. Physiology applied to stretching is also discussed together with different related techniques and practical aspects. A proposed model stretching regime is presented based on the literature reviewed.

304 citations


Journal ArticleDOI
TL;DR: It is concluded that young athletes continue to improve their psychomotor performance during exercise even at heavy work loads exceeding anaerobic, and plasma adrenaline thresholds and a relationship between reaction time and plasma catecholamines fits the U-shape curve.
Abstract: Twenty-two male soccer players (mean age 21.3 yrs) performed an incremental, multistage bicycle ergometer exercise test with work load increasing by 50 W, until volitional exhaustion. The exercise stages lasted 3 min and were separated by 1 min resting periods. Before exercise and during each load an audio-visual five-choice reaction task was administered to assess subjects' psychomotor performance. During resting intervals venous blood samples were taken for lactate (LA), adrenaline (A) and noradrenaline (NA) determinations. It was found that reaction time (RT) decreased gradually during exercise reaching its minimum (approx. 87% of pre-exercise value) at load 236 W (approx. 75% VO2max, HR 164 beats/min). Then, it increased rapidly, exceeding the resting level by 18%. The work load and heart rate (HR) associated with the minimal RT were higher (p < 0.001) than work load and HR associated with the LA threshold (by 46 W and 17 beats/min, respectively). Plasma A and NA showed an exponential increase during exercise with thresholds at 204 and 208 W, respectively (HR 149 and 154 beats/min). Work load at which plasma NA threshold occurred was significantly higher than the LA threshold but it did not differ from the work load associated with the minimal RT. Conversely, plasma A threshold was lower than the load of the minimal RT but did not differ significantly from LA threshold. It is concluded that young athletes continue to improve their psychomotor performance during exercise even at heavy work loads exceeding anaerobic, and plasma adrenaline thresholds. A relationship between reaction time and plasma catecholamines fits the U-shape curve.

277 citations


Journal ArticleDOI
TL;DR: This article finds strongly depressed production of interferon gamma (in response to mitogen or endotoxin) following strenuous exercise, and the potential significance of cytokine modulation for exercise-related immunological problems is discussed.
Abstract: Several groups have now investigated the cytokine response to strenuous exercise. In this article we try to summarize known data on this topic. Significant, albeit mild increases in plasma levels of the monokines IL-1, TNF-alpha, IL-6, and of soluble IL-2 receptor have been reported following strenuous exercise. Increased excretion of cytokines after exercise can also be shown in the urine of athletes. Modulation of cytokine release by strenuous exercise can also be demonstrated using in vitro cell cultures. Several authors have shown an increase in endotoxin-stimulated monokine release following exercise. In contrast, using whole blood cultures we found strongly depressed production of interferon gamma (in response to mitogen or endotoxin) following strenuous exercise. The potential significance of cytokine modulation for exercise-related immunological problems is discussed.

277 citations


Journal ArticleDOI
TL;DR: It is demonstrated that Cr ingestion can increase whole body exercise performance during the initial two, but not a third, successive bout of maximal exercise lasting 30 s, and the lower accumulation of plasma ammonia under these conditions suggests this response is achieved by an effect on muscle ATP turnover.
Abstract: The effect of dietary creatine (Cr) supplementation on performance during 3, 30 s bouts maximal isokinetic cycling and on plasma ammonia and blood lactate accumulation during exercise was investigated. Placebo (P) ingestion had no effect on peak power output (PPO), mean power output (MPO) and total work output during each bout of exercise. Cr ingestion (4 x 5 g.day-1 for 5 days) significantly increased PPO in exercise bout 1 (p < 0.05) and MPO and total work output in exercise bouts 1 (p < 0.05, p < 0.05, respectively) and 2 (p < 0.05, p < 0.05, respectively). Cr ingestion had no effect on any of the measures of performance during exercise bout 3. No difference was observed in peak plasma ammonia accumulation before (146 + 30 mumol.l-1) and after (122 +/- 17 mumol.l-1) P ingestion, however the corresponding concentration was lower following Cr ingestion (129 +/- 22 mumol.l-1) compared with before Cr ingestion (160 +/- 18 mumol.l-1, p < 0.05), despite subjects performing more work. No difference in peak blood lactate accumulation was observed before and after P or Cr ingestion. The results demonstrate that Cr ingestion can increase whole body exercise performance during the initial two, but not a third, successive bout of maximal exercise lasting 30 s. The lower accumulation of plasma ammonia under these conditions suggests this response is achieved by an effect on muscle ATP turnover.

259 citations


Journal ArticleDOI
TL;DR: It is suggested that deficits in GH secretion do not underlie the time-dependent leveling off of muscle strength seen with training in the elderly and provide no support for the popular view of GH as an ergogenic aid.
Abstract: Normal aging is characterized by detrimental changes in body composition, muscle strength, and somatotropic function. Reduction in muscle strength contributes to frailty and risk for fracture in the elderly. Although older adults increase muscle strength as a result of resistance exercise training, the strength gains quickly level off, with only modest increases thereafter despite continued training. To investigate whether age-related deficits in the somatotropic axis limit the degree to which muscle strength can improve with resistance training in older individuals, we conducted a double blind, placebo-controlled exercise trial. Eighteen healthy elderly men (65-82 yr) initially underwent progressive weight training for 14 weeks to invoke a trained state. Subjects were then randomized to receive either 0.02 mg/kg BW.day recombinant human GH (rhGH) or placebo, given sc, while undertaking a further 10 weeks of strength training. Sequential measurements were made of muscle strength (one repetition maximum), body composition (dual energy x-ray absorptiometry), and circulating levels of insulin-like growth factor-I (IGF-I) and IGF-binding protein-3. For each exercise, strength increased for both groups (P = 0.0001) through 14 weeks of training, with little improvement thereafter. Increases in muscle strength ranged from 24-62% depending on the muscle group. Baseline plasma IGF-I concentrations were similar in both groups (mean +/- SEM, 106 +/- 9 micrograms/L), approximately half that observed in healthy young adults. In the rhGH group, IGF-I levels increased to 255 +/- 32 micrograms/L at week 15 and 218 +/- 21 micrograms/L at week 24 (P < 0.001). In the placebo group, IGF-I increased slightly to 119 +/- 6 micrograms/L at 24 weeks. IGF-binding protein-3 also increased in the rhGH group (P < 0.05). rhGH had no effect on muscle strength at any time, and no systematic difference in muscle strength was observed between groups throughout the study. Body weight did not change in either group, but lean body mass increased, and fat mass decreased (P < 0.05) in the rhGH group. Supplementation with rhGH does not augment the response to strength training in elderly men. These results suggest that deficits in GH secretion do not underlie the time-dependent leveling off of muscle strength seen with training in the elderly and provide no support for the popular view of GH as an ergogenic aid.

Book
15 Jan 1994
TL;DR: Structural Considerations: Overview of Performance and Sports Medicine Comparative Aspects of Exercise Physiology and Practical Consideration: Nutrition and the Athletic Horse.
Abstract: Structural Considerations: Overview of Performance and Sports Medicine. Comparative Aspects of Exercise Physiology. Conformation, Gait, And Biomechanics. Energetics and Performance. Hematology and Biochemistry. Respiratory System- Anatomy, Physiology and Adaptations to Exercise and Training. Cardiovascular System- Anatomy, Physiology and Adaptations to Exercise and Training. Muscle-Anatomy, Physiology and Adaptations to Exercise and Training. Thermoregulation. Practical Considerations: Nutrition and the Athletic Horse. Evaluation of Performance Potenital. Clinical Exercise Testing. Assessing Fitness During Trainign. Assessment of the Poor Performance Horse. New Diagnostic Modalities in Equine Sports Medicine. Lameness- Approaches to Therapy and Rehabilitation. Transport Stress. Training Regimens- Overview, Throroughbred Training, Standardbred Training, Endurance Training, Eventing Training, Showjumping. Drugs and Performance.

Journal Article
TL;DR: The three types of pain related to exercise are 1) pain experienced during or immediately following exercise, 2) delayed onset muscle soreness, and 3) pain induced by muscle cramps.
Abstract: The three types of pain related to exercise are 1) pain experienced during or immediately following exercise, 2) delayed onset muscle soreness, and 3) pain induced by muscle cramps. Each is characterized by a different time course and different etiology. Pain perceived during exercise is considered to result from a combination of factors including acids, ions, proteins, and hormones. Although it is commonly believed that lactic acid is responsible for this pain, evidence suggests that it is not the only factor. However, no single factor has ever been identified. Delayed onset muscle soreness develops 24-48 hours after strenuous exercise biased toward eccentric (muscle lengthening) muscle actions or strenuous endurance events like a marathon. Soreness is accompanied by a prolonged strength loss, a reduced range of motion, and elevated levels of creatine kinase in the blood. These are taken as indirect indicators of muscle damage, and biopsy analysis has documented damage to the contractile elements. The exact cause of the soreness response is not known but thought to involve an inflammatory reaction to the damage. Muscle cramps are sudden, intense, electrically active contractions elicited by motor neuron hyperexcitability. Although it is commonly assumed that cramps during exercise are the result of fluid electrolyte imbalance induced by sweating, two studies have not supported this. Moreover, participants in occupations that require chronic use of a muscle but do not elicit profuse sweating, such as musicians, often experience cramps. Fluid electrolyte imbalance may cause cramps if there is profuse prolonged sweating such as that found in working in a hot environment. Thus, despite the common occurrence of pain associated with exercise, the exact cause of these pains remains a mystery.

Journal ArticleDOI
TL;DR: An acute insulin-like growth factor I response to 10 min of above-lactate threshold cycle ergometer exercise led to brief and small increases in circulating IGF-I that were independent of circulating GH.
Abstract: An acute insulin-like growth factor I (IGF-I) response to 10 min of above-lactate threshold cycle ergometer exercise was studied in 10 subjects (age 22-35 yr). Each subject exercised on three separate mornings after ingesting one of two isocaloric isovolemic liquid meals high in either fat or glucose or an isovolemic noncaloric placebo. The high-fat meal attenuated the growth hormone (GH) response (Cappon et al., J. Clin. Endocrinol. Metab. 76: 1418-1422, 1993). In contrast, IGF-I increased equally for all protocols [e.g., after the placebo meal IGF-I increased from 21,716 (SE) ng/ml preexercise to 25,316 ng/ml at 10 min of exercise; P < 0.05]. IGF-I peaked by the 10th min of exercise, like GH, and remained significantly elevated for only 20 min of recovery. We tested for possible GH-dependent mechanisms in which circulating IGF-I would increase 12-24 h after exercise. Ten subjects (age 23-32 yr) performed 10 min of above-lactate threshold exercise at 9, 10, and 11 A.M. GH was elevated after the first exercise bout (peak GH 6.05 +/- 1.45 ng/ml; P < 0.001) but was significantly reduced for the second and third bouts (peak GH 2.52 +/- 0.76 and 1.50 +/- 0.40 ng/ml, respectively). No increase in IGF-I was observed by 8 A.M. on the following day. Heavy ergometer exercise led to brief and small increases in circulating IGF-I that were independent of circulating GH.(ABSTRACT TRUNCATED AT 250 WORDS)

Journal ArticleDOI
TL;DR: It is suggested that sports massage will reduce DOMS and CK when administered 2 hours after the termination of eccentric exercise, due to a reduced emigration of neutrophils and/or higher levels of serum cortisol.
Abstract: It was hypothesized that athletic massage administered 2 hours after eccentric exercise would disrupt an initial crucial event in acute inflammation, the accumulation of neutrophils. This would result in a diminished inflammatory response and a concomitant reduction in delayed onset muscle soreness (DOMS) and serum creatine kinase (CK). Untrained males were randomly assigned to a massage (N = 7) or control (N = 7) group. All performed five sets of isokinetic eccentric exercise of the elbow flexors and extensors. Two hours after exercise, massage subjects received a 30-minute athletic massage; control subjects rested. Delayed onset muscle soreness and CK were assessed before exercise and at 8, 24, 48, 72, 96, and 120 hours after exercise. Circulating neutrophils were assessed before and immediately after exercise, and at 30-minute intervals for 8 hours; cortisol was assessed at similar times. A trend analysis revealed a significant (p < 0.05) treatment by time interaction effect for 1) DOMS, with the massa...

Journal ArticleDOI
TL;DR: In this study, aerobic exercise performed four or five times per week beginning six to eight weeks post partum had no adverse effect on lactation and significantly improved the cardiovascular fitness of the mothers.
Abstract: Background The potential risks and benefits of regular exercise during lactation have not been adequately evaluated. We investigated whether regular aerobic exercise had any effects on the volume or composition of breast milk. Methods Six to eight weeks post partum, 33 sedentary women whose infants were being exclusively breast-fed were randomly assigned to an exercise group (18 women) or a control group (15 women). The exercise program consisted of supervised aerobic exercise (at a level of 60 to 70 percent of the heart-rate reserve) for 45 minutes per day, 5 days per week, for 12 weeks. Energy expenditure, dietary intake, body composition, and the volume and composition of breast milk were assessed at 6 to 8, 12 to 14, and 18 to 20 weeks post partum. Maximal oxygen uptake and the plasma prolactin response to nursing were assessed at 6 to 8 and 18 to 20 weeks. Results The women in the exercise group expended about 400 kcal per day during the exercise sessions but compensated for this energy expenditure w...

Journal ArticleDOI
TL;DR: A review of the literature suggests that caffeine at doses of approximately 6 mg/kg is not of ergogenic benefit to high intensity exercise performance, but similar doses are ergogenic in endurance exercise performance.
Abstract: Caffeine is consumed in many beverages and foods throughout the world. It is the most commonly used drug in North America and, probably, in many other countries. The short term consumption of caffeine may result in increased urination, gastrointestinal distress, tremors, decreased sleep, and anxiety symptoms in certain individuals. The long term consumption of caffeine at < 5 cups/day does not appear to increase the risk of cancer, cardiovascular disease, peptic ulcer disease or cardiac arrhythmias. At the cellular level, caffeine is a competitive antagonist of adenosine receptors and probably acts directly on the ryanodine receptor (Ca++ release channel) to potentiate Ca++ release from skeletal muscle sarcoplasmic reticulum. As a result of these 2 cellular mechanisms of action, caffeine causes increased lipolysis, a facilitation of central nervous system transmission, a reduction in plasma potassium during exercise, an increased force of muscle contraction at lower frequencies of stimulation, and a sparing of muscle glycogen (partially or wholly due to an increase in free fatty acid oxidation). These mechanisms of action would predict that caffeine should be of ergogenic benefit during endurance exercise performance, especially when glycogen depletion would be rate limiting to performance. A review of the literature suggests that caffeine at doses of approximately 6 mg/kg is not of ergogenic benefit to high intensity exercise performance, but similar doses are ergogenic in endurance exercise performance. These doses (approximately 6 mg/kg) would result in urinary caffeine concentrations less than the current International Olympic Committee restricted level of 12 mg/L, and consideration should be given to lowering this level.

Journal ArticleDOI
01 May 1994-Chest
TL;DR: In this paper, the relationship between heart rate and oxygen uptake throughout exercise (HR:VO2) was determined using a statistical technique that included each data point from each subject, and prediction equations for maximal heart rate (HRmax) and maximal oxygen uptake (VO2max) were developed by linear regression and were selected from all possible combinations of parameters.

Journal ArticleDOI
TL;DR: The nature of cardiovascular adaptations to strenuous endurance exercise of long duration and the mechanisms underlying increased stroke volume and cardiac output in highly trained older endurance athletes are delineated.
Abstract: BACKGROUND The age-associated decline in aerobic exercise capacity is partially reversible by endurance exercise training. Moderate-intensity endurance exercise training increases aerobic exercise capacity mediated, in part, by improvement of stroke volume and left ventricular performance in older men. The present study was designed to characterize the nature of cardiovascular adaptations to strenuous endurance exercise of long duration and to delineate the mechanisms underlying increased stroke volume and cardiac output in highly trained older endurance athletes. METHODS AND RESULTS Nine male master athletes (MA: 64 +/- 2 years old, mean +/- SEM) and 9 older sedentary healthy men (controls: 63 +/- 1 year) were studied. Left ventricular systolic function was evaluated with the use of cardiac blood pool imaging and echocardiography. Maximal O2 uptake (VO2max) was 50.4 +/- 1.7 mL.kg-1 x min-1 in the MA and 29.6 +/- 1.4 mL.kg-1 x min-1 (P = .0001) in controls. Systolic and mean blood pressures at rest and during exercise were not different in the two groups. Left ventricular systolic function at peak exercise was higher in the MA than in sedentary controls as evidenced by (1) a higher left ventricular functional reserve (delta EF: 12.4 +/- 2 versus 5.6 +/- 2.5, P = .05), (2) a large decrease in end-systolic volume during exercise (MA: 56 +/- 4 mL at rest and 42 +/- 5 mL at peak exercise, P = .007; controls: 43 +/- 2 mL at rest and 42 +/- 6 mL at peak exercise, P = .35) with no differences in systolic blood pressure, (3) a higher left ventricular fractional shortening at peak exercise (MA: 52 +/- 2.6%; controls: 45 +/- 1%, P = .046) at comparable values for end-systolic wall stress (MA: 56 +/- 12 g/cm2; controls: 53 +/- 7 g/cm2, P = .50), and (4) a greater decrease in end-systolic diameter at peak exercise in the MA than in controls (MA: -1.2 +/- 0.16 cm versus -0.57 +/- 0.13 cm, P = .014) despite no significant differences between the changes in end-systolic wall stress during exercise (MA: -15.5 +/- 7.5 g/cm2, controls: -11.0 +/- 9.0 g/cm2, P = .6). MA had a larger end-diastolic volume at rest (153 +/- 6 versus 132 +/- 4 mL, P = .009) with a normal wall thickness-to-radius ratio (0.34 +/- 0.02). Peak exercise stroke volume was higher (P = .023) in the MA (132 +/- 6 mL/min) than in the sedentary controls (111 +/- 6 mL/min). Changes in stroke volume correlated strongly with changes in ejection fraction in the MA (r = .80, P = .010) but not in sedentary controls (r = .59, P = .097). Further, changes in stroke volume from rest to exercise correlated strongly with changes in end-diastolic volume in both MA (r = .78, P = .013) and sedentary controls (r = .73, P = .026), suggestive of reliance of stroke volume on end-diastolic volume and preload. However, for a given increase in end-diastolic volume, the rise in stroke volume during exercise was significantly larger in the MA than in controls, which, in the absence of differences in mean blood pressures, indicates that enhanced left ventricular systolic function independent of preload plays an additional role in maintaining a higher stroke volume at peak exercise in the highly trained older men. CONCLUSIONS Cardiac adaptations in older endurance trained men are characterized by volume-overload left ventricular hypertrophy and enhancement of left ventricular systolic performance at peak exercise. These adaptive responses contribute to enhanced stroke volume at peak exercise in older endurance trained men.

Journal ArticleDOI
TL;DR: The present data suggest that a lowered blood lactate level during active recovery is due to an elevated muscle lactate metabolism and is not caused by a transient higher release of lactate from the exercising muscles coupled with greater uptake in other tissues.
Abstract: This study examined the effect of low-intensity exercise on lactate metabolism during the first 10 min of recovery from high-intensity exercise. Subjects exercised (61.0 +/- 5.4 W) one leg to exhaustion (approximately 3.5 min), and after 1 h of rest they performed the same exhaustive exercise with the other leg. For one leg the intense exercise was followed by rest [passive (P) leg], and for the other leg the exercise was followed by a 10-min period with low-intensity exercise at a work rate of 10 W [active (A) leg]. The muscle lactate concentration after the intense exercise was the same in the P and A legs, but after 10 min of recovery, the lactate concentration and the arterial blood lactate level were higher for the P leg than for the A leg (both P < 0.05). During the recovery, the mean blood flow was lower for the P leg than for the A leg (P < 0.05), whereas the mean lactate efflux was not significantly different. During the 10 min of recovery, lactate release accounted for approximately 60% of the change in muscle lactate for either leg. The leg excess postexercise O2 consumption during 10 min of recovery was 440 and 750 ml for the P and A legs, respectively. The present data suggest that a lowered blood lactate level during active recovery is due to an elevated muscle lactate metabolism and is not caused by a transient higher release of lactate from the exercising muscles coupled with greater uptake in other tissues.(ABSTRACT TRUNCATED AT 250 WORDS)

Journal ArticleDOI
TL;DR: To investigate the effects of exercise intensity on resting blood pressure (BP) in normotensive elderly subjects, 44 sedentary healthy subjects aged 60 to 79 years of age were studied during 6 months of walking exercise.
Abstract: To investigate the effects of exercise intensity on resting blood pressure (BP) in normotensive elderly subjects, 44 sedentary healthy subjects aged 60 to 79 years of age were studied during 6 months of walking exercise. Subjects were ranked according to maximal oxygen consumption and randomly stratified to groups that trained at 70% (n = 19) or 80% to 85% (n = 14) of maximal heart rate reserve, or to a control group (n = 11) that did not train. Initial BP was established during a 2- to 3-week control period. During the first 3 months, both exercise groups progressed to 70% of heart rate reserve for 40 minutes 3 times each week. The moderate-intensity group continued to train at 70% (45-minute duration) for an additional 3 months, whereas the high-intensity group progressed to training at 85% of heart rate reserve (35-minute duration). Maximal oxygen consumption increased (p < or = 0.05) during the initial 3 months in both exercise groups (25.2 to 28.1 ml.kg-1.min-1 and 26.3 to 29.3 ml.kg-1.min-1) and continued to increase (p < or = 0.05) after 3 additional months of training, but the increase was greater (p < or = 0.05) in the high-intensity group (28.1 to 29.4 ml.kg-1.min-1 and 29.3 to 32.8 ml.kg-1.min-1). Systolic BP decreased (p < or = 0.05) similarly at 6 months in both training groups (120 to 111 mm Hg and 120 to 112 mm Hg).(ABSTRACT TRUNCATED AT 250 WORDS)

Journal ArticleDOI
TL;DR: A rationale for the use of RPE and other exertional symptoms as an alternative to traditional exercise prescription procedures for healthy adults is described and important areas that have not received enough research attention are summarized.
Abstract: Rating of perceived exertion (RPE) is endorsed by the American College of Sports Medicine as a useful adjuvant for prescribing and monitoring exercise intensity. In this paper, I describe a rationale for the use of RPE and other exertional symptoms as an alternative to traditional exercise prescription procedures for healthy adults. Errors associated with using RPE for producing exercise intensity are discussed along with limitations with the use of HRReserve as the standard for judging the accuracy of RPE for prescribing relative exercise intensity. The concept of preferred exertion is discussed as a prescription paradigm that is complementary to the use of perceived exertion and physiological indicators of relative exercise intensity. Important areas that have not received enough research attention are summarized.

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TL;DR: Characterizing oxygen uptake (VO2) kinetics yields valuable information regarding both a) the effectiveness of the coupling of O2 delivery to tissue metabolic demands, and b) the ability of the muscle itself to utilize O2 for oxidative phosphorylation.
Abstract: Characterizing oxygen uptake (VO2) kinetics yields valuable information regarding both a) the effectiveness of the coupling of O2 delivery to tissue metabolic demands, and b) the ability of the muscle itself to utilize O2 for oxidative phosphorylation During moderate exercise VO2 reaches a new steady state within 3 min in normal subjects, with little or no sustained rise in blood lactate The steady state VO2 increases linearly with work rate The time constant for VO2 in Phase 2 (after first 15-20 s) is constant across work intensities, and appears to reflect muscle oxygen utilization kinetics However, when heavier exercise is performed, which elevates blood lactate throughout the exercise, the VO2 response becomes more complex The predominant, Phase 2 response continues to rise exponentially with about the same time constant as for moderate exercise, and the amplitude continues to be linearly related to work rate However, an additional, slowly developing rise in VO2 is also usually observed, beginning 100-200 s into exercise This additional VO2 delays attainment of a steady state, increases the overall O2 "cost" of the exercise, and is statistically associated with the rate and magnitude of increase in blood lactate Interestingly, in children, neither the slow component nor blood lactate rise as much during heavy exercise

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TL;DR: Clinical exercise testing is an important tool in assessment of exercise limitation in COPD patients, in Assessment of physiologic and psychological factors that contribute to exercise limitation, and in the differential diagnosis of cardiorespiratory disease.


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TL;DR: In older humans, aerobic exercise training lowers heart rate at rest, reduces levels of heart rate and plasma catecholamines at the same absolute submaximal workload, and, at least in men, improves left ventricular performance during peak exercise, but does not reduce, and may even increase, basal sympathetic nerve activity.
Abstract: This review describes age-related changes in autonomic control of the circulation during exercise and the associated effects on exercise capacity. The increase in heart rate during exercise becomes smaller with aging probably due to both less withdrawal of cardiac vagal tone and diminished beta-adrenergic responsiveness. The latter also appears to contribute to an attenuation in the left ventricular contractile response to exercise despite greater beta-adrenergic stimulation. At rest, muscle sympathetic nerve activity and arterial plasma norepinephrine spillover rates are elevated in older humans. With aging, sympathetically mediated vasoconstriction in nonactive muscle is augmented during brief dynamic exercise. Paradoxically, during more prolonged exercise increases in plasma norepinephrine concentrations/spillover rates are not greater with age. These age-related changes do not adversely affect submaximal exercise performance at a particular % maximal oxygen consumption. However, the lower peak heart rate and attenuated left ventricular contractile response reduce maximal cardiac output, oxygen consumption, and exercise capacity. In older humans, aerobic exercise training lowers heart rate at rest, reduces levels of heart rate and plasma catecholamines at the same absolute submaximal workload, and, at least in men, improves left ventricular performance during peak exercise, but does not reduce, and may even increase, basal sympathetic nerve activity.

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TL;DR: It is suggested that strenuous resistive exercise results in a greater excess postexercise oxygen consumption compared to steady-state endurance exercise of similar estimated energy cost.
Abstract: Postexercise energy metabolism was examined in male subjects age 22-35 years in response to three different treatments: a strenuous bout of resistive exercise (REx), a bout of stationary cycling (AEx) at 50% peak VO2, and a control condition (C) of quiet sitting. Resting metabolic rate (RMR) was measured the morning of and the morning following each condition. Recovery oxygen consumption (RcO2) was measured for 5 hr following each treatment. Total 5-hr RcO2 was higher for the REx treatment relative to both AEx and C, with the largest treatment differences occurring early during recovery. There were no large treatment differences in postexercise respiratory exchange ratio values, except for the first hour of recovery following REx. RMR measured 14.5 hr postexercise for the REx condition was significantly elevated compared to C. These results suggest that strenuous resistive exercise results in a greater excess postexercise oxygen consumption compared to steady-state endurance exercise of similar estimated energy cost.

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TL;DR: The results indicate that, in this model of soleus muscle functional overload, the GLUT-4 protein level may initially regulate insulin-stimulated glucose transport activity in the absence of changes in other modifying factors, however, this regulation of glucose Transport activity by GLUT -4 protein may be subsequently overridden by elevated glycogen concentration.
Abstract: Voluntary wheel running (WR) by juvenile female rats was used as a noninterventional model of soleus muscle functional overload to study the regulation of insulin-stimulated glucose transport activ...

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TL;DR: Nonswimming exercises appear to be a viable and effective means to improve cardiorespiratory function and physical work capacity of the elderly.
Abstract: Exercise in a water medium reduces weight-bearing stresses on the skeletal joints, which may be advantageous for older individuals needing rehabilitation. The purpose of this study was to determine the effects of nonswimming exercises on muscle endurance, % body fat, and aerobic work capacity of an older adult population. Twelve subjects were in an exercise group (10 females and two males), and eight were in a control group (five females and three males). The mean ages of the groups were 65 (+/- 5.29) years and 56 (+/- 6.78) years, respectively. Before and after 12 weeks of training, subjects were measured three times weekly for resting heart rate, maximum heart rate, VO2 max, body composition, and work capacity in water. A general linear model ANCOVA was used with age as the covariate. The exercise group improved significantly (p < .05) on all dependent variables examined except body composition after 12 weeks. However, the control group experienced no significant changes on any variable over this period. In the comparisons between groups, the exercise group significantly surpassed the control group on all variables except body composition, where neither group experienced change. Nonswimming exercises appear to be a viable and effective means to improve cardiorespiratory function and physical work capacity of the elderly.

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TL;DR: Endurance training can greatly improve endurance in old age, at least in part by the same mechanism originally described in youth, i.e., an increase in muscle oxidative capacity, which contributes to reduced glycogen depletion.
Abstract: The mass of many weight-bearing muscles declines in old rats, secondary to the atrophy of fibers, particularly of type IIb, with relatively little loss of muscle fibers during most of the adult life span. In humans, muscle atrophy is the result of a combination of progressive fiber loss and fiber atrophy. In both species, the proportion of histochemically determined fiber types is relatively stable across the adult portion of the life span. The loss of strength in old age is predominantly accounted for by reduced muscle mass in humans and rats. Resistance training leads to increased muscle mass and strength in old humans and rats, primarily by increasing fiber CSA. Muscle capillarity is unchanged in old rats but decreases in old dogs. Apparently, capillarity declines in truly sedentary older people. Endurance training enhances capillarity, and old rats and humans can attain levels of capillarity comparable to their active young counterparts, even when performing considerably less exercise. Blood flow during contractile activity is reduced in male rats and humans but not in old female rats or dogs. Oxidative capacity declines in many muscles of sedentary old rats and humans. With endurance training, old individuals from both species attain levels of muscle oxidative capacity quite similar to those in identically training young individuals. Muscle insulin-stimulated glucose transport is enhanced in rats after a bout of exercise, regardless of age. Endurance training elevates muscle GLUT-4 levels in young and middle-aged, but not old, rats, perhaps because the old rats trained at slower treadmill speeds. Middle-aged (47-62 yr) men and women can substantially increase muscle GLUT-4 with relatively brief (12-14 wk) endurance training; older humans (> 70-80 yr) have not been studied. Endurance training leads to reduced LDH activity without altering PFK or phosphorylase in old rats and humans. Muscle glycogen depletion, CP depletion, and lactate accumulation during contractile activity are exaggerated in old rats, apparently secondary to reduced muscle oxidative capacity and blood flow. Resting muscle glycogen concentration is diminished in older humans, probably in part because of a more sedentary lifestyle. Although several months of endurance training raises muscle glycogen concentration in older people, it does not restore it to youthful levels. Endurance training can greatly improve endurance in old age, at least in part by the same mechanism originally described in youth, i.e., an increase in muscle oxidative capacity, which contributes to reduced glycogen depletion.(ABSTRACT TRUNCATED AT 400 WORDS)