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Showing papers on "Exercise physiology published in 2000"


Journal ArticleDOI
TL;DR: It is suggested that IL‐6 produced by skeletal contracting muscle contributes to the maintenance of glucose homeostasis during prolonged exercise.
Abstract: 1. Plasma interleukin (IL)-6 concentration is increased with exercise and it has been demonstrated that contracting muscles can produce IL-The question addressed in the present study was whether the IL-6 production by contracting skeletal muscle is of such a magnitude that it can account for the IL-6 accumulating in the blood. 2. This was studied in six healthy males, who performed one-legged dynamic knee extensor exercise for 5 h at 25 W, which represented 40% of peak power output (Wmax). Arterial-femoral venous (a-fv) differences over the exercising and the resting leg were obtained before and every hour during the exercise. Leg blood flow was measured in parallel by the ultrasound Doppler technique. IL-6 was measured by enzyme-linked immunosorbent assay (ELISA). 3. Arterial plasma concentrations for IL-6 increased 19-fold compared to rest. The a-fv difference for IL-6 over the exercising leg followed the same pattern as did the net IL-6 release. Over the resting leg, there was no significant a-fv difference or net IL-6 release. The work was produced by 2.5 kg of active muscle, which means that during the last 2 h of exercise, the median IL-6 production was 6.8 ng min-1 (kg active muscle)-1 (range, 3.96-9.69 ng min-1 kg-1). 4. The net IL-6 release from the muscle over the last 2 h of exercise was 17-fold higher than the elevation in arterial IL-6 concentration and at 5 h of exercise the net release during 1 min was half of the IL-6 content in the plasma. This indicates a very high turnover of IL-6 during muscular exercise. We suggest that IL-6 produced by skeletal contracting muscle contributes to the maintenance of glucose homeostasis during prolonged exercise.

937 citations


Journal ArticleDOI
TL;DR: Hormonal changes include a reduced insulin sensitivity, a possible increase in testosterone and growth hormone levels in strength athletes, and a reversal of short term training-induced adaptations in fluid-electrolyte regulating hormones.
Abstract: Detraining is the partial or complete loss of training-induced adaptations, in response to an insufficient training stimulus. Detraining characteristics may be different depending on the duration of training cessation or insufficient training. Short term detraining (less than 4 weeks of insufficient training stimulus) is analysed in part I of this review, whereas part II will deal with long term detraining (more than 4 weeks of insufficient training stimulus). Short term cardiorespiratory detraining is characterised in highly trained athletes by a rapid decline in maximal oxygen uptake (VO2max) and blood volume. Exercise heart rate increases insufficiently to counterbalance the decreased stroke volume, and maximal cardiac output is thus reduced. Ventilatory efficiency and endurance performance are also impaired. These changes are more moderate in recently trained individuals. From a metabolic viewpoint, short term inactivity implies an increased reliance on carbohydrate metabolism during exercise, as shown by a higher exercise respiratory exchange ratio, and lowered lipase activity, GLUT-4 content, glycogen level and lactate threshold. At the muscle level, capillary density and oxidative enzyme activities are reduced. Training-induced changes in fibre cross-sectional area are reversed, but strength performance declines are limited. Hormonal changes include a reduced insulin sensitivity, a possible increase in testosterone and growth hormone levels in strength athletes, and a reversal of short term training-induced adaptations in fluid-electrolyte regulating hormones.

595 citations


Journal ArticleDOI
TL;DR: It is concluded that physical training can be considered to play an important, if not essential role in the treatment and prevention of insulin insensitivity.
Abstract: Physical activity has a beneficial effect on insulin sensitivity in normal as well as insulin resistant populations. A distinction should be made between the acute effects of exercise and genuine training effects. Up to two hours after exercise, glucose uptake is in part elevated due to insulin independent mechanisms, probably involving a contraction-induced increase in the amount of GLUT4 associated with the plasma membrane and T-tubules. However, a single bout of exercise can increase insulin sensitivity for at least 16 h post exercise in healthy as well as NIDDM subjects. Recent studies have accordingly shown that acute exercise also enhances insulin stimulated GLUT4 translocation. Increases in muscle GLUT4 protein content contribute to this effect, and in addition it has been hypothesized that the depletion of muscle glycogen stores with exercise plays a role herein. Physical training potentiates the effect of exercise on insulin sensitivity through multiple adaptations in glucose transport and metabolism. In addition, training may elicit favourable changes in lipid metabolism and can bring about improvements in the regulation of hepatic glucose output, which is especially relevant to NIDDM. It is concluded that physical training can be considered to play an important, if not essential role in the treatment and prevention of insulin insensitivity.

562 citations


Journal ArticleDOI
TL;DR: Results continue to indicate that exercise training decreases blood pressure (BP) in approximately 75% of individuals with hypertension, with systolic and diastolic BP reductions averaging approximately 11 and 8mm Hg, respectively.
Abstract: Hypertension is a very prevalent cardiovascular (CV) disease risk factor in developed countries. All current treatment guidelines emphasise the role of nonpharmacological interventions, including physical activity, in the treatment of hypertension. Since our most recent review of the effects of exercise training on patients with hypertension, 15 studies have been published in the English literature. These results continue to indicate that exercise training decreases blood pressure (BP) in approximately 75% of individuals with hypertension, with systolic and diastolic BP reductions averaging approximately 11 and 8mm Hg, respectively. Women may reduce BP more with exercise training than men, and middle-aged people with hypertension may obtain greater benefits than young or older people. Low to moderate intensity training appears to be as, if not more, beneficial as higher intensity training for reducing BP in individuals with hypertension. BP reductions are rapidly evident although, at least for systolic BP, there is a tendency for greater reductions with more prolonged training. However, sustained BP reductions are evident during the 24 hours following a single bout of exercise in patients with hypertension. Asian and Pacific Island patients with hypertension reduce BP, especially systolic BP, more and more consistently than Caucasian patients. The minimal data also indicate that African-American patients reduce BP with exercise training. Some evidence indicates that common genetic variations may identify individuals with hypertension likely to reduce BP with exercise training. Patients with hypertension also improve plasma lipoprotein-lipid profiles and improve insulin sensitivity to the same degree as normotensive individuals with exercise training. Some evidence also indicates that exercise training in hypertensive patients may result in regression of pathological left ventricular hypertrophy. These results continue to support the recommendation that exercise training is an important initial or adjunctive step that is highly efficacious in the treatment of individuals with mild to moderate elevations in BP.

528 citations


Journal ArticleDOI
TL;DR: It follows that exhaustive whole-body VE elicits a mild cardiovascular exertion, and that neural as well as muscular mechanisms of fatigue may play a role.
Abstract: Summary Vibration exercise (VE) is a new neuromuscular training method which is applied in athletes as well as in prevention and therapy of osteoporosis. The present study explored the physiological mechanisms of fatigue by VE in 37 young healthy subjects. Exercise and cardiovascular data were compared to progressive bicycle ergometry until exhaustion. VE was performed in two sessions, with a 26 Hz vibration on a ground plate, in combination with squatting plus additional load (40% of body weight). After VE, subjectively perceived exertion on Borg’s scale was 18, and thus as high as after bicycle ergometry. Heart rate after VE increased to 128 min ‐1 , blood pressure to 132/ 52 mmHg, and lactate to 3AE 5m M. Oxygen uptake in VE was 48AE8% of VO2max in bicycle ergometry. After VE, voluntary force in knee extension was reduced by 9AE2%, jump height by 9AE1%, and the decrease of EMG median frequency during maximal voluntary contraction was attenuated. The reproducibility in the two VE sessions was quite good: for heart rate, oxygen uptake and reduction in jump height, correlation coefficients of values from session 1 and from session 2 were between 0AE67 and 0AE7. Thus, VE can be well controlled in terms of these parameters. Surprisingly, an itching erythema was found in about half of the individuals, and an increase in cutaneous blood flow. It follows that exhaustive whole-body VE elicits a mild cardiovascular exertion, and that neural as well as muscular mechanisms of fatigue may play a role.

490 citations


Journal ArticleDOI
TL;DR: The re-establishment of EV is associated with healing, improved life quality, and exercise capabilities for these injured/sick persons, and the influence of several perturbations on adaptations of blood volume, erythrocyte volume, and plasma volume is reviewed.
Abstract: This paper reviews the influence of several perturbations (physical exercise, heat stress, terrestrial altitude, microgravity, and trauma/sickness) on adaptations of blood volume (BV), erythrocyte volume (EV), and plasma volume (PV). Exercise training can induced BV expansion; PV expansion usually occurs immediately, but EV expansion takes weeks. EV and PV expansion contribute to aerobic power improvements associated with exercise training. Repeated heat exposure induces PV expansion but does not alter EV. PV expansion does not improve thermoregulation, but EV expansion improves thermoregulation during exercise in the heat. Dehydration decreases PV (and increases plasma tonicity) which elevates heat strain and reduces exercise performance. High altitude exposure causes rapid (hours) plasma loss. During initial weeks at altitude, EV is unaffected, but a gradual expansion occurs with extended acclimatization. BV adjustments contribute, but are not key, to altitude acclimatization. Microgravity decreases PV and EV which contribute to orthostatic intolerance and decreased exercise capacity in astronauts. PV decreases may result from lower set points for total body water and central venous pressure, which EV decrease bay result form increased erythrocyte destruction. Trauma, renal disease, and chronic diseases cause anemia from hemorrhage and immune activation, which suppressions erythropoiesis. The re-establishment of EV is associated with healing, improved life quality, and exercise capabilities for these injured/sick persons.

440 citations


Journal ArticleDOI
TL;DR: Although Cr supplementation exhibits small but significant physiological and performance changes, the increases in performance are realized during very specific exercise conditions, suggesting that the apparent high expectations for performance enhancement, evident by the extensive use of Cr supplementation, are inordinate.
Abstract: Creatine (Cr) supplementation has become a common practice among professional, elite, collegiate, amateur, and recreational athletes with the expectation of enhancing exercise performance. Research indicates that Cr supplementation can increase muscle phosphocreatine (PCr) content, but not in all individuals. A high dose of 20 g x d(-1) that is common to many research studies is not necessary, as 3 g x d(-1) will achieve the same increase in PCr given time. Coincident ingestion of carbohydrate with Cr may increase muscle uptake; however, the procedure requires a large amount of carbohydrate. Exercise performance involving short periods of extremely powerful activity can be enhanced, especially during repeated bouts of activity. This is in keeping with the theoretical importance of an elevated PCr content in skeletal muscle. Cr supplementation does not increase maximal isometric strength, the rate of maximal force production, nor aerobic exercise performance. Most of the evidence has been obtained from healthy young adult male subjects with mixed athletic ability and training status. Less research information is available related to the alterations due to age and gender. Cr supplementation leads to weight gain within the first few days, likely due to water retention related to Cr uptake in the muscle. Cr supplementation is associated with an enhanced accrual of strength in strength-training programs, a response not independent from the initial weight gain, but may be related to a greater volume and intensity of training that can be achieved. There is no definitive evidence that Cr supplementation causes gastrointestinal, renal, and/or muscle cramping complications. The potential acute effects of high-dose Cr supplementation on body fluid balance has not been fully investigated, and ingestion of Cr before or during exercise is not recommended. There is evidence that medical use of Cr supplementation is warranted in certain patients (e.g.. neuromuscular disease); future research may establish its potential usefulness in other medical applications. Although Cr supplementation exhibits small but significant physiological and performance changes, the increases in performance are realized during very specific exercise conditions. This suggests that the apparent high expectations for performance enhancement, evident by the extensive use of Cr supplementation, are inordinate.

438 citations


Journal ArticleDOI
TL;DR: Results from animal research seem to indicate that there are multiple analgesia systems, including opioid and non-opioid systems, and that properties of the exercise stressor are important in determining which analgesic system is activated during exercise.
Abstract: Over the past 20 years a number of studies have examined whether analgesia occurs following exercise. Exercise involving running and cycling have been examined most often in human research, with swimming examined most often in animal research. Pain thresholds and pain tolerances have been found to increase following exercise. In addition, the intensity of a given pain stimulus has been rated lower following exercise. There have been a number of different noxious stimuli used in the laboratory to produce pain, and it appears that analgesia following exercise is found more consistently for studies that used electrical or pressure stimuli to produce pain, and less consistently in studies that used temperature to produce pain. There is also limited research indicating that analgesia can occur following resistance exercise and isometric exercise. Currently, the mechanism(s) responsible for exercise-induced analgesia are poorly understood. Although involvement of the endogenous opioid system has received mixed support in human research, results from animal research seem to indicate that there are multiple analgesia systems, including opioid and non-opioid systems. It appears from animal research that properties of the exercise stressor are important in determining which analgesic system is activated during exercise.

427 citations


Journal ArticleDOI
TL;DR: A maintained substrate uptake by the brain after exercise suggests a role for brain glycogen in cerebral activation, but the fate of brain substrate uptake has not yet been determined.

407 citations


Journal ArticleDOI
TL;DR: It appears plausible that muscular adaptation to physical exercise occurs without preceding muscle inflammation, and modes of stress other than eccentric cycling should therefore be evaluated as a myositis model in human.
Abstract: 1. A role of the immune system in muscular adaptation to physical exercise has been suggested but data from controlled human studies are scarce. The present study investigated immunological events in human blood and skeletal muscle by immunohistochemistry and flow cytometry after eccentric cycling exercise and multiple biopsies. 2. Immunohistochemical detection of neutrophil- (CD11b, CD15), macrophage- (CD163), satellite cell- (CD56) and IL-1beta-specific antigens increased similarly in human skeletal muscle after eccentric cycling exercise together with multiple muscle biopsies, or multiple biopsies only. 3. Changes in immunological variables in blood and muscle were related, and monocytes and natural killer (NK) cells appeared to have governing functions over immunological events in human skeletal muscle. 4. Delayed onset muscle soreness, serum creatine kinase activity and C-reactive protein concentration were not related to leukocyte infiltration in human skeletal muscle. 5. Eccentric cycling and/or muscle biopsies did not result in T cell infiltration in human skeletal muscle. Modes of stress other than eccentric cycling should therefore be evaluated as a myositis model in human. 6. Based on results from the present study, and in the light of previously published data, it appears plausible that muscular adaptation to physical exercise occurs without preceding muscle inflammation. Nevertheless, leukocytes seem important for repair, regeneration and adaptation of human skeletal muscle.

392 citations


Journal ArticleDOI
TL;DR: In this paper, a literature search over the past 15 years was conducted using Medline and selected papers to review results on exercise induced changes in the immune system following strenuous and moderate exercise.
Abstract: Objectives —To review results on exercise induced changes in the immune system following strenuous and moderate exercise. Methods —A literature search over the past 15 years was conducted using Medline and selected papers. Results —After intense long term exercise, the immune system is characterised by concomitant impairment of the cellular immune system and increased inflammation. Thus low concentrations of lymphocytes, suppressed natural immunity, suppressed lymphocyte proliferation, and suppressed levels of secretory IgA in saliva are found simultaneously with high levels of circulating proinflammatory and anti-inflammatory cytokines. The underlying mechanisms are multifactorial and include neuroendocrinological and metabolic factors. The clinical consequences of the exercise induced immune changes have not formally been identified, but the exercise effect on lymphocyte dynamics and immune function may be linked to the exercise effects on resistance to infections and malignancy and the cytokine response may be linked to muscle damage or muscle cell growth. Conclusions —Moderate exercise across the life span seems to increase resistance to upper respiratory tract infections, whereas repeated strenuous exercise suppresses immune function. It is premature to offer advice on nutrition to athletes in order to alter the exercise induced immunosuppression found after exercise.

Journal ArticleDOI
09 Feb 2000-JAMA
TL;DR: It is suggested that testosterone and resistance exercise promote gains in body weight, muscle mass, muscle strength, and lean body mass in HIV-infected men with weight loss and low testosterone levels.
Abstract: ContextPrevious studies of testosterone supplementation in HIV-infected men failed to demonstrate improvement in muscle strength. The effects of resistance exercise combined with testosterone supplementation in HIV-infected men are unknown.ObjectiveTo determine the effects of testosterone replacement with and without resistance exercise on muscle strength and body composition in HIV-infected men with low testosterone levels and weight loss.Design and SettingPlacebo-controlled, double-blind, randomized clinical trial conducted from September 1995 to July 1998 at a general clinical research center.ParticipantsSixty-one HIV-infected men aged 18 to 50 years with serum testosterone levels of less than 12.1 nmol/L (349 ng/dL) and weight loss of 5% or more in the previous 6 months, 49 of whom completed the study.InterventionsParticipants were randomly assigned to 1 of 4 groups: placebo, no exercise (n = 14); testosterone enanthate (100 mg/wk intramuscularly), no exercise (n = 17); placebo and exercise (n = 15); or testosterone and exercise (n = 15). Treatment duration was 16 weeks.Main Outcome MeasuresChanges in muscle strength, body weight, thigh muscle volume, and lean body mass compared among the 4 treatment groups.ResultsBody weight increased significantly by 2.6 kg (P<.001) in men receiving testosterone alone and by 2.2 kg (P = .02) in men who exercised alone but did not change in men receiving placebo alone (−0.5 kg; P = .55) or testosterone and exercise (0.7 kg; P = .08). Men treated with testosterone alone, exercise alone, or both experienced significant increases in maximum voluntary muscle strength in leg press (range, 22%-30%), leg curls (range, 18%-36%), bench press (range, 19%-33%), and latissimus pulls (range, 17%-33%). Gains in strength in all exercise categories were greater in men assigned to the testosterone-exercise group or to the exercise-alone group than in those assigned to the placebo-alone group. There was a greater increase in thigh muscle volume in men receiving testosterone alone (mean change, 40 cm3; P<.001 vs zero change) or exercise alone (62 cm; P = .003) than in men receiving placebo alone (5 cm3; P = .70). Average lean body mass increased by 2.3 kg (P = .004) and 2.6 kg (P<.001), respectively, in men who received testosterone alone or testosterone and exercise but did not change in men receiving placebo alone (0.9 kg; P = .21).Hemoglobin levels increased in men receiving testosterone but not in those receiving placebo.ConclusionOur data suggest that testosterone and resistance exercise promote gains in body weight, muscle mass, muscle strength, and lean body mass in HIV-infected men with weight loss and low testosterone levels. Testosterone and exercise together did not produce greater gains than either intervention alone.

Journal ArticleDOI
TL;DR: Compared with untrained persons exercising at the same absolute intensity, persons who have undergone endurance training have greater fat oxidation during exercise without increased lipolysis, and available evidence suggests that the training-induced increase in fat oxidation is due primarily to increased oxidation of non-plasma-derived fatty acids, perhaps from intramuscular triacylglycerol stores.

Journal ArticleDOI
TL;DR: Exercise at a higher intensity for only 20 min leads to increases in AMPK alpha2 activity but not alpha1 activity, suggesting that the alpha2-containing AMPK complex, rather than alpha1, may be involved in the metabolic responses to exercise in human skeletal muscle.

Journal ArticleDOI
TL;DR: Football-specific intermittent exercise did not increase the demands placed on the aerobic energy systems compared to continuous exercise performed at the same average speed, although the results indicate that anaerobic energy provision is more important during intermittent than during continuous exercise at thesame average speed.
Abstract: The aim of this study was to devise a laboratory-based protocol for a motorized treadmill that was representative of work rates observed during soccer match-play. Selected physiological responses to this soccer-specific intermittent exercise protocol were then compared with steady-rate exercise performed at the same average speed. Seven male university soccer players (mean +/- s: age 24 +/- 2 years, height 1.78 +/- 0.1 m, mass 72.2 +/- 5.0 kg, VO2max 57.8 +/- 4 ml x kg(-1) x min(-1)) completed a 45-min soccer-specific intermittent exercise protocol on a motorized treadmill. They also completed a continuous steady-rate exercise session for an identical period at the same average speed. The physiological responses to the laboratory-based soccer-specific protocol were similar to values previously observed for soccer match-play (oxygen consumption approximately 68% of maximum, heart rate 168 +/- 10 beats x min(-1)). No significant differences were observed in oxygen consumption, heart rate, rectal temperature or sweat production rate between the two conditions. Average minute ventilation was greater (P < 0.05) in intermittent exercise (81.3 +/- 0.2 l x min(-1)) than steady-rate exercise (72.4 +/- 11.4 l x min(-1)). The rating of perceived exertion for the session as a whole was 15 +/- 2 during soccer-specific intermittent exercise and 12 +/- 1 for continuous exercise (P < 0.05). The physiological strain associated with the laboratory-based soccer-specific intermittent protocol was similar to that associated with 45 min of soccer match-play, based on the variables measured, indicating the relevance of the simulation as a model of match-play work rates. Soccer-specific intermittent exercise did not increase the demands placed on the aerobic energy systems compared to continuous exercise performed at the same average speed, although the results indicate that anaerobic energy provision is more important during intermittent than during continuous exercise at the same average speed.

Journal ArticleDOI
TL;DR: It is likely that IL‐6 plays a beneficial role and may be involved in mediating exercise‐related metabolic changes and there appears to be a logarithmic relationship.
Abstract: Strenuous exercise induces increased levels in a number of pro-inflammatory and anti-inflammatory cytokines, naturally occurring cytokine inhibitors and chemokines. Thus, increased plasma levels of TNF-alpha, IL-1, IL-6, IL-1 receptor antagonist, TNF receptors, IL-10, IL-8 and macrophage inflammatory protein-1 are found after strenuous exercise. The concentration of IL-6 increases up to 100-fold after a marathon race. The increase in IL-6 is tightly related to the duration of the exercise and there appears to be a logarithmic relationship. Furthermore, the increase in IL-6 is related to the intensity of exercise. Given the facts that IL-6, more than any other cytokine, is produced in large amounts in response to exercise, that IL-6 is produced locally in the skeletal muscle in response to exercise and that IL-6 is known to have growth factor abilities, it is likely that IL-6 plays a beneficial role and may be involved in mediating exercise-related metabolic changes.

Journal ArticleDOI
TL;DR: This brief advisory will highlight the major clinical and research applications of functional capacity assessment and the impact of age, sex, conditioning status, and the presence of diseases or medications that influence its components.
Abstract: Afundamental requirement for many of the activities of daily living is the ability to perform predominantly aerobic, ie, oxygen-using, work. Such activities require the integrated efforts of the heart, lungs, and circulation to deliver oxygen to the metabolically active muscle mass. Thus, the assessment of functional or aerobic exercise time or peak oxygen consumption provides important diagnostic and prognostic information in a wide variety of clinical settings. Furthermore, numerous clinical trials, especially those in patients with heart failure, have used aerobic exercise time or peak oxygen consumption as a primary or secondary end point. This brief advisory will highlight the major clinical and research applications of functional capacity assessment. For a comprehensive review of exercise testing, the reader is referred to the American College of Cardiology/American Heart Association Guidelines for Exercise Testing.1 The maximal capacity of an individual to perform aerobic work is defined by the maximal oxygen consumption (Vo2max), the product of cardiac output (CO) and arteriovenous oxygen (AV O2) difference at exhaustion. Although Vo2max is measured in liters per minute, it is usually expressed per kilogram of body weight to facilitate intersubject comparisons. Functional capacity, particularly when estimated rather than measured directly, is often expressed in metabolic equivalents (METs); 1 MET represents resting energy expenditure and approximates 3.5 mL O2 · kg−1 · min−1. Because Vo2max is typically achieved by exercise that involves only about half of the total body musculature, it is generally believed that Vo2max is limited by maximal CO rather than peripheral factors.2 Vo2max is affected by age, sex, conditioning status, and the presence of diseases or medications that influence its components. Vo2max in a young world-class male …

Journal ArticleDOI
TL;DR: It is concluded that muscle damage is similar between genders, yet the inflammatory response is attenuated in women vs. men, and exercise may stimulate the expression of proteins involved in apoptosis in skeletal muscle.
Abstract: Unaccustomed exercise is followed by delayed-onset muscle soreness and morphological changes in skeletal muscle. Animal studies have demonstrated that women have an attenuated response to muscle da...

Journal ArticleDOI
TL;DR: Exercise training in individuals with elevated cardiovascular risk or established disease can increase NO bioavailability and may represent an important mechanism by which exercise training conveys benefit in the setting of secondary prevention.
Abstract: Accumulating data suggest that nitric oxide (NO) is important for both coronary and peripheral hemodynamic control and metabolic regulation during exercise. Although still controversial, NO of endothelial origin may potentiate exercise-induced hyperemia. Mechanisms of release include both acetylcholine derived from the neuromuscular junction and elevation in vascular shear stress. A splice variant of neuronal nitric oxide synthase (NOS), nNOSmu, is expressed in human skeletal muscle. In addition to being a potential modulator of blood flow, NO from skeletal muscle regulates muscle contraction and metabolism. In particular, recent human data indicate that NO plays a role in muscle glucose uptake during exercise independently of blood flow. Exercise training in healthy individuals elevates NO bioavailability through a variety of mechanisms including increased NOS enzyme expression and activity. Such adaptations likely contribute to increased exercise capacity and cardiovascular protection. Cardiovascular risk factors including hypercholesterolemia, hypertension, diabetes, and smoking as well as established disease are associated with impairment of the various NO systems. Given that NO is an important signaling mechanism during exercise, such impairment may contribute to limitations in exercise capacity through inadequate coronary or peripheral perfusion and via metabolic effects. Exercise training in individuals with elevated cardiovascular risk or established disease can increase NO bioavailability and may represent an important mechanism by which exercise training conveys benefit in the setting of secondary prevention.

Journal ArticleDOI
TL;DR: It has been suggested that hyperhydration (increased total body water) may reduce physiologic strain during exercise heat stress, but data supporting that notion are not robust.

Journal ArticleDOI
TL;DR: It is concluded that the patterns of changes in substrate kinetics during moderate- and high-intensity exercise are similar in trained men and women.
Abstract: We have studied eight endurance-trained women at rest and during exercise at 25, 65, and 85% of maximal oxygen uptake. The rate of appearance (Ra) of free fatty acids (FFA) was determined by infusi...

Journal ArticleDOI
TL;DR: Exercise training improves endothelium-dependent and -independent vascular function and peak vasodilator capacity in patients with CHF and effects on the vasculature are generalized, as they were evident in a vascular bed not directly involved in the exercise stimulus.
Abstract: Exercise training of a muscle group improves local vascular function in subjects with chronic heart failure (CHF). We studied forearm resistance vessel function in 12 patients with CHF in response ...

Journal ArticleDOI
TL;DR: The OUES is an objective, reproducible measure of cardiopulmonary reserve that does not require a maximal exercise effort and integrates cardiovascular, musculoskeletal and respiratory function into a single index that is largely influenced by pulmonary dead space ventilation and exercise-induced lactic acidosis.

Journal ArticleDOI
TL;DR: Neither moderate- nor heavy-intensity exercise had an effect on the VO(2) kinetic response to subsequent moderate exercise, suggesting phase II VO( 2) kinetics are not speeded by prior heavy exercise.
Abstract: We tested the hypothesis that heavy-exercise phase II oxygen uptake (VO(2)) kinetics could be speeded by prior heavy exercise Ten subjects performed four protocols involving 6-min exercise bouts on a cycle ergometer separated by 6 min of recovery: 1) moderate followed by moderate exercise; 2) moderate followed by heavy exercise; 3) heavy followed by moderate exercise; and 4) heavy followed by heavy exercise The VO(2) responses were modeled using two (moderate exercise) or three (heavy exercise) independent exponential terms Neither moderate- nor heavy-intensity exercise had an effect on the VO(2) kinetic response to subsequent moderate exercise Although heavy-intensity exercise significantly reduced the mean response time in the second heavy exercise bout (from 652 +/- 41 to 470 +/- 31 s; P < 005), it had no significant effect on either the amplitude or the time constant (from 239 +/- 19 to 253 +/- 29 s) of the VO(2) response in phase II Instead, this "speeding" was due to a significant reduction in the amplitude of the VO(2) slow component These results suggest phase II VO(2) kinetics are not speeded by prior heavy exercise

Journal ArticleDOI
TL;DR: Vitamin E was shown to significantly increase circulating neutrophils in older, but not younger, subjects performing eccentric exercise that causes an increase in skeletal muscle damage and causes a greater increase in circulating creatine kinase activity, perhaps indicating increased skeletal muscle repair.

Journal ArticleDOI
TL;DR: In both trials, IGF-1 concentrations were significantly lower after exercise as compared to concentrations found at 0800 hours the morning before exercise, and it is not known if this reduction observed 22 hours after exercise is of physiological significance.
Abstract: The hormonal responses of nine male, strength athletes to strength exercise were examined. The athletes performed one moderate- and one high-intensity strength exercise workout. In the high-intensity workout, the load was 100% of each subject's three-repetition maximum (3-RM) for squats and front squats, and 100% of each subject's six-repetition maximum (6-RM) for leg extensions. In the moderate-intensity workout, the load was 70% of the high-intensity protocol. Rest periods between sets were 4-6 min for both workouts. Blood samples were taken before, 30 min into, and every 15 min for the 1st h after exercise, and then 3, 7, 11, 22 and 33 h after exercise, thus allowing examination of both the acute and prolonged hormonal responses. Blood samples were analyzed for testosterone, luteinizing hormone (LH), follicle stimulating hormone (FSH), cortisol, adrenocorticotrophic hormone (ACTH), growth hormone (GH), insulin-like growth factor (IGF-1), insulin, sex hormone binding globulin, creatine kinase, total protein, glucose and lactate. The acute responses of testosterone and cortisol were greater during the high-intensity protocol as compared to the moderate-intensity protocol. The cortisol response was associated with an increase in ACTH concentration. LH and FSH showed no response to either protocol. Acute GH responses were not different between protocols. There were great inter-individual differences in acute GH responses to both protocols. There were no significant differences between protocols with regard to prolonged responses for any hormone. In both trials, IGF-1 concentrations were significantly lower at 0800 hours the morning after exercise as compared to concentrations found at 0800 hours the morning before exercise. The mechanisms responsible for reducing IGF-1 concentration in these trials are unclear, and it is not known if this reduction observed 22 hours after exercise is of physiological significance.

Journal ArticleDOI
TL;DR: Xanthine oxidase is involved in free‐radical formation in exercise in humans and inhibition of this enzyme with allopurinol decreases oxidative stress and muscle damage associated with exhaustive exercise.
Abstract: Moderate exercise is a healthy practice. However, exhaustive exercise generates free radicals. This can be evidenced by increases in lipid peroxidation, glutathione oxidation, and oxidative protein damage. It is well known that activity of cytosolic enzymes in blood plasma is increased after exhaustive exercise. This may be taken as a sign of damage to muscle cells. The degree of oxidative stress and of muscle damage does not depend on the absolute intensity of exercise but on the degree of exhaustion of the person who performs exercise. Training partially prevents free radical-formation in exhaustive exercise. Treatment with antioxidants such as vitamins C or E protects in part against free radical-mediated damage in exercise. Xanthine oxidase is involved in free-radical formation in exercise in humans and inhibition of this enzyme with allopurinol decreases oxidative stress and muscle damage associated with exhaustive exercise. Knowledge of the mechanism of free-radical formation in exercise is important because it will be useful to prevent oxidative stress and damage associated with exhaustive physical activity.

Journal ArticleDOI
TL;DR: First order decay is an inadequate model for HR recovery following max exercise, but may be reasonable for sub-max levels.
Abstract: The time constant (T) obtained by fitting post-exercise heart rate (HR) recovery to a first order exponential decay curve has been promoted as an index of parasympathetic activity. However, acceptance has been limited because reported data are inadequate to assess goodness of fit for the model, determine the best exercise protocol, or optimize the duration of post exercise monitoring. Consequently, we evaluated T for nine healthy volunteers (age 24-46) following treadmill exercise at maximal (max) and two stages sub-max exercise (Bruce protocol). T stabilized only after 3 min of post-exercise monitoring. With max exercise, T varied unacceptably with small changes in onset of monitoring, e.g. -16.7+/-16.6 (-13.2%) in the first 5 s, and residuals of the fitted curve were non-random. In contrast, sub-max exercise produced consistent T values, e.g. -1.9+/-3.2 (-4.2%) in the first 5 s, and residuals were more nearly random. In conclusion, first order decay is an inadequate model for HR recovery following max exercise, but may be reasonable for sub-max levels.

Journal ArticleDOI
TL;DR: It is possible that the combined effects of small changes in several immune parameters may compromise resistance to minor illnesses such as URTI, and whether moderate exercise training is helpful in preventing infectious illness among the wider population is uncertain.
Abstract: MACKINNON. L. T. Chronic exercise training effects on immune function. Med. Sri. Sports Exerc., Vol. 32, No. 7, Suppl., pp. S369-S376. 2000. Purpose: This paper reviews the recent literature on the chronic effects of exercise training. on immune function in humans. There is a general perception by athletes and other physically active individuals that regular moderate activity enhances, whereas intense exercise suppresses, resistance to minor illnesses such as upper respiratory tract infection (URTI). This perception is supported by epidemiological data in endurance athletes and limited data from intervention studies using moderate exercise in previously untrained individuals. The apparently high incidence of URTI among endurance athletes has prompted interest the relationship between chronic exercise training and immune function. Whereas immune cell number is generally normal during intense exercise training, recent evidence suggests that prolonged periods of intense training may lead to slight impairment in immune parameters such as neutrophil function, serum and mucosal immunoglobulin levels, plasma glutamine concentration, and possibly natural killer cell cytotoxic activity. In contrast, moderate exercise training has either no effect on, or may stimulate, these immune parameters. Conclusion: Whereas athletes are not clinically immune deficient, it is possible that the combined effects of small changes in several immune parameters may compromise resistance to minor illnesses such as URTI. Strategies to prevent URTI in athletes include avoiding overtraining, providing adequate rest and recovery during the training cycle and after competition, limiting exposure to sources of infection, ensuring adequate nutrition, and possibly vitamin C supplementation. It is uncertain at present whether moderate exercise training is helpful in preventing infectious illness among the wider population.

Journal ArticleDOI
TL;DR: In previously sedentary, moderately obese females, continuous or intermittent exercise performed long-term may be effective for preventing weight gain and for improving some measures of metabolic fitness.
Abstract: The effects of 18 months of intermittent vs continuous exercise on aerobic capacity, body weight and composition, and metabolic fitness in previously sedentary, moderately obese females