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PubMed1998

Endurance exercise training increases peripheral vascular response in human fingers.

The purpose of this study was to clarify whether peripheral vascular response to alteration of transmural pressure is changed by endurance exercise training. The healthy male subjects (training group; n = 6) performed endurance exercise training that consisted of cycle ergometer exercise 5 d.week-1 and 30 min.d-1 for a period of 8 weeks. Changes in the peripheral vascular response to alteration of transmural pressure in the human finger were measured by a differential digital photoplethysmogram (DeltaDPG) and blood pressure during passive movement of the arm to different vertical hand positions relative to heart level. Following 8 weeks of endurance training, percent changes in DeltaDPG from heart level in the training group increased significantly (mean +/- SD, -48.1 +/- 7. 3 to -58.7 +/- 9.3% at the lowered position, 46.1 +/- 13.4 to 84.6 +/- 8.8% at the elevated position, p<0.05). Similarly, the arterial compliance index, which was calculated from DeltaDPG-P wave amplitude and arterial pulse pressure, also significantly changed in the training group over the 8 weeks (5.6 +/- 1.3 to 2.7 +/- 1.6 mV. V-1.s-1.mmHg-1 at the lowered position, 30.0 +/- 12.4 to 54.4 +/- 18. 9 mV.V-1.s-1.mmHg-1 at the elevated position ). Maximal oxygen uptake (V.O2 max) was significantly increased in the training group. On the other hand, the control group (n = 6) showed no significant changes in all parameters for 8 weeks. Therefore these results suggest that endurance exercise training induces an increase in peripheral vascular response to alteration of transmural pressure in the human finger.

Adult↗

PubMed2006

Chronic L-arginine supplementation enhances endurance exercise tolerance in heart failure patients.

The purpose of the study was to determine the potential beneficial effect of six weeks oral L-arginine supplementation (LAS) on endurance exercise, an important determinant of daily-life activity in patients with chronic stable heart failure (CHF). After an initial incremental maximal exercise test, CHF patients performed an identical thirty-minute interval endurance exercise test before and after six weeks with (L-arginine group; ARG) or without LAS (control group; CTL). Hemodynamic, respiratory, and metabolic parameters were determined at rest, during exercise, and during recovery. Mean heart rate decreased throughout exercise and recovery after LAS (- 8.2 +/- 1.4 b x min(-1); p = 0.003 and - 6.7 +/- 1.6 b x min(-1); p < 0.001, respectively), systemic blood pressure and respiratory parameters remaining unchanged. Resting L-argininaemia increased from 102 +/- 11 to 181 +/- 37 micromol x l(-1) (p < 0.004) and exercise-induced peak increase in plasma lactate was blunted after LAS (4.13 +/- 0.75 vs. 3.13 +/- 0.39 mmol x l(-1); p = 0.02). No significant change was observed in the control group. In heart failure patients, six weeks oral LAS enhances endurance exercise tolerance, reducing both heart rate and circulating lactates. This suggests that chronic LAS might be useful as a therapeutic adjuvant in order to improve the patient's physical fitness.

Administration, Oral↗

PubMed1978

Time course of sympathoadrenal adaptation to endurance exercise training in man.

One possible reason for the lower exercise heart rate after endurance exercise training is that the sympathetic drive to the heart is reduced. We have studied the relationship between plasma catecholamines and heart rate during exercise in the course of a 7-wk training program. Six untrained subjects exercised vigorously (on bicycle ergometers and by running) 30--50 min/day for 7 wk. Prior to the beginning of training and at weekly intervals thereafter, participants were subjected to a 5-min strenuous bicycle ergometer test. In the test prior to training, plasma epinephrine increased to 0.5 ng/ml and norepinephrine increased to 3.0 ng/ml. The major proportion of the training-induced decrement in catecholamine response was reached at the end of the 3rd wk when epinephrine increased to 0.17 ng/ml and norepinephrine increased to 1.5 ng/ml in response to the same test. Heart rate during exercise continued to decrease even after the catecholamine response had plateaued, implying that the reduced sympathetic response is not solely responsible for the reduced exercise heart rate.

Adaptation, Physiological↗

PubMed2006

Ultra-endurance exercise and oxidative damage : implications for cardiovascular health.

At least 30 minutes of moderate-intensity physical activity accumulated on most, preferably all days is considered the minimum level necessary to reduce the risk of developing cardiovascular disease. Despite an unclear explanation, some epidemiological data paradoxically suggest that a very high volume of exercise is associated with a decrease in cardiovascular health. Although ultra-endurance exercise training has been shown to increase antioxidant defences (and therefore confer a protective effect against oxidative stress), an increase in oxidative stress may contribute to the development of atherosclerosis via oxidative modification of low-density lipoprotein (LDL). Research has also shown that ultra-endurance exercise is associated with acute cardiac dysfunction and injury, and these may also be related to an increase in free radical production. Longitudinal studies are needed to assess whether antioxidant defences are adequate to prevent LDL oxidation that may occur as a result of increased free radical production during very high volumes of exercise. In addition, this work will assist in understanding the accrued effect of repeated ultra-endurance exercise-induced myocardial damage.

Antioxidants↗

PubMed1999

Neuroendocrine activation in heart failure is modified by endurance exercise training.

OBJECTIVES: The purpose of this study was to determine whether endurance exercise training could buffer neuroendocrine activity in chronic heart failure patients. BACKGROUND: Neuroendocrine activation is associated with poor long-term prognosis in heart failure. There is growing consensus that exercise may be beneficial by altering the clinical course of heart failure, but the mechanisms responsible for exercise-induced benefits are unclear. METHODS: Nineteen heart failure patients (ischemic disease; New York Heart Association [NYHA] class II or III) were randomly assigned to either a training group or to a control group. Exercise training consisted of supervised walking three times a week for 16 weeks at 40% to 70% of peak oxygen uptake. Medications were unchanged. Neurohormones were measured at study entry and after 16 weeks. RESULTS: The training group (n = 10; age = 61 +/- 6 years; EF = 30 +/- 6%) and control group (n = 9; age = 62 +/- 7 years; EF = 29 +/- 7%) did not differ in clinical findings at study entry. Resting levels of angiotensin II, aldosterone, vasopressin and atrial natriuretic peptide in the training and control groups did not differ at study entry (5.6 +/- 1.3 pg/ml; 158 +/- 38 pg/ml; 6.1 +/- 2.0 pg/ml; 37 +/- 8 pg/ml training group vs. 4.8 +/- 1.2; 146 +/- 23; 4.9 +/- 1.1; 35 +/- 10 control group). Peak exercise levels of angiotensin II, aldosterone, vasopressin and atrial natriuretic peptide in the exercise and control groups did not differ at study entry. After 16 weeks, rest and peak exercise hormone levels were unchanged in control patients. Peak exercise neurohormone levels were unchanged in the training group, but resting levels were significantly (p < 0.001) reduced (angiotensin -26%; aldosterone -32%; vasopressin -30%; atrial natriuretic peptide -27%). CONCLUSIONS: Our data indicate that 16 weeks of endurance exercise training modified resting neuroendocrine hyperactivity in heart failure patients. Reduction in circulating neurohormones may have a beneficial impact on long-term prognosis.

Aged↗

PubMed2004

Effects of high-intensity endurance exercise training in the G93A mouse model of amyotrophic lateral sclerosis.

The G93A transgenic mouse has a mutation in copper/zinc superoxide dismutase (CuZnSOD) that results in oxidative stress and motor neuron loss. Endurance exercise training is known to increase antioxidant capacity in skeletal muscle. Therefore, we hypothesized that endurance training may extend onset of disease or survival in the G93A mouse. We examined the effects of high-intensity endurance exercise training (45 min/day, 5 times/week, progressive increase from 9 to 22 m/min) on disease onset and survival in G93A mice. Endurance training did not affect clinical onset, although it hastened death in male mice (P < 0.05). Endurance-trained males had a statistically significant decrease in rotarod performance at 112 days (P < 0.05), whereas sedentary males decreased at 119 days (P < 0.05). Endurance-trained and sedentary females decreased at 126 days and 129 days, respectively (P < 0.05). Female mice lived longer than males (P < 0.05), and there was a trend for hastened clinical onset in males (P = 0.062). We conclude that high-intensity endurance exercise training does not affect onset of clinical symptoms in G93A mice but hastens a decrease in motor performance and death following onset of clinical symptoms in male mice only. In light of a recent report describing increased survival following low-intensity endurance training, it appears that training intensity is an important determinant of survival in the G93A mouse.

Alanine↗

PubMed1999

Ventilatory assistance improves exercise endurance in stable congestive heart failure.

We postulated that ventilatory assistance during exercise would improve cardiopulmonary function, relieve exertional symptoms, and increase exercise endurance (T(lim)) in patients with chronic congestive heart failure (CHF). After baseline pulmonary function tests, 12 stable patients with advanced CHF (ejection fraction, 24 +/- 3% [mean +/- SEM]) performed constant-load exercise tests at approximately 60% of their predicted maximal oxygen consumption (V O(2)max) while breathing each of control (1 cm H(2)O), continuous positive airway pressure optimized to the maximal tolerable level (CPAP = 4.8 +/- 0.2 cm H(2)O) or inspiratory pressure support (PS = 4.8 +/- 0.2 cm H(2)O), in randomized order. Measurements during exercise included cardioventilatory responses, esophageal pressure (Pes), and Borg ratings of dyspnea and leg discomfort (LD). At a standardized time near end-exercise, PS and CPAP reduced the work of breathing per minute by 39 +/- 8 and 25 +/- 4%, respectively (p < 0. 01). In response to PS: T(lim) increased by 2.8 +/- 0.8 min or 43 +/- 14% (p < 0.01); slopes of LD-time, V O(2)-time, V CO(2)-time, and tidal Pes-time decreased by 24 +/- 10, 20 +/- 11, 28 +/- 8, and 44 +/- 9%, respectively (p < 0.05); dyspnea and other cardioventilatory parameters did not change. CPAP did not significantly alter measured exercise responses. The increase in T(lim) was explained primarily by the decrease in LD- time slopes (r = -0.71, p < 0.001) which, in turn, correlated with the reductions in V O(2)-time (r = 0.61, p < 0.01) and tidal Pes-time (r = 0.52, p < 0.01). in conclusion, ventilatory muscle unloading with PS reduced exertional leg discomfort and increased exercise endurance in patients with stable advanced CHF.

Double-Blind Method↗

PubMed2000

Lipid metabolism during endurance exercise.

Endogenous triacylglycerols represent an important source of fuel for endurance exercise. Triacylglycerol oxidation increases progressively during exercise; the specific rate is determined by energy requirements of working muscles, fatty acid delivery to muscle mitochondria, and the oxidation of other substrates. The catecholamine response to exercise increases lipolysis of adipose tissue triacylglycerols and, presumably, intramuscular triacylglycerols. In addition, increases in adipose tissue and muscle blood flow decrease fatty acid reesterification and facilitate the delivery of released fatty acids to skeletal muscle. Alterations in fatty acid mobilization and the relative use of adipose and intramuscular triacylglycerols during exercise depend, in large part, on degree of fitness and exercise intensity. 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. 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. Fat oxidation is lower in high-intensity exercise than in moderate-intensity exercise, in part because of decreased fatty acid delivery to exercising muscles. Parenteral lipid supplementation during high-intensity exercise increases fat oxidation, but the effect of ingesting long-chain or medium-chain triacylglycerols on substrate metabolism during exercise is less clear. This review discusses the relation between fatty acid mobilization and oxidation during exercise and the effect of endurance training, exercise intensity, and lipid supplementation on these responses.

Adipose Tissue↗

PubMed2003

Effects of endurance exercise on three-dimensional trabecular bone microarchitecture in young growing rats.

Appropriate endurance exercise is capable of increasing bone mass and strength in both animals and humans. We examined the skeletal changes induced by treadmill running exercise in young growing rats with a particular emphasis on three-dimensional trabecular bone microarchitecture. Fourteen male Wistar rats were divided into sedentary (CON; n = 7) and exercised (RUN; n = 7) groups at the age of 4 weeks. The rats in the RUN group performed the treadmill running exercise of 30 m/min for 60 min, 5 times a week. After 10 weeks of exercise, bone mineral density (BMD), cortical geometry, diaphyseal breaking force, and trabecular bone microarchitecture in the femur were measured. Three-dimensional trabecular bone microarchitecture was evaluated at the distal femoral metaphysis using microcomputed tomography. The running exercise significantly increased BMD, bone volume, bone volume fraction, trabecular thickness, and trabecular number, whereas trabecular bone pattern factor, the parameter associated with decreased trabecular connectivity, was significantly lower in the RUN group than the CON group. On the other hand, no significant difference in the degree of anisotropy and structure model index was observed between the two groups. At the femoral diaphysis, running exercise significantly increased cortical bone area, width, and maximum load without affecting bending stress, implying that the material properties of bone had not changed in the exercised rats. These results suggest that the increase in bone strength induced by endurance exercise is mediated by changes in trabecular bone microarchitecture as well as density and cortical geometry.

Animals↗

PubMed1993

Endurance exercise training augments diastolic filling at rest and during exercise in healthy young and older men.

BACKGROUND: Diastolic filling at rest is altered markedly with advancing age. Whether exercise training can improve diastolic filling at rest or during exercise in either healthy older or healthy young men has not been determined. The purpose of this study was to determine if 6 months of aerobic exercise training improves diastolic filling. METHODS AND RESULTS: Radionuclide diastolic filling parameters were measured at rest and during exercise in 14 older (age, 60 to 82 years) and 17 young (age, 24 to 32 years) rigorously screened healthy males before exercise training and in 13 older and 11 young men after 6 months of endurance exercise training. Diastolic filling rates were expressed in two ways, as absolute milliliters of blood (mL.s-1.m-2) and normalized to the end-diastolic volume. At baseline, the peak early filling rates were lower in the older group compared with the young group as expressed in absolute milliliters of blood (older, 85 +/- 7 mL.s-1.m-2; young, 173 +/- 10 mL.s-1.m-2; P < or = .0001) and in end-diastolic volume per second (1.66 +/- 0.11 versus 2.55 +/- 0.08, P < .0001), whereas the peak atrial filling rates were greater in absolute milliliters of blood (85 +/- 5 versus 56 +/- 7 mL.s-1.m-2, P = .003) and in end-diastolic volume per second (1.70 +/- 0.12 versus 0.80 +/- 0.06, P < .0001). During exercise, at any given heart rate, the older group had a lower peak filling rate than the young group. Also, at peak exercise, the single peak filling rate was decreased in the older group in mL.s-1.m-2 (384 +/- 19 versus 565 +/- 36 mL.s-1.m-2, P = .0002) and in end-diastolic volume per second (6.01 +/- 0.25 versus 7.91 +/- 0.28 end-diastolic volume per second, P < .0001). Six months of intensive aerobic exercise training had similar effects in the old and young groups overall. Maximal oxygen consumption increased 19% (ANOVA training effect, P < or = .0001) and echocardiographic left ventricular mass increased 8% (ANOVA training effect, P = .002). Training increased the resting peak early filling rate in absolute milliliters of blood by +14% (ANOVA training effect, P = .02). During exercise, the peak early or single peak filling rate at any given heart rate was increased. At peak exercise, the single peak filling rate was increased by 14% in mL.s-1.m-2 (ANOVA training effect, P = .0004). The only age-related differential effect of training was on the peak atrial filling rate in end-diastolic volume per second, which decreased by 27% in the older group but was unchanged in the young (+5%) (ANOVA young versus older, P = .001). The independent predictors of a greater maximal oxygen consumption by multivariate analysis were a higher peak exercise heart rate, a greater resting peak early filling rate, the exercise trained state, and a younger age. CONCLUSIONS: Healthy older men have reduced early diastolic filling at rest and during exercise compared with young men. Endurance exercise training enhances early diastolic filling at rest and during exercise in both the old and the young. Training reduces the elevated resting atrial filling rate in the old, whereas the young were unchanged. The training-induced augmentation of early diastolic filling at rest and during exercise may be an important adaptation to allow an increase in stroke volume at rest and an increase in stroke volume, cardiac output, and maximal oxygen consumption during exercise.

Adult↗

PubMed1999

Effects of endurance exercise training on muscle glycogen accumulation in humans.

The purpose of this investigation was to determine whether endurance exercise training increases the ability of human skeletal muscle to accumulate glycogen after exercise. Subjects (4 women and 2 men, 31 +/- 8 yr old) performed high-intensity stationary cycling 3 days/wk and continuous running 3 days/wk for 10 wk. Muscle glycogen concentration was measured after a glycogen-depleting exercise bout before and after endurance training. Muscle glycogen accumulation rate from 15 min to 6 h after exercise was twofold higher (P < 0.05) in the trained than in the untrained state: 10.5 +/- 0.2 and 4.5 +/- 1.3 mmol. kg wet wt(-1). h(-1), respectively. Muscle glycogen concentration was higher (P < 0.05) in the trained than in the untrained state at 15 min, 6 h, and 48 h after exercise. Muscle GLUT-4 content after exercise was twofold higher (P < 0.05) in the trained than in the untrained state (10.7 +/- 1.2 and 4.7 +/- 0.7 optical density units, respectively) and was correlated with muscle glycogen concentration 6 h after exercise (r = 0.64, P < 0.05). Total glycogen synthase activity and the percentage of glycogen synthase I were not significantly different before and after training at 15 min, 6 h, and 48 h after exercise. We conclude that endurance exercise training enhances the capacity of human skeletal muscle to accumulate glycogen after glycogen-depleting exercise.

Adult↗

PubMed2006

Effects of dorsiflexor endurance exercises on foot drop secondary to multiple sclerosis: a pilot study.

PURPOSE: This is a pilot study to determine if endurance exercises for dorsiflexors will improve walking for people with foot drop secondary to MS, and if improvement in muscle endurance for persons with MS can be predicted based on the amount of central fatigue (CF) in the muscle. SUBJECTS: Five individuals with foot drop secondary to MS and five age-matched controls. METHODS: The intervention was 4 sets of 10 isometric contractions, at 60% of MVC, 3X/week, 8 weeks. Pretests-posttests included a dorsiflexor endurance test with superimposed electrical stimulation to measure CF, and a gait assessment including measurement of dorsiflexion at initial contact. RESULTS: Two of 5 subjects with MS had significant improvement in muscle endurance in both legs and in dorsiflexor control during walking. Correlation between CF and improved endurance was not significant (r=-0.07). One of the subjects with significant improvement in endurance had a significant decrease in central activation failure. CONCLUSIONS AND DISCUSSION: For individuals with foot drop secondary to MS, endurance exercises for the dorsiflexors can result in improved walking. CF may not be useful in predicting whether a muscle will improve in endurance with exercise. Improvement may result from either a peripheral training effect, a central learning effect, or both.

Adult↗

PubMed2005

Estrogen supplementation reduces whole body leucine and carbohydrate oxidation and increases lipid oxidation in men during endurance exercise.

Healthy active men exhibit higher rates of carbohydrate (CHO) and leucine oxidation and lower rates of lipid oxidation compared with their female counterparts both at rest and during moderate intensity endurance exercise. We postulated that this reduced dependence on amino acids as a fuel source in women was due to the female sex hormone estrogen. In a randomized, double-blind, placebo-controlled, cross-over design, we investigated the effect of supplementing 12 recreationally active men with estrogen on whole body substrate oxidation and leucine kinetics at rest and during moderate intensity endurance exercise. Subjects cycled for 90 min at an intensity of 65% maximum O(2) consumption after 8 d of either estrogen supplementation (2 mg 17beta-estradiol/d) or placebo (polycose). After a 2-wk washout period, they repeated the test after 8 d of the alternate treatment. On the test day, after a primed continuous infusion of l-[(13)C]leucine, O(2) consumption, CO(2) production, steady-state breath (13)CO(2), and plasma alpha-[(13)C]ketoisocaproate enrichments were measured at rest and at 60, 75, and 90 min during exercise in the postabsorptive state. Exercise increased energy expenditure more than 5-fold, CHO oxidation more than 6-fold, lipid oxidation more than 4-fold, and leucine oxidation 2.2-fold (all P < 0.0001), whereas it decreased the ratio of lipid to CHO oxidation by 50-70% (P = 0.003) compared with values at rest. Estrogen supplementation decreased respiratory exchange ratio during exercise (P = 0.03). Estrogen supplementation significantly decreased CHO oxidation by 5-16% (P = 0.04) and leucine oxidation by 16% (P = 0.01), whereas it significantly increased lipid oxidation by 22-44% (P = 0.024) at rest and during exercise. We conclude that estrogen influences fuel source selection at rest and during endurance exercise in recreationally active men, characterized by a reduced dependence on amino acids and CHO and an increased reliance on lipids as a fuel source.

Adult↗

PubMed2000

Gender differences in substrate metabolism during endurance exercise.

Females show a lower respiratory exchange ratio (RER) than males during submaximal endurance exercise, which translates into a proportionately lower carbohydrate and higher fat oxidation. Data from rodents show that 17-beta-estradiol may mediate these metabolic differences. 17-beta-estradiol supplementation in humans is less convincing; however, two studies found a reduction in glucose rate of appearance during exercise. No difference is found between genders in muscle glycogen content; however, lipid content in muscle is higher in females. Evidence shows that short chain OH-acyl CoA-dehydrogenase (SCHAD) maximal enzyme activity is higher in females. The rate of leucine oxidation is lower in females at rest and during endurance exercise. This is not apparently related to gender differences in branched chain-2-oxo-dehydrogenase (BCOAD) activity in skeletal muscle, which may implicate hepatic control. Important muscle proteins to examine in future research are hormone sensitive lipase, the enzymes of beta-oxidation, and fatty acid transporters.

Animals↗

PubMed2005

Testosterone and endurance exercise: development of the "exercise-hypogonadal male condition".

During the last 30 years a large number of research studies have been conducted examining reproductive endocrine dysfunction in exercising women. The number of similar studies examining men is still relatively small. Nevertheless, an increasing amount of research studies in men indicate endurance exercise training has significant effects upon the major male reproductive hormone, testosterone, and the hypothalamic-pituitary-testicular axis that regulates reproductive hormones. This review article addresses one reproductive endocrine dysfunction found in exercising men, what has been deemed the "exercise-hypogonadal male condition". Specifically, men with this condition exhibit basal (resting-state) free and total testosterone levels that are significantly and persistently reduced. The exact physiological mechanism inducing the reduction of testosterone is currently unclear, but is postulated to be a dysfunction (or perhaps a readjustment) within the hypothalamic-pituitary-testicular regulatory axis. The time course for the development of the "exercise-hypogonadal condition" or the threshold of exercise training necessary to induce the condition remains unresolved. The potential exists for these reduced testosterone levels within the exercise-hypogonadal male to disrupt and be detrimental to some anabolic or androgenic testosterone-dependent physiological processes. Unfortunately, extremely few research studies have addressed whether such processes are affected, and thus findings are inconclusive. Conversely, the alterations in testosterone levels brought about by endurance exercise training have the potential for cardiovascular protective effects and thus could be beneficial to the health of these men. Current evidence suggests this condition is limited to men who have been persistently involved in chronic endurance exercise training for extended periods of time (i.e., years). Many questions, however, regarding the male reproductive endocrine adaptive process to exercise and exercise training remain unanswered, necessitating the need for further research on this topic.

Cumulative Trauma Disorders↗

PubMed2002

Metabolic response to provision of mixed protein-carbohydrate supplementation during endurance exercise.

The interaction of substrates and hormones in response to ingestion of intact proteins during endurance exercise is unknown. This study characterized substrate and hormone responses to supplementation during endurance exercise. Nine male runners participated in 3 trials in which a non-fat (MILK), carbohydrate (CHO), or placebo (PLA) drink was consumed during a 2-hour treadmill run at 65% VO2max. Circulating levels of insulin, glucagon, epinephrine, norepinephrine, growth hormone, testosterone, and cortisol were measured. Plasma substrates included glucose, lactate, free fatty acids, and select amino acids. Except for insulin and cortisol, hormones increased with exercise. While post-exercise insulin concentrations declined similarly in all 3 trials, the glucagon increase was greatest following MILK consumption. CHO blunted the post-exercise increase in growth hormone compared to levels in MILK. Free fatty acids and plasma amino acids also were responsive to nutritional supplementation with both CHO and MILK attenuating the rise in free fatty acids compared to the increase observed in PLA. Correspondingly, respiratory exchange ratio increased during CHO. Essential amino acids increased significantly only after MILK and were either unchanged or decreased in CHO. PLA was characterized by a decrease in branched-chain amino acid concentrations. Modest nutritional supplementation in this study altered the endocrine response as well as substrate availability and utilization following and during an endurance run, respectively.

Adult↗

PubMed1999

Increased concentrations of interleukin 1-beta in whole blood cultures supernatants after 12 weeks of moderate endurance exercise.

The aim of the study was to investigate whether a regular moderate endurance exercise programme influenced the in vitro cytokine synthesis by stimulated whole blood cultures. To this end, eight healthy subjects exercised moderately by running for 3-5 h a week over a period of 12 weeks, whilst seven other healthy subjects served as the control group. The intensity of the exercise was determined by lactic acid concentrations in the blood which were maintained between 1.8 and 2.5 mmol x l(-1). Over the period of training the running velocity producing the 4 mmol x l(-1) lactic acid threshold increased from 2.86 (SD 0.83) m x s(-1) to 3.06+/-0.79 m x s(-1) (P < or = 0.008). Blood samples were taken at rest before and after the training programme. The following blood parameters were determined: leucocyte count, differential leucocyte count, lymphocyte subpopulations [CD14 positive (+)/CD45+, CD4+/ CD25+, CD8+, CD16+/CD122+]. Whole blood cultures were stimulated with lipopolysaccarides [interleukin (IL)-1 beta and IL-6] and staphylococcal enterotoxin B [IL-2, soluble interleukin 2 receptor (sIL2-R) and interferon (IFN)-gamma]. Cytokine concentrations in the supernatants were measured using an enzyme-linked immunosorbent assay. The white blood cell count, differential leucocyte count, lymphocyte subset distribution and the expression of the CD25 and CD122 antigen on lymphocytes were unchanged by training. After the training programme the IL-1 beta production changed significantly [1496 (SD 264) pg ml(-1) before, compared to 2127 (SD 672) pg ml(-1) after training, P < or = 0.008]. In the control group these parameters remained unchanged. With respect to changes in the values in both groups the syntheses of IL-1 beta (P < or = 0.023) and IL-6 (P < or = 0.021) were significantly higher after regular training. The syntheses of IL-2, sIL-2 and INF-gamma were not significantly influenced. Regular endurance exercise influenced the in vitro production of monocyte derived cytokines, while the effect of exercise on the cytokines synthesized by T-cells appeared to be of lesser importance.

Adult↗

PubMed1988

Effect of cocaine on exercise endurance and glycogen use in rats.

To determine the effects of cocaine on exercise endurance, male rats were injected intraperitoneally with cocaine (20 mg/kg body wt) or saline and then run to exhaustion 20 min later at 22 m/min and 15% grade. Saline-injected animals ran 74.9 +/- 16.5 (SD) min, whereas cocaine-treated rats ran only 29 +/- 11.6 min. The drug had no effect on resting blood glucose or lactate levels, nor did it affect resting glycogen levels in liver or red and white vastus muscle. However, it did reduce resting soleus glycogen content by 30%. During exercise liver and soleus glycogen depletion occurred at the same rate in saline- and cocaine-treated animals. In contrast, the rate of glycogen depletion during exercise in red and white vastus was markedly increased in cocaine-treated rats with a corresponding elevation in blood lactate (12 vs. only 5 mM in saline group) at exhaustion. These data suggest that cocaine administration (20 mg/kg) before submaximal exercise dramatically alters glycogen metabolism during exercise, and this effect has a negative impact on exercise endurance.

Animals↗