Abstract: Fatigue of voluntary muscular effort is a complex phenomenon. To date, relatively little attention has been placed on the role of the central nervous system (CNS) in fatigue during exercise despite the fact that the unwillingness to generate and maintain adequate CNS drive to the working muscle is the most likely explanation of fatigue for most people during normal activities. Several biological mechanisms have been proposed to explain CNS fatigue. Hypotheses have been developed for several neurotransmitters including serotonin (5-HT; 5-hydroxytryptamine), dopamine, and acetylcholine. The most prominent one involves an increase in 5-HT activity in various brain regions. Good evidence suggests that increases and decreases in brain 5-HT activity during prolonged exercise hasten and delay fatigue, respectively, and nutritional manipulations designed to attenuate brain 5-HT synthesis during prolonged exercise improve endurance performance. Other neuromodulators that may influence fatigue during exercise include cytokines and ammonia. Increases in several cytokines have been associated with reduced exercise tolerance associated with acute viral or bacterial infection. Accumulation of ammonia in the blood and brain during exercise could also negatively effect the CNS function and fatigue. Clearly fatigue during prolonged exercise is influenced by multiple CNS and peripheral factors. Further elucidation of how CNS influences affect fatigue is relevant for achieving optimal muscular performance in athletics as well as everyday life.

Abstract: Objective. —To determine the effects of moderate-intensity exercise training on self-rated (subjective) sleep quality among healthy, sedentary older adults reporting moderate sleep complaints. Design. —Randomized controlled trial of 16 weeks' duration. Setting. —General community. Participants. —Volunteer sample of 29 women and 14 men (of 67 eligible subjects) aged 50 to 76 years who were sedentary, free of cardiovascular disease, and reported moderate sleep complaints. No participant was withdrawn for adverse effects. Intervention. —Randomized to 16 weeks of community-based, moderate-intensity exercise training or to a wait-listed control condition. Exercise consisted primarily of four 30- to 40-minute endurance training sessions (low-impact aerobics; brisk walking) prescribed per week at 60% to 75% of heart rate reserve based on peak treadmill exercise heart rate. Main Outcome Measure. —Pittsburgh Sleep Quality Index (PSQI). Results. —Compared with controls (C), subjects in the exercise training condition (E) showed significant improvement in the PSQI global sleep score at 16 weeks (baseline and posttest values in mean [SD] for C=8.93 [3.1] and 8.8 [2.6]; baseline and posttest values for E=8.7 [3.0] and 5.4 [2.8]; mean posttest difference between conditions=3.4; P Conclusions. —Older adults with moderate sleep complaints can improve selfrated sleep quality by initiating a regular moderate-intensity exercise program.

Abstract: We determined the effect on exercise tolerance and physiological exercise responses of rigorous rehabilitative exercise training in chronic obstructive pulmonary disease (COPD). Fifteen men and 10 women (mean age, 68 +/- 6 yr; FEV1, 0.93 +/- 0.27 L) participated in a rehabilitation program with an exercise component of three per week 45-min sessions of cycle ergometer training for 6 wk with exercise intensity kept near maximal targets. Before and after rehabilitation, patients performed an incremental test and a constant work rate (CWR) test at 80% of the peak work rate in the preprogram incremental test. Ventilation (V(E)) and gas exchange were measured breath by breath; arterialized venous blood was analyzed for blood gas determinations and lactate. Rehabilitation yielded an average increase in peak work rate in the incremental test of 36% (p < 0.001), and in the duration of the CWR test of 77% (p < 0.001). In the CWR test, the kinetics of O2 uptake, CO2 output, V(E), and heart rate were markedly slower than those of healthy subjects. After training, mean response time decrease averaged 17, 22, 34, and 29%, respectively (p < 0.02), evidence of a physiologic training effect. Further, for identical CWR tasks, V(E) was 10% lower (p < 0.02) after training, attributable to altered breathing pattern: tidal volume increased by 8% and respiratory rate decreased by 19%, yielding lower V(D) /V(T) (0.46 versus 0.53 p < 0.005). Rigorous exercise training for patients with severe COPD yields more efficient exercise breathing pattern and lower V(E); this is associated with improved exercise tolerance.

Abstract: Exercise increases the rate of glucose uptake into the contracting skeletal muscles. This effect of exercise is similar to the action of insulin on glucose uptake, and the mechanism through which b...

Abstract: The applicability of high-intensity training and the possibility of inducing physiologic adaptation to training are still uncertain in patients with severe chronic obstructive pulmonary disease (COPD). The purposes of this study were to evaluate the proportion of patients with moderate to severe COPD in whom high-intensity exercise training (30-min exercise session at 80% of baseline maximal power output [Wmax]) is feasible, and the response to training in these patients. We also sought to evaluate the possible influence of disease severity on the training intensity achieved and on the development of physiologic adaptation following endurance training. Forty-two patients with COPD (age = 66 +/- 7 yr, FEV1 = 38 +/- 13% predicted, [mean +/- SD]) were evaluated at baseline and after a 12-wk endurance training program. Each evaluation included a stepwise exercise test on an ergocycle up to the individual maximal capacity during which minute ventilation (VE), oxygen consumption (VO2), carbon dioxide production (VCO2), and arterial lactic acid concentrations were measured. The training consisted of 25 to 30-min exercise sessions on a calibrated ergocycle three times a week, with a target training intensity at 80% of Wmax. The training intensity was adjusted with the objective of reaching the target intensity, but also to ensure that the cycling exercise could be maintained for the specified duration. The training intensity sustained for the duration of each exercise session averaged 24.5 +/- 12.6, 51.7 +/- 17.4, 63.8 +/- 22.4, and 60.4 +/- 22.7% of Wmax at Weeks 2, 4, 10, and 12, respectively. High-intensity training was achieved in zero, three, five, and five patients at Weeks 2, 4, 10, and 12, respectively. A significant increase in VO2max and Wmax occurred with training (p or = 40% or or = 40% predicted. We conclude that although most patients were unable to achieve high-intensity training as defined in this study, significant improvement in their exercise capacity was obtained and physiologic adaptation to endurance training occurred. The training intensity expressed as a percent of the individual maximum exercise capacity, and the relative effectiveness of training, were not influenced by the severity of airflow obstruction.

Abstract: Recent epidemiological studies indicate that individuals who maintain a physically active lifestyle are much less likely to develop impaired glucose tolerance and non-insulin-dependent diabetes mellitus (NIDDM). Moreover, it was found that the protective effect of physical activity was strongest for individuals at highest risk of developing NIDDM. Reducing the risk of insulin resistance and NIDDM by regularly performed exercise is also supported by several aging studies. It has been found that older individuals who vigorously train on a regular basis exhibit a greater glucose tolerance and a lower insulin response to a glucose challenge than sedentary individuals of similar age and weight.

Abstract: We used meta-analytic methods to examine the influence of acute exercise on sleep. Thirty-eight studies were reviewed yielding 211 effects on 401 subjects. Mean effect sizes were calculated for sleep onset latency (SOL), stage 2, slow-wave sleep (SWS), rapid eye movement (REM) sleep, REM latency (REM-L), total sleep time (TST), and wakefulness after sleep onset (WASO). Moderating influences of subject fitness, heat load, exercise duration, time of day, associated light environment (i.e. indoor or outdoor), sleep schedule, and the scientific quality of the studies were examined. Effect sizes for SWS, REM, REM-L, and TST were moderate [0.18-0.52 standard deviation (SD)] and their associated 95% confidence intervals did not include zero. Exercise duration and time of day were the most consistent moderator variables. In contrast with previous hypotheses, heat load had little influence on sleep. The results of our quantitative synthesis of the literature are inconsistent with previous narrative reviews (1,2) which suggested that exercise elicits larger changes in sleep than those quantified in this meta-analysis. A major delimitation of published studies on the effects of acute exercise has been an exclusive focus on good sleepers. Hence, the effects we report herein may be underestimates of the efficacy of exercise for enhancing sleep among people with sleep disturbances.

Abstract: OBJECTIVE To evaluate the effects of an intense physical training program on abdominal fat distribution, glycemic control, and insulin sensitivity in patients with NIDDM and to determine whether branched-chain amino acid (BCAA) supplements influence these effects. RESEARCH DESIGN AND METHODS Twenty-four patients (ages 45 ± 2 [mean ± SE] years, BMI 30.2 ± 0.9 kg/m 2 , HbA 1c 7.9 ± 0.3%) were randomly assigned to four groups: training plus BCAA supplement ( n = 6), training plus placebo ( n = 6), sedentary plus BCAA supplement ( n = 6), and sedentary plus placebo ( n = 6). Physical training consisted of a supervised 45-min cycling exercise at 75% of their oxygen uptake peak (VO 2 peak) two times per week and an intermittent exercise one time per week for 2 months. RESULTS Patients who exercised increased their VO2 peak by 41% and their insulin sensitivity by 46%. Physical training significantly decreased abdominal fat evaluated by magnetic resonance imaging (umbilicus), with a greater loss of visceral adipose tissue (VAT) (48%) in comparison with the loss of subcutaneous adipose tissue (18%), but did not significantly affect body weight. The change in visceral abdominal fat was associated with the improvement in insulin sensitivity ( r = 0.84, P = 0.001). BCAA supplementation had no effect on abdominal fat and glucose metabolism. CONCLUSIONS Physical training resulted in an improvement in insulin sensitivity with concomitant loss of VAT and should be included in the treatment program for patients with NIDDM.

Abstract: Background The ventilatory response to exercise in patients with chronic heart failure (HF) is greater than normal for a given metabolic rate. The objective of the present study was to determine the mechanism(s) for the high ventilatory output in patients with chronic HF. Methods and Results Centers in Germany, Italy, Japan, and the United States participated in this study. Each center contributed studies on patients and normal subjects of similar age and sex. One hundred thirty patients with chronic HF and 52 healthy subjects participated. Spirometric and breath-by-breath gas exchange measurements were made during rest and increasing cycle exercise. Arterial blood was sampled for measurement of pH, Paco2, Pao2, and lactate during exercise in 85 patients. Resting forced expiratory volume in 1 second (FEV1) and vital capacity (VC) were proportionately reduced at all levels of impairment. Patients with more severe HF had greater tachypnea and a smaller tidal volume (Vt) at a given exercise expired volume per unit time (Ve). This was associated with an expiratory flow pattern characteristic of lung restriction. Ve and Vco2 as a function of Vo2 were increased during exercise in HF patients. The increases were greater the lower the peak Vo2 per kilogram of body weight. The ratio of Vd (physiological dead space) to Vt and the difference between arterial and end tidal Pco2 at peak Vo2 also increased inversely with peak Vo2/kg. In contrast, the difference between alveolar and arterial Po2 and PaCO2 were both normal, on average, at peak Vo2 regardless of the level of impairment. The more severe the exercise limitation, the higher the lactate and the lower the HCO3− at a given Vo2, although pH was tightly regulated. Conclusions The increase in Ve in chronic HF patients is caused by an increase in Vd/Vt due to high ventilation/perfusion mismatching, an increase in Vco2 relative to Vo2 resulting from HCO3− buffering of lactic acid, and a decrease in Paco2 due to tight regulation of arterial pH. With regard to the excessive Ve in HF patients, the increases in Vd/Vt and Vco2 relative to Vo2 are more important as the patient becomes more exercise limited. Regional hypoperfusion but not hypoventilation typifies lung gas exchange in HF. This and other mechanisms might account for the restrictive changes leading to exercise tachypnea in HF patients.

Abstract: Fitzgerald, Margaret D., Hirofumi Tanaka, Zung V. Tran, and Douglas R. Seals. Age-related declines in maximal aerobic capacity in regularly exercising vs. sedentary women: a meta-analysis.J. Appl. ...

Abstract: The objectives were: (i) to present a method for assessing muscle pain during exercise, (ii) to provide reliability and validity data in support of the measurement tool, (iii) to test whether leg muscle pain threshold during exercise was related to a commonly used measure of pain threshold pain during test, (iv) to examine the relationship between pain and exertion ratings, (v) to test whether leg muscle pain is related to performance, and (vi) to test whether a large dose of aspirin would delay leg muscle pain threshold and/or reduce pain ratings during exercise. In study 1, seven females and seven males completed three 1-min cycling bouts at three different randomly ordered power outputs. Pain was assessed using a 10-point pain scale. High intraclass correlations (R from 0.88 to 0.98) indicated that pain intensity could be rated reliably using the scale. In study 2, 11 college-aged males (age 21.3 +/- 1.3 yr) performed a ramped (24 W.min-1) maximal cycle ergometry test. A button was depressed when leg muscle pain threshold was reached. Pain threshold occurred near 50% of maximal capacity: 50.3 (+/- 12.9% Wmax), 48.6 (+/- 14.8% VO2max), and 55.8 (+/- 12.9% RPEmax). Pain intensity ratings obtained following pain threshold were positively accelerating function of the relative exercise intensity. Volitional exhaustion was associated with pain ratings of 8.2 (+/- 2.5), a value most closely associated with the verbal anchor "very strong pain." In study 3, participants completed the same maximal exercise test as in study 2 as well as leg cycling at 60 rpm for 8 s at four randomly ordered power outputs (100, 150, 200, and 250 W) on a separate day. Pain and RPE ratings were significantly lower during the 8-s bouts compared to those obtained at the same power outputs during the maximal cycle test. The results suggest that noxious metabolites of muscle contraction play a role in leg muscle pain during exercise. In study 4, moderately active male subjects (N = 19) completed two ramped maximal cycle ergometry tests. Subjects drank a water and Kool-Aid mixture, that either was or was not (placebo) combined with a 20 mg.kg-1 dose of powdered aspirin 60 min before exercise. Paired t-tests revealed no differences between conditions for the measures of exercise intensity at pain threshold [aspirin vs placebo mean (+/- SD)]: power output: 150 (+/- 60.3 W) versus 153.5 (+/- 64.8 W); VO2: 21.3 (+/- 8.6 mL.kg-1.min-1) versus 22.1 (+/- 10.0 mL.kg-1.min-1); and RPE: 10.9 (+/- 3.1) versus 11.4 (+/- 2.9). Repeated measures ANOVA revealed no significant condition main effect or condition by trial interaction for pain responses during recovery or during exercise at 60, 70, 80, 90, and 100% of each condition's peak power output. It is concluded that the perception of leg muscle pain intensity during cycle ergometry: (i) is reliably and validly measured using the developed 10-point pain scale, (ii) covaries as a function of objective exercise stimuli such as power output, (iii) is distinct from RPE, (iv) is unrelated to performance of the type employed here, and (v) is not altered by the ingestion of 20 mg.kg-1 acetylsalicylic acid 1 h prior to the exercise bout.

Abstract: We tested the hypothesis that exercise would improve subjective sleep quality and activity in depressed elders. A 10-week randomized controlled trial was utilized. Participants consisted of a volunteer sample, aged > 60 with a diagnosis of major or minor depression or dysthymia. A total of 32 subjects aged 60-84 years with a mean age of 71.3 +/- 1.2 years was used. Intervention consisted of a supervised weight-training program three times a week or an attention-control group. Main outcome measures were Pittsburgh Subjective Sleep Quality Index (PSQI), Likert Scale of Subjective Sleep Quality and Quantity. Paffenbarger Activity Index. Geriatric Depression Scale (GDS). Beck Depression Inventory (BDI), Hamilton Rating Scale of Depression (HRSD), and the Medical Outcomes Survey Short Form 36 (SF-36). Results showed that exercise significantly improved all subjective sleep-quality and depression measures. Depression measures were reduced by approximately twice that of controls. Habitual activity was not significantly increased by exercise. Quality of life subscales significantly improved. In a forward stepwise multiple regression, percent improvement in GDS and percent increase in strength remained significant predictors of the improvement in total PSQI score (r = 0.71, p = 0.0002). In conclusion, weight lifting exercise was effective in improving subjective sleep quality, depression, strength, and quality of life without significantly changing habitual activity.

Abstract: Jungersten, Lennart, Anneli Ambring, Bjorn Wall, andAke Wennmalm. Both physical fitness and acute exercise regulate nitric oxide formation in healthy humans. J. Appl. Physiol. 82(3): 760–764, 1997....

Abstract: Exercise training elevates arterial compliance at rest, but the effects of acute exercise in this regard are unknown. This study investigated the effects of a single, 30-min bout of cycling exercis...

Abstract: beta-Endorphin, a 31-amino-acid peptide, is primarily synthesised in the anterior pituitary gland and cleaved from pro-opiomelanocortin, its larger precursor molecule. beta-Endorphin can be released into the circulation from the pituitary gland or can project into areas of the brain through nerve fibres. Exercise of sufficient intensity and duration has been demonstrated to increase circulating beta-endorphin levels. Previous reviews have presented the background of opioids and exercise and discussed the changes in beta-endorphin levels in response to aerobic and anaerobic exercise. The present review is to update the response of beta-endorphin to exercise. This review suggests that exercise-induced beta-endorphin alterations are related to type of exercise and special populations tested, and may differ in individuals with health problems. Additionally, some of the possible mechanisms which may induce beta-endorphin changes in the circulation include analgesia, lactate or base excess, and metabolic factors. Based on the type of exercise, different mechanisms may be involved in the regulation of beta-endorphin release during exercise.

Abstract: This review suggests that there is little or no effect of elevating pre-exercise muscle glycogen contents above normal resting values on a single exhaustive bout of high-intensity exercise lasting less than 5 minutes. Nor is there any benefit of increasing starting muscle glycogen content on moderate-intensity running or cycling lasting 60 to 90 minutes. In such exercise substantial quantities of glycogen remain in the working muscles at the end of exercise. However, elevated starting muscle glycogen content will postpone fatigue by approximately equal to 20% in endurance events lasting more than 90 minutes. During this type of exercise, exhaustion usually coincides with critically low (25 mmol/kg wet weight) muscle glycogen contents, suggesting the supply of energy from glycogen utilisation cannot be replaced by an increased oxidation of blood glucose. Glycogen supercompensation may also improve endurance performance in which a set distance is covered as quickly as possible. In such exercise, high carbohydrate diets have been reported to improve performance by 2 to 3%.

Abstract: Aerobic endurance exercise has traditionally been advocated in the treatment of type 2 diabetes, while the potential role of resistance training has often been overlooked. The aim of the present study was to determine the effect of circuit-type resistance training on blood pressure, lipids and long-term glycaemic control (HbA1c) in type 2 diabetic subjects. Thirty-eight type 2 diabetic subjects were enrolled in the study; 18 participated in a 5-month individualized progressive resistance training programme (moderate intensity, high volume) twice a week, while the remaining 20 served as controls. The exercise group showed improvements in total cholesterol (6.0±.3 vs 5.3±.3 mM; P<0.01), low density lipoprotein (LDL)-cholesterol (3.90±.22 vs 3.35±.21 mM; P<0.01) and triglycerides (1.91±.25 vs 1.53±.22 mM; P<0.01). Also, the difference in the change in HbA1c between the groups (0.5%) achieved statistical significance (P<0.01). Circuit-type resistance training seems to be feasible in moderately obese, sedentary type 2 diabetic subjects and the inclusion of circuit-type resistance training in exercise training programmes for type 2 diabetic subjects seems appropriate.

Abstract: Background The influence of age, skeletal muscle function and peripheral blood flow on exercise capacity in chronic heart failure patients is controversial, possibly due to variations in skeletal muscle atrophy. Methods and results To assess predictors of exercise capacity in patients with clinical cardiac cachexia, we studied 16 cachectic and 39 non-cachectic male chronic heart failure patients of similar age and ejection fraction. All cachectic patients were wasted (% ideal body weight: 81 1·9 vs 105·2±2·1, P <0· mean±SEM) and had documented weight loss (5–30 kg). Peak oxygen consumption (14·9±1·4 vs 16·3±0·6 ml.kg−1, min −1, resting, and peak blood flow (plethysmography) and 20 min fatigability (% baseline strength) were all similar between the two groups. Quadriceps strength, muscle size (all P <0·0001), strength per unit muscle (right: P <0·05; left: P <0·0·01) and 5 min fatigability ( P <0·05) were all lower in cachectic patients. In non-cachectic patients, age (R=0·48 and quadriceps strength ( R =0·43, all P <0·01) predicted peak oxygen consumption. Only in cachectic patients did peak blood flow predict peak oxygen consumption significantly (R=0·72, P 0·005), whereas age and strength did not. Similar findings were confirmed using other previously published definitions of cardiac cachexia. Conclusion The predictors of exercise capacity change with the development of cardiac cachexia from age and strength to peak blood flow. This shift may be caused by additional endocrine or catabolic abnormalities active in end stage heart failure.

Abstract: At a time of increased obesity, decreased physical activity, and high food consumption, the relationship between physical activity and appetite control needs to be examined. Many people believe that the energy expended as a result of physical activity generates a drive to eat. However, a counterintuitive conclusion arises since there is no compelling evidence that increased physical activity increases energy intake. A suppression of hunger occurs following intense exercise; however, this effect is brief and has no influence on energy intake. Indeed, there does not appear to be any within-day effect of exercise on energy intake. Day-to-day effects of exercise on energy intake could occur, but only a few provocative data exist showing a delayed effect of exercise on energy intake 2 d later. Therefore, there appears to be only a weak short-term coupling between energy expenditure and energy intake. What about the effects of increased physical activity on food selection? The natural hypothesis would be that the energy reserves used during exercise would estimate a drive for a particular nutrient. There is no clear consistent evidence to indicate that in the short-term, exercise induces changes in food or nutrient preferences. In the long-term there is some evidence that physical activity is associated with an increase in carbohydrate intake, but it is uncertain whether these changes are biologically driven for a result of changes of a psychological nature. Contrary to a popularly held view, food selection and nutrient intake constitute patterns of behavior held in place by environmental contingencies and short-acting post-ingestive physiological responses; these patterns of behavior are relatively immune to modulation by the metabolic effects of exercise.

Abstract: This investigation examined predictors of compliance with exercise therapy in a clinical trial involving older adults with knee osteoarthritis (OA). The study sample was partitioned into tertiles by level of compliance to determine its effect on several clinical outcome measures in the trial (i.e., knee pain, difficulty with activities of daily living, and performance-related disability). The participants (N = 439) first completed all baseline assessments and were then randomly assigned to one of three treatment conditions: health education control, aerobic exercise, or resistance exercise. The two exercise treatments involved a 3-month center-based phase and a 15-month home-based phase. Variables in five categories (i.e., demographic, fitness, health-related quality of life, performance-related disability, and prior exercise behavior) were entered as predictors of attendance and time spent exercising during each session for three different periods of time across the course of the study. Results of these analyses revealed that it was possible to explain more variance for time spent exercising (approximately 40%) during the first 3 months than for attendance (approximately 10%). Furthermore, once participants completed the first 3 months of their training, prior behavior was the strongest predictor of exercise compliance. In most cases, the regression models accounted anywhere from 26 to 46% of the variance in attendance or time spent exercising (7 of the 8 P values < 0.01). In general, demographic, fitness, psychosocial, and disability-related measures did not predict compliance with any consistency across the various phases of the trial. Analysis of the dose-response data suggest that, in the use of aerobic exercise to deter disability in older people with knee OA, consideration should be given to prescribing frequent bouts of activity (at least 3 times each week) of moderate duration (approximately 35 min).

Abstract: Recent research has suggested that cardiovascular recovery from stress can play a potential role in hypertension pathogenesis. Sixty-nine studies were included in a meta-analytic review to evaluate the effect of various hypertension risk factors (e.g., race, lack of exercise) on cardiovascular recovery from stress. Small mean effect sizes were observed for studies examining hypertension status and race as risk factors associated with delayed diastolic blood pressure recovery. Lack of fitness was also associated with delayed heart rate recovery. These results revealed that, for the specified risk factors and cardiovascular variables, high-risk individuals exhibited delayed cardiovascular recovery as compared with low-risk individuals. Further, the relationships between hypertension status, race, and cardiovascular recovery were typically associated with the use of "active" laboratory stressors. The relationship between lack of fitness and cardiovascular recovery was also associated with the use of "active" and exercise laboratory stressors.

Abstract: The authors assessed the cross-sectional association between intensity of exercise in later life and coronary heart disease risk factors and subclinical disease among 2,274 men and women, 65 years of age and older, who were participants in the Cardiovascular Health Study (CHS) during 1989-1990. Subjects were free of prior clinical cardiovascular disease or impairment of physical function. Exercise intensity was characterized as low, moderate, or high, based on highest intensity exercise reported over the 2 weeks prior to the CHS baseline examination. After adjustment for age, education, and postmenopausal hormone therapy (among women), there was an inverse dose-response relationship of exercise intensity with selected risk factors. By low, moderate, and high exercise intensity, respectively: fasting insulin-men, 15.6 microU/ml, 14.1 microU/ml, and 12.6 microU/ml, p for trend <0.001; women, 14.8 microU/ml, 13.8 microU/ml, and 12.0 microU/ml, p for trend = 0.01; serum fibrinogen-men, 316.2 mg/dl, 315.4 mg/dl, and 300.0 mg/dl, p for trend = 0.01; women, 327.3 mg/dl, 317.0 mg/dl, and 310.7 mg/dl, p for trend = 0.01; lower extremity arterial disease by percent with ankle-arm index <0.9-men, 18.3, 5.5, and 3.7, p for trend = 0.01; women, 10.0, 5.7, and 2.8, p for trend = 0.02; evidence of myocardial injury by cardiac infarction/injury score (CIIS)-men, 8.0, 6.0, 3.9, p for trend <0.001; women, 4.6, 3.9, and 3.6, p for trend = 0.03. Adjustment for smoking, alcohol consumption, and total kilocalories expended in exercise altered the findings only slightly. The authors conclude that intensity of exercise in later life is associated with favorable coronary disease risk factor levels and a reduced prevalence of several markers of subclinical disease.

Abstract: The aim of this study was to assess the psychosocial effects of exercise training on hemodialysis (HD) patients. Thirty-one uremic patients, aged 50.6+/-11.6 years, on maintenance HD were studied. Twenty patients were selected at random for a 6-month exercise renal rehabilitation program (ERRP) consisting of 3 weekly sessions of exercise training. The other 11 patients were assigned to sedentary control status. A formal psychosocial assessment, which included affective (Beck Depression Inventory, BDI), quality of life (Quality of Life Index, QLI) and personality (Eysenck Personality Questionnaire, EPQ) parameters, was performed with validated questionnaires at the beginning and the end of the ERRP. After training significant improvement occurred in physical capacity (VO2max increased from 16.8+/-6.2 to 23.2+/-7.6 ml/kg/min, p < 0.05). Although the level of depression did not differ betwen the 2 groups at pretesting, the ERRP group showed a decrease in their self-report of depression (decrease in BDI score value, from 21.0+/-10.4 to 13.7+/-9.5, p < 0.05) after the training program. From the relationship between the baseline levels of BDI depression and changes in VO2max in the ERRP group it was suggested that the most severely depressed patients got the greatest beneficial effects from exercise training. Moreover, trained patients demonstrated an improvement in QLI (from 6.3+/-1.5 to 9.0+/-0.9, p < 0.05). This improvement was found to be dependent on the participation in ERRP, the effects of the training and the improvement in the depression. All the above functional and psychosocial parameters remained unchanged in the controls. The results demonstrate that ERRP is an effective emotional therapeutic method for HD patients and improves their quality of life.

Abstract: Fifteen athletes were investigated 24 h before, 1 h after, and 20 h after an exhaustive exercise stress test (mean duration 68 min). Testing for cytokines was done in serum, urine, and the supernatants of whole blood cell cultures, which were stimulated with lipopolysaccharide (LPS), concanavalin A (Con A), or phythaemagglutinin (PHA). Elevated levels of interleukin 6 (IL-6) and soluble IL-2 receptor (sIL-2R) were found 1 h after the run in both serum and urine samples. TNF-alpha in serum was also increased, whereas IL-2 in urine was decreased after the exercise. All other testings in serum and urine (including IFN-gamma) gave borderline or negative results. In cell cultures, the LPS-induced release of the inflammatory cytokines TNF-alpha, IL-1, and IL-6 was suppressed 1 h after exercise. Also, the Con-A-induced and LPS-induced release of IFN-gamma, and the PHA-induced release of IL-2 were suppressed 1 h after exercise. In contrast, Con-A-induced release of IL-2 was mildly increased after the run. We conclude that exercise of the intensity and duration described here causes an activation of the immune system, which is immediately counter-regulated. Twenty hours after the exercise, most of the observed changes were back to pre-exercise levels, indicating only a short duration for this suppressive counter-regulation.