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PubMed1999

Short-arm (1.9 m) +2.2 Gz acceleration: isotonic exercise load-O2 uptake relationship.

BACKGROUND: The deconditioning syndrome from prolonged bed rest (BR) or spaceflight includes decreases in maximal oxygen uptake (VO2max), muscular strength and endurance, and orthostatic tolerance. In addition to exercise training as a countermeasure, +Gz (head-to-foot) acceleration training on 1.8-2.0 m centrifuges can ameliorate the orthostatic and acceleration intolerances induced by BR and immersion deconditioning. PURPOSE: Study A was designed to determine the magnitude and linearity of the heart rate (HR) response to human-powered centrifuge (HPC) acceleration with supine exercise vs. passive (no exercise) acceleration. Study B was designed to test the hypothesis that moderate +Gz acceleration during exercise will not affect the respective normal linear relationships between exercise load and VO2max, HR, and pulmonary ventilation (VEBTPS). Study C: To determine if these physiological responses from the HPC runs (exercise + on-platform acceleration) will be similar to those from the exercise + off-platform acceleration responses. METHODS: In Study A, four men and two women (31-62 yr) were tested supine during exercise + acceleration and only passive acceleration at 100% [maximal acceleration (rpm) = Amax] and at 25%, 50%, and 75% of Amax. In Studies B and C, seven men (33+/-SD 7 yr) exercised supine on the HPC that has two opposing on-platform exercise stations. A VO2max test and submaximal exercise runs occurred under three conditions: (EX) exercise (on-platform cycle at 42%, 61%, 89% and 100% VO2max) with no acceleration; (HPC) exercise + acceleration via the chain drive at 25%,50%, and 100% Gzmax (35%, 72% and 100% VO2max); and (EXA) exercise (on-platform cycle at 42%, 61%, 89%, and 100% VO2max) with acceleration performed via the off-platform cycle operator at +2.2+/-0.2 Gz [50% of max (rpm) G]. RESULTS: Study A: Mean (+/-SE) Amax was 43.7+/-1.3 rpm (mean = +3.9+/-0.2, range = 3.3 to 4.9 Gz). Amax run time for exercise +acceleration was 50-70 s, and 40-70 s for passive acceleration. Regression of X HR on Gz levels indicated explained variances (r2) of 0.88 (exercise) and 0.96 (passive). The mean exercise HR of 107+/-4 (25%), to 189+/-13 (100%) bpm were 43-50 bpm higher (p < 0.05) than comparable passive HR of 64+/-2 to 142+/-22 bpm, respectively. Study B: There were no significant differences in VO2, HR or VEBTPS at the submaximal or maximal levels between the EX and EXA runs. Mean (+/-SE) VO2max for EX was 2.86+/-0.12 L x min(-1)(35+/-2 ml x min(-1) x kg(-1)) and for EXA was 3.09+/-0.14 L x min(-1) (37+/-2 ml-min(-1) x kg(-1)). Study C: There were no significant differences in the essentially linear relationships between the HPC and EXA data for VO2 (p = 0.45), HR (p < 0.08), VEBTPS (p = 0.28), or the RE (p = 0.15) when the exercise load was % VO2max. CONCLUSION: Addition of + 2.2 Gz acceleration does not significantly influence levels of oxygen uptake, heart rate, or pulmonary ventilation during submaximal or maximal cycle ergometer leg exercise on a short-arm centrifuge.

Acceleration↗

PubMed2003

[Evaluation of physiological index on treadmill exercise testing of 294 healthy children in Shanghai area].

OBJECTIVE: Dynamic exercise is often used to evaluate the backlog function of cardiovascular system, and the treadmill test is a commonly used dynamic exercise protocol. The study aimed to assess the exercise capacity and cardiovascular response to treadmill exercise in healthy children, and create normal reference values of exercise testing in native children. METHODS: Two huadveds and ninety-four healthy children aged 5 to 14 years were tested using the Bruce protocol on treadmill. RESULTS: Mean exercise capacity in boys increased from 12.2 METs at the age of 5 to 6 years, to 15.2 METs at the age of 13 to 14 years. Mean exercise capacity in girls increased from 11.7 METs at the age of 5 to 6 years, to 12.6 METs at the age of 13 to 14 years. Sex difference was obvious in exercise capacity of children except those at the age of 5 to 6 years. There was no obvious correlation between exercise capacity and the ratio of weight to height. Maximal heart rate ranged from 187 to 235 beats/min. Systolic blood pressure increased gradually until peak exercise was achieved. The mean systolic blood pressure of boys at maximal exercise increased by 38.6 percent compared to resting level, and the girls increased by 34.4 percent. After maximal exercise, mean systolic blood pressure reached resting level in 6 minutes but diastolic blood pressure varied. All children had sinus rhythm at rest. No arrhythmia was recorded during treadmill exercise. However, arrhythmia was found in five children in early recovery period. The incidence of exercise-induced arrhythmia was 1.7 percent. CONCLUSION: Sex difference and age difference was obvious in exercise capacity. In the 21st century, the exercise capacity of children in Shanghai area has approached to the developed country. Using MET as the standardized criterion of exercise capacity is advantageous to standardize maximal or submaximal exercise workloads of all kinds of protocols. Exercise-induced arrhythmia in the early recovery period in children without structural heart disease may not be pathological, but it is necessary for those children to be followed-up.

Adolescent↗

PubMed2004

[Clinical use of ventilation measurement during early phase of exercise in patients with chronic heart failure].

BACKGROUND: In patients with chronic heart failure (CHF) augmented exercise ventilation is related to functional severity and increased mortality. Nevertheless, the optimal approach to the assessment of ventilatory response to controlled exercise has not been established. AIM: The study was carried out to evaluate the clinical application of the measurement of ventilatory response to the early phase of exercise in the non-selected group of patients with CHF. MATERIAL AND METHODS: We investigated 180 consecutive patients with CHF (155 men, age: 59 +/- 11 years, left ventricle ejection fraction: 31 +/- 7%; NYHA class I/II/III/IV: 13/90/60/17). All patients underwent the cardiopulmonary exercise testing (CPX) with RER > 1.0 (mean peak oxygen consumption [peakVO2]: 15.5 +/- 4.8 ml/kg/min). Ventilatory response to exercise was assessed: 1) during the whole exercise--expressed as a correlation coefficient of linear regression describing the relationship between minute ventilation (VE) and carbon dioxide production (VCO2) during the whole exercise (VE-VCO2 100%); 2) during the early phase of exercise--expressed as VE-VCO2 derived from VE and VCO2 during first 180 seconds of exercise (VE-VCO2 180 s). RESULTS: Ventilatory responses to early and maximal exercise were significantly augmented in CHF patients (VE-VCO2 100% -36.1 +/- 9.8, VE-VCO2 180% -34.4 +/- 10.3; p < 0.0001 vs values in the reference group without CHF). Ventilatory responses to early and whole exercise were strongly interrelated (r = 0.88, p < 0.0001). Indices of exercise ventilation correlated with the severity of CHF expressed as NYHA class (for VE-VCO2 100% and VE-VCO2 180 s -r = 0.52 and r = 0.51) and peak VO2 (for VE-VCO2 100% and VE-VCO2 180 s, r = -0.49 and r = -0.47, respectively) (p < 0.0001 for all correlations). Among echocardiographic parameters only right ventricular systolic pressure correlated with indices of exercise ventilation (for VE-VCO2 100% -r = 0.45, p = 0.001; for VE-VCO2 180 s -r = 0.35, p = 0.01). The reproducibility of indices of exercise ventilation was assessed in 19 CHF patients (another CPX during 2-9 days), and variability coefficients reached 7.8% for VE-VCO2 100% and 8.5% for VE-VCO2 180 s. CONCLUSIONS: Indices of ventilatory response to both early and maximal exercise can significantly differentiate the CHF patients with regard to their exercise capacity, are highly reproducible, and may therefore constitute useful parameters carrying an important clinical message. The assessment of ventilatory response during the early stage of exercise seems to be of a particular significance in CHF patients who are unable to perform the maximal exercise effort, as diagnostic data obtained during first 180 seconds of exercise are in accordance to those derived from the standard maximal CPX.

Disease Progression↗

PubMed1997

Prognostic implications of exercise echocardiography in women with known or suspected coronary artery disease.

OBJECTIVES: The purpose of this study was to define the value of exercise echocardiography as an independent predictor of cardiac events in women with known or suspected coronary artery disease (CAD), incremental to the data provided by clinical evaluation and exercise testing. BACKGROUND: Exercise echocardiography is more accurate than exercise electrocardiography for the identification of CAD in women. However, the prognostic implications of exercise echocardiography, especially relative to exercise electrocardiography, are undefined. METHODS: Symptom-limited exercise echocardiography was performed in 549 consecutive women between 1989 and 1993. Echocardiography and electrocardiography were performed before and after treadmill exercise; an abnormal result on exercise electrocardiography was defined by ST segment depression > 0.1 mV, ischemia by exercise echocardiography as a new or worse wall motion abnormality after exercise and scar by akinesia or dyskinesia at rest. After exclusion of six patients with uninterpretable studies (1%) and 35 (6%) lost to follow-up, 508 women (mean [+/-SD] age 55 +/- 11 years) were followed up for 41 +/- 10 months for cardiac-related death, infarction or late revascularization. RESULTS: The group attained 92 +/- 10% of age-predicted maximal heart rate, with an exercise capacity of 7 +/- 2 metabolic equivalents. Of 420 women with an interpretable electrocardiogram, significant ST segment changes were present in 68 (16%). Results of exercise echocardiography were normal in 413 (81%) women, positive for ischemia in 66 (13%) and scar only in 29 (6%). No events occurred in 444 patients (89%), and 19 underwent primary revascularization (within 3 months of exercise test). Cardiac events occurred in 36 women (7%), including 17 who died of cardia causes and 19 who had a myocardial infarction or required late revascularization for progressive symptoms. On univariate analysis, the variables associated with cardiac mortality and total cardiac events were a history of CAD, diabetes, left ventricular hypertrophy, exercise capacity and echocardiographic evidence of myocardial ischemia and infarction. A Cox proportional hazards model showed the independent predictors of outcome to be known CAD (odds ratio [OR] 6.6, 95% confidence interval [CI] 3.2 to 13.7, p < 0.00001) and echocardiographic ischemia (OR 4.3, 95% CI 2.1 to 8.7, p < 0.0001). The prognostic value of exercise echocardiography incremental to clinical and exercise variables was demonstrated using sequential Cox models. CONCLUSIONS: In this large cohort of women, exercise echocardiography provided key prognostic information incremental to clinical and exercise testing data.

Coronary Disease↗

PubMed1991

Prevention of postmenopausal osteoporosis. A comparative study of exercise, calcium supplementation, and hormone-replacement therapy.

BACKGROUND: Osteoporosis among older women is a major public health problem. We studied the effects of three approaches to the prevention of osteoporosis in women with low bone density. METHODS: One hundred twenty postmenopausal women (mean [+/- SD] age, 56 +/- 4) who were selected because they had low forearm bone density were enrolled in a double-blind, placebo-controlled, randomized study comparing the effects of an exercise regimen (exercise group, n = 41), exercise plus dietary calcium supplementation (exercise-calcium group, n = 39), and exercise plus continuous replacement of estrogen and progesterone (exercise-estrogen group, n = 40). Periodically during the two-year study period, we measured the women's bone density at three forearm sites, measured indexes of calcium metabolism, and recorded symptom scores. A comparison group of 42 women (mean age, 55.5 +/- 3.1) with normal bone density was also followed for two years. RESULTS: Significant bone loss in the distal forearm occurred in the group with normal bone density (control group) and the exercise group (change, -2.7 percent and -2.6 percent of the base-line value per year, respectively). Bone loss at the distal forearm site was significantly lower in the exercise-calcium group (-0.5 percent of the base-line value per year), and bone density increased at this site in the exercise-estrogen group (+2.7 percent of the base-line value per year). Bone loss at the median forearm site was significantly lower in the exercise-calcium group (-1.3 percent of the base-line value per year) than in the exercise group (-2.4 percent), and bone density at this site increased significantly in the exercise-estrogen group (+0.8 percent of the base-line value per year). Breast tenderness occurred in 47 percent of the women in the exercise-estrogen group but in only 20 percent in the other two treatment groups. Vaginal bleeding occurred at some time in 52 percent of the women who had not had a hysterectomy in the exercise-estrogen group, as compared with 11 percent and 12.5 percent, respectively, in the exercise and exercise-calcium groups. CONCLUSIONS: In postmenopausal women with low bone density, bone loss can be slowed or prevented by exercise plus calcium supplementation or estrogen-progesterone replacement. Although the exercise-estrogen regimen was more effective than exercise and calcium supplementation in increasing bone mass, it also caused more side effects.

Bone Density↗

PubMed2002

Does exercise reduce the burden of fractures? A review.

The null hypothesis that exercise has no effect on fracture rates in old age cannot be rejected on the basis of any published, randomized, prospective data. The view that exercise reduces the number of fractures is based on prospective and retrospective, observational cohort studies and case-control studies, all hypothesis-generating, not hypothesis-testing. Consistently replicated sampling bias may confirm the finding when evaluating other than randomized prospective studies. Better health, better muscle function, more muscle mass, better coordination may lead to exercise. The causal relationship could be between better health and exercise and better health and fewer fractures, not exercise and fewer fractures. The hypothesis should be tested in prospective, randomized studies evaluating hip, spine and other fragility fractures separately. Blinded studies assessing the effects of exercise can obviously not be done, but open trials can and should be undertaken to increase the level of evidence within the evidence-based system. There are firm data supporting the view that exercise during growth builds a stronger skeleton. Exercise during growth seems to result in high peak BMD and high muscle strength. However, the Achilles heel of exercise is its cessation. Are the skeletal and muscular benefits attained during growth retained after the cessation of exercise and can any residual benefits be found in old age, the period when fragility fractures rise exponentially? Does exercise during adulthood produce any biologically important reduction in surrogate end-points for fractures other than BMD, since BMD can be influenced only marginally by exercise after completion of growth? Recommendations for exercise should be based on evidence, not on opinion. Can continued recreational exercise maintain some of the benefits in BMD and muscle function achieved in youth? What level of recreational exercise is needed to retain these benefits, if not fully, then at least to some extent? Dose-response relationships should be quantified. Furthermore, the effect of exercise on independent, surrogate end-points for fractures, such as bone size, shape, architecture, muscle function, fall frequency and frequency of injurious falls during defined periods in the life cycle must be determined. Absence of evidence is not evidence of absence of effect, but if we recommend exercise then should this be to children, adults, elderly, men and women with fractures, all persons? What type of exercise? For how long? Lifelong? If exercise could be implemented for most persons in society, would this reduce the number of fractures? Would the increased costs associated with the efforts to increase the activity level be lower than the reduced costs associated with any reduction in fractures? Our inability to answer these questions must be acknowledged before recommendations are made at the community level.

Accidental Falls↗

PubMed1990

Plasma potassium changes with high intensity exercise.

1. Exercise seems to change the extracellular potassium concentration far beyond the narrow limits seen in resting subjects. To examine alterations in plasma potassium concentration during exercise, twenty healthy, well-trained men ran on the treadmill at 6 deg inclination with catheters inserted in the femoral vein and artery. 2. During 1 min exhausting exercise plasma potassium concentration rose in parallel in the vein and artery, reaching peak post-exercise values of 8.34 +/- 0.23 mmol l-1 and 8.17 +/- 0.29 mmol l-1. After 3 min recovery the potassium concentration was 0.50 +/- 0.05 mmol l-1 below pre-exercise values. Both the rise of plasma potassium concentration during exercise and the decline during recovery followed exponential time courses with a half-time of 25 s. 3. Exercise at reduced intensity showed that the peak post-exercise potassium concentration was linearly related to the exercise intensity. Individual resting, peak and nadir values were proportionally related. 4. The increased potassium concentration during exercise can be explained in full by the electrical activity in the exercising muscles. Repeated 1 min exhausting exercise bouts revealed no relationship between potassium concentration and plasma pH nor glycogen break-down. 5. All of the observations fit a simple model of potassium efflux from active muscle and elimination from blood with the following characteristics: the efflux increases (decreases) stepwise at the onset (end) of exercise, and the efflux rate during exercise increases with exercise intensity. Potassium is eliminated from blood by a proportional regulator which may be the Na(+)-K+ pump of the exercising muscle. Extracellular potassium is indirectly linked to the pump stimulus, and the rate of reuptake is proportional to the extracellular accumulation. Thus no limited maximal power for potassium uptake was found. The post-exercise undershoot of 0.5 mmol l-1 can be explained by a higher gain of the pump after exercise. 6. The large, rapid changes in the plasma potassium concentration during and after exercise is due to the first order kinetics of the reuptake mechanism rather than to a limited power to take up potassium.

Adolescent↗

PubMed1993

Ventilatory responses to exercise in humans lacking ventilatory chemosensitivity.

1. In healthy humans during aerobic exercise ventilation increases and mean arterial PCO2 usually remains constant over a wide range of CO2 production. 2. Congenital central hypoventilation syndrome (CCHS) is associated with ineffective chemoreceptor regulation of breathing and severe hypoventilation during sleep (requiring mechanical ventilation) reflecting abnormalities in the brainstem respiratory complex or its chemoreceptor input. Such patients can have adequate spontaneous ventilation during resting wakefulness and participate in normal activities. 3. If children with CCHS have normal ventilatory responses to exercise then chemoreceptors are not necessary for this ventilatory response or the resultant control of Pa,CO2 during exercise. We studied five children with CCHS (aged 8-17 years) with abnormally low ventilatory responses to steady-state increased end-tidal PCO2 (< 9 ml min-1 kg-1 mmHg-1) and five age-matched controls. 4. Depth and rate of breathing, end-tidal PCO2, end-tidal PO2, CO2 production, O2 utilization and heart rate were monitored during the following conditions: whilst subjects stood at rest; following the onset of treadmill exercise (4 m.p.h.); during steady-state exercise (4 m.p.h.); during an incremental maximal exercise test; and during recovery from exercise. 5. There were no significant differences in the ventilatory responses between CCHS subjects and controls during the onset of treadmill exercise, in the dynamic response in achieving the steady-state exercise, during steady-state exercise, in the recovery from steady-state exercise, or during incremental exercise (up to the point of presumed blood lactate accumulation, as indicated by gas exchange criteria). There was a very small mean increase in PCO2 in both groups during steady-state exercise (controls 1.4 mmHg; CCHS 2.2 mmHg). 6. The only differences which emerged between groups were (i) slightly more variability in PCO2 in the CCHS group during steady-state exercise, and (ii) the CCHS subjects did not hyperventilate, as the controls did, at exercise levels above the point of presumed blood lactate accumulation. 7. Breath-by-breath coefficient of variation of ventilation was significantly reduced in both groups during steady-state exercise compared to rest. There were no differences between groups in either state. 8. We conclude that chemoreceptors are not necessary for an appropriate ventilatory response to aerobic exercise. Hence, other stimuli, such as afferent information from the exercising limbs or signals related to activation of the motor cortex, can increase alveolar ventilation in close proportion to CO2 production. 9. The lack of hyperventilatory response to blood lactate accumulation during heavy exercise provides good evidence that these CCHS patients have ineffective peripheral chemoreception.

Adolescent↗

PubMed1992

Oxidation of carbohydrate ingested during prolonged endurance exercise.

Classic studies conducted in the 1920s and 1930s established that the consumption of a high carbohydrate (CHO) diet before exercise and the ingestion of glucose during exercise delayed the onset of fatigue, in part by preventing the development of hypoglycaemia. For the next 30 to 40 years, however, interest in CHO ingestion during exercise waned. Indeed, it was not until the reintroduction of the muscle biopsy technique into exercise physiology in the 1960s that a series of studies on CHO utilisation during exercise appeared. Investigations by Scandinavian physiologists showed that muscle glycogen depletion during prolonged exercise coincided with the development of fatigue. Despite this finding, attempts to delay fatigue during prolonged exercise focused principally on techniques that would increase muscle glycogen storage before exercise. The possibility that CHO ingestion during exercise might also delay the development of muscle glycogen depletion and hence, at least potentially, fatigue, was not extensively investigated. This, in part, can be explained by the popular belief that water replacement to prevent dehydration and hyperthermia was of greater importance than CHO replacement during prolonged exercise. This position was strengthened by studies in the early 1970s which showed that the ingestion of CHO solutions delayed gastric emptying compared with water, and might therefore exacerbate dehydration. As a result, athletes were actively discouraged from ingesting even mildly concentrated (greater than 5 g/100ml) CHO solutions during exercise. Only in the early 1980s, when commercial interest in the sale of CHO products to athletes was aroused, did exercise physiologists again begin to study the effects of CHO ingestion during exercise. These studies soon established that CHO ingestion during prolonged exercise could delay fatigue; this finding added urgency to the search for the optimum CHO type for ingestion during exercise. Whereas in the earlier studies, estimates of CHO oxidation were made using respiratory gas exchange measurements, investigations since the early 1970s have employed stable 13C and radioactive 14C isotope techniques to determine the amount of ingested CHO that is oxidised during exercise. Most of the early interest was in glucose ingestion during exercise. These studies showed that significant quantities of ingested glucose can be oxidised during exercise. Peak rates of glucose oxidation occur approximately 75 to 90 minutes after ingestion and are unaffected by the time of glucose ingestion during exercise. Rates of oxidation also appear not to be influenced to a major extent by the use of different feeding schedules.(ABSTRACT TRUNCATED AT 400 WORDS)

Dietary Carbohydrates↗

PubMed2004

Exercise-induced behavioral recovery and neuroplasticity in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-lesioned mouse basal ganglia.

Physical activity has been shown to be neuroprotective in lesions affecting the basal ganglia. Using a treadmill exercise paradigm, we investigated the effect of exercise on neurorestoration. The 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-lesioned mouse model provides a means to investigate the effect of exercise on neurorestoration because 30-40% of nigrostriatal dopaminergic neurons survive MPTP lesioning and may provide a template for neurorestoration to occur. MPTP-lesioned C57 BL/6J mice were administered MPTP (four injections of 20 mg/kg free-base, 2 hr apart) or saline and divided into the following groups: (1). saline; (2). saline + exercise; (3). MPTP; and (4) MPTP + exercise. Mice in exercise groups were run on a motorized treadmill for 30 days starting 4 days after MPTP lesioning (a period after which MPTP-induced cell death is complete). Initially, MPTP-lesioned + exercise mice ran at slower speeds for a shorter amount of time compared to saline + exercise mice. Both velocity and endurance improved in the MPTP + exercise group to near normal levels over the 30-day exercise period. The expression of proteins and genes involved in basal ganglia function including the dopamine transporter (DAT), tyrosine hydroxylase (TH), and the dopamine D1 and D2 receptors, as well as alterations on glutamate immunolabeling were determined. Exercise resulted in a significant downregulation of striatal DAT in the MPTP + exercise compared to MPTP nonexercised mice and to a lesser extent in the saline + exercised mice compared to their no-exercise counterparts. There was no significant difference in TH protein levels between MPTP and MPTP + exercise groups at the end of the study. The expression of striatal dopamine D1 and D2 receptor mRNA transcript was suppressed in the saline + exercise group; however, dopamine D2 transcript expression was increased in the MPTP + exercise mice. Immunoelectron microscopy indicated that treadmill exercise reversed the lesioned-induced increase in nerve terminal glutamate immunolabeling seen after MPTP administration. Our data demonstrates that exercise promotes behavioral recovery in the injured brain by modulating genes and proteins important to basal ganglia function.

Animals↗

PubMed2002

Effect of decreased physical activity on bone mass in exercise-trained young rats.

The aim of this study was to determine whether decreased physical activity in exercise-trained young rats would result in a lower rate of bone gain or a reversal of the benefits of exercise. Thirty-five female Wistar rats, 6 weeks of age, were randomized into seven groups: 7 weeks of exercise (7EX), 7 weeks of sedentary control (7CN), 11 weeks of exercise (11EX), 7 weeks of exercise followed by 4 weeks of exercise cessation (7EX4C), 7 weeks of exercise followed by 4 weeks of decreased exercise frequency (7EX4F), 7 weeks of exercise followed by 4 weeks of decreased exercise intensity (7EX4I), and 11 weeks of sedentary control (11CN). The running intensity (speed) and duration were 25 m/min for 60 min/day at a frequency of 5 days/week. During the last 4 weeks, exercise frequency was reduced to 1 day/week in the 11EX4F group, and exercise intensity (speed) was reduced to 12 m/min in the 7EX4I group. After each period of exercise, the bone mineral content (BMC) of the proximal, middle, and distal tibiae, determined by dual-energy X-ray absorptiometry (DXA), was significantly greater in the 7EX and 11EX groups than in the 7CN and 11CN groups, respectively, but it was significantly lower in the 7EX4C group than in the 11EX group and did not differ significantly from the values of the 11CN group. Although the BMC of the proximal and middle tibiae did not differ significantly among the 7EX4F, 7EX4I, 7EX4C, and 11CN groups, the BMC of the distal tibia was significantly greater in the 7EX4F and 7EX4I groups than in the 11CN group and tended to be greater than in the 7EX4C group. The results of this study suggest that the effect of decreased exercise intensity and frequency on bone mass appears to be site specific in the tibia of the exercise-trained young rats. This study shows that exercise-trained young rats lose the benefits gained from exercise when exercise is completely ceased, resulting in the reduction of bone mass to levels that do not differ significantly from those of sedentary controls. At least, continuous exercise appears to be necessary for the maintenance of high bone mass.

Absorptiometry, Photon↗

PubMed1998

Contemporary exercise physiology: fifty years after the closure of Harvard Fatigue Laboratory.

The relationships between the discipline of exercise physiology and the activities of the Harvard Fatigue Laboratory were examined. Even though 5 decades have elapsed since the Laboratory's closure, its existence, leaders, and accomplishments continue to be revered by exercise physiologists. The Laboratory was unique because it was the first research facility of its type and because no single exercise physiology laboratory in the United States since 1947 has been able to attract the stature of the national and international investigators that conducted the interdisciplinary research published by the Laboratory. Despite the inference from its name, the Laboratory's purpose was not to advance the discipline of exercise physiology; rather, it was to advance our understanding and interactions of applied physiology, physiology, and sociology. Consequently, its contributions to the critical mass of exercise physiology literature were limited even though may of the publications were seminal in nature. As documented by the Horvaths, the closure resulted in the establishment of many different research laboratories by former Laboratory staff members and associates (R.E. Johnson at Illinois, Horvath at Santa Barbara, and Dill at Nevada); however, their impact on exercise physiology was delayed because Keys and Robinson had left for Minnesota and Indiana, respectively, well in advance of closing. Unfortunately, the administrative structure and organization of the Laboratory was not conducive to the training of Ph.D candidates with an interest in exercise physiology. Consequently, only two individuals graduated during its existence. Since departments of physiology or biology had limited faculty or interest in preparing students for such a future before and after closure, departments of physical education with specialization graduate programs in exercise physiology assumed this responsibility, which was facilitated by post-World War II funding that supported mass education, graduate training, health related research, and facility development. Today, the majority of the leaders in exercise physiology are the "products" of the specialization movement. Although undergraduates were encouraged to participate in the research activities, the talented faculty of the Laboratory did not offer formal courses in exercise physiology. Thus, the development of an academic discipline in exercise physiology was left to institutions that required a science-oriented curriculum in their undergraduate and graduate degree programs in physical education, exercise science, or kinesiology. The emergence of exercise physiology as a discipline in the United States was enhanced by the publications of the Journal of Applied Physiology in 1948 and by Medicine and Science in Sports in 1969. These were peer-reviewed journals that were interested in publishing research studies on exercise topics. Two other reasons contributed to its development. The first was the creation of an Applied Physiology Study Section at the National Institute of Health in 1964, whose purpose was to evaluate grant proposals in subject matter area intrinsic to exercise physiology, while the second reason was the formation of the American College of Sports Medicine in 1954. ACSM was an important for the establishment of the discipline because it had an organizational structure that encouraged exercise physiologists to join, provided opportunities for members to present at regional and national meetings, and would publish their findings. Although the American Physiological Society had been established more than a 100 years ago, only a limited number of its members were interested and active in exercise physiology at the time of the Laboratory's closure or at the beginning of the specialization era (1963). However, in 1977, APS created a membership section that included exercise physiology in its title. Currently, both APS and ACSM are effectively representing the professional interests of exercise ph

Boston↗

PubMed2004

Acute effects of a short bout of moderate versus light intensity exercise versus inactivity on tobacco withdrawal symptoms in sedentary smokers.

RATIONALE: A previous study found that a 10-min bout of moderate intensity exercise reduced cigarette withdrawal symptoms and desire to smoke in sedentary smokers but the effect may have been due to participants focusing attention on physical activity rather than the activity itself. OBJECTIVES: This study examined the effect of 5 min of moderate intensity exercise and 5 min of light intensity exercise on tobacco withdrawal symptoms amongst sedentary smokers. METHODS: Eighty-four smokers attended a laboratory session having abstained from smoking for between 11 and 14 h. Participants were randomly allocated to one of three conditions: (i) light intensity exercise [ n=28; 10-20% of heart rate reserve (HRR)]; (ii) moderate intensity exercise ( n=28; 40-60% HRR), (iii) a passive control condition ( n=28). Both exercise conditions involved 5 min of stationary cycling and participants rated tobacco withdrawal symptoms and cravings immediately before exercise (baseline), during exercise at 2.5 min, immediately following exercise, then after 5 and 10 min of rest. Control participants made the same ratings across an equivalent time period. RESULTS: For moderate intensity exercise compared to light intensity exercise and control there was a significant reduction in strength of desire to smoke, relative to baseline, both during exercise and up to 5 min post-exercise. Relative to baseline, there were also significant reductions in restlessness, stress, tension and poor concentration at 5 and 10 min post-exercise, for moderate intensity exercise compared to light intensity exercise and control. CONCLUSIONS: Five minutes of moderate intensity exercise is associated with a short-term reduction in desire to smoke and tobacco withdrawal symptoms. Very brief bouts of exercise may therefore be useful as an aid to smoking cessation.

Adolescent↗

PubMed1998

The effects of high-intensity intermittent exercise on the plasma concentrations of glutamine and organic acids.

Glutamine is an essential substrate for the proper functioning of cells of the immune system. Falls in plasma glutamine concentration after exercise may have deleterious consequences for immune cell function and render the individual more susceptible to infection. The purpose of the present study was to examine changes in plasma glutamine concentration (measured using a validated enzymatic spectrophotometric method) following an acute bout of intermittent high-intensity exercise. Eight well-trained male games players took part in the study. Subjects reported to the laboratory following an overnight fast and performed a 1-h cycle exercise task consisting of 20 1-min periods at 100% maximal O2 consumption (VO2max) each separated by 2 min of recovery at 30% VO2max. Venous blood samples were taken before exercise and at 5 min, 1 h, 2.5 h, 5 h and 24 h post-exercise. Glutamine was measured by enzymatic spectrophotometric determination of the ammonia concentration before and after treatment of the plasma with glutaminase (EC 3.5.1.2). Plasma glutamine concentration did not fall in the immediate post-exercise period [pre-exercise 681 (23) microM compared with 663 (46) microM at 5 min post-exercise, mean (SEM)], but fell to 572 (35) microM at 5 h post-exercise (P < 0.05 compared with pre-exercise). Plasma lactate concentration rose to 8.8 (1.0) mM at the end of exercise and fell to 1.8 (0.4) mM at 1 h post-exercise, but plasma concentrations of free fatty acids and beta-hydroxybutyrate both rose substantially in the post-exercise period (to 240% and 400% of pre-exercise levels, respectively). The circulating leucocyte count increased significantly during exercise (P < 0.01), continued to increase in the hours following exercise and peaked at 2.5 h post-exercise (mainly due to a neutrophilia). The fall in the plasma glutamine concentration at 5 h post-exercise could be due to increased renal uptake of glutamine, which generally occurs in conditions of metabolic acidosis or due to a greater removal of glutamine from the plasma resulting from the elevated circulating leucocyte count.

3-Hydroxybutyric Acid↗

PubMed1995

Dissociation between peak exercise oxygen consumption and hemodynamic dysfunction in potential heart transplant candidates.

OBJECTIVES: The purpose of this study was to determine how often peak exercise oxygen consumption (VO2) misclassifies the severity of cardiac dysfunction in potential heart transplant candidates. BACKGROUND: Cardiopulmonary exercise testing is being used to help select heart transplant candidates on the basis of the assumption that a low peak exercise VO2 indicates severe hemodynamic dysfunction and a poor prognosis. However, noncardiac factors, such as muscle deconditioning, can also influence exercise capacity. Therefore, peak exercise VO2 may overestimate the severity of cardiac dysfunction in some patients. METHODS: Hemodynamic and respiratory responses to maximal treadmill exercise were measured in 64 sequential patients undergoing evaluation for heart transplantation, all of whom had an ejection fraction < 35% and reduced peak exercise VO2 levels (mean [+/- SD] 13.3 +/- 2.7 ml/min per kg). RESULTS: Twenty-eight (44%) of 64 patients exhibited a reduced cardiac output response to exercise and pulmonary wedge pressure > 20 mm Hg at peak exercise, consistent with severe hemodynamic dysfunction. Twenty-three patients (36%) exhibited a normal cardiac output response to exercise but a wedge pressure > 20 mm Hg at peak exercise, suggesting moderate hemodynamic dysfunction. Thirteen patients (20%) exhibited a normal cardiac output and wedge pressure < 20 mm Hg at peak exercise, suggesting mild hemodynamic dysfunction. Despite these markedly different hemodynamic responses, all three groups exhibited similar peak exercise VO2 levels (mild dysfunction 14.2 +/- 3.5 ml/min per kg, moderate dysfunction 13.9 +/- 2.7 ml/min per kg, severe dysfunction 12.4 +/- 2.1 ml/min per kg). A peak exercise VO2 level < 14 ml/min per kg, considered to reflect severe hemodynamic dysfunction, was observed in 18 of the patients with a normal cardiac output response to exercise, whereas 7 patients with severe hemodynamic dysfunction had a peak VO2 level > 14 ml/min per kg. CONCLUSIONS: More than 50% of potential heart transplant candidates with a reduced peak exercise VO2 level exhibit only mild or moderate hemodynamic dysfunction during exercise. Hemodynamic responses to exercise should be directly measured in potential transplant candidates to confirm severe circulatory dysfunction.

Adult↗

PubMed1999

Effects of exercise training on chronotropic incompetence in patients with heart failure.

OBJECTIVE: To describe the effects of exercise training on chronotropic incompetence in patients with stable heart failure, as measured by their inability to achieve a peak exercise heart rate greater than 85% of maximum. BACKGROUND: Exercise intolerance and chronotropic incompetence are characteristic of patients with heart failure. Exercise training improves exercise capacity in these patients; however, to what extent reversal of chronotropic incompetence contributes to such a response remains uncertain. METHODS: Fifty-one patients undergoing standard medical therapy were randomly assigned to a 24-week exercise training program or a no exercise control group. Twenty-one of 26 patients assigned to the exercise group and 22 of 25 control patients completed the study. Peak oxygen consumption, resting and exercise plasma norepinephrine level, and quality of life (Living With Heart Failure Questionnaire) were assessed. RESULTS: A significant (P <.05) increase in peak heart rate was observed in the exercise group (9 +/- 3 beats/min) when compared with the control group (1 +/- 3 beats/min). Among exercise-trained patients with chronotropic incompetence at baseline (n = 14), the increase in peak heart rate at week 24 was 12 +/- 3 beats/min. Peak oxygen consumption was significantly (P <.05) increased in the exercise group (204 +/- 57 mL/min) versus the control group (72 +/- 33 mL/min). Health-related quality of life was not significantly changed with exercise training. Twenty-four weeks of exercise training induced a greater (P <.05) reduction in plasma norepinephrine at rest and during exercise in patients with a nonischemic cardiomyopathy versus those with ischemic cardiomyopathy. CONCLUSIONS: Exercise training results in an increase in peak heart rate and partial reversal of chronotropic incompetence among patients with stable heart failure. These responses contribute, in part, to the exercise training-induced increase in exercise capacity that occurs in these patients.

Cardiac Output↗

PubMed1998

Effects of regular exercise in management of chronic idiopathic constipation.

Regular physical exercise has long been considered in the management of chronic constipation. This recommendation is probably based on the assumption that exercise shortens the transit time through the gastrointestinal tract. However, on the basis of previous studies, the effect of exercise on the transit remains controversial at best. Therefore, it was the goal of the present study to assess the influence of regular physical exercise, what average people may consider routine exercise, in the management of chronic idiopathic constipation. The study population consisted of eight patients, seven women and a man, with chronic idiopathic constipation. They were studied for six weeks, including two weeks of rest and four weeks of regular exercise. Patients had a submaximal exercise test, before and after the exercise period, to determine their rate of perceived exertion (RPE), the target heart rate, and the intensity of exercise they can perform. In addition to their routine daily activities, they exercised 1 hr a day, five days a week according to their performance at the initial exercise tolerance test. They kept a daily activity log and maintained their normal dietary intake during this period. The patients overall physical activity was assessed by a pedometer. They also maintained a diary of the number and consistency of their bowel movements and the amount of straining required for defecation. The impact of exercise on constipation was assessed by utilizing an index that took into consideration all three parameters of bowel function. Results of the study revealed that patients covered 1.8+/-0.33 and 3.24+/-0.28 miles/day in the rest period and during the exercise period, respectively (P = 0.007). The intensity of exercise may have improved the level of training as reflected on the mean maximum time before and after exercise period (P = 0.039). This level of exercise did not improve their constipation indices, which were 9.11+/-0.65 and 8.57+/-1.08 in the rest and exercise periods, respectively (P = 0.68). In conclusion, physical activity, to the extent that people consider "regular exercise," does not play a role in the management of chronic idiopathic constipation.

Adult↗

PubMedDate not supplied

Arm exercise capacity and dyspnea ratings in subjects with chronic obstructive pulmonary disease.

PURPOSE: This study aimed to compare the metabolic, ventilatory, and dyspnea responses to unsupported arm exercise, supported arm exercise and leg exercise between subjects with chronic obstructive pulmonary disease (COPD) and healthy age-matched controls. METHODS: For this study, 21 subjects with COPD (mean age, 62 +/- 2 years; predicted forced expiratory volume in 1 second [FEV(1)], 37 +/- 3%) and 7 healthy age-matched control subjects (% pred FEV(1) = 109 +/- 5%) were included in the analyses of three incremental exercise tests to peak work capacity: unsupported arm exercise, supported arm exercise (arm ergometry), and leg exercise (cycle ergometry). Work level, oxygen consumption (VO(2)), minute ventilation (V(E)), dyspnea, and rate of perceived exertion were measured each minute. RESULTS: Peak work level and peak VO(2) were significantly reduced in the subjects with COPD for all exercise tests (P <.01 for all), as compared with the control subjects. Within the COPD group, the VO(2) and V(E) at peak exercise were significantly lower for unsupported arm exercise than for both the leg and supported arm exercises (both P <.001). The ratio of V(E) to maximal voluntary ventilation was high for leg exercise (96%), supported arm exercise (91%), and unsupported arm exercise (77%) among the subjects with COPD. At a given percentage of VO(2) peak, dyspnea scores were similar for all the exercise tests. CONCLUSIONS: Ventilatory constraints limit exercise performance in COPD. The lowest amount of work, in terms of VO(2,), was during unsupported arm exercise. Because the subjects with COPD had scores showing similar levels of dyspnea at the same percentage of VO(2) peak, it is suggested that patients be encouraged to reach equivalent dyspnea levels when performing unsupported and supported arm exercise training and leg training.

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