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The positive effect of exercise on physical health has been given much attention. Research has shown it is also beneficial for mental health, and there is increasing evidence to suggest it could be used as an alternative therapy to antidepressants and psychotherapy.
The development and progress of antidiabetic drugs (e.g., insulin preparations and hypoglycemic drugs) are retrospectively investigated in Japan. Their influences on the treatment of diabetes mellitus (DM) and its epidemiological aspects are also discussed. 1) Insulin preparations: Insulin was introduced for DM therapy in 1925, two or three years after its discovery in Canada. The preparations were raw extracts of bovine or porcine pancreas. These did not prevail widely in Japan because of the low incidence of DM before World Wan II. After the war, a shortage of mammalian materials compelled the use of fish pancreatic tissues such as bonito and/or tuna for insulin production. Insulin infection, so-called regular insulin, was first promoted in the 6th "Pharmacopoeia Japonica" (JP6) in 1951 and has been maintained to the present edition (JP14, 2001). Although depot-type insulin preparations were developed in the USA and Europe during the war, the introduction of those preparations to Japan was delayed until 1951, when Protamine zinc insulin appeared. Globin zinc insulin and Isophane insulin were introduced for clinical use in 1952 and 1955, respectively. These were also adopted for JP7 (1961). Biphasic-type insulin, which has a rapid onset and long duration of activity, appeared in 1965. Purified preparations from bovine or porcine sources have been available since 1980, which might be a strong reason for the decrease in insulin allergy. Insulin from animal origin has been supplied for almost 60 years since its discovery. Amino acid sequences of insulins from various species of animals were determined by the pioneering studies of Sanger and his associates. Human insulin, which differs from porcine insulin by only one amino acid, was produced by Novo researchers in 1982 using a semi-synthetic method. Then the Lilly group soon succeeded in obtaining human insulin by recombinant DNA technology in the same year. Both products were introduced to Japan in 1985, and the recombinant products prevailed throughout the 1990s. Human insulin analogues (i.e., Insulin lispro and Insulin aspart) appeared in 2001. These are applied for after-meal glycosmia owing to their ultrarapid onset of activity. Self-injection by DM patients was legalized in 1981. To make the infection technique sure and easy, cartridge (pen-type) and disposable kit-type needles were devised in the 1990s. 2) Oral hypoglycemic drugs: Instead of the exclusive parenteral usage of insulins, there was also demand for oral dosage forms. The first of the sulfonyrlurea (SU) group, BZ-55, was used for DM clinically in 1955 in Germany. But it was soon withdrawn because of its antibacterial action. This led to the development of various SU groups. Tolbutamide (1956), chlorpropamide (1959), acetohexamide (1964) and tolazamide (1961) were introduced to Japan as first-generation SUs. Then glyclopyramide (Kyorin, 1965), glybenclamide (1971), gliclazide (1984) and glimepiride (1999) appeared as the second-generation SUs. These were used orally for Type 2 diabetes. Biguanide (BG) group, phenformin HC1 (1959), metformin HC1 (1961) and buformin HC1 (1961) had also been in use by oral treatment of Type 2 diabetes. SU appears to act by increasing the sensitivity of b-cells, which secrete insulin. BG probably exerts by increasing glucose transport across the membranes of target organs. 3) New types of antidiabetic drugs: a-Glucosidase inhibitors (i.e., acarbose: Bayer, 1993; and voglibose: Takeda, 1994) act on hyperglycemia after meals by decreasing glucose absorption. Thiazolidinedione compounds, such as troglitazone (Sankyo, 1995) and pioglitazone HC1 (Takeda, 1994) act by increasing the insulin sensitivity of the target tissues. These are useful for Type 2 DM patients when SUs are ineffective. Nevertheless, troglitazone was discontinued in 2000 due to severe liver damage. Nateglinide (Ajinomoto Co., 1999), which is a D-phenylalanine derivative acting similar to SUs, is useful orally for after-meal hyperglycemia of Type 2 diabetes. Epalrestat (Ono Yakuhin Co., 1992) is effective for diabetic neuropathy by reducing the formation of sorbitol. These anti-DM drugs were recently studied and developed in Japan. 4) The Japan Diabetes Society proposed a guideline on diagnostic criteria and treatment of diabetes mellitus (DM) in 1999 and revised it in 2002. DM is classified as insulin-dependent DM (Type l) and non-insulin dependent DM (Type 2). Type 1, juvenile onset DM, requires insulin therapy to prevent ketosis and to sustain life. Treatment of type 2, adult onset DM, is recommended as a step-by-step method, starting with dietary-exercise therapy, followed by oral hypoglycemic drugs and then insulin therapy. DM patients with complications should have a therapy devised to match their circumstances. 5) Epidemiological aspects: The mortality rate of DM compared to the time of drug appearance was traced from 1920 to 2000. The curve goes down slowly in the time frame of World War II, but rises from 1950 to 1970. The elevation could not be suppressed by the appearance of SUs, BGs or improved insulin preparations. The curve runs flat from 1980 to 1990, which might be related to the use of purified insulin or human insulin therapy. The mortality rate of DM indicates that death by hyperglycemic coma and other deaths resulting from complications are excluded. The survey of the principal cause of death by DM during the period of 1981-1990 indicates that the death rate due to hyperglycemic coma is only 1.7% of the total deaths caused by DM. The effect of drug therapy on all of the death resulting from DM is not detected. Hospital visitation and admission rates of the DM patients have been recorded since 1952 in Japan. This curve is rising continuously, and none of the antidiabetic drugs has been able to suppress it. These data show that the antidiabetic drugs relieve DM symptoms through their effective hypoglycemic actions, but that they cannot suppress the mortality rate of DM. It is possible that none of the drugs currently available can suppress the increasing tendency of DM patients.
INTRODUCTION: National cardiac guidelines recommend that patients with intermittent claudication should be managed in the same way as those with established coronary heart disease. This survey aimed to determine the attitudes of vascular consultants to risk factor management in new patients attending their out-patient clinic. METHODS: An anonymous postal questionnaire was sent to all 394 members of the Vascular Surgical Society in June 2002. Questions were asked about the following measures: serum cholesterol levels, the presence of diabetes, antiplatelet therapy, exercise regimens, blood pressure, thrombophilia, smoking and the availability of local guidelines and expertise. RESULTS: A response rate of 65% was obtained. Most (85%) consultants would measure a random cholesterol, but 34% would only treat claudicants if the cholesterol was greater than 5.5 mmol/l. Furthermore, 23% would inappropriately use diet alone as initial cholesterol lowering therapy. Over a quarter of consultants would not screen for diabetes or measure blood pressure. Nearly all (99%) would recommend aspirin and 66% would recommend nicotine replacement therapy. Only 55% had access to a smoking cessation clinic, and 34% to a formal exercise program. The majority (56%) did not have local risk factor management guidelines, only 16% had access to a vascular physician, and 65% would prefer to have this expertise available for difficult cases. DISCUSSION: Management of major risk factors was found to be sub-optimal. Thus guidelines for the prevention of coronary disease in clinical practice are not being applied to claudicants.
Arthrolysis plays an important part in the treatment of stiffened elbow joints after fractures. The article reports on the technical details of surgery and postoperative positional-change and exercise therapy, basing on the experience collected with a group of 30 patients. The intra-operatively detected causes of stiffening, postoperative complications and, finally, the mobility growth rates obtained in this manner, are shown and discussed while comparing these results with those achieved by other authors. This comparison also serves as a basis for a detailed discussion. The authors suggest as a standard measure for assessing the success of arthrolysis, an extent of mobility amounting to 0-30-110 degrees; in any case, a bending capacity (flexion) of 110 degrees should be accepted as a standard measure for such an assessment.
A survey of 47 cystic fibrosis referral centers was conducted to study the use of exercise in the management of patients with cystic fibrosis (CF). A questionnaire with 5 brief questions concerning the prescription and application of exercise therapy was sent to the first 47 centers (38.5%) listed in the 1988 CF Foundation Directory, and 46 (97.9%) were returned. While all but one of the respondents recommend exercise at least to selected patients, and while 80.4% of the centers refer patients to summer camp programs, only 43.5% offer exercise stress testing and only 21.7% offer an exercise program for their patients. Most of the respondents who recommend exercise prescribe aerobic exercise, swimming being the most frequently chosen type. Although there is a large discrepancy between those centers that acknowledge the benefits of exercise and those that have arranged for regularly available exercise services, inroads have been made in utilizing this therapeutic tool for patients with CF.
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Deep-water running is performed in the deep end of a swimming pool, normally with the aid of a flotation vest. The method is used for purposes of preventing injury and promoting recovery from strenuous exercise and as a form of supplementary training for cardiovascular fitness. Both stroke volume and cardiac output increase during water immersion: an increase in blood volume largely offsets the cardiac decelerating reflex at rest. At submaximal exercise intensities, blood lactate responses to exercise during deep-water running are elevated in comparison to treadmill running at a given oxygen uptake (VO2). While VO2, minute ventilation and heart rate are decreased under maximal exercise conditions in the water, deep-water running nevertheless can be justified as providing an adequate stimulus for cardiovascular training. Responses to training programmes have confirmed the efficacy of deep-water running, although positive responses are most evident when measured in a water-based test. Aerobic performance is maintained with deep-water running for up to 6 weeks in trained endurance athletes; sedentary individuals benefit more than athletes in improving maximal oxygen uptake. There is some limited evidence of improvement in anaerobic measures and in upper body strength in individuals engaging in deep-water running. A reduction in spinal loading constitutes a role for deep-water running in the prevention of injury, while an alleviation of muscle soreness confirms its value in recovery training. Further research into the applications of deep-water running to exercise therapy and athletes' training is recommended.
This study examined the unique contribution of acute exercise to perceptions of pain in 32 older, overweight, or obese adults with knee osteoarthritis (OA), statistically controlling for the effect of diurnal variation, supplemental medication intake, and stress. Using an ecological momentary assessment method, 964 pain appraisals were recorded and coded into experience samplings that occurred either on a nonexercise day or before or following scheduled activity on an exercise day. Univariate and multivariate multilevel modeling analyses controlling for supplemental medication intake and stress revealed a quadratic trend in diurnal pain variations with the peak occurring mid-afternoon. Although pain was significantly elevated following exercise in comparison with the predicted diurnal pattern, pain reports later in the day following exercise were significantly lower than immediately following exercise. We conclude that the pain associated with acute exercise by older, overweight, or obese adults who have knee OA is transient. Findings are discussed in terms of the implications of exercise therapy for patients with knee OA.
Prescribing exercise for cardiac patients is comparable in many ways to prescribing medications; that is, one recommends an optimal dosage according to individual needs and limitations. For in-patients, simple exposure to orthostatic or gravitational stress can obviate much of the deterioration in exercise tolerance that normally follows a cardiovascular event or intervention. On the other hand, the continuum of exercise therapy for outpatients may range from brisk walking to marathon running. Upper body and resistance training also have been shown to be safe and effective for clinically stable patients. Moderate intensity exercise training can produce beneficial changes in functional capacity, cardiac function, coronary risk factors, psychosocial well being, and possibly improve survival in patients with coronary artery disease. These findings may be especially relevant for the previously sedentary patient, in whom the subjective discomfort of vigorous exercise may serve as a deterrent to long-term compliance with physical training. (c) 2000 by CHF, Inc.
The purpose of this study was to evaluate the remaining effects of 12-month intervention of alendronate and exercise on selected risk factors of fragility fractures in 15-month follow-up after withdrawal of intervention among early postmenopausal women. The trial consisted four experimental groups: (1) 5 mg of alendronate daily + exercise (Al+Ex+), (2) 5 mg alendronate daily (Al+Ex-), (3) placebo + exercise (Al-Ex+), and (4) placebo (Al-Ex-). At the follow-up measurements, bone mass and physical fitness of 102 women (mean age 53.5 +/- 2.5 years) out of initial 150 subjects could be evaluated. Alendronate increased bone mass significantly [mean; 95% confidence interval (CI)] during the intervention at the lumbar spine (3.9%; 2.2% to 5.7%) and femoral neck (2.1%; 0.9% to 3.4%). After withdrawal of alendronate, bone loss resumed to the rate comparable to that evident in the placebo group. Despite the declining bone mass, the between-group mean difference (3.2%; 1.0% to 5.4%) remained at the lumbar spine. However, the benefits at the femoral neck had disappeared 15 months after the withdrawal of alendronate. The 12-month exercise training resulted in significant increases in muscle power, dynamic balance, and aerobic capacity with no benefits on bone mass. Fifteen months later, these performance variables had declined among both the exercisers and nonexercisers. Although the between-group differences were no longer statistically significant, muscle power, dynamic balance, and aerobic capacity of those who exercised still remained above the pretraining levels. In conclusion, 12-month treatment with alendronate prevented postmenopausal bone loss, and residual effect was seen 15 months after withdrawal of the drug at the lumbar spine. Similarly, exercise improved muscle power, agility, and aerobic capacity during the intervention, but the improvement was lost after the cessation of the exercise program. Based on these results, it was evident that to maintain the benefits of alendronate or exercise, therapy should be continued.
From January 1, 1981 until August 31, 1983, 27 fractures of the corpus humeri were treated with bunch nailing, according to Hackethal. 23 Patients had one or more further injuries and/or accompanying diseases, which did not allow conservative therapy. Only 4 patients had nothing but a corpus humeri fracture, and only for professional reasons they asked for surgery. The operation method was secure and without complications. After a few days, exercise therapy was possible; and in the average full load capacity was reached after 6 weeks. 3-18 months after surgery 85% of the patients with aftercare (n = 18) said that the treatment brought "good" or even "very good" results; in all cases the functional and anatomic results were good.
The paper is concerned with comparative estimation of the effect of different therapeutic methods (hypocaloric diet, physiotherapeutic, drug and exercise therapy, reflexotherapy) on loss of body mass. The experience of reflexotherapy of 86 patients showed its positive effect on the psychoemotional activities of patients with obesity, a rise of adaptation capabilities of the body under physical exercise, improved external respiration function, an increase in oxygen saturation of tissues, the stimulation of metabolism (by the basal metabolism findings) by way of increasing the secretion of hypophyseal tropic hormones, triiodothyronine and thyroxin, and potentiation of the time course of loss of body mass.
Antianginal efficacy and improved exercise performance with timolol, a new beta-adrenergic blocking agent, was assessed in 23 patients with chronic stable angina pectoris in an 11-week double-blind, placebo-controlled study. Twenty-two of the 23 subjects completed the open-label phase of this investigation (weeks 0 to 6) while receiving 10 to 30 mg of timolol twice daily to optimize exercise capacity. Weekly anginal episodes and nitroglycerin consumption declined from 8.9 +/- 9.1 episodes/week and 8.1 +/- 10.6 tablets/week, respectively, with placebo to 2.7 +/- 5.2 episodes/week and 2.6 +/- 6.0 tablets/week with optimal timolol dose (p less than 0.05). Resting heart rate (HR) and systolic blood pressure (SBP) also decreased from 75.2 +/- 14.0 beats/min and 139.1 +/- 15.7 mm Hg with placebo to 55.1 +/- 8.9 beats/min and 130.5 +/- 15.9 mm Hg with timolol (p less than 0.05). Peak exercise HR, peak exercise SBP, and peak exercise double product (HR X SBP) were significantly (p less than 0.05) reduced when evaluated 12 to 13 hours after administration of timolol compared with placebo (101.5 +/- 21.1 beats/min verus 193.3 +/- 96.2 beats/min, 161.5 +/- 26.7 mm Hg versus 175.6 + 20.8 mm Hg, and 16.6 +/- 5.1 X 10(-3) versus 21.7 +/- 5.4 X 10(-3), respectively). Exercise duration was prolonged from 263.3 +/- 90.2 seconds to 330.3 +/- 73.9 seconds (p less than 0.05), while time to onset of 1 mm S-T segment depression was delayed in 15 patients from 231.8 +/- 86.4 seconds to 298.7 +/- 68.4 seconds (p less than 0.05). During the double-blind phase (weeks 7 to 10), 8 subjects received timolol and 11 patients received placebo. Nitroglycerin consumption at weeks 8 and 10 and anginal frequency at week 8 were unchanged compared with initial placebo treatment. Resting HR, peak exercise HR, and peak exercise double product were significantly attenuated at weeks 8 and 10 in timolol patients compared with their initial placebo exposure. However, these variables were unchanged in placebo subjects compared with their initial placebo therapy. Exercise duration was again prolonged at week 8 in timolol subjects compared with initial placebo results (315.1 +/- 61.2 seconds versus 261.3 +/- 68.8 seconds, p less than 0.05), but not at week 10. Placebo patients demonstrated no difference at week 8 or 10 in exercise performance compared with initial placebo treatment. Timolol twice daily, therefore, is potentially useful in some patients with angina pectoris. Other patients may, however, require a shorter dose interval for optimal angina control and maximal improvement in exercise capacity.
Insulin resistance is associated with the circulating free fatty acid (FFA) level and intracellular lipid content in muscle and liver. We investigated the effect of 2-wk diet and exercise therapy on total adiposity, circulating FFA, intracellular lipid content in muscle and liver, and peripheral insulin sensitivity. Type 2 diabetic patients were divided into a diet group (n = 7) and a diet plus exercise group (n = 7). We performed a hyperinsulinemic-euglycemic clamp study before and after treatment. Intramyocellular lipid (IMCL) in the tibialis anterior muscle and intrahepatic lipid (IHL) were evaluated by (1)H-magnetic resonance spectroscopy. Fasting FFA were not altered, and total body fat showed a slight, but significant, decrease in both groups after treatment. IMCL was decreased by 19%, and the glucose infusion rate was increased by 57% in the diet plus exercise group, whereas neither IMCL nor glucose infusion rate was significantly altered in the diet group. However, IHL showed a significant decrease in both groups. In summary, we found that 2 wk of diet and exercise decreased IMCL and increased muscle insulin-mediated glucose uptake, whereas diet with or without exercise decreased IHL. These effects were evident despite a small decrease in body fat and were observed independently of fasting FFA levels.
Physical fitness through exercise is the rage of today. Almost everybody is indulging in various forms of exercise from weight lifting to marathons. These regimens presuppose a normal muscle metabolism. However, a significant number of so-called normals end up with the symptoms of cramps, fatigue, and, in advanced cases, myoglobinuria. Exercise forms the mainstay of rehabilitation of patients with neurologic disorders manifesting as paresis or paralysis, and certain rheumatologic or metabolic problems are also handled via the medium of exercise therapy. It is, thus, imperative that there should be a clear understanding of normal muscle composition and metabolic responses. We will summarize the histology, histochemistry, physiology and metabolic responses of normal muscle to exercise and put this information in perspective in the light of various muscle disorders.
BACKGROUND: Training therapy with its manifold effects should be part of a modern and multi modular treatment of the COPD. Because of the specific symptoms (e. g. muscle atrophy, dyspnea, low testosterone levels) and the deconditioning of these patients, a resistance training might meet the demands of a COPD-exercise-therapy rather than an endurance training. The aim of this research project was to evaluate the efficiency of a hypertrophic maximal strength training on various COPD relevant parameters. METHODS: 28 patients with moderate to severe COPD (m12/f16) were randomized and divided in a treatment and a control group. The patients in the treatment group underwent a resistance training (hypertrophic maximal strength training) for 12 weeks, initially two times, then three times a week. RESULTS: Considering the results of the daily Peak-Flow-Measurement, there was no significant change in both groups, but a trend towards an improvement could be found in the treatment group. There was no difference in the change of FEV 1. The performance on the ergo cycle showed a highly significant improvement (p < 0.001) in the treatment group of 18.7 % (21.9 Watt). The results of the SGRQ showed a significant improvement (p < 0.05) of the HRQL in the treatment group. A change of the HRQL in the control group was not found. CONCLUSIONS: These data support the hypotheses that a short term high intensity strength training programme is suitable to improve performance measures of patients with moderate to severe COPD and it might also improve pulmonary function. The conclusion can be drawn, that this kind of resistance training can be prefered as COPD-specific training therapy and offers new treatment perspectives.
Congestive heart failure occurs when myocardial dysfunction is advanced. Although clinical manifestations and diminished functional capacity can be traced back to the poor cardiac contractile state, there are major modifying influences from a complex series of compensatory responses. These particularly involve the heart, vessels, kidneys, sympathetic nervous system, the renin-angiotensin system, and other hormone systems. Functional capacity is, therefore, determined by the sum of the effects of the original cardiac insult and the effects, beneficial and adverse, of the secondary events. Functional capacity relates closely to prognosis only in the most severely disabled patients. The latter is mainly related to the extent of ventricular dysfunction, and there can be independent contributions from arrhythmias and sympathetic activity. Measures of resting parameters of cardiac contractility, hemodynamics, or neurohumoral responses are, therefore, of no value in predicting functional capacity but can be useful in examining outlook or examining mechanisms of disease and therapy. Exercise measurements are necessary because adequate resting performance can disguise major limitations in cardiac reserve. Measurement of functional capacity can be used to quantify the effects of therapy on daily living and to give an indication of the overall response of the body to major cardiac inadequacy. Limitation of exercise capacity, the earliest symptom of heart failure, can be quantified during a graded exercise test. Measurements of cardiac output and hemodynamic variables during exercise quantify the extent to which the cardiovascular system can increase performance to meet the demands of exercise. Work capacity and maximum oxygen capacity indicate the limits of physical performance, whereas determination of the anaerobic threshold indicates the highest level of exercise at which cardiorespiratory mechanisms are able to provide adequate oxygen supply to maintain aerobic metabolism in working skeletal muscle.
The prophylactic value of physical activity for arteriosclerotic diseases is generally accepted. Regular exercise is also the most effective therapy for intermittent claudication although drug treatment is more popular in general practice. Recent findings show that exercise and drug treatments complement each other.