Man's responses to breath-hold exercise in air and in water.
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Twenty-four patients suffering from chronic obstructive pulmonary disease (COPD) exercised on a bicycle with a progressive increase in load (30 W/min) until dyspnea or exhaustion occurred. Seven subjects were CO2 retainers: PaCO2 greater than or equal to 45 mm Hg at rest and/or during exercise. Fifteen normal subjects were submitted to the same protocol. To make comparison possible, all the parameters studied were calculated at 60 watts. It was concluded that CO2 retention during exercise is not secondary to a decreased respiratory drive but mainly to a lesser increase in VE and to higher VD/VT ratios.
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This paper reviewed in short neural and humoral factors which might be responsible for inducing exercise hyperpnea. As one of the neural factors afferent signals which arise in the exercising limbs and are transmitted via group III or IV high threshold sensory fibres were involved. The other neural factor is command signals originating in the central nervous system and being fed onto the respiratory center. Hypothalamic locomotor region is assumed to be a possible locus to integrate these peripheral and central neural signals. There are enough evidences to believe that humoral factors mediated via cardiac output is also essential for the hyperpnea. Changes in VCO2 is well correlated with those of VE in dynamic as well as in steady-state response. Oscillations in PaCO2 can be assumed to play a role to link metabolic CO2 changes to those in ventilation. Thus, no single factor can explain the whole process of exercise hyperpnea. Poon's optimization model may give a key to integrate complicated and coflicting experimental results in a unique concept.
The increase in ventilation caused by exercise is controlled by a combination of neural and chemical events, although the precise contribution and relative importance of these signals is still debated. It is generally agreed that the genesis of exercise hyperpnoea lies within the central nervous system and that peripheral reflexes, both chemical and neural, modulate central drive. Recently, attention has once again focused on the idea that circulating factors, in particular potassium, may play an important role in this modulation by stimulating known areas of peripheral chemoreception. Arterial chemoreceptors, muscle chemoreflex and slowly adapting pulmonary stretch receptors are all excited by hyperkalaemia. When potassium is raised to mimic exercise concentrations it increases ventilation in anaesthetised animals. This response is abolished by surgical denervation of the arterial chemoreceptors and is markedly reduced by chemical denervation with hyperoxia. Hypoxia enhances the ventilatory response to hyperkalaemia, and the stimulatory effects of potassium are further increased when combined with lactic acid or raised concentrations of noradrenaline. Hyperkalaemia can also increase the hypoxic sensitivity of the arterial chemoreflex in exercise. There is a close temporal relationship between potassium and ventilation during exercise, but changes in potassium are not proportionally related to changes in ventilation. When all data are taken together, there is good evidence that potassium has a supporting role in the control of exercise hyperpnoea, predominantly through modulation of the arterial chemoreflex.
General principles of physical medicine and rehabilitation of rheumatic diseases are described. In knee and hip osteoarthritis it is important to protect full extension and in evolutive phase treat with drugs, unloading and physical therapy. Rest and ice are efficacious in active rheumatoid arthritis and in chronic phase all procedures and exercises are recommended with respect to pain threshold. Physical therapy for spondy larthropathies is directed to maintenance range of motion exercise for spine and breathing exercises. Swimming is the most appropriate recreational activity for spondylarthropathies.
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We studied cardiovascular and respiratory changes during yogic breathing exercise kapalabhati (KB) in 17 advanced yoga practitioners. The exercise consisted in fast shallow abdominal respiratory movements at about 2 Hz frequency. Blood pressure, ECG and respiration were recorded continuously during three 5 min periods of KB and during pre- and post-KB resting periods. The beat-to-beat series of systolic blood pressure (SBP) and diastolic blood pressure (DBP), R-R intervals and respiration were analysed by spectral analysis of time series. The mean absolute power was calculated in three frequency bands--band of spontaneous respiration, band of 0.1 Hz rhythm and the low-frequency band greater than 15 s in all spectra. The mean modulus calculated between SBP and R-R intervals was used as a parameter of baroreceptor-cardiac reflex sensitivity (BRS). Heart rate increased by 9 beats per min during KB. SBP and DBP increased during KB by 15 and 6 mmHg respectively. All frequency bands of R-R interval variability were reduced in KB. Also the BRS parameter was reduced in KB. The amplitude of the high-frequency oscillations in SBP and DBP increased during KB. The low-frequency blood pressure oscillations were increased after KB. The results point to decreased cardiac vagal tone during KB which was due to changes in respiratory pattern and due to decreased sensitivity of arterial baroreflex. Decreased respiratory rate and increased SBP and low-frequency blood pressure oscillations after KB suggest a differentiated pattern of vegetative activation and inhibition associated with KB exercise.
The aim of this survey was to characterize respiratory rehabilitation programmes for patients with COPD in Switzerland. Rate of return of questionnaires was 94%. In 2001, 2238 patients with COPD followed an inpatient (1790) or outpatient (448) respiratory rehabilitation programme. This corresponds to 1% of all patients with COPD in Switzerland. Physical exercise is estimated to be significantly more important compared to breathing exercises, patient education and psychosocial support although this prioritization is not as pronounced as in the current literature. Disease-specific instruments to measure health related quality of life that represents the most important outcome measure for patients with COPD should be implemented in practice. Thereby both the components of rehabilitation programmes and predictive factors for a successful rehabilitation could be evaluated.
Previous studies have shown both worsening ventilation-perfusion (VA/Q) relationships and the development of diffusion limitation during exercise at simulated altitude and suggested that similar changes could occur even at sea level. We used the multiple-inert gas-elimination technique to further study gas exchange during exercise in healthy subjects at sea level. Mixed expired and arterial respiratory and inert gas tensions, cardiac output, heart rate, minute ventilation, respiratory rate, and blood temperature were recorded at rest and during steady-state exercise in the following order: rest, minimal exercise (75 W), heavy exercise (300 W), heavy exercise breathing 100% O2, repeat rest, moderate exercise (225 W), and light exercise (150 W). Alveolar-to-arterial O2 tension difference increased linearly with O2 uptake (VO2) (6.1 Torr X min-1 X 1(-1) VO2). This could be fully explained by measured VA/Q inequality at mean VO2 less than 2.5 l X min-1. At higher VO2, the increase in alveolar-to-arterial O2 tension difference could not be explained by VA/Q inequality alone, suggesting the development of diffusion limitation. VA/Q inequality increased significantly during exercise (mean log SD of perfusion increased from 0.28 +/- 0.13 at rest to 0.58 +/- 0.30 at VO2 = 4.0 l X min-1, P less than 0.01). This increase was not reversed by 100% O2 breathing and appeared to persist at least transiently following exercise. These results confirm and extend the earlier suggestions (8, 21) of increasing VA/Q inequality and O2 diffusion limitation during heavy exercise at sea level in normal subjects and demonstrate that these changes are independent of the order of performance of exercise.
Twelve subjects with mild asthmatic episodes in the form of nocturnal precipitation were studied. A two-week schedule of placebo administration, pranayamic breathing exercises using a Pink City lung exerciser alone, and exercises using the lung exerciser with hot, humid air were performed. Five of the 12 asthmatics showed highly significant increases in peak expiratory flow rate (PEFR) with the lung exerciser alone, while eight of the 12 cases showed highly significant increases in PEFR with exercise using hot, humid air. The frequency of nocturnal wheezing also declined. It can be inferred that slow breathing alone and in combination with hot, humid air has a nonspecific bronchoprotective or bronchorelaxing effect.
In this original method of improving muscle tone in the perineum the author adapts the technique used for strengthening the quadriceps muscles. In that method the muscles progressively pull against an increasing weight. This method adapted to the perineum can be performed if a tampon is inserted into the vagina and the patient is instructed to contract her muscles so that increasingly heavy weights attached to the thread by which the tampon is normally removed are applied and the patient is taught how to contract so that the tampon is held in place. Furthermore the patient is taught breathing exercises together with abdomino-perineal muscle development, using H. Stapfer's method which was first described in his book published in 1912. Two case histories illustrate how the method has been applied and there are also diagrams showing how to carry out the exercises and how not to carry them out.