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Results for “BREATHING EXERCISES”

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At least 613 records · Page 34Linked to original sources
PubMed1981

Control of breathing during prolonged exercise.

Ventilation (VE) climbs steadily throughout prolonged heavy exercise. While this VE "drift" has implications for the adequacy of gas exchange in long-term exercise, its mechanism remains unknown. We examined the behavior of previously proposed mediators of VE drift during one hour of cycle ergometer exercise at constant work rate requiring 2/3 VO2 max in 10 subjects. VE increased 13% from 12 to 61 min of exercise (P less than 0.05). Although body core temperature rose as VE rose, equal elevation of core temperature by passive means failed to increase exercise VE. Rising VE during the hour of exercise occurred despite unchanged arterial pH, PCO2, and lactate and despite unchanged VCO2. Thus, all of the VE increase was calculated to be due to increased dead space ventilation (VD). Tidal volume (VT) was unchanged, while VD/VT rose from 0.16 to 0.24 from 12 to 61 min of work (P less than 0.05). These results show that increased body core temperature does not mediate VE drift, and that changes in previously proposed mediators (arterial pH, arterial lactate, and VCO2) are not necessary for a slow VE rise to occur in prolonged heavy exercise.

Body Temperature↗
PubMed1984

Role of VCO2 in control of breathing of awake exercising dogs.

Steady-state ventilatory responses to CO2 inhalation, intravenous CO2 loading (loading), and intravenous CO2 unloading (unloading) were measured in chronic awake dogs while they exercised on an air-conditioned treadmill at 3 mph and 0% grade. End-tidal PO2 was maintained at control levels by manipulation of inspired gas. Responses obtained in three dogs demonstrated that the response to CO2 loading [average increase in CO2 output (Vco2) of 216 ml/min or 35%] was a hypercapnic hyperpnea in every instance. Also, the response to CO2 unloading [average decrease in Vco2 of 90 ml/min or 15% decrease] was a hypocapnic hypopnea in every case. Also, the analysis of the data by directional statistics indicates that there was no difference in the slopes of the responses (change in expiratory ventilation divided by change in arterial Pco2) for loading, unloading, and inhalation. These results indicate that the increased CO2 flow to the lung that occurs in exercise does not provide a direct signal to the respiratory controller that accounts for the exercise hyperpnea. Therefore, other mechanisms must be important in the regulation of ventilation during exercise.

Animals↗
PubMed1991

The effect of obliterative bronchiolitis on breathing pattern during exercise in recipients of heart-lung transplants.

The more rapid and shallow ventilation pattern seen during exercise in patients with obstructive and/or restrictive lung disease has been attributed by some investigators to the effects of vagal afferents from intrapulmonary receptors. Recipients of heart-lung transplants (HLTR) offer a unique opportunity to test this hypothesis since they have denervated lungs and may develop obliterative bronchiolitis after organ rejection. We thus compared the ventilation responses to incremental bicycle ergometry of five HLTR with relatively normal pulmonary function (HLTR-N) and four with bronchiolitis obliterans (HLTR-O). We compared the slopes of the linear portion of the tidal volume versus inspired minute ventilation relationship of both groups. The rate of rise of tidal volume (VT) (slope of VT versus VI) was greater in HLTR-N (0.31 +/- 0.004) than in HLTR-O (0.023 +/- 0.007) (p less than 0.05). This corresponded to a slower increase in respiratory rate (RR) (slope of RR versus Vl/cm) in HLTR-N (0.055 +/- 0.005) than in HLTR-O (0.083 +/- 0.019) (p less than 0.01). Furthermore, values for VT, inspiratory time (TI), and duty cycle (TI/Ttot) measured during exercise at the VT break point were all significantly lower in the HLTR-O than in HLTR-N. We also evaluated the ability of HLTR with lung disease to regulate their ultimate level of ventilation during maximal exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2004

Dyspnoea in health and obstructive pulmonary disease : the role of respiratory muscle function and training.

A consistent finding of recent research on respiratory muscle training (RMT) in healthy humans has been an attenuation of respiratory discomfort (dyspnoea) during exercise. We argue that the neurophysiology of dyspnoea can be explained in terms of Cambell's paradigm of length-tension inappropriateness. In the context of this paradigm, changes in the contractile properties of the respiratory muscles modify the intensity of dyspnoea predominantly by changing the required level of motor outflow to these respiratory muscles. Thus, factors that impair the contractile properties of the respiratory muscles (e.g. the pattern of tension development, functional weakening and fatigue) have the potential to increase the intensity of dyspnoea, while factors that improve the contractile properties of these respiratory muscles (e.g. RMT) have the potential to reduce the intensity of dyspnoea. In patients with obstructive pulmonary disease, functional weakening of the inspiratory muscles in response to dynamic lung hyperinflation appears to be a central component of dyspnoea. A decrease in the intensity of respiratory effort sensation (during exercise and loaded breathing) has been observed in both healthy individuals and patients with obstructive pulmonary disease after RMT. We conclude that RMT has the potential to reduce the severity of dyspnoea in healthy individuals and in patients with obstructive pulmonary disease, and that this probably occurs via a reduction in the level of motor outflow. Further work is required to clarify the role of RMT in the management of other disease conditions in which the function of the respiratory muscles is impaired, or the loads that they must overcome are elevated (e.g. cardiorespiratory and neuromuscular disorders).

Asthma↗
PubMed1981

Physiological responses to resistance breathing during short and prolonged exercise.

Respirators which impose a resistance to breathing may cause a limitation in maximum exercise intensity. This limitation is of particular concern when respirators are used in emergency situations requiring high levels of exercise intensity. Many studies have defined the limitations of exercise intensity imposed by breathing resistance as the point where the subject feels "uncomfortable". Perhaps of greater importance is the true physiological limit. Using motivated subjects, the physiological limits of exercise intensity and related respiratory responses resistances of 11, 16, 25, 40, and 57 cm H2O pressure at a flow rate of 120 L.min-1 exercise limits were 72, 72, 79, 60, and 54 percent of maximum aerobic capacity (% VO2 max) for the short term and 58, 60, 49, 43, and 35% VO2max for the prolonged exercise (1 hour). The presence of significant external resistance to breathing was found to influence the traditional relationship between exercise intensity and duration.

Adult↗
PubMed2026

The Human Breath Volatilome Responds to Exercise and Recovery: An Untargeted Profiling Study.

Exercise induces metabolic and physiological changes across multiple organs. These changes have been studied via several human biofluids, including urine and blood; however, they remain mainly underexplored in exhaled breath. In this exploratory pilot study, we performed untargeted profiling of breath volatile compounds (VCs) to investigate how exercise and recovery influence breath chemical composition. Breath samples were collected from 71 university athletes from three sporting disciplines. Across 143 breath samples, a total of 1,204 unique breath VCs were detected. There were distinct volatilomic responses to physical activity and recovery, regardless of the athlete's sport. Comparison of paired samples using volcano analysis collected before and during exercise identified 80 breath VCs that significantly increased and 182 that significantly decreased. Similarly, a comparison of samples collected before and after exercise identified 11 compounds that decreased significantly. These findings demonstrate that exercise induces measurable changes in the breath volatilome. However, due to the lack of standardized exercise intensity measures and physiological monitoring, the results should be considered exploratory and interpreted cautiously within the field of exercise science.

Exhaled breath analysis↗
PubMed1978

The contribution of the reflex hypoxic drive to the hyperpnoea of exercise.

Oxygen breath tests have been applied to six normal subjects at rest and during steady state exercise on a bicycle ergometer (200, 400 and 600 kpm) to estimate the contribution of the reflex hypoxic drive to total ventilation. The subjects were changed without their knowledge from air to 100% oxygen for 4--5 breaths, the fall in ventilation was recorded and expressed as a percentage of total ventilation (hypoxic drive). The average reflex hypoxic drive was 16.2% (SE +/- 2.6; n = 35) this remianed unaltered during all levels of steady state exercise. The maximum fall in ventilation occurred earlier in exercise (P less than 0.0005). At rest the maximum fall occurred on average 31.2 s (SE +/- 2.6) from the start of the first breath of oxygen. During the first level of steady state exercise the maximum fall occurred 19.4 s (SE +/- 0.5) from the start of the first breath of oxygen. It is concluded that the contribution of the reflex hypoxic drive to the total ventilation is unaltered by exercise although a substantial part of the hyperpnoea can be accounted for by the presence of this drive.

Adult↗
PubMed2005

Inspiratory muscle training compared with other rehabilitation interventions in adults with chronic obstructive pulmonary disease: a systematic literature review and meta-analysis.

The purpose of this systematic review was to determine the effect of inspiratory muscle training (IMT) (alone or combined with exercise and/or pulmonary rehabilitation) compared to other rehabilitation interventions such as: exercise, education, other breathing techniques or exercise and/or pulmonary rehabilitation among adults with chronic obstructive pulmonary disease (COPD). A systematic review of the literature on IMT and COPD was conducted according to the Cochrane Collaboration protocol. Inclusion criteria for the review included randomized controlled trials, published in English, comparing IMT or combined IMT and exercise/pulmonary rehabilitation with other rehabilitation interventions such as general exercise, education, other breathing techniques or exercise/pulmonary rehabilitation among adults with COPD. 274 articles were retrieved, and 16 met the inclusion criteria. Seven meta-analyses were performed that compared targeted or threshold IMT to exercise (n = 3) or to education (n = 4). Results showed significant improvements in inspiratory muscle strength and endurance, and in the dyspnea scale on a quality of life measure, for participants in the IMT versus education group. In other instances where meta-analyses could not be performed, a qualitative review was performed. IMT results in improved inspiratory muscle strength and endurance compared to education. Further trials are required to investigate the effect of IMT (or combined IMT) compared to other rehabilitation inventions for outcomes such as dyspnea, exercise tolerance, and quality of life.

Adult↗