Changes in ventilation in response to ramp changes in treadmill exercise load

Kelsey, Carol J.; Duffin, James

doi:10.1007/bf00243518

Cited by 20 publications

(17 citation statements)

References 17 publications

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“…Moreover several investigators have found that for the same increase in metabolic rate, the tachypnea and hyperpnea are greater when the treadmill speed or cycling frequency is increased as opposed to an increase in treadmill grade or cycling resistance (5,32,53,67,179,193,194,242). Furthermore during sinusoidal changes in work rate, investigators have found greater amplitudes and lower phase lags for ventilation when limbmovement frequency is varied compared to variations in treadmill grade or cycle resistance (64,65,342).…”

Section: Breathing Frequency and Limb-movement Frequencymentioning

confidence: 92%

Control of Breathing During Exercise

Forster

Haouzi

Dempsey

2012

Comprehensive Physiology

198

203

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During exercise by healthy mammals, alveolar ventilation and alveolar-capillary diffusion increase in proportion to the increase in metabolic rate to prevent PaCO2 from increasing and PaO2 from decreasing. There is no known mechanism capable of directly sensing the rate of gas exchange in the muscles or the lungs; thus, for over a century there has been intense interest in elucidating how respiratory neurons adjust their output to variables which can not be directly monitored. Several hypotheses have been tested and supportive data were obtained, but for each hypothesis, there are contradictory data or reasons to question the validity of each hypothesis. Herein, we report a critique of the major hypotheses which has led to the following conclusions. First, a single stimulus or combination of stimuli that convincingly and entirely explains the hyperpnea has not been identified. Second, the coupling of the hyperpnea to metabolic rate is not causal but is due to of these variables each resulting from a common factor which link the circulatory and ventilatory responses to exercise. Third, stimuli postulated to act at pulmonary or cardiac receptors or carotid and intracranial chemoreceptors are not primary mediators of the hyperpnea. Fourth, stimuli originating in exercising limbs and conveyed to the brain by spinal afferents contribute to the exercise hyperpnea. Fifth, the hyperventilation during heavy exercise is not primarily due to lactacidosis stimulation of carotid chemoreceptors. Finally, since volitional exercise requires activation of the CNS, neural feed-forward (central command) mediation of the exercise hyperpnea seems intuitive and is supported by data from several studies. However, there is no compelling evidence to accept this concept as an indisputable fact.

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Section: Breathing Frequency and Limb-movement Frequencymentioning

confidence: 92%

Control of Breathing During Exercise

Forster

Haouzi

Dempsey

2012

Comprehensive Physiology

198

203

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“…Thus, phase I ventilatory response might be regulated so that it is always maintained in the same in individual. On the other hand, some researchers have revealed that initial exercise hyperpnea is changed by various factors such as muscle pain and limb frequency (Kelsey and Duffin, 1992;Cerretelli et al, 1995;Hotta et al, 2006Hotta et al, , 2007aWells et al, 2007). Further study will be needed to clarify this contradiction.…”

Section: The Effect Of Increase In Imp On Phase I Ventilatory Responsementioning

confidence: 98%

“…Thus, an increase in exercise intensity or workload is expected to augment both central command and feedback signals from the exercising muscles, resulting in an exaggerated initial exercise hyperpnea. However, it has been well documented that phase I ventilatory response is unaffected by the alteration of exercise intensity or workload (Kelsey and Duffin, 1992;Cerretelli et al, 1995;Wells et al, 2007).…”

Section: The Effect Of Increase In Imp On Phase I Ventilatory Responsementioning

confidence: 99%

“…Many investigators have revealed that the phase I ventilatory response is not affected by changes in exercise intensity or workload, which is likely to influence both central activity and feedback from exercising muscles (Kelsey and Duffin, 1992;Cerretelli et al, 1995;Wells et al, 2007). Ventilatory response at the onset of exercise has been thought to be controlled not additively but redundantly by the dual modulations in which signals are received from the motor center and the periphery into the respiratory center through neural occlusion (Waldrop et al, 1986).…”

Section: Introductionmentioning

confidence: 99%

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The Effect of External Cuff Pressure on Initial Exercise Hyperpnea

Hotta

Yamamoto

Ishida

2009

J Physiol Anthropol

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The purpose of this study was to investigate the effect of an increase in intramuscular pressure on ventilatory response at the onset of exercise. Seven subjects participated in this study. We measured ventilatory responses to a 20-s singlearm extension-flexion exercise and passive movement. Each subject performed two kinds of exercise and passive movement in random order: in one, the exercising arm was encircled with a deflated cuff placed around the upper arm; in the other, the exercising arm was compressed by a cuff placed around the upper arm, which was inflated to 25 mmHg. We found that neither ventilatory response during exercise nor during passive movement was significantly changed even though the cuff compressed the arm. In conclusion, the increased intramuscular pressure caused by the 25-mmHg pressure of the cuff did not have a significant influence on ventilatory response at the onset of exercise.

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“…For example, in treadmill walking, the incline of the treadmill can be paired with different treadmill speeds so that subjects walk with the same oxygen consumption at very different rates of limb movement. In all cases, the magnitude of the initial increase in ventilation (i.e., breath-by-breath measures of l/min) was associated with the rate of the movement rather than the load (Casey et al 1987;Duffin and Bechbache 1983;Kelsey and Duffin 1992;Wells et al 2007). Other studies in which the load of the movement (bicycling) is changed without a change in the rate of the movement also indicate that there is no rapid change in the minute ventilation when the load is altered (e.g., Whipp et al 1982).…”

Section: Rate Of Breathing Is a Function Of The Rate Of Steppingmentioning

confidence: 99%

Breathing Frequency Changes at the Onset of Stepping in Human Infants

Noah¹,

Boliek²,

Lam³

et al. 2008

Journal of Neurophysiology

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Breathing frequency increases at the onset of movement in a wide rage of mammals including adult humans. Moreover, the magnitude of increase in the rate of breathing appears related to the rate of the rhythmic movement. We determined whether human infants show the same type of response when supported to step on a treadmill. Twenty infants (ages 9.7 Ϯ 1.2 mo) participated in trials consisting of sitting, stepping on the treadmill, followed by sitting again. Breathing frequency was recorded with a thermocouple, positioned under one naris and taped to a soother that the infant held in his/her mouth. A video camera, electrogoniometers, and force platforms under the treadmill belts recorded stepping movements. We found that the rate of breathing changed at the beginning of stepping. Most surprisingly, we found that when infants stepped at a frequency slower than their breathing frequency in sitting, the breathing frequency decreased. Average breathing frequency during stepping was positively correlated with stepping frequency. There was no evidence of entrainment between stepping and breathing. In conclusion, the rapid change in breathing frequency at the beginning of movement is functional in infants. The direction and magnitude of change in breathing is associated with the leg movements.

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Changes in ventilation in response to ramp changes in treadmill exercise load

Cited by 20 publications

References 17 publications

Control of Breathing During Exercise

Control of Breathing During Exercise

The Effect of External Cuff Pressure on Initial Exercise Hyperpnea

Breathing Frequency Changes at the Onset of Stepping in Human Infants

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