Reflexes Controlling Circulatory, Ventilatory and Airway Responses to Exercise

Kaufman, Marc P.; Forster, H. V.

doi:10.1002/cphy.cp120110

Cited by 226 publications

(325 citation statements)

References 430 publications

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“…The standard of care Rating of perceived exertion 0.5 kg 7 (6-9) 6 (6-9) 6 (6-7) 6 (6-7) 1.0 kg 9 (6-11) 8 (6-10) 7 (6-9) 7 (6-7) 1.5 kg 10 (8-13) 9 (8-13)* 8 (6-11) 7 (6-9) 2.0 kg 11 (9)(10)(11)(12)(13)(14) 10 (9-14)* 9 (7-12) 9 (7-10) 7.0 kg 15 (13)(14)(15)(16)(17) Data are shown as medians with ranges in parentheses; n ϭ 7 PAD patients and 7 healthy control subjects. *Significant difference between groups at the specific time point.…”

Section: Discussionmentioning

confidence: 99%

“…This information is projected to the spinal cord and brain stem; eventually, sympathetic outflow increases, mean arterial pressure (MAP) increases, and heart rate (HR) increases (16). Prostanoids are produced during skeletal muscle contraction and subsequently stimulate muscle afferent nerves, thereby contributing to the exercise pressor reflex (32)(33)(34)38).…”

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Inhibition of cyclooxygenase attenuates the blood pressure response to plantar flexion exercise in peripheral arterial disease

Müller

Drew

Ross

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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Muller MD, Drew RC, Ross AJ, Blaha CA, Cauffman AE, Kaufman MP, Sinoway LI. Inhibition of cyclooxygenase attenuates the blood pressure response to plantar flexion exercise in peripheral arterial disease. Am J Physiol Heart Circ Physiol 309: H523-H528, 2015. First published June 8, 2015 doi:10.1152/ajpheart.00267.2015.-Prostanoids are produced during skeletal muscle contraction and subsequently stimulate muscle afferent nerves, thereby contributing to the exercise pressor reflex. Humans with peripheral arterial disease (PAD) have an augmented exercise pressor reflex, but the metabolite(s) responsible for this augmented response is not known. We tested the hypothesis that intravenous injection of ketorolac, which blocks the activity of cyclooxygenase, would attenuate the rise in mean arterial blood pressure (MAP) and heart rate (HR) evoked by plantar flexion exercise. Seven PAD patients underwent 4 min of single-leg dynamic plantar flexion (30 contractions/min) in the supine posture (workload: 0.5-2.0 kg). MAP and HR were measured on a beat-by-beat basis; changes from baseline in response to exercise were determined. Ketorolac did not affect MAP or HR at rest. During the first 20 s of exercise with the most symptomatic leg, ⌬MAP was significantly attenuated by ketorolac (2 Ϯ 2 mmHg) compared with control (8 Ϯ 2 mmHg, P ϭ 0.005), but ⌬HR was similar (6 Ϯ 2 vs. 5 Ϯ 1 beats/min). Importantly, patients rated the exercise bout as "very light" to "fairly light," and average pain ratings were 1 of 10. Ketorolac had no effect on perceived exertion or pain ratings. Ketorolac also had no effect on MAP or HR in seven age-and sex-matched healthy subjects who performed a similar but longer plantar flexion protocol (workload: 0.5-7.0 kg). These data suggest that prostanoids contribute to the augmented exercise pressor reflex in patients with PAD. PERIPHERAL ARTERIAL DISEASE (PAD) is a form of atherosclerosis that preferentially affects the lower extremity. Because leg blood flow is impaired in PAD, it is not surprising that dynamic exercise, such as walking, provokes pain in the calf, thigh, or buttocks, termed "intermittent claudication." Clinical exercise testing (e.g., the Bruce treadmill protocol) also causes a large increase in blood pressure (BP) in PAD patients, and studies (10, 11) have linked this augmented pressor response to cardiovascular morbidity and mortality. In recent years, our laboratory has focused on BP control in patients with PAD. Specifically, we found that 1) the BP response to single-leg dynamic plantar flexion exercise was augmented in PAD patients compared with healthy control subjects; 2) the pressor response occurred at very low workloads and before the onset of pain; 3) the pressor response correlated with the anklebrachial index (ABI), suggesting that disease severity plays a role; and 4) intravenous infusion of ascorbic acid lowered the pressor response to exercise in PAD (13,28). To date, the mechanisms for these findings are largely unknown. Understanding BP regulation during exercise in PAD ...

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Inhibition of cyclooxygenase attenuates the blood pressure response to plantar flexion exercise in peripheral arterial disease

Müller

Drew

Ross

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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“…In marine mammals, it has been proposed that depth and exercise may also promote such autonomic conflict, and that behavioral modification of exercise (decreased stroke effort) during dives can minimize the risk of arrhythmias (Williams et al, 2015a,b). andForster, 1996;Mitchell et al, 1983;Smith et al, 2006;Waldrop et al, 1996;Waldrop and Iwamoto, 2006). Of course, the initiation and intensity of exercise are under voluntary control.…”

Section: Neuroregulation Of the Exercise Responsementioning

confidence: 99%

Heart rate regulation in diving sea lions: the vagus nerve rules

Ponganis

McDonald

Tift

et al. 2017

Journal of Experimental Biology

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Recent publications have emphasized the potential generation of morbid cardiac arrhythmias secondary to autonomic conflict in diving marine mammals. Such conflict, as typified by cardiovascular responses to cold water immersion in humans, has been proposed to result from exercise-related activation of cardiac sympathetic fibers to increase heart rate, combined with depth-related changes in parasympathetic tone to decrease heart rate. After reviewing the marine mammal literature and evaluating heart rate profiles of diving California sea lions (Zalophus californianus), we present an alternative interpretation of heart rate regulation that de-emphasizes the concept of autonomic conflict and the risk of morbid arrhythmias in marine mammals. We hypothesize that: (1) both the sympathetic cardiac accelerator fibers and the peripheral sympathetic vasomotor fibers are activated during dives even without exercise, and their activities are elevated at the lowest heart rates in a dive when vasoconstriction is maximal, (2) in diving animals, parasympathetic cardiac tone via the vagus nerve dominates over sympathetic cardiac tone during all phases of the dive, thus producing the bradycardia, (3) adjustment in vagal activity, which may be affected by many inputs, including exercise, is the primary regulator of heart rate and heart rate fluctuations during diving, and (4) heart beat fluctuations (benign arrhythmias) are common in marine mammals. Consistent with the literature and with these hypotheses, we believe that the generation of morbid arrhythmias because of exercise or stress during dives is unlikely in marine mammals.

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“…Lactic acidosis is considered an important mediator of the compensatory hyperventilation that normally occurs at high-intensity exercise by stimulation of carotid chemoreceptors (55), and thus would be presumed to be an important contributor to the ventilatory response to exercise in MM patients. Exercise ventilation is also regulated by feedforward mechanisms via central command (15) and by feedback reflexes mediated by activation of metaboreceptors or mechanoreceptors (ergoreflexes) in working muscle (2,13,23,31). Peak increases in blood lactate and maximal decreases in pH occur during the first minutes of recovery from exercise when the influence of central command ceases and ergoreflexes are rapidly withdrawn.…”

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confidence: 99%

Exertional dyspnea in mitochondrial myopathy: clinical features and physiological mechanisms

Heinicke

Taivassalo

Wyrick

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

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-Exertional dyspnea limits exercise in some mitochondrial myopathy (MM) patients, but the clinical features of this syndrome are poorly defined, and its underlying mechanism is unknown. We evaluated ventilation and arterial blood gases during cycle exercise and recovery in five MM patients with exertional dyspnea and genetically defined mitochondrial defects, and in four control subjects (C). Patient ventilation was normal at rest. During exercise, MM patients had low V O2peak (28 Ϯ 9% of predicted) and exaggerated systemic O 2 delivery relative to O2 utilization (i.e., a hyperkinetic circulation). High perceived breathing effort in patients was associated with exaggerated ventilation relative to metabolic rate with high V E/V O2peak, (MM ϭ 104 Ϯ 18; C ϭ 42 Ϯ 8, P Յ 0.001), and V E/V CO2peak, (MM ϭ 54 Ϯ 9; C ϭ 34 Ϯ 7, P Յ 0.01); a steeper slope of increase in ⌬V E/⌬V CO2 (MM ϭ 50.0 Ϯ 6.9; C ϭ 32.2 Ϯ 6.6, P Յ 0.01); and elevated peak respiratory exchange ratio (RER), (MM ϭ 1.95 Ϯ 0.31, C ϭ 1.25 Ϯ 0.03, P Յ 0.01). Arterial lactate was higher in MM patients, and evidence for ventilatory compensation to metabolic acidosis included lower Pa CO 2 and standard bicarbonate. However, during 5 min of recovery, despite a further fall in arterial pH and lactate elevation, ventilation in MM rapidly normalized. These data indicate that exertional dyspnea in MM is attributable to mitochondrial defects that severely impair muscle oxidative phosphorylation and result in a hyperkinetic circulation in exercise. Exaggerated exercise ventilation is indicated by markedly elevated V E/V O2, V E/V CO2, and RER. While lactic acidosis likely contributes to exercise hyperventilation, the fact that ventilation normalizes during recovery from exercise despite increasing metabolic acidosis strongly indicates that additional, exercise-specific mechanisms are responsible for this distinctive pattern of exercise ventilation.hyperventilation; lactic acidosis; metaboreflex; exercise; oxidative phosphorylation EXERTIONAL DYSPNEA WAS FIRST described as a symptom that limited exercise in mitochondrial myopathy (MM) in patients with a familial disorder studied by Linderholm and coworkers in the 1960s (36, 38), a disease now recognized to be attributable to a mutation in the iron-sulfur cluster scaffold (ISCU) gene (40, 42) and associated with deficiency of multiple iron-sulfur proteins, including succinate dehydrogenase and aconitase (20,21). Exertional dyspnea has since been described as a dominant feature of exercise intolerance in other mitochondrial myopathies that severely restrict muscle oxidative phosphorylation (3a, 22). Moreover, mitochondrial disease has been suggested to be an underrecognized cause of unexplained exertional dyspnea (16,25), although, these reports lacked genetic confirmation and, in most cases, did not include biochemical assessment to indicate the presence and severity of the putative mitochondrial defect (16). To better define the physiological manifestations of exertional dyspnea in mitochondrial myopathy, we have evalu...

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Reflexes Controlling Circulatory, Ventilatory and Airway Responses to Exercise

Cited by 226 publications

References 430 publications

Inhibition of cyclooxygenase attenuates the blood pressure response to plantar flexion exercise in peripheral arterial disease

Inhibition of cyclooxygenase attenuates the blood pressure response to plantar flexion exercise in peripheral arterial disease

Heart rate regulation in diving sea lions: the vagus nerve rules

Exertional dyspnea in mitochondrial myopathy: clinical features and physiological mechanisms

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