Ventilatory Response To Exercise Research Articles

Comparative ergoespirometric adaptations to a treadmill exercise test in untrained show Andalusian and Arabian horses

Significant differences exist in the respiratory adaptation to exercise in different equine breeds. This research describes the ergoespirometric response to exercise of Andalusian (AN) and Arabian (A) horses, both selected according to morphological criteria. Thirteen untrained male horses (6 AN and 7 A) performed a treadmill exercise test (TET) with a slope of 6%, with workloads starting from 5 m/s and increasing 1 m/s every 3 min until the horses were not able to keep the required velocity. Tidal volume (TV), respiratory rate, minute ventilation (VE), oxygen uptake (VO2), carbon dioxide production, peak oxygen uptake (VO2peak), respiratory exchange ratio (RER), exercise time to fatigue (ETF) and respiratory aerobic threshold (RAT) were determined. AN horses presented higher TV and VE, whereas respiratory rate, VO2 and VCO2 were lower at the same velocities. RER was similar between breeds. ETF was longer in A horses (556.7 ± 66.5 in AN vs. 607.1 ± 71.1 s in A) and no significant differences were found in RAT (5.50 ± 0.50 in AN vs. 5.86 ± 1.07 m/s in A). In summary, despite the more intense ventilatory response to exercise at the same velocity, AN horses had lower VO2. The AN horse develops a more intense ventilatory response to fixed velocities than the A horse and it could be interesting to clarify the role of the locomotion characteristics in this response.

Cardiopulmonary Response and Body Composition Changes after Prolonged High Altitude Exposure in Women

Weight loss in men is commonly observed during prolonged high altitude exposure as a result of a daily negative energy balance. Its amount depends mainly on duration of exposure, altitude reached, and level of physical activity. This reduction in body weight often comes with a loss of muscular mass, likely contributing to the decreased physical performance generally reported. Limited data is, however, available on body composition, functional capacity, and cardiopulmonary response to exercise after high altitude exposure in women. The aim of this study was to evaluate the effects of prolonged high altitude exposure on body composition and on cardiopulmonary response to maximal exercise in a group of young, moderately active women. Twelve female subjects, aged 21.5 ± 3.1 (mean ± SD), BMI 22.1 ± 1.9 kg · m(-2) and Vo(2max) 33.8 ± 3.5 mL · kg(-1) · min(-1), participated in this study, by residing for 21 days at high altitude (5050 m, Pyramid, EV-K(2)-CNR laboratory). Before and after high altitude exposure, all subjects underwent both a body composition evaluation using two methods (bioimpedance analysis and DEXA) and a functional evaluation based on a maximal exercise test on a cycle ergometer with breath-by-breath gas analysis. After high altitude exposure, data showed a slight, nonsignificant reduction in body weight, with an average 3:2 reduction ratio between fat and fat-free mass evaluated by DEXA, in addition to a significant decrease in Vo(2max) on the cycle ergometer test (p<0.01). Changes in Vo(2max) correlated to changes of leg muscle mass, evaluated by DEXA (r(2) = 0.72; p<0.0001). No changes were observed in the maximal heart rate, work capacity, and ventilatory thresholds, while the Vo(2)/W slope was significantly reduced (p<0.05). Finally, Ve/Vo(2) and VE/Vco(2max) slopes were increased (p<0.01), suggesting a possible long-term modulation of the exercise ventilatory response after prolonged high altitude exposure.

Short-term modulation of the exercise ventilatory response in younger and older women

The exercise ventilatory response (EVR; defined as the slope of the relationship between ventilation and CO(2) production) is reversibly augmented within a single exercise trial with increased respiratory dead space (DS) in both younger (Wood, H.E., Mitchell, G.S., Babb, T.G., 2008. Short-term modulation of the exercise ventilatory response in young men. J. Appl. Physiol. 104, 244-252) and older (Wood, H.E., Mitchell, G.S., Babb, T.G., 2010. Short-term modulation of the exercise ventilatory response in older men. Respir. Physiol. Neurobiol. 173, 37-46) men. The neural mechanism accounting for this augmentation is known as short-term modulation (STM) of the EVR. Since the effects of female sex hormones on STM are unknown, we examined the capacity for STM in healthy adult women of two age groups; nine younger (29±3 yrs, eumenorrheic) and seven older (69±3 yrs, postmenopausal) women were studied at rest and during cycle exercise (10 W, 30 W; not randomized) in control conditions and with added external DS (200 mL, 400 mL; randomized). Within groups, the main effects of DS and work rate on EVR were analyzed with a two-way repeated measures ANOVA; EVR comparisons between groups were made with unpaired t-tests. In both groups, EVR increased progressively with increasing DS volume (e.g. at 10 W 31±4 and 35±6 in control, 40±11 and 40±6 with 200 mL, 48±12 and 49±11 with 400 mL DS in younger and older women, respectively). In younger women, the effects of DS on EVR differed between work rates (significant interaction, p<0.05), although this was not the case for older women. In both groups, [Formula: see text] regulation was similar between DS and control; hence, increased EVR was not due to altered chemoreceptor feedback from rest to exercise. EVR with and without added DS did not differ between age groups. We conclude that the capacity for STM of the EVR with added DS is similar in healthy younger and older women.

Short- and Long-Term Modulation of the Exercise Ventilatory Response

The importance of adaptive control strategies (modulation and plasticity) in the control of breathing during exercise has become recognized only in recent years. In this review, we discuss new evidence for modulation of the exercise ventilatory response in humans, specifically, short- and long-term modulation. Short-term modulation is proposed to be an important regulatory mechanism that helps maintain blood gas homeostasis during exercise.

Short-term modulation of the exercise ventilatory response in older men

During exercise with added dead space (DS), the exercise ventilatory response (DeltaV(E)/ DeltaV(CO(2))) is augmented in younger men, via short-term modulation (STM) of the exercise ventilatory response. We hypothesized that STM would be diminished or absent in older men due to age-related changes in respiratory function and ventilatory control. Men were studied at rest and during cycle exercise with and without added DS. DeltaV(E)/ DeltaV(CO(2)) increased progressively with increasing DS volume (p<0.01), such that CO(2) was not retained with added DS versus without. Hence, the increase in DeltaV(E)/ DeltaV(CO(2)) was not due to increased chemoreceptor feedback from rest to exercise. Increasing exercise intensity diminished the DeltaV(E)/ DeltaV(CO(2)) (p<0.01), and the size of this effect varied by DS volume (p<0.05). We conclude that STM of the exercise ventilatory response is robust in older men; hence, despite age-related changes in lung function and ventilatory control, the exercise ventilatory response can still adapt to increased DS, in order to maintain isocapnia during exercise relative to rest.

Breathing mechanics during exercise with added dead space reflect mechanisms of ventilatory control

Small increases in external dead space (V(D)) augment the exercise ventilatory response via a neural mechanism known as short-term modulation (STM). We hypothesized that breathing mechanics would differ during exercise, increased V(D) and STM. Men were studied at rest and during cycle exercise (10-50W) without (Control) and with added V(D) (200-600ml). With added V(D), V(T) increased via increased end-inspiratory lung volume (EILV), with no change in end-expiratory lung volume (EELV), indicating recruitment of inspiratory muscles only. With exercise, V(T) increased via both decreased EELV and increased EILV, indicating recruitment of both expiratory and inspiratory muscles. A significant interaction between the effects of exercise and V(D) on mean inspiratory flow indicated that the augmented exercise ventilatory response with added V(D) (i.e. STM) resulted from increased drive to the inspiratory muscles. These results reveal different patterns of respiratory muscle recruitment among experimental conditions. Hence, we conclude that fundamental differences exist in the neural control of ventilatory responses during exercise, increased V(D) and STM.

Increased Ventilatory Response To Submaximal Exercise After 5 Weeks Of Head-down Bed Rest

Previously, ventilation (VE) during incremental exercise was found to be elevated after 7 days of horizontal bed rest (FASEB J 1991, 5:A1477). We investigated the effects of 5 weeks of head-down bed rest (HDBR) on the exercise ventilatory response (EVR), defined as the slope of the relationship between VE and CO2 production (VCO2), to submaximal constant load exercise. To further explore the effects of HDBR, we examined short-term modulation (STM) of the EVR before and after HDBR. STM is defined as a neural mechanism where EVR is augmented in the presence of increased respiratory dead space (DS; J Appl Physiol 2008, 104: 244-252). PURPOSE: To examine the effects of 5 weeks of HDBR on EVR and the capacity for STM. METHODS: 25 subjects (3 female) spent 5 weeks in HDBR. As part of a larger study, subjects were assigned to 3 groups, 2 of which undertook exercise training during HDBR (semi-recumbent rowing 3 days/wk and horizontal strength training 2 days/wk) while the third remained inactive. The EVR was measured at rest and during upright cycle exercise (30W) without (Control) and with 400ml added external DS, before and after HDBR. The main effects of group and HDBR were analyzed with a two-way repeated measures ANOVA. RESULTS: The main effect of group was not significant for any of the variables tested. The physical characteristics for the 25 subjects were: age 33±11 yr, height 175±10 cm, weight 74±12 kg and BMI 24±2 kg/m2. EVR both with and without added DS was elevated post HDBR (Control: 27.9±4.5 and 30.3±5.6; DS: 31.4±7.2 and 36.0±8.1; pre and post HDBR, respectively; p<0.05). EVR was significantly augmented with DS vs. Control both pre and post (p<0.05), indicating STM of the EVR, and this capacity to augment the EVR was unaffected by HDBR. The increase in EVR was due to a significant decrease in VCO2 (Control: 0.79±0.15 and 0.73±0.11; DS: 0.75±0.11 and 0.70±0.10 l/min; at 30W pre and post HDBR, respectively; p<0.05), with no affect of HDBR on VE during exercise. CONCLUSION: HDBR appears to alter the EVR mainly by a reduction in VCO2, which we speculate might be associated with a change in substrate metabolism. However, HDBR does not appear to affect the capacity for STM to augment the EVR with added DS. Supported by NASA grant CA00701, the King Charitable Foundation Trust, Cain Foundation.

Short- and Long-term Modulation of the Exercise Ventilatory Response

Short- and Long-term Modulation of the Exercise Ventilatory Response

Ventilatory Responses to Exercise and Hypercapnia Following 18 Days of Head-Down Rest

The effects of head-down rest (HDR) and microgravity on cardiovascular control have been widely studied; however, their effects on ventilatory control are less clear. An increased ventilatory response to exercise and/or to hypercapnia (HCVR) could cause significantly increased ventilatory demand and/or dyspnea, and thus limit the ability of flight crew to perform high-intensity exercise during or after spaceflight. Based on limited previous studies, we hypothesized that the ventilatory response to exercise would be increased, while the HCVR would be decreased after HDR. In 21 healthy subjects, ventilatory responses to submaximal exercise and to hypercapnia were tested before and immediately after 18 d of HDR. Subjects were randomly assigned to either daily supine cycle exercise (Exercise group; N = 14, 2 women) or no exercise (Rest group; N = 7, 1 woman) during HDR. The exercise ventilatory response (DeltaV(E)/DeltaV(CO2)) and the HCVR were unchanged following HDR in both groups. However, ventilation was significantly elevated after HDR at rest, during submaximal exercise, and while breathing 6% CO2. End-tidal P(CO2) was significantly reduced at rest, during submaximal exercise, and while breathing 3% CO2, indicating a decrease in the CO2 set point. Although HDR had no effect on the ventilatory responses to exercise and hypercapnia, the CO2 set point appeared to be reduced, suggesting an increase in drive to breathe that occurred regardless of whether or not subjects undertook exercise during HDR. These preliminary results indicate that further study of the effects of HDR on ventilatory control is warranted.

Reply to Dr. Poon

to the editor: Thank you for the opportunity to respond to the letter from Dr. Poon ([7][1]) regarding our manuscript ([10][2]). Our purpose was to translate work establishing short-term modulation (STM) of the exercise ventilatory response in an animal model (goats) to healthy humans using similar

The classic potentiation of exercise ventilatory response by increased dead space in humans is more than short-term modulation

to the editor: Wood et al. ([9][1]) report that end-tidal Pco2 (PetCO2) in young men increases with increased external dead space (DS) at rest and equally so during moderate exercise, such that the slope of the resultant ventilation (Ve)-metabolic CO2 production (Vco2) relationship is

Short‐term modulation of the exercise ventilatory response is not diminished in older men

We have previously shown that the exercise ventilatory response (EVR; defined as the slope of the relationship between ventilation and CO2 production) is reversibly augmented within a single exercise trial in the presence of added dead space (DS) in healthy young men. This augmentation arises from a mechanism known as short‐term modulation (STM; FASEB J. 21, 765.18. 2007), independent of changes in chemoreceptor (CR) feedback from rest to exercise. We hypothesized that the capacity for STM to augment the EVR with added DS is diminished in healthy older men due to age‐dependent decreases in pulmonary function and increases in EVR. Eleven men (age 69 ± 3 years) were studied at rest and during cycle exercise (10, 30, 50W; not randomized) in Control conditions (no added DS) and with added DS (200, 400, 600ml; randomized). The EVR increased sufficiently with the increasing DS volume (p&lt;0.01), e.g. at 10W, from 33 ± 6 in Control to 47 ± 10 with 600ml DS, such that CO2 was not retained with added DS vs. Control. Hence, the increase in the EVR was not due to increased CR feedback from rest to exercise. Increasing exercise intensity diminished the EVR (p&lt;0.01), e.g. with 400ml DS, from 40 ± 7 at 10W to 34 ± 5 at 50W; and the size of this effect varied by DS level (p&lt;0.05). A very similar response pattern was observed in younger men. We conclude that the capacity for STM to augment the EVR with added DS is not diminished with age in healthy men.Support: The Cain Foundation, The King Foundation, and Presbyterian Hospital of Dallas

Spinal serotonin receptor activation modulates the exercise ventilatory response with increased dead space in goats

Small increases in respiratory dead space (VD) augment the exercise ventilatory response by a serotonin-dependent mechanism known as short-term modulation (STM). We tested the hypotheses that the relevant serotonin receptors for STM are in the spinal cord, and are of the 5-HT2-receptor subtype. After preparing adult female goats with a mid-thoracic (T6-T8) subarachnoid catheter, ventilation and arterial blood gases were measured at rest and during treadmill exercise (4.8 km/h; 5% grade) with and without an increased VD (0.2-0.3 L). Measurements were made before and after spinal or intravenous administration of a broad-spectrum serotonin receptor antagonist (methysergide, 1-2mg total) and a selective 5-HT2-receptor antagonist (ketanserin, 5-12 mg total). Although spinal methysergide had no effect on the exercise ventilatory response in control conditions, the augmented response with increased VD was impaired, allowing Pa(CO)(2) to increase from rest to exercise. Spinal methysergide diminished both mean inspiratory flow and frequency responses to exercise with increased VD. Spinal ketanserin impaired Pa(CO)(2) regulation with increased VD, although its ventilatory effects were less clear. Intrathecal dye injections indicated CSF drug distribution was caudal to the upper cervical spinal cord and intravenous drugs at the same total dose did not affect STM. We conclude that spinal 5-HT2 receptors modulate the exercise ventilatory response with increased VD in goats.

Exercise Oscillatory Ventilation: Instability of Breathing Control Associated With Advanced Heart Failure

Instability of breathing control due to heart failure (HF) manifests as exercise oscillatory ventilation (EOV). Prior descriptions of patients with EOV have not been controlled and have been limited to subjects with left ventricular ejection fraction (LVEF) of <or= 0.40. The aim of this study was to compare clinical characteristics including ventilatory responses of subjects with EOV to those of control subjects with HF matched for LVEF. Subjects (n = 47) were retrospectively identified from 1,340 consecutive patients referred for cardiopulmonary exercise testing. Study inclusion required EOV without consideration of LVEF while control subjects (n = 47) were composed of HF patients with no EOV matched for LVEF. Characteristics for each group were summarized and compared. For EOV subjects, the mean LVEF was 0.37 (range, 0.11 to 0.70), and 19 subjects (41%) had an LVEF of >or= 0.40. Compared to control subjects, EOV subjects had increased left atrial dimension, mitral E-wave velocity, and right heart pressures as well as decreased exercise tidal volume response, functional capacity, rest and exercise end-tidal carbon dioxide, and increased ventilatory equivalent for carbon dioxide and dead space ventilation (all p < 0.05). Multivariate analysis demonstrated atrial fibrillation (odds ratio, 6.7; p = 0.006), digitalis therapy (odds ratio, 0.27; p = 0.02), New York Heart Association class (odds ratio, 3.5; p = 0.0006), rest end-tidal carbon dioxide (odds ratio, 0.87; p = 0.005), and peak heart rate (odds ratio, 0.98; p = 0.02) were independently associated with EOV. Patients with EOV have clinical characteristics and exercise ventilatory responses consistent with more advanced HF than patients with comparable LV systolic function; EOV may occur in HF patients with an LVEF of >or= 0.40.

275: Preferential Improvement in Exercise Time, Oxygen Consumption and Ventilatory Response in Patients Supported with Pneumatic Versus Electric LVADs

275: Preferential Improvement in Exercise Time, Oxygen Consumption and Ventilatory Response in Patients Supported with Pneumatic Versus Electric LVADs

Short-term modulation of the exercise ventilatory response in young men

Arterial isocapnia is a hallmark of moderate exercise in humans and is maintained even when resting arterial Pco(2) (Pa(CO(2))) is raised or lowered from its normal level, e.g., with chronic acid-base changes or acute increases in respiratory dead space. When resting ventilation and/or Pa(CO(2)) are altered, maintenance of isocapnia requires active adjustments of the exercise ventilatory response [slope of the ventilation (Ve)-CO(2) production (Vco(2)) relationship, DeltaVe/DeltaVco(2)]. On the basis of animal studies, it has been proposed that a central neural mechanism links the exercise ventilatory response to the resting ventilatory drive without need for changes in chemoreceptor feedback from rest to exercise, a mechanism referred to as short-term modulation (STM). We tested the hypothesis that STM is elicited by increased resting ventilatory drive associated with added external dead space (DS) in humans. Twelve young men were studied in control conditions and with added DS (200, 400, and 600 ml; randomized) at rest and during mild-to-moderate cycle exercise. DeltaVe/DeltaVco(2) increased progressively as DS volume increased (P < 0.0001). While resting end-tidal Pco(2) (Pet(CO(2))) increased with DS, the change in Pet(CO(2)) from rest to exercise was not increased, indicating that increased chemoreceptor feedback from rest to exercise cannot account for the greater exercise ventilatory response. We conclude that STM of the exercise ventilatory response is induced in young men when resting ventilatory drive is increased with external DS, confirming the existence of STM in humans.

Improvement in Quadriceps Muscle Strength and Fucntional Capacities after a 3-month home-based Endurance Training in Lung Transplant Recipients

Background: Peripheral muscle dysfunction and reduced exercise capacity are well recognized in lung transplant recipients (LTR) in spite of improved lung function. However, the effect of exercise training in this specific population is still poor studied. We investigated the benefits of training on muscle function and cardio-ventilatory response during exercise in LTR. &#x0D; &#x0D; Methods: Twelve patients after lung transplantation (FEV1: 74 ± 24 % of predicted value) and 12 healthy subjects (C) were studied before and after a 3-month home-based endurance training. Quadriceps strength and fatigability were assessed by maximal twitch tension (TwQ) using magnetic stimulation of the femoral nerve and fiber diameters were obtained after biopsy of the vastus lateralis. Cardio-ventilatory responses were measured during both maximal and constant workload (W) cycle exercise and quality of life was assessed by the Chronic Respiratory Questionnaire. &#x0D; &#x0D; Results: At baseline, LTR had lower percentage of type I fibers, TwQ, Wmax, VO2max, VEmax and endurance time than C (&lt; 50% of C each). After training, significant improvement in TwQ (+44 ± 26 N), Wmax (+13 ± 19 W), endurance time (+11.5 ± 11.1 min) and dyspnea score (CRQdyspnea: +3.1 ± 4.4 points) were observed in LTR (p &lt; 0.05). Furthermore, VE was reduced at submaximal (VE at ventilatory threshold: -4.5 ± 6.8 L/min) and constant (65% Wmax) exercise (-6.4 ± 5.2 L/min) (P &lt; 0.05). Decrease in exercise-induced fatigability correlated with decrease in VE at initial maximal workload in LTR (r = 0.72, P = 0.06) and in LTR + C (r = 0.56, P = 0.02) and increase in TwQ correlated to increase in CRQdyspnea in LTR (r = 0.74, P = 0.04). &#x0D; &#x0D; Conclusion: Gains in exercise capacity and in quadriceps strength were observed after endurance training in LTR. The latter may have been involved in improving exercise ventilatory response and dyspnea, supporting the benefit of peripheral muscle strength improvement in exercise tolerance in LTR and even the larger field of chronic respiratory diseases.

The exercise ventilatory response does not differ between obese women with and without dyspnea on exertion

We tested the hypothesis that the exercise ventilatory response (EVR) differed between otherwise healthy obese women with and without dyspnea on exertion (DOE). In fourteen obese women we determined EVR (defined as slope of VE vs. VCO2) during cycling at 30W and 60W, O2 cost of breathing (from measurements of VO2 and VE at rest and during eucapnic voluntary hyperpnea at 40 and 60 L/min; slope was calculated in ml/L) and O2 uptake of the respiratory muscles (VO2RESP) at 30W and 60W (calculated from O2 cost multiplied by VE at each exercise level). Subjects were grouped according to RPB (Borg 0–10) during cycling at 60W (Control, n = 7, RPB ≤ 2; DOE, n = 7, RPB ≥ 4). Age, ht, wt and % body fat were similar between groups. RPB and O2 cost of breathing were significantly higher in DOE than Control (p<0.05). The EVR at 30W and 60W was similar between groups. VO2RESP was significantly higher in DOE than Control at 30W and 60W (30W 66±19 and 37±6, 60W 115±44 and 63±12 ml/min, respectively; p<0.02). There were significant correlations between RPB at 60W and VO2RESP at 30W and 60W (30W r = 0.91, 60W r = 0.88; p<0.01). The EVR did not differ between groups, and hence did not appear to account for the DOE. However, VO2RESP during exercise was significantly higher in obese women with DOE, suggesting that VO2RESP may play an important role in DOE. Support: American Heart Association, The King Foundation, The Cain Foundation, Presbyterian Hospital of Dallas

Short‐term modulation of the exercise ventilatory response in humans

Short‐term modulation of the exercise ventilatory response in humans

Layers of exercise hyperpnea: Modulation and plasticity

Despite the fundamental biological significance of the ventilatory response to mild or moderate physical activity (the exercise hyperpnea), we still know remarkably little concerning its underlying mechanisms. Part of the difficulty in revealing those mechanisms may arise due to confusion between multiple mechanistic layers, each contributing to the impressive degree of regulation achieved. The primary, feedforward exercise stimulus or stimuli increase ventilation in approximate proportion to changes in metabolic rate. Chemoreceptor feedback then minimizes deviations from optimal blood gas regulation, most often preventing excessive hypocapnia in non-human mammals. Recent evidence has accumulated, suggesting that adaptive control strategies including modulation and plasticity may adjust the feedforward and/or feedback contributions when blood gas homeostasis proves inadequate. In this review, we present evidence from a goat model of exercise hyperpnea concerning the existence of modulation and plasticity, and specifically mechanisms known as short-term and long-term modulation of the exercise ventilatory response. Throughout the review, we consider available evidence concerning the relevance of these mechanisms to humans. Plasticity is a property only recently recognized in the neural system subserving respiratory control, and the application of these concepts to the exercise ventilatory response in humans is in its infancy. Modulation and plasticity may confer an ability of individuals to adapt their exercise ventilatory response so that it remains appropriate in the face of life-long changes in endogenous (e.g. development, aging, onset of disease) or exogenous (e.g. altitude, wearing a breathing apparatus during physical exertion) physiological conditions.