Role of the carotid bodies in the respiratory compensation for the metabolic acidosis of exercise in humans.

Rausch, Stefan; Whipp, Brian J.; Wasserman, Karlman; Huszczuk, A

doi:10.1113/jphysiol.1991.sp018894

Cited by 67 publications

(44 citation statements)

References 23 publications

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“…The strategy utilized by Rausch, Whipp, Wasserman & Huszczuk (1991) for normalizing the intensity of cycle ergometer exercise in terms of the degree of metabolic-acidaemic stress, AE-LE protocol (left) in the same subject; the response from Bout 2 of the AE-LE protocol (0) is superimposed upon that of Bout 1 of the LE-LE protocol (0) (right). Note the slower Vco response profile for Bout 2, in contrast to the initial LE work bout, consistent with a smaller exercise-induced lactic acidaemia; this effect is more marked for the LE-LE protocol than for the AE-LE protocol.…”

Section: Discussionmentioning

confidence: 99%

Effects of prior arm exercise on pulmonary gas exchange kinetics during high‐intensity leg exercise in humans

Bohnert

Ward

Whipp

1998

Experimental Physiology

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SUMMARYFor moderate work rates (i.e. below the lactate threshold, OL), oxygen uptake (VO2) approaches the steady state mono-exponentially. At higher work rates, the VO2 kinetics are more complex, reflecting the delayed superimposition of an additional, slow component. The mechanisms of this 'slow' component are poorly understood. It has been demonstrated, however, that while a prior bout of supra-OL cycling (with a 6 min recovery) does not significantly affect the VO. time course for a subsequent sub-OL bout, it significantly speeds the VO2 response to a subsequent supra-OL bout (Gausche, Harmon, Lamarra & Whipp, 1989;Gerbino, Ward & Whipp, 1996). These investigators proposed that this speeding was a result of improved muscle perfusion during the exercise transient, possibly related to the residual metabolic acidaemia still present at the start of the subsequent exercise bout. To determine whether speeding of the VO2 kinetics could also be induced by a bout of prior high-intensity exercise performed at a remote site (e.g. the arms), subjects each performed two 6 min bouts of high-intensity cycling (leg exercise: LE) at a work rate equivalent to 50% of 'ALE' (the difference between maximum 1VO2LE and oLLE). On one occasion this was preceded by a 6 min period of cycling at 50 % ALE and, on another, by a similar period of arm-crank exercise (arm exercise: AE) at 50% AAE; in each case, the work bouts were separated by 6 min of unloaded pedalling. Pulmonary gas exchange variables were derived breath-by-breath. During unloaded pedalling and at minute 6 of each work bout, arterialized venous blood samples were drawn from the dorsum of the heated hand or at the wrist for analysis of pH, lactate, pyruvate, noradrenaline (NAdr), adrenaline (Adr), and potassium (K+). The difference in V02 between minute 6 and 3 of each work bout (AVO ) and the 'partial' 02 deficit (02 Def) provided indices of the slow phase of V02 kinetics. The initial AE and LE bouts resulted in similar degrees of metabolic (lactic) acidaemia; the residual acidaemia at the end of the subsequent 6 min recovery phase was also similar for the two protocols, as were [K+], [Adr] and [NAdr]. The subsequent LE bouts were associated with reductions in both A1!02, and 02 Def, relative to control, with the effect being more marked when the work was preceded by a prior LE bout than a prior AE bout: AV02, averaging 32 and 56 % of control, respectively, and 02 Def 71 and 81 %. Consequently, the increase in [lactate] and decrease in pH induced in this second LE bout were smaller when preceded by prior leg exercise than prior arm exercise. It is therefore concluded that while metabolic acidaemia induced at a site remote from the legs is associated with a less prominent slow phase of the V0 kinetics for high-intensity leg exercise, a component specific to the involved contractile units appears to exert the dominant effect. The mechanisms underlying this response are, however, presently uncertain.

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Section: Discussionmentioning

confidence: 99%

Effects of prior arm exercise on pulmonary gas exchange kinetics during high‐intensity leg exercise in humans

Bohnert

Ward

Whipp

1998

Experimental Physiology

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“…In addition, PaCO 2pred during IE 2nd was significantly lower than that during IE 1st . Although these observations concerning blood acid-base balance suggest that ventilatory chemoreflex via central and peripheral chemoreceptors (Rausch et al 1991;Ward 1994;Ward 2007) and perhaps via muscle afferents (Oelberg et al 1998) (Yamanaka et al 2012). We observed a significant increase in ESL from IE 1st to IE 2nd .…”

Section: Discussionmentioning

confidence: 97%

“…This hyperventilatory response is considered to be respiratory compensation to minimize a decrease in blood pH (Kowalchuk et al 1988;Rausch et al 1991;Ward 2007;Wasserman et al 1986;Yunoki et al 1999), and the decrease in blood pH per se has been regarded as an important factor enhancing ventilation during exercise above the lactate threshold (Stringer et al 1992;Wasserman et al 1975). However, by using a glycogen-reduction procedure (Gollnick et al 1974;Heigenhauser et al 1983; Sabapathy et al 2006), which can manipulate the degree of metabolic acidosis, we found that hyperventilatory response to IE is not dependent on blood pH but is associated with effort sense of exercising muscle (Yamanaka et al 2011;Yamanaka et al 2012).…”

Section: Introductionmentioning

confidence: 99%

Relationship between motor corticospinal excitability and ventilatory response during intense exercise

et al. 2016

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2 Abstract PurposeEffort sense has been suggested to be involved in the hyperventilatory response during intense exercise (IE). However, the mechanism by which effort sense induces an increase in ventilation during IE has not been fully elucidated. The aim of this study was to determine the relationship between effort-mediated ventilatory response and corticospinal excitability of lower limb muscle during IE. MethodsEight subjects performed 3 min of cycling exercise at 75-85% of maximum workload twice (IE 1st and IE 2nd ). IE 2nd was performed after 60 min of resting recovery following 45 min of submaximal cycling exercise at the workload corresponding to ventilatory threshold. Vastus lateralis muscle response to transcranial magnetic stimulation of the motor cortex (motor evoked potentials, MEPs), effort sense of legs (ESL, Borg 0-10 scale), and ventilatory response were measured during the two IEs. ResultsThe slope of ventilation (l/min) against CO 2 output (l/min) during IE 2nd (28.0 ± 5.6) was significantly greater than that (25.1 ± 5.5) during IE 1st . Mean ESL during IE was significantly higher in IE 2nd (5.25 ± 0.89) than in IE 1st (4.67 ± 0.62). Mean MEP (normalized to maximal M-wave) during IE was significantly lower in IE 2nd (66 ± 22%) than in IE 1st (77 ± 24%). The difference in mean ESL between the two IEs was significantly (p < 0.05, r = -0.82) correlated with the difference in mean MEP between the two IEs. ConclusionsThe findings suggest that effort-mediated hyperventilatory response to IE may be associated with a decrease in corticospinal excitability of exercising muscle.

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“…It follows that in individuals with higher HVR, the fall in pH due to lactic acidosis at a given level of heavy work rate would be restricted to a smaller extent because compensatory hyperventilation could start at lower levels of work rate as compared with individuals with lower HVR. Rausch et al [29] have evidenced the importance of the carotid chemoreceptor sensitivity in constraining the fall of arterial pH by demonstrating a more rapid restoration of arterial pH toward the normal level during heavy exercise while breathing 12% O 2 and a slower restoration while breathing 80% O 2 as compared to restoration while breathing air.…”

Section: Discussionmentioning

confidence: 99%

Respiratory Compensation Point during Incremental Exercise as Related to Hypoxic Ventilatory Chemosensitivity and Lactate Increase in Man.

Takano

2000

JJP

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During incremental exercise in normal humans, pulmonary ventilation (V E) linearly increases with increasing O 2 uptake (V O 2 ), but the increment of V E against V O 2 becomes steeper at two V O 2 points [1]. The first inflection point, occurring at a lower V O 2 , is termed the ventilatory threshold (VT) [2], above which various kinds of ventilatory stimuli such as a fall in arterial pH due to lactic acidosis, hyperkalemia and augumentation of arterial PCO 2 oscillation are newly induced [3][4][5][6]. With further increases in the ventilatory stimuli as exercise becomes heavier, a steeper increase in V E against V O 2 occurs. The V O 2 point of the onset of this V E augmentation is termed the respiratory compensation point (RCP), above which the V E augmentation (hyperventilation) induces a fall in arterial PCO 2 , with resulting constraint of further falls of arterial pH due to severer lactic acidosis [7]. Peripheral chemoreceptors have been implicated as the site at which the ventilatory stimuli act because of the absence of compensatory hyperventilation and subsequent fall in PCO 2 during heavy exercise in carotid body-resected patients [8,9]. Japanese Journal of Physiology, 50, 449-455, 2000 Key words: heavy exercise, respiratory compensation point, exercise hyperpnea, carotid body, lactic acidosis. Abstract:The pulmonary ventilation-O 2 uptake (V E-V O 2 ) relationship during incremental exercise has two inflection points: one at a lower V O 2 , termed the ventilatory threshold (VT); and another at a higher V O 2 , the respiratory compensation point (RCP). The individuality of RCP was studied in relation to those of the chemosensitivities of the central and peripheral chemoreceptors, which were assessed by resting estimates of hypercapnic ventilatory response (HCVR) and hypoxic ventilatory response (HVR), respectively, and the rate of lactic acid increase during exercise, which was estimated as a slope difference (⌬slope) between a lower slope of V CO 2 -V O 2 relationship (V CO 2 : CO 2 output) obtained at work rates below VT and a higher slope at work rates between VT and RCP. Twenty-two male and sixteen female subjects underwent a 1 min incremental exercise test until exhaustion, in which VT, RCP and ⌬slope were determined. All measures were normalized for body surface area. In the males, the individual difference in RCP was inversely correlated with those of HVR and ⌬slope (pϽ0.05), and in the females, similar tendencies persisted, while the correlation did not reach statistically significant levels (0.05ϽpϽ 0.1). There was no significant correlation between RCP and HCVR in either sex. A multiple linear regression analysis showed that 40 to 50% of the variance of RCP was accounted for by those of HVR and ⌬slope, both of which were related linearly and additively to RCP, this relation being manifested in the males but not in the females without consideration of the menstrual cycle. These results suggest that the individuality of RCP depends partly on the chemosensitivity of the carotid bodies and th...

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Role of the carotid bodies in the respiratory compensation for the metabolic acidosis of exercise in humans.

Cited by 67 publications

References 23 publications

Effects of prior arm exercise on pulmonary gas exchange kinetics during high‐intensity leg exercise in humans

Effects of prior arm exercise on pulmonary gas exchange kinetics during high‐intensity leg exercise in humans

Relationship between motor corticospinal excitability and ventilatory response during intense exercise

Respiratory Compensation Point during Incremental Exercise as Related to Hypoxic Ventilatory Chemosensitivity and Lactate Increase in Man.

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