HbO2 dissociation in man during prolonged work in chronic hypoxia

Dempsey, Jerome A.; Thomson, J. M.; Forster, H. V.; Cerny, F. C.; Chosy, L. W.

doi:10.1152/jappl.1975.38.6.1022

Cited by 28 publications

(14 citation statements)

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“…These results speak against the hypothesis than an exercise-induced tissue hypoxia causes the lactate release seen during exercise in normal subjects, since that lactate release occurs even at venous oxygen pressures that are clearly quite higher than in the present two subjects. The im- portance of tissue hypoxia in lactate production during exercise in man has also been questioned by others (37,38).…”

Section: Discussionmentioning

confidence: 99%

Tissue oxygenation and muscular substrate turnover in two subjects with high hemoglobin oxygen affinity.

Wranne¹,

Berlin²,

Jorfeldt³

et al. 1983

J. Clin. Invest.

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A B S T R A C T Oxygen transport to and substrate turnover in leg muscle were studied at rest and during light and heavy upright bicycle exercise in two brothers with a hereditary hemoglobinopathy associated with high oxygen affinity (P50 = 13 mmHg). Femoral venous oxygen tension was below normal and femoral venous oxygen saturation above normal at rest and during exercise. Thus, the arterial-femoral venous oxygen saturation difference was decreased. Despite a compensatory increase in hemoglobin concentration, the arterial-femoral venous oxygen content difference tended to be below normal at heavy exercise. Approximately 25% of the oxygen was delivered via the abnormal hemoglobin at relative heavy exercise. Arterial lactate levels, lactate release, and muscle lactate concentration were not increased at any level of exercise. Glucose, alanine, pyruvate, and glycerol turnover were essentially normal, but the glycogen and creatine phosphate stores were abnormally depleted at the termination of heavy exercise. The exercise electrocardiogram (ECG) was normal, indicating that myocardial oxygenation was adequate. Muscle-surface oxygen pressure fields were normal at rest (not investigated during exercise). It is concluded that the high oxygen affinity of the hemoglobin in our two subjects did not lead to heart or skeletal muscle hypoxia during heavy exercise, as judged from the ECG and from the leg lactate turnover. Despite the lack of evidence for muscle hypoxia, the subjects experienced leg muscle fatigue and the creatine phosphate and glycogen stores were depleted more than normally.

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Section: Discussionmentioning

confidence: 99%

Tissue oxygenation and muscular substrate turnover in two subjects with high hemoglobin oxygen affinity.

Wranne¹,

Berlin²,

Jorfeldt³

et al. 1983

J. Clin. Invest.

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“…The target venous P O 2 corresponding to the calculated S vO 2 was considered to be the mixed venous P O 2 in the case of a normal P 50 . It is assumed that any right shift in the O 2 -haemoglobin dissociation curve as a result of acidosis and hyperthermia in the exercising muscles is similar in subjects with variant and with normal Hb (Thomson et al 1974;Dempsey et al 1975;Dempsey et al 1984;Dempsey & Wagner, 1999).…”

Section: Mathematical Modellingmentioning

confidence: 99%

“…There are certainly differences and challenges of in vivo vs. in vitro measurements of the oxygen dissociation curve dynamics at both the lungs and muscles in response to variables such as temperature, pH, and 2,3-biphosphoglycerate. J Physiol 597.16 A few studies (Thomson et al 1974;Dempsey et al 1975;Dempsey et al 1984;Calbet et al 2015b) show that the additive effects of temperature and pH are responsible for shifting the oxygen dissociation curve affinity, especially with prolonged exercise. However, it is still not well understood how significant of contribution this makes to oxygen delivery and exchange.…”

Section: Limitations Of Our Modelmentioning

confidence: 99%

Modelling the relationships between haemoglobin oxygen affinity and the oxygen cascade in humans

Shepherd

Dominelli

Roy

et al. 2019

The Journal of Physiology

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Key points Haemoglobin affinity is an integral concept in exercise physiology that impacts oxygen uptake, delivery and consumption. How chronic alterations in haemoglobin affinity impact physiology is unknown. Using human haemoglobin variants, we demonstrate that the affinity of haemoglobin for oxygen is highly correlated with haemoglobin concentration. Using the Fick equation, we model how altered haemoglobin affinity and the associated haemoglobin concentration influences oxygen consumption at rest and during exercise via alterations in cardiac output and mixed‐venous PnormalO2. The combination of low oxygen affinity haemoglobin and reduced haemoglobin concentration seen in vivo may be unable to support oxygen uptake during moderate or heavy exercise. Abstract The physiological implications, with regard to exercise, of altered haemoglobin affinity for oxygen are not fully understood. Data from the Mayo Clinic Laboratories database of rare human haemoglobin variants reveal a strong inverse correlation (r = −0.82) between blood haemoglobin concentration and P50, an index of oxygen affinity [Hb = −0.3135(P50) + 23.636]. In the present study, observed P50 values for high, normal and low oxygen‐affinity haemoglobin variants (13, 26 and 39 mmHg) and corresponding haemoglobin concentrations (19.5, 15.5 and 11.4 g dL−1 respectively) are used to model oxygen consumption as a fraction of delivery at rest (V̇O2 = 0.25 L min−1, cardiac output = 5.70 L min−1) and during exercise (V̇O2 = 2.75 L min−1, cardiac output = 18.9 l min−1). With high‐affinity haemoglobin, the model shows that normal levels of oxygen consumption can be achieved at rest and during exercise at the assumed cardiac output levels, with reduced oxygen extraction both at rest (16.8% high affinity vs. 21.7% normal) and during exercise (55.8% high affinity vs. 72.2% normal). With low‐affinity haemoglobin, which predicts low haemoglobin concentration, oxygen consumption at rest can be sustained with the assumed cardiac output, with increased oxygen extraction (31.1% low affinity vs. 21.7% normal). However, exercise at 2.75 l min−1 cannot be achieved with the assumed cardiac output, even with 100% oxygen extraction. In conclusion, the model indicates chronic alterations in P50 associate directly with Hb concentration, highlighting that human Hb variants can serve as ‘experiments of nature’ to address fundamental hypotheses on oxygen transport and exercise.

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“…19 Heavy exercise at 3100 m induces a further increase in the P 50 to approximately 38 mm Hg, a response similar to that at sea level. 29 This seemingly paradoxical increase may be beneficial at rest or during submaximal exercise, as long as oxygen loading can be maintained by raising the alveolar oxygen tension through ventilatory stimulation. 30 However, under conditions of severe hypoxia or at extremely high altitude, hyperventilation cannot adequately augment the alveolar oxygen tension, but the associated respiratory alkalosis causes a large decrease in P 50 .…”

Section: Adaptation To High Altitudementioning

confidence: 99%