Effect of Exercise-Induced Reductions in Blood Volume on Cardiac Output and Oxygen Transport Capacity

Abstract

We wanted to demonstrate the relationship between blood volume, cardiac size, cardiac output and maximum oxygen uptake (V.O2max) and to quantify blood volume shifts during exercise and their impact on oxygen transport. Twenty-four healthy, non-smoking, heterogeneously trained male participants (27 ± 4.6 years) performed incremental cycle ergometer tests to determine V.O2max and changes in blood volume and cardiac output. Cardiac output was determined by an inert gas rebreathing procedure. Heart dimensions were determined by 3D echocardiography. Blood volume and hemoglobin mass were determined by using the optimized CO-rebreathing method. The V.O2max ranged between 47.5 and 74.1 mL⋅kg–1⋅min–1. Heart volume ranged between 7.7 and 17.9 mL⋅kg–1 and maximum cardiac output ranged between 252 and 434 mL⋅kg–1⋅min–1. The mean blood volume decreased by 8% (567 ± 187 mL, p = 0.001) until maximum exercise, leading to an increase in [Hb] by 1.3 ± 0.4 g⋅dL–1 while peripheral oxygen saturation decreased by 6.1 ± 2.4%. There were close correlations between resting blood volume and heart volume (r = 0.73, p = 0.002), maximum blood volume and maximum cardiac output (r = 0.68, p = 0.001), and maximum cardiac output and V.O2max (r = 0.76, p < 0.001). An increase in maximum blood volume by 1,000 mL was associated with an increase in maximum stroke volume by 25 mL and in maximum cardiac output by 3.5 L⋅min–1. In conclusion, blood volume markedly decreased until maximal exhaustion, potentially affecting the stroke volume response during exercise. Simultaneously, hemoconcentrations maintained the arterial oxygen content and compensated for the potential loss in maximum cardiac output. Therefore, a large blood volume at rest is an important factor for achieving a high cardiac output during exercise and blood volume shifts compensate for the decrease in peripheral oxygen saturation, thereby maintaining a high arteriovenous oxygen difference.

The Effects of Sodium Phosphate Supplementation on the Cardiorespiratory System and Gross Efficiency during Exercise under Hypoxia in Male Cyclists: A Randomized, Placebo-Controlled, Cross-Over Study

“…Since the SV is also largely determined by blood volume [27,62], it is possible that an increase in SV after SP supplementation results from an increase in PV caused by an increase in serum sodium concentration [63,64]. During our experiment, blood sodium concentration was not determined.…”

Preoperative Hemoglobin Level, Oxygen Saturation and Postoperative Outcomes in Children With Cyanotic Congenital Heart Disease: A Propensity-Score Matching Analysis

“…However, this regression equation was restricted to children with sufficient iron stores and oxygen saturation >75% (21). Based on the theory of an inverse relationship between the severity of compensatory erythrocytosis and resting oxygen saturation (14) and the estimation formula of CaO 2 (18), we presumed that the value of preoperative Hb × SpO 2 can evaluate whether cyanotic children achieved adequate Hb compensation. If the value of preoperative Hb × SpO 2 of cyanotic children was below the lower limit of normal Hb of each age group, this indicated that the preoperative Hb concentration was not sufficient to obtain similar CaO 2 to healthy children, and preoperative anemia would be considered.…”

“…Physically dissolved oxygen is rare, and noninvasive SpO 2 could replace invasive arterial oxygen saturation (SaO 2 ) tests (18), so the arterial oxygen content (CaO 2 ) for blood with normal Hb quality could be estimated according to the formula: CaO 2 (ml/dl) = 1.39(ml/g)×Hb(g/dl)×SpO 2 (%)÷100 (a)…”

Nedocromil sodium and diphenhydramine HCl ameliorate exercise‐induced arterial hypoxemia in highly trained athletes

“…Recent data from Durand et al (Durand et al, 2020 ) found that athletes with EIAH had higher PAPs than similarly trained athletes without EIAH, further supporting a hemodynamic initiating mechanism of EIAH in this cohort. Additionally, Schierbauer and colleagues found that, when corrected for body mass, maximal Q̇ C , but not V̇O 2max , was correlated with the decline in S p O 2 from rest to maximal exercise ( Schierbauer et al, ). It is possible that the highly trained subjects in our study approached maximal Q̇ C values meeting or, more likely, exceeding 30–35 L·min −1 (Table 1 ) (Zhou et al, 2001 ).…”

“…This could be exacerbated by the considerably larger Q̇ C values of trained athletes (Ekblom & Hermansen, 1968 ; Zhou et al, 2001 ), and it has been demonstrated that intense exercise can cause stress failure of the BGB in this population (Hopkins et al, 1997 ). Indeed, recent data demonstrated that, when corrected for body mass, maximal Q̇ C , but not V̇O 2max , was correlated with the decline in S p O 2 from rest to maximal exercise ( Schierbauer et al, ). These observations suggest that extravascular fluid may accumulate in the interstitium of the lung, at least transiently, enough so that decreases in S a O 2 during exercise are evident until the pulmonary lymphatics can clear the interstitial space of the excess fluid post‐exercise (McKenzie et al, 2005 ).…”