Exercise-Induced Blood Lactate Increase Does Not Change Red Blood Cell Deformability in Cyclists

Abstract

BackgroundThe effect of exercise-induced lactate production on red blood cell deformability and other blood rheological changes is controversial, given heavy-exercise induces biochemical processes (e.g., oxidative stress) known to perturb haemorheology. The aim of the present study was to examine the haemorheological response to a short-duration cycling protocol designed to increase blood lactate concentration, but of duration insufficient to induce significant oxidative stress.MethodsMale cyclists and triathletes (n = 6; 27±7 yr; body mass index: 23.7±3.0 kg/m2; peak oxygen uptake 4.02±0.51 L/min) performed unloaded (0 W), moderate-intensity, and heavy-intensity cycling. Blood was sampled at rest and during the final minute of each cycling bout. Blood chemistry, blood viscosity, red blood cell aggregation and red blood cell deformability were measured.ResultsBlood lactate concentration increased significantly during heavy-intensity cycling, when compared with all other conditions. Methaemoglobin fraction did not change during any exercise bout when compared with rest. Blood viscosity at native haematocrit increased during heavy-intensity cycling at higher-shear rates when compared with rest, unloaded and moderate-intensity cycling. Heavy-intensity exercise increased the amplitude of red blood cell aggregation in native haematocrit samples when compared with all other conditions. Red blood cell deformability was not changed by exercise.ConclusionAcute exercise perturbs haemorheology in an intensity dose-response fashion; however, many of the haemorheological effects appear to be secondary to haemoconcentration, rather than increased lactate concentration.

Eryptosis and hemorheological responses to maximal exercise in athletes: Comparison between running and cycling

“…6,7,10,21 Although blood viscosity measurements were not performed at 37°C, as recommended, 22 the same exercise blood viscosity responses have been reported at 25°C or 37°C. 8,10,21,25,26 The increase in blood viscosity during cycling may be partly explained by the increase in hematocrit and white blood cell count subsequent to water loss, spleen contraction, and fluid shifts between vascular and tissue compartments. 8,16,27 In contrast, blood viscosity remained unchanged after the progressive and maximal running test compared to resting value, despite a rise in hematocrit and white blood cell count equivalent to the one found during the cycling test.…”

“…8,10,21,25,26 The increase in blood viscosity during cycling may be partly explained by the increase in hematocrit and white blood cell count subsequent to water loss, spleen contraction, and fluid shifts between vascular and tissue compartments. 8,16,27 In contrast, blood viscosity remained unchanged after the progressive and maximal running test compared to resting value, despite a rise in hematocrit and white blood cell count equivalent to the one found during the cycling test. While this finding could seem surprising, it is in agreement with previous studies showing no change in blood viscosity after a marathon 12 or a 10-km running competition performed in the hot and wet environment.…”

“…Most of the studies have been performed during cycling exercises (both submaximal and maximal tests). 7 These works reported an increase in blood viscosity at the end of the exercise mainly in relation with the rise in hematocrit, 8 subsequent to water loss, fluid shift, and the release of spleen trapped RBC 9,10 In contrast and surprisingly, previous studies conducted on running exercises, such as a marathon or a 10-km running competition, did not find any change in blood viscosity. [11][12][13] Authors hypothesized that this lack of change could be due to the absence of hematocrit variations presumably explained by RBC foot strike hemolysis during running.…”

Shear‐thinning behaviour of blood in response to active hyperaemia: Implications for the assessment of arterial shear stress‐mediated dilatation

“…Conceptually, the haematocrit‐to‐blood viscosity ratio is based on the rationale that an increase in circulating erythrocytes is beneficial for arterial oxygen‐carrying capacity, but negatively increases blood viscosity (at a given shear rate) and, in turn, vascular and blood flow resistance (Poiseuille's law) (Crowell & Smith, ). The haemoconcentration that accompanies an acute bout of cycling exercise, secondary to fluid shifts, has been observed to explain directly the hyperviscosity of blood (Simmonds et al., ), while also increasing arterial oxygen content (i.e. haemoglobin concentration; Ahmadizad et al., ).…”

“…The latter point is important given that blood viscosity is measured in vitro at ‘steady‐state’ shear rates in a rotational viscometer. Furthermore, it is known that the determinants of blood viscosity (haematocrit, plasma viscosity, and erythrocyte aggregation and deformability; Baskurt & Meiselman, ) are sensitive to alterations in peripheral and central haemodynamics, such as shear stress and mean arterial blood pressure (Ahmadizad et al., ; Connes, Simmonds, Brun, & Baskurt, ; Simmonds, Atac, Baskurt, Meiselman, & Yalcin, ; Simmonds, Connes, & Sabapathy, ).…”