Sickle cell anemia (SCA) is a hemoglobinopathy leading to major hematologic, hemorheologic, and hemodynamic disorders that induce various complications, including organ failure, and ultimately lead to death. Here, we assessed for the first time repercussions of SCA on skeletal muscle and its microvasculature. Twenty-seven sedentary Cameroonian volunteer men participated in the study. They were assigned to one of three groups according to their hemoglobin status (healthy control subjects, n = 10; sickle cell trait carriers, n = 10; and SCA patients, n = 7) and underwent muscle biopsy of the vastus lateralis. SCA was associated with microvessel rarefaction, decrease in capillary tortuosity, and widening of microvessel diameter. The absence of capillary wall reinforcement was shown by lack of wall thickening and lack of fibrous tissue or smooth muscle in their constitution. We also observed changes in fiber type distribution, muscle atrophy, an increase in satellite cell number, and a decrease in activity of creatine kinase and several oxidative enzymes. No signs of tissue necrosis, inflammatory stress, fibrosis, or segmented fibers were observed. The present study highlighted marked effects of SCA on microvascular, structural, and energetic characteristics of skeletal muscle.

Arterial blood lactate concentrations were measured on 19 subjects before, during, and after a 3-min bicycle exercise at several work rates, and the concentrations during the recovery phases were fitted to a biexponential time function consisting of a rapidly increasing and a slowly decreasing component. Highly significant correlations with the work rate of the exercise preceding the recovery were found for all the parameters of the fitted equation. The two velocity constants show inverse linear relationships, whereas the other parameters vary according to a definite power function. A functional meaning has been given to the two velocity constants, namely the ability of the tissues to exchange and to remove lactate. For the group of subjects studied, after exercises at work rates below about 3.5 W/kg, the tissue's ability to utilize, and possibly to exchange lactate, increases over values generally reported for resting conditions, whereas after exercises at higher work rates the inverse occurs. Lactate kinetics during recovery appear to be the result of two underlying processes, one enhancing the ability of the tissues to exchange and remove lactate and the other restraining it.

The influence of sickle cell trait and/or α-thalassemia on skeletal muscle microvascular network characteristics was assessed and compared with control subjects [hemoglobin (Hb) AA] in 30 Cameroonian residents [10 HbAA, 5 HbAA α-thalassemia (α-t), 6 HbAS, and 9 HbASα-t] matched for maximal work capacity and daily energy expenditure. Subjects performed an incremental exercise to exhaustion and underwent a muscle biopsy. Muscle fiber type and surface area were not different among groups. However, sickle cell trait (SCT) was associated with lower capillary density ( P < 0.05), lower capillary tortuosity ( P < 0.001), and enlarged microvessels ( P < 0.01). SCT carriers had reduced counts of microvessels <5-μm diameter, but a higher percentage of broader microvessels, i.e., diameter >10 μm ( P < 0.05). α-Thalassemia seemed to be characterized by a higher capillary tortuosity and unchanged capillary density and diameter. Thus, while SCT is a priori clinically benign, we demonstrate for the first time that significant remodeling of the microvasculature occurs in SCT carriers. These modifications may possibly reflect protective adaptations against hemorheological and microcirculatory dysfunction induced by the presence of HbS. The remodeling of the microvascular network occurs to a lesser extent in α-thalassemia. In α-thalassemic subjects, increased capillary tortuosity would promote oxygen supply to muscle tissues and might compensate for the lower Hb content often reported in those subjects.

Arterial blood lactate concentrations and pH were measured on seven black male sickle cell trait (SCT) carriers before, during and after incremental exhaustive bicycle exercise (25 W increments per minute) and compared with those of six control individuals of the same ethnic origin having a similar physical fitness level. The object of the experiment was to determine if SCT has an effect on lactate kinetics. At volitional exhaustion which was reached at a comparable overall mean absolute work rate for both groups, oxygen consumption expressed per kilogram body mass was significantly lower for the SCT carriers than for the control volunteers. Lactate concentrations were higher for the SCT carriers after the 150 W exercise step but differences reached statistical significance only at exhaustion. Concentrations were distinctly higher for the SCT group during the following 40 minutes of recovery. While there were no observable differences in blood pH between the SCT and control subjects during the exercise, this variable became significantly lower for the SCT than for the control group 8 minutes after the end of exercise. Lactate recovery curves were fitted by a biexponential time function where the two velocity constants inform on the body's overall ability to exchange and remove lactate. The ability to remove lactate was comparable for the two groups. The present results do not warrant drawing a definite conclusion on impairment of the ability to exchange lactate in the presence of SCT. However, SCT carriers are likely to produce more lactate than control subjects reaching exhaustion at similar mean absolute work rate during exhaustive incremental bicycle exercise.

Venous blood lactate concentrations [1ab] were measured every 30 s in five athletes performing prolonged exercise at three constant intensities: the aerobic threshold (Thaer), the anaerobic threshold (Than) and at a work rate (IWR) intermediate between Thaer and Than. Measurements of oxygen consumption (VO2) and heart rate (HR) were made every min. Most of the subjects maintained constant intensity exercise for 45 min at Thaer and IWR, but at Than none could exercise for more than 30 min. Relationships between variations in [1ab] and concomitant changes in VO2 or HR were not statistically significant. Depending on the exercise intensity (Thaer, IWR, or Than) several different patterns of change in [1ab] have been identified. Subjects did not necessarily show the same pattern at comparable exercise intensities. Averaging [1ab] as a function of relative exercise intensity masked spatial and temporal characteristics of individual curves so that a common pattern could not be discerned at any of the three exercise levels studied. The differences among the subjects are better described on individual [1ab] curves when sampling has been made at time intervals sufficiently small to resolve individual characteristics.