RESUMEN

Exercise training is known (1) to enhance the function of the GH-IGF-I system, which has profound effects on body fluid status; (2) to increase blood fluidity. Thus, we investigated during an exercise-test in 39 male elite sportsmen (age 23.7+/-0.72 years; body mass index 23.7+/-0.28 kg/m2) the possible relationships between GH and IGF-I status and the rheological properties of blood. Two correlations indicate a relationship between body hydration and fitness: isometric handgrip strength is correlated with the percentage of extracellular water in total body water (r = 0.432, p = 0.02) and the aerobic working capacity W170 is negatively correlated with hematocrit (r = -0.341, p = 0.039). Water loss during exercise appears to be inversely related to fitness as evaluated by W170 (r = -0.529, p = 0.05), and is positively correlated with the score of signs of overtraining (r = 0.725, p = 0.003) and with the red blood cell aggregation index (r = 0.584, p = 0.036). Finally, while the GH peak value is correlated with the extracellular water volume (r = 0.393, p = 0.02), IGF-I is correlated with blood viscosity (r = 0.546, p = 0.0003), suggesting that when IGF-I values are within the upper quintile (>340 ng/ml) IGF-I may unfavourably affect blood rheology. Among factors of blood viscosity, IGF-I exhibits a borderline correlation (p = 0.05) with "Tk" and the ratio IGF1/IGFBP3 which reflects free circulating IGF-I is correlated with red cell aggregability measured with the Myrenne "M" (r = 0.485, p = 0.014) and S60 (r = 0.396, p = 0.494). These findings confirm the importance of hydration and dehydration as determinants of both blood rheology and exercise performance. Moreover, they suggest that values of IGF-I within the upper quintile are associated with an impairment of blood fluidity, possibly due to a direct effect of IGF-I on red cell deformability and aggregability.

Asunto(s)

RESUMEN

The paradox of hematocrit in exercise physiology is that artificially increasing it by autotransfusion or erythropoietin doping improves VO2 max and performance, while in normal conditions there is a strong negative correlation between hematocrit and fitness, due to a training-induced "autohemodilution". We aimed at investigating: (a) which is the physiological range of hematocrit in highly trained professional footballers; (b) what are the characteristics of athletes with high vs low hematocrit? We determined in 77 healthy male footballers the physiological range (mean +/- sd) of hematocrit: 42.3+/-2.74, (range -2sigma/+2sigma = 36.8-47.8%) thus defining boundaries of quintiles of distribution for this parameter: 40, 41.6, 42.9, 44.6. In another sample of 42 male footballers we compared three groups: lowest quintile (n = 8), highest quintile (n = 5) and the three middle quintiles considered together (n = 29). Athletes in the lowest quintile compared to those in the four other quintiles had a lower value of blood viscosity (-8%, p < 0.01) but this difference disappeared after correction for hematocrit. These subjects with low hematocrit had also higher values of the following parameters: aerobic working capacity (p < 0.01); isometric adductor strength (p = 0.02); crossover point of carbohydrate oxidation (70% carbohydrates/30% lipids) (p < 0.05); insulin like growth factor binding protein 1 (p < 0.0001). Athletes in the highest quintile had higher red cell aggregability (Myrenne index "M1" 8.45+/-0.38 vs 6.82+/-0.62, p < 0.04) and a higher disaggregability threshold gammaD (72.6+/-22.63 vs 44.49+/-1.37, p < 0.01) and a lower percentage of water in fat-free mass (p < 0.02). On the whole sample hematocrit was negatively correlated with aerobic working capacity (W170 r = -0.329, p = 0.007; Wmax (% of expected value) r = -0.552, p = 0.008; VO2 max (% of expected value) r = -0.543, p = 0.009) and with ferritin (r = -0.33, p = 0.031), and positively correlated with the overtraining score (r = 0.352, p = 0.019) which was in turn negatively correlated with ferritin r = -0.312, p = 0.02). Besides, hematocrit behaves as a major determinant of blood viscosity (correlation with blood viscosity r = 0.997, p < 10(-7)) and erythrocyte disaggregability gammaD (r = 0.384, p = 0.03), but the hematocrit/viscosity ratio (h/eta index of O2 delivery) remains maintained almost constant over the range of values studied. These results show that (a) physiological values of hematocrit in these athletes are comprised between 36 and 48%; (b) "low" hematocrit (<40%) was associated with a higher aerobic capacity; (c) subjects with the higher hematocrits (>44.6%) were frequently overtrained and/or iron-deficient, and their blood viscosity (and red cell disaggregability) tended to be increased.

Asunto(s)

RESUMEN

Growth hormone deficiency (GHD) in adults results in alterations of body composition and metabolism associated with a lowered insulin sensitivity and an increased cardiovascular risk. Since hemorheologic disturbances (putative factors of vascular risk) are found in the insulin-resistance syndrome, we investigated blood rheology in 9 adults GHDs (5 men, 4 women; age 37.9+/-4.7 years; body mass index 30.23+/-3.2 kg/m2) compared with 23 lean controls and 37 controls matched for sex, age and body mass index. While this sample of GHDs exhibits the typical metabolic picture of this syndrome (upper body overweight with a waist-to-hip ratio at 0.91+/-0.07; low HDL cholesterol at 1.07+/-0.09 mmol x l(-1); low insulin sensitivity with the minimal model technique at 3.3+/-1.29 min(-1)/(microU/ml) x 10(-4)) they have similar values of blood viscosity at either native or corrected hematocrit, similar hematocrit, similar red cell rigidity viscometric index, similar red cell aggregation parameters than overweight matched controls. There is only a nonsignificant tendency for plasma viscosity to be higher in GHDs: this tendency becomes significant when women are considered alone (GHDs: 1.44+/-0.04 mPa.s; controls: 1.31+/-0.04 mPa.s, p<0.05) while it is no longer found in men. This study suggests that GHDs exhibit the classical hemorheological disturbances of non-GHD individuals with the same degree of obesity. There is no evidence for a further impairment of blood rheology associated with the specific metabolic and endocrine pattern of GHDs that may be involved in their increased vascular risk.

Asunto(s)

Asunto(s)