No abstract

To describe the time course of plasma volume alterations and the changes in the plasma concentrations of hormones regulating water balance in relation to a marathon race, six experienced marathon runners (five men, one women) aged 28 (SD 6) years were studied during and for the 3 days following a treadmill marathon run at 68 (SD 5) percent of maximal oxygen consumption. Haematocrit, haemoglobin, plasma protein (Prot) and electrolyte (Na+, K+) concentration, osmolality (osm), plasma concentrations of renin (Ren), aldosterone (Ald) and atrial natriuretic peptide (ANP) were determined at rest in a sitting position (T(-30)), and then after 30 min in an upright posture (R(0)), while running a marathon at 10 km (R(10)), 30 km (R(30)) and 42.2 km (R end), and after the marathon at 30 min (T(30)), 60 min (T(60)), 120 min (T(120)) and 24 h (TD(+1)), 48 h (TD(+2)) and 72 h (TD(+3)). The changes in plasma volume (PV), Prot, osm and Na+ observed during the race were nonsignificant. Significant increases in plasma concentration of K+ [4.8 (SD 0.6) vs 5.5 (SD 0.6) mmol*1(-1); P <0.01], Ren [38(SD 57) vs 197 (SD 145) pmol*1(-1); P <0.02] and Ald [175 (SD 142) vs 1632 (SD 490) pmol*1(-1); P <0.01] were observed at R(end). A significant increase of ANP (P <0.05) was only found after R(10). Body mass significantly decreased by 2.0 kg (P <0.01) during the race in spite of the ingestion of 1.46 (SD 0.34)1 of a 5 percent glucose solution. Urinary volume and Na+ excretion dropped significantly after the completion of the marathon in comparison with the day before [2600 vs 1452 ml*day(-1)(P <0.02) and 161.3 vs 97.1 mmol*1(-1) (P <0.05)]. At TD(+1) and TD(+2) a significant increase in PV was noted, compared to T(-30). The lack of a decrease in PV during the marathon may have been due to the production of 402 g of metabolic water and by the release of 1280 g of water stored in glycogen complexes in muscle and liver. Thus, the hormone response during the marathon may have been due to the effects of the exercise itself and not to the effects of dehydration. The postmarathon PV expansion may be explained by a protein shift to the intravascular space and by renal sodium retention.

To highlight the influences of age, sex, body mass (mb) and running training on the energy cost of running (Cr) young basketball players [38 boys (BB) and 14 girls (BG), aged 14.2 (SD 0.3) and 12.2 (SD 1.9) years, respectively] were selected to be compared to middle-distance runners [27 men (MR) and 14 women (FR) aged 23.7 (SD 3.4) and 23.9 (SD 4.1) years, respectively]. The Cr was measured during a maximal treadmill test. In each group Cr and body mass (mb) and body height were negatively and significantly correlated. A stepwise regression showed that among both the body dimensions measured, mb was the most important factor in determining the variations of Cr. For the whole group (n = 93) the correlation coefficient was 0.72 (P < 0.0001). For a given mb, there was no significant difference between the Cr of BG, BB and MR: this result would support the hypothesis that the differences in Cr currently attributed to age, running training or sex differences are mainly related to mb. On the other hand, for a given mb, FR showed a significantly lower Cr than the basketball players (P < 0.01 for BG and BB) and than MR (P < 0.05), thus suggesting that women decrease their Cr as a response to running training more efficiently than do men.

An increased carotid arterial intima-media thickness (IMT) has been reported in hypopituitary adults untreated for GH deficiency. In the present study, the effect of GH replacement on IMT and cardiovascular risk factors was prospectively investigated, in GH deficiency patients treated at a mean dose of 1 UI/day during 1 yr (n = 22) and 2 yr (n = 11). The IMT measurements were performed by the same experienced physician, and the coefficient of variation (calculated in two control groups) was below 6.5%. IMT at baseline was related to conventional risk factors. After 1 yr GH treatment, IMT decreased from 0.78 +/- 0.03 mm to 0.70 +/- 0.03 mm (P < 0.001). The decrement was observed in 21 of 22 patients. After 2 yr GH treatment, IMT had stabilized at 0.70 +/- 0.04 mm and remained significantly different from baseline values (P < 0.003). GH treatment resulted in a moderate decrease in waist circumference and body fat mass and an increase in VO2 max. Conventional cardiovascular risk factors were unmodified except for a transient 10% decrease in low-density lipoprotein cholesterol at 6 months. The contrast between the limited metabolic effect of treatment and the importance and precocity of the changes in IMT suggests that the decrease in IMT was not exclusively attributable to a reversal in the atherosclerotic process. A direct parietal effect of GH replacement on the arterial wall might also be involved. The consequences, in terms of cardiovascular risk, should be established by randomized prospective trials.