Blood pressure responses to 1 week of low-salt (20 mmol sodium/d) and high-salt (300 mmol sodium/d) intake were investigated in a single-blind randomized study in 163 white, nonobese normotensive subjects (65 women and 98 men; mean age, 38±1.2 years). The individuals were classified as salt sensitive when mean arterial blood pressure rose by at least 5 mm Hg during high-salt intake, as salt resistant when mean arterial blood pressure changed by less than 5 mm Hg, and as "counterregulator" when mean arterial blood pressure fell by at least 5 mm Hg during the high-salt diet. Reexamination of 31 subjects showed that this approach to the testing of salt sensitivity was reliable and reproducible. Thirty subjects (18.4%) were classified as salt sensitive, 108 (66.3%) as salt resistant, and 25 (15.3%) as counterregulators. Multiple regression analysis revealed that age, body weight, and family history of hypertension contributed significantly to the change in blood pressure after the diets. Salt sensitivity was more frequent in older subjects and in those with a positive family history of hypertension. An increase in blood pressure after salt restriction was more likely in younger individuals and in those with a negative family history of hypertension. Plasma renin activity and plasma aldosterone concentrations were lower in salt-sensitive compared with salt-resistant and counterregulating subjects. The rise in plasma renin activity during salt restriction was most pronounced in counterregulating subjects. Plasma norepinephrine concentrations were not different among the groups. Plasma levels of atrial natriuretic peptide increased during high-salt intake in all groups, the rise being most pronounced in salt-sensitive subjects. The increase in blood pressure during salt restriction in counterregulating subjects may be partially due to an overstimulation of the renin-angiotensin system. The exaggerated response of the secretion of atrial natriuretic peptide to high-salt intake in salt-sensitive subjects may point to an impaired capability of the kidney to excrete a salt load. 7 It has been assumed recently that the effect of a concerted health care program directed toward lowering salt intake of the general population would be extremely small. 6 The blood pressure response to sodium chloride is heterogeneous, at least during relatively short-term changes in salt intake. Salt sensitivity, defined as a significant rise in blood pressure when individuals switch from a low to a high sodium chloride intake, is seen in a considerable number of patients with essential hypertension and, although less frequent, in normotensive subjects.8 On the other hand, some individuals increase their blood pressure with sodium depletion 910 and therefore could be at higher risk when ingesting a salt-restricted diet.Little attention has focused so far on this issue. This may partially be due to the design of most of the previous studies dealing with salt sensitivity in which subjects reacting to low-salt intake with no change or a rise in pre...

Seventeen male physical education students performed three types of treadmill exercise: (1) progressive exercise to exhaustion, (2) prolonged exercise of 50 min duration at the anaerobic threshold of 4 mmol . l-1 blood lactate (AE), (3) a single bout of short-term high-intensity exercise at 156% of maximal exercise capacity in the progressive test, leading to exhaustion within 1.5 min (ANE). Immediately before and after ANE and before, during, and after AE adrenaline, noradrenaline, growth hormone, cortisol, insulin, testosterone, and oestradiol were determined in venous blood, and glucose and lactate were determined in arterialized blood from the earlobe. Adrenaline and noradrenaline increased 15 fold during ANE and 3--4 fold and 6--9 fold respectively during AE. The adrenaline/noradrenaline ratio was 1 : 3 during ANE and 1 : 10 during AE. Cortisol increased by 35% in ANE (12% of which appeared in the postexercise period) and 54% in AE. Insulin increased during ANE but decreased during AE. Testosterone and oestradiol increased by 14% and 16% during ANE and by 22% and 28% during AE. The results point to a markedly higher emotional stress and higher sympatho-adrenal activity in anaerobic exercise. Growth hormone and cortisol appear to be the more affected by intense prolonged exercise. Taking plasma volume changes and changes of metabolic clearance rates into consideration, neither of the exercise tests appeared to affect secretion of testosterone and oestradiol.

A detailed theory for the Zeeman splitting of shallow acceptors in cubic semiconductors is presented, allowing for cubic contributions from the band stmct-, magnetic field orientations B 11 [OOl], [lll], [110] and large magnetic fields B.Practically exact solutions are achieved by taking the contributions of higher angular momenta into account. We calculate the Zeeman splitting of the ground state and the first excited odd-parity states. By also determining the probability for transitions between these states we succeed in a reasonable interpretation of the experimental results for Ge and GaAs. We tabulate g-values for *wide range of Lutt-parame.ters. A description of the Zeeman splitting in terms of a linear field dependence only proves to be accurate for limited field strengths.

To examine the metabolic and hormonal responses to non-exhaustive steady-state exercise at the individual anaerobic threshold (IAT), 12 male physical education students performed treadmill exercise of 50 min duration. The treadmill speed equaled that at the IAT as assessed in a standardized progressive exercise test (75 +/- 2% of maximal oxygen uptake). Heart rate averaged 177.0 +/- 12.2 min-1 at 15 min and 184.5 +/- 11.5 min-1 at 50 min. After the initial adjustment, arterial lactate stabilized at individually different levels between 2.70 and 6.00 mmol/l without any substantial trend in the individual curves. Arterial glucose was unchanged throughout the test. Glycerol increased continuously to 157% above the preexercise value (P less than 0.001). The FFA blood level was not depressed but rather showed an increasing tendency between 25 and 50 min (P less than 0.05). Between 0 and 25 min, insulin decreased (P less than 0.01), growth hormone increased to 8 times its pre-exercise value (P less than 0.001), and cortisol did not show any significant changes. Between 25 and 50 min, no significant additional changes were detected for these hormones. At 15 min epinephrine and norepinephrine had increased 2.8- and 7-fold above the respective pre-exercise values (P less than 0.001); both catecholamines continued to increase until 50 min (P less than 0.001 and P less than 0.01). It is concluded that prolonged exercise at the IAT is associated with a steady-state condition in carbohydrate supply and turnover, as is suggested by the stable blood levels of glucose and lactate. The stably elevated blood level of lactate did not result in depression of the FFA blood level, suggesting unimpaired supply of FFA from extramuscular sources. Exercise at the IAT places a high load on aerobic metabolism without encountering progressive lactate accumulation and the associated metabolic effects.

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