Eleven weight-trained athletes (age X +/- SD = 33 +/- 5 yrs, weight = 72 +/- 10 kg) with a maximal performance in bench press at the beginning of the study (116 +/- 19 kg) were studied at rest, after a standardized submaximal training session, and after a maximal session once a month for 4 months to study the blood metabolites and hormonal changes during weight lifting. The submaximal load was six series of eight bench presses at 70% of maximal performance presses, and the maximal load was the maximal number of repetitions at the same work load. The levels of several metabolites (lactate, glycerol, triglycerides, beta-OH-butyrate) and hormones (norepinephrine and epinephrine) increased (P less than 0.05) after submaximal work and more after maximal work. Glucose, FFA, acetoacetate, insulin, testosterone, and cortisol did not change significantly or consistently. Lactate after maximal work was higher after the 4th training month (P less than 0.05). Other variables did not change much with training while the maximal number of repetitions in the last series increased slightly (P less than 0.05). In general, the changes observed were smaller than the ones reported for endurance or interval running, which use larger muscle groups. Nevertheless, weight lifting induced changes in blood metabolites which reflect a mobilization of both carbohydrates and lipids stores for energy.

The hypothesis of a blunted chronotropic response of cardiac beta-adrenergic receptors in altitude hypoxia was tested in nine subjects at sea level (SL) by infusion of isoproterenol. Observations were made at SL, in acute hypoxia (2 days at 4,350 m, condition H1), in more prolonged hypoxia [13 days between 850 and 4,800 m, condition H2] and in chronic hypoxia [21 days at 4,800 m, condition H3]. Resting heart rate was higher in all hypoxic conditions. Resting norepinephrine concentrations were found to be significantly higher in conditions H2 (1.64 +/- 0.59) and H3 (1.74 +/- 0.76) than at SL (0.77 +/- 0.18 ng/ml). Isoproterenol, diluted in saline, was infused at increasing doses of 0.0, 0.02, 0.04, and 0.06 micrograms.kg-1.min-1. For the highest dose, there was a significantly smaller increase in heart rate in conditions H1 (35 +/- 9), H2 (33 +/- 11), and H3 (31 +/- 11) than at SL (45 +/- 8 min-1). The increase in pulse (systolic/diastolic) pressure, considered as the vascular response to isoproterenol infusion, was smaller in condition H3 (29 +/- 16) than at SL (51 +/- 24 mmHg). There was a significant increase in the dose of isoproterenol required to increase heart rate by 25 min-1 and decrease in slope of heart rate increase vs. log(dose) relationship in conditions H2 and H3. Thus an hypoxia-related attenuated response of beta-adrenergic receptors to exogenous stimulation was found in humans.(ABSTRACT TRUNCATED AT 250 WORDS)

In a number of pathological states a decrease in the plasma protein binding of drugs is observed. This may be due to many factors related either to the protein, or the ligand (drug), or to the binding conditions. The most important of these disease states quantitatively are probably hypoalbuminaemia, conditions resulting in modification of the albumin compartment volume and the presence on albumin binding sites of pathological inhibitors of drug binding. A decrease in the extent of drug plasma protein binding does not necessarily lead to enhanced drug effects and therefore raises two important therapeutic questions. Firstly, does reduced protein binding have a clinically significant influence on the pharmacological effects of the drug? Secondly, if it does, is it preferable to modify the dosage regimen of the drug or to correct the plasma protein concentration prior to the administration of the drug? At present, only tentative answers can be given.