The triathlon has come to be recognized as a distinct endurance event and although a substantial body of research information exists with regard to the individual components (canoeing, cycling, running, etc.), the physiologic demands imposed by combining the respective activities into one continuous event have not yet been assessed. Twenty-three male athletes (age = 33 +/- 5.2 yr; mass = 71.79 +/- 7.42 kg; height = 176.0 +/- 7.21 cm; means +/- SD) participated in the study on the basis of informed consent. Venous blood samples, taken immediately prior to and on completion of the Iron Man Triathlon held in Johannesburg during 1983, were assayed for parameters of energy metabolism, fluid and electrolyte balance, and stress (tissue enzymes in serum). On the basis of post-race blood glucose (6.17 mmol. l-1), free fatty acids (1943 mumol. l-1), and blood lactate (3.45 mmol. l-1) changes, it was concluded that the triathlon is primarily, in an overall sense, an aerobic event. With the exception of magnesium and iron, serum electrolyte changes agreed with literature findings. However, body mass reductions (average 3.23 kg, i.e., 4.5%) indicated that the extent of dehydration is more severe in the triathlon than in comparable endurance events. Post-race enzyme levels (LD, CK, and AST) were significantly elevated, and LD negatively correlated with total performance time (P less than 0.01). The general conclusion is that the physiologic demand of the triathlon exceeds that of other comparable endurance events.

The effect of clinically used equipotent doses of nonselective (beta 1/beta 2; propranolol) and selective (beta 1; atenolol) beta-adrenoceptor blockers on thermoregulation was studied during prolonged exercise in the heat. Oral propranolol (160 mg/day), atenolol (100 mg/day) or matching placebo were taken for 6 days each by 11 healthy young adult caucasian males. Subjects participated in 2 h of block-stepping at a work rate of 54 W in an environmental chamber with a temperature of 33.2 +/- 0.3 degree C dry bulb and 31.7 /+- 0.3 degree C wet bulb, 2 h after ingestion of the final dose of each drug. Both active agents produced similar marked (P less than 0.001) increases in subjective perception of effort, the mechanism of which was not immediately evident from changes in serum electrolytes, blood glucose, blood lactate, or ventilatory parameters. Propranolol did, however, cause a greater rise in serum K+ than placebo (P less than 0.02) and atenolol (P = NS) after exercise. Although rectal and mean skin temperatures were insignificantly altered by beta-adrenoceptor blockade, an increased total sweat production was noted with propranolol (P less than 0.01 vs. placebo) and to a lesser degree atenolol (P = NS vs. placebo) therapy. Analysis of the time course of sweat production showed the propranolol-mediated enhancement of sweating to ensue largely during the initial hour of block-stepping and to be transient in nature. The scientific and clinical implications of this observation will be dependent upon the precise underlying mechanism, a factor not identified by the present study.

SUMMARY The effect of the beta1 selective adrenoceptor blocker, atenolol, on the physiological response to exercise was studied in 12 healthy young men. Oral atenolol (100 mg) and placebo were administered in a randomised double blind crossover fashion an hour and a half before an intermittent multistage cycle ergometer exercise test. At maximal effort oxygen consumption, pulmonary ventilation, carbon dioxide output, and respiratory exchange ratio were not modified by atenolol. In contrast, maximal heart rate and performance time were significantly reduced after atenolol. Nevertheless, because the relation of percentage of maximal oxygen consumption to percentage of maximal heart rate was not changed by atenolol both the absolute and relative oxygen consumption corresponding to 70% and 85%h of the maximal heart rate remained unaltered.These data suggest that recommendations of exercise intensity may be determined on the basis of a calculated percentage of the predetermined maximal heart rate in persons without symptomatic coronary heart disease receiving beta1 selective adrenoceptor blockers.

The effect of clinically used doses of propranolol, atenolol, nifedipine, propranolol plus nifedipine, and atenolol plus nifedipine on thermoregulatory responses of 11 healthy men was studied during 2-h block-stepping in heat. Drug intervention did not alter ventilation during exercise. In contrast, propranolol and atenolol produced equivalent reductions in exercise tachycardia, implying a similar level of beta 1-adrenoceptor blockade. The heart rate response to exercise was unaffected by nifedipine and during dual beta-adrenoceptor blockade and calcium antagonism was equivalent to that with beta-adrenoceptor blockade alone. While rectal temperature rises were not modified by drug ingestion, propranolol and, to a lesser degree, atenolol and combination therapy, but not nifedipine alone, attenuated skin temperature rises. Moreover, although atenolol, nifedipine, and their combination did not alter sweating, propranolol and its combination with nifedipine enhanced sweating during the 1st and 2nd h of exercise. This study concludes that nifedipine does not modify thermoregulation during exercise and allows for greater confidence of its use during cardiac rehabilitation. Furthermore, the present data confirm that propranolol does enhance sweating during exercise and demonstrate that this effect is not mediated simply by an earlier onset of rapid sweating nor abolished by concomitant calcium antagonism.

Cardiorespiratory responses of 11 healthy males were studied, with placebo and propranolol, during a continuous and an intermittent multistage maximal treadmill test. With placebo, equivalent maximal heart rates were attained for the disparate test modes, and the intermittent protocol yielded a slightly higher (2%, P less than 0.01) maximal O2 consumption. In contrast, during beta-adrenoceptor blockade, higher maximal heart rates (5.1%, P less than 0.01) and O2 consumptions (4.4%, P less than 0.02) were reached with intermittent compared with continuous testing. Values were, however, markedly lower (P less than 0.001) for both protocols than with placebo. These results demonstrate that the precise degree of attenuation of maximal heart rate and O2 consumption observed in physically active persons receiving propranolol is partly dependent upon the actual test protocol utilized. Furthermore, the present data suggest an advantage for intermittent testing when accurate evaluation of the maximal cardiorespiratory capacity is desired in such individuals.