Interval training at VO2max: effects on aerobic performance and overtraining markers.

PURPOSE: Between inefficient training and overtraining, an appropriate training stimulus (in terms of intensity and duration) has to be determined in accordance with individual capacities. Interval training at the minimal velocity associated with VO2max (vVO2max) allows an athlete to run for as long as possible at VO2max. Nevertheless, we don't know the influence of a defined increase in training volume at vVO2max on aerobic performance, noradrenaline, and heart rate. METHODS: Eight subjects performed 4 wk of normal training (NT) with one session per week at vVO2max, i.e., five repetitions run at 50% of the time limit at vVO2max, with recovery of the same duration at 60% vVO2max. They then performed 4 wk of overload training (OT) with three interval training sessions at vVO2max. RESULTS: Normal training significantly improved their velocity associated with VO2max (20.5+/-0.7 vs 21.1+/-0.8 km x h(-1), P = 0.02). As a result of improved running economy (50.6+/-3.5 vs 47.5+/-2.4 mL x min(-1) x kg(-1), P = 0.02), VO2max was not significantly different (71.6+/-4.8 vs 72.7+/-4.8 mL x min(-1) x kg(-1)). Time to exhaustion at vVO2max was not significantly different (301+/-56 vs 283+/-41 s) as was performance (i.e., distance limit run at vVO2max: 2052.2+/-331 vs 1986.2+/-252.9 m). Heart rate at 14 km x h(-1) decreased significantly after NT (162+/-16 vs 155+/-18 bpm, P < 0.01). Lactate threshold remained the same after normal training (84.1+/-4.8% vVO2max). Overload training changed neither the performance nor the factors concerning performance. However, the submaximal heart rate measured at 14 km x h(-1) decreased after overload training (155+/-18 vs 150+/-15 bpm). The maximal heart rate was not significantly different after NT and OT (199+/-9.5, 198+/-11, 194+/-10.4, P = 0.1). Resting plasma norepinephrine (veinous blood sample measured by high pressure liquid chromatography), was unchanged (2.6 vs 2.4 nm x L(-1), P = 0.8). However, plasma norepinephrine measured at the end of the vVO2max test increased significantly (11.1 vs 26.0 nm x L(-1), P = 0.002). CONCLUSION: Performance and aerobic factors associated with the performance were not altered by the 4 wk of intensive training at vVO2max despite the increase of plasma noradrenaline.

Clinical chronopharmacology of ACTH 1-17. II. Effects on plasma testosterone, plasma aldosterone, plasma and urinary electrolytes (K, Na, Ca and Mg).

The aim of the investigation was to study the effects of ACTH 1-17 on plasma testosterone, plasma aldosterone as well as on both plasma and urinary electrolytes (K, Na, Mg and Ca) in healthy young adult males with regard to the time (clock hours) at which this polypeptide was injected. Eight healthy adults (males from 28 to 30 years) volunteered for the study. The were synchronized with a diurnal activity from 0700 to midnight and a nocturnal rest. Each week, during 6 consecutive weeks (January 19 to February 25, 1980) a 3-day test was performed on Saturday, Sunday and Monday. On Sundays 3 control-tests and the 3 ACTH-tests were programmed during which either saline or 100 microgram ACTH 1-17 were injected i.m. at respectively 0700, 1400 and 2100. During each 3 day-test period (72 h) the urinary excretion of K, Na, Mg and Ca was determined every 4 h at fixed clock hours. In addition, on Sundays, venous blood was sampled prior to control or ACTH injections at respectively 0700, 1400 and 2100 and 20, 40, 60, 90, 120, 150 and 180 min thereafter. Plasma testosterone, aldosterone (radioimmunoassays) K, Na (flame photometry), Mg and Ca (photocolorimetric methods) were determined in the collected samples. Both conventional and cosinor methods were used for statistical analyses. The injection of ACTH at 0700 was followed by a clear and statistically significant rise of plasma testosterone. No change with regard to control occurred when ACTH was injected at either 1400 or at 2100. A statistically significant rise of plasma aldosterone was observed after each of the ACTH injections. However, the highest plasma aldosterone level was reached when ACTH was administered at 1400 and the lowest level at 2100. ACTH-induced changes in plasma electrolytes were either nil (for Na and Ca) or small (for K and Mg). A more or less important increase of urinary K occurred after the ACTH injection at each of the 3 considered times. The highest values of excreted K occurred after the injection of ACTH at 0700, without shift of the acrophase. In contrast, injections of ACTH at 1400 and 2100 induced a dramatic alteration of the K rhythms. ACTH induced an important fall in the Na urinary excretion. This fall was the greatest when ACTH was injected at 1400. Na rhythm alterations also occurred, particularly after ACTH injections at 2100. However, this effect was less pronounced after ACTH injection at 0700 than at other considered time points. The urinary amount of excreted Ca did not seem to be affected by ACTH. Rhythm alterations occurred after ACTH injections at 1400 and 2100. Peaks of plasma testosterone, plasma aldosterone as well as plasma cortisol (reported in a previous paper) resulting from ACTH stimulation coincided in time with the acrophase of the physiological circadian rhythm in plasma levels of these hormones...