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In the present study, we analysed the training-intensity distribution and physiological adaptations over a 6-month period preceding an Ironman triathlon race. Ten athletes (mean ± s: age 43 ± 3 years, mass 78.3 ± 10.3 kg, stature 1.79 ± 0.05 m) participated in the study. The study consisted of three training periods (A, B, C), each of approximately 2 months' duration, and four testing weeks. Testing consisted of incremental tests to exhaustion for swimming, cycling and running, and assessments for anthropometry plus cardiovascular and pulmonary measures. The lactate threshold and the lactate turnpoint were used to demarcate three discipline-specific, exercise-intensity zones. The mean percentage of time spent in zones 1, 2, and 3 was 69 ± 9%, 25 ± 8%, and 6 ± 2% for periods A-C combined. Only modest physiological adaptation occurred throughout the 6-month period, with small to moderate effect sizes at best. Relationships between the training volume/training load and the training-intensity distribution with the changes in key measures of adaptation were weak and probably reflect differences in initial training status. Our results suggest that the effects of intensity distribution are small over short-term training periods and future experimental research is needed to clarify the potential impact of intensity distribution on physiological adaptation.

The aim of this study was to determine if inducing metabolic alkalosis would alter neuromuscular control after 50 min of standardized submaximal cycling. Eight trained male cyclists (mean age 32 years, s = 7; [Vdot]O(2max) 62 ml . kg(-1) x min(-1), s = 8) ingested capsules containing either CaCO(3) (placebo) or NaHCO(3) (0.3 g x kg(-1) body mass) in eight doses over 2 h on two separate occasions, commencing 3 h before exercise. Participants performed three maximal isometric voluntary contractions (MVC) of the knee extensors while determining the central activation ratio by superimposing electrical stimulation both pre-ingestion and post-exercise, followed by a 50-s sustained maximal contraction in which force, EMG amplitude, and muscle fibre conduction velocity were assessed. Plasma pH, blood base excess, and plasma HCO(3) were higher (P < 0.01) during the NaHCO(3) trial. After cycling, muscle fibre conduction velocity was higher (P < 0.05) during the 50-s sustained maximal contraction with NaHCO(3) than with placebo (5.1 m x s(-1), s = 0.4 vs. 4.2 m x s(-1), s = 0.4) while the EMG amplitude remained the same. Force decline rate was less (P < 0.05) during alkalosis-sustained maximal contraction and no differences were shown in central activation ratio. These data indicate that induced metabolic alkalosis can increase muscle fibre conduction velocity following prolonged submaximal cycling.

A high ambient temperature reduces the capacity to perform prolonged exercise. Total carbohydrate oxidation is less, and thus glycogen depletion is not limiting. Fluid ingestion in the heat should, therefore, focus on maintenance of hydration status rather than on substrate provision. Six healthy males cycled to exhaustion at 60% of maximum oxygen consumption (VO2max) with no drink, ingestion of a 15% carbohydrate-electrolyte drink (1.45+/-0.29 litres) or ingestion of a 2% carbohydrate-electrolyte drink (3.12+/-0.47 litres). The ambient temperature was 30.2+/-0.6 degrees C (mean +/- s), with a relative humidity of 71+/-1% and an air speed of approximately 0.7 m x s(-1) on all trials. Weighted mean skin temperature, rectal temperature and heart rate were recorded and venous samples drawn for determination of plasma volume changes, blood metabolites, serum electrolytes and osmolality. Expired gas was collected to estimate rates of fuel oxidation. Exercise capacity was significantly (P < 0.05) different in all trials. The median (range) time to exhaustion was 70.9 min (39.4-97.4 min) in the no-drink trial, 84.0 min (62.7-145 min) in the 15% carbohydrate trial and 118 min (82.6-168 min) in the 2% carbohydrate trial. The 15% carbohydrate drink resulted in significantly (P < 0.05) elevated blood glucose and total carbohydrate oxidation compared with the no-drink trial. The 2% carbohydrate drink restored plasma volume to pre-exercise values by the end of exercise. No differences were observed in other thermoregulatory or cardiorespiratory responses between trials. These results suggest that fluid replacement with a large volume of a dilute carbohydrate drink is beneficial during exercise in the heat, but the precise mechanisms for the improved exercise capacity are unclear.