Overtrained horses alter their resting pulsatile growth hormone secretion.

The influence of intensified and reduced training on nocturnal growth hormone (GH) secretion and elimination dynamics was studied in young (1.5 yr) Standardbred geldings to detect potential markers indicative for early overtraining. Ten horses trained on a treadmill for 32 wk in age-, breed-, and gender-matched fixed pairs. Training was divided into four phases (4, 18, 6, and 4 wk, respectively): 1) habituation to high-speed treadmill trotting, 2) normal training, in which speed and duration of training sessions were gradually increased, 3) in this phase, the horses were divided into 2 groups: control (C) and intensified trained (IT) group. In IT, training intensity, duration, and frequency were further increased, whereas in control these remained unaltered, and 4) reduced training (RT). At the end of phases 2, 3, and 4, blood was sampled overnight every 5 min for 8 h for assessment of GH secretory dynamics using pulse detection, deconvolution analysis, and approximate entropy (ApEn). Intensified training induced overtraining (performance decreased by 19% compared with C), which was associated with an increase in concentration peaks number (3.6 vs. 2.0, respectively), a smaller peak secretion pattern with a prolonged half-life (15.2 vs. 7.3 min, respectively), and an increased ApEn (0.89 vs. 0.49, respectively). RT did not lead to full recovery for the overtrained horses. The increased irregularity of nocturnal GH pulsatility pattern is indicative of a loss of coordinated control of GH regulation. Longer phases of somatostatin withdrawal are hypothesized to be the underlying mechanism for the observed changes in GH pulsatility pattern.

The influence of training on oxygen isotope fractionation in healthy subjects.

We determined the oxygen isotope fractionation in expired alveolar gas relative to inspired air (delta(A-I)) in eight young, healthy subjects at rest and at five levels of exercise up to maximal workload both before and after a training period of about 4 weeks which increased maximum oxygen uptake by about 10%. The data for delta(A-I) were used to compute the relative difference (deltaU) between the resistances of 16O18O and 16O2 for oxygen transport from the alveolar space and utilization in the mitochondria. Prior to training, deltaU decreased from 15 per thousand at rest to 5 per thousand at the highest level of exercise and after training from 12 to 5 per thousand. The difference between the results for deltaU before and after training was significant for rest (P < or = 5) but not for exercise conditions. Accordingly, we conclude that for exercise conditions the non-fractionating oxygen transport by blood flow to and the fractionating oxygen transport by diffusion in the muscles have improved by training to more or less the same degree. The decrease in deltaU in rest after training suggests that oxygen transport by diffusion in other tissues also benefits from the effects of training.