Castration inhibits exercise-induced accumulation of Hsp70 in male rodent hearts.

Intense exercise leads to accumulation of the inducible member of the 70-kDa family of heat shock proteins, Hsp70, in male, but not female, hearts. Estrogen is at least partially responsible for this difference. Because androgen receptors are expressed in the heart and castration leads to decreases in calcium regulatory proteins and altered cardiac function, testosterone (T) or its metabolites could also be involved. We hypothesized that removal of endogenous T production through castration would reduce cardiac Hsp70 accumulation after an acute exercise bout, whereas castrated animals supplemented with 5alpha-dihydrotestosterone (DHT) would show the intact male response. Fifty-four 8-wk-old male Sprague-Dawley rats were divided into intact, castrated, or castrated + DHT groups (n = 18/group). At 11 wk of age, 12 animals in each group undertook a 60-min bout of treadmill running at 30 m/min (2% incline) while the remaining 6 in each group remained sedentary. At 30 min or 24 h after exercise (n = 6/time point), blood and hearts were harvested for analysis. Serum T was undetectable in castrated and DHT-treated castrated rats, whereas serum DHT was significantly reduced in castrated animals only (approximately 60% reduction) (P < 0.05). Although there were no differences in constitutive levels of Hsp70 protein, exercise significantly increased cardiac hsp70 mRNA and protein in intact and DHT-supplemented rats, but not in castrated animals (P < 0.05). To examine whether castration eliminated the ability to respond to stress, another six intact and six castrated animals were subjected to a 15-min period of hyperthermia (core temperature raised to 42 degrees C) and killed 24 h later. As opposed to exercise, castrated animals subjected to heat shock exhibited increases in Hsp70 above nonshocked (i.e., sedentary) animals, similarly to intact males (P < 0.05). These data suggest that androgens, in addition to estrogen, play a role in the sexual dimorphism observed in the stress response to exercise but not heat shock.

Determinants of oxygen uptake kinetics in older humans following single-limb endurance exercise training.

We hypothesised that the observed acceleration in the kinetics of exercise on-transient oxygen uptake (VO2) of five older humans (77 +/- 7 years (mean +/- S.D.) following 9 weeks of single-leg endurance exercise training was due to adaptations at the level of the muscle cell. Prior to, and following training, subjects performed constant-load single-limb knee extension exercise. Following training VO2 kinetics (phase 2, tau) were accelerated in the trained leg (week 0, 92 +/- 44 s; week 9, 48 +/- 22 s) and unchanged in the untrained leg (week 0, 104 +/- 43 s; week 9, 126 +/- 35 s). The kinetics of mean blood velocity in the femoral artery were faster than the kinetics of VO2, but were unchanged in both the trained (week 0, 19 +/- 10 s; week 9, 26 +/- 11 s) and untrained leg (week 0, 20 +/- 18 s; week 9, 18 +/- 10 s). Maximal citrate synthase activity, measured from biopsies of the vastus lateralis muscle, increased (P < 0.05) in the trained leg (week 0, 6.7 +/- 2.0 micromol x (g wet wt)(-1) x min(-1); week 9, 11.4 +/- 3.6 micromol x (g wet wt)(-1) x min(-1)) but was unchanged in the untrained leg (week 0, 5.9 +/- 0.5 micromol x (g wet wt)(-1) x min(-1); week 9, 7.9 +/- 1.9 micromol x (g wet wt)(-1) x min(-1)). These data suggest that the acceleration of VO2 kinetics was due to an improved rate of O2 utilisation by the muscle, but was not a result of increased O2 delivery.