l-Carnitine supplementation can stimulate erythropoiesis, reduce exercise-induced plasma lactate concentrations and decrease post-exercise muscle damage. Next to horses, Greyhounds represent the premier animal racing species and perform short-duration, very high-intensity exercise that has the potential to incur substantial muscle damage. Under resting and standard racing conditions (5/16 mile), we tested the novel hypotheses that l-carnitine supplementation in Greyhounds would: (1) elevate haematocrit at rest and immediately post-exercise; (2) reduce peak post-exercise plasma lactate; and (3) reduce indices of muscle damage (plasma creatine phosphokinase, CPK and aspartate aminotransferase, AST). Six conditioned Greyhounds (30.1 ± 1.6 kg) underwent a randomized placebo-controlled crossover study to determine the effects of 6 weeks of l-carnitine supplementation (100 mg kg− 1 of body weight/day) at rest and following a maximal speed 5/16 mile race. In accordance with our hypotheses, l-carnitine elevated resting and immediately post-race haematocrit (control, 60.1 ± 1.7, l-carnitine, 63.6 ± 1.7; P < 0.05) and reduced peak post-race plasma CPK and AST concentrations (both P < 0.05). Those dogs with the highest peak post-exercise plasma CPK concentrations under placebo conditions evidenced the greatest reduction with l-carnitine supplementation (r = 0.99, P < 0.01). However, contrary to our hypotheses, l-carnitine did not change peak post-exercise plasma lactate concentrations (control, 27.0 ± 2.1, l-carnitine, 27.7 ± 1.3; P>0.05). We conclude that l-carnitine supplementation increases the potential for oxygen transport and reduces plasma indicators of muscle damage, CPK and AST in racing Greyhounds.

We evaluated the concentrations of brain natriuretic peptide in the plasma as a marker of systolic ventricular function before and after maximal exercise in 15 surgically palliated patients with functionally univentricular hearts, with apparently good ventricular function. Of the patients, 6 with median age of 14.6 years, and a range from 12.5 to 17.9 years, had been palliated by construction of a total cavopulmonary connection, while the other 9 patients, with a median age of 32.1 years, and a range from 15.6 to 54.2 years, had undergone the classical Fontan procedure. We used 8 healthy individuals, with a median age of 13.9 years, and a range from 12.8 to 14.2 years, as a control group for the measurements of brain natriuretic peptide. The values of the peptide were significantly higher in those with the classical Fontan procedure, both before, when the median value was 131.8 nanogram per litre, with a range from 0.5 to 296.4, and after maximal exercise, when the median value was 108.1, with a range from 0.1 to 235.9. The comparable values in those with a total cavopulmonary connection were a median of 12.8, and a range from 0.5 to 39.1 before, and a median of 9.7, with a range from 2.7 to 26.2 after maximal exercise. The median value for the control group was 13.1, with a range from 2.6 to 38.7 before exercise (p = 0.016), and a median of 24.1, with a range from 5.8 to 66.7 after maximal exercise (p = 0.03), respectively. In the control subjects, the level of the peptide increased by a median of 9.7 nanograms per litre, with a range from 1.2 to 28.0 after maximal exercise (p = 0.008). The level was unchanged after maximal exercise in those with classical Fontan procedures and total cavopulmonary connections, with a difference between levels before and after exercise of a median of 5.9 nanogram per litre, and a range from −23.7 to 31.0 (p = 0.96), and a median of −1.0 nanogram per litre, with a range from −12.0 to 3.9 (p > 0.99), respectively. We conclude that maximal exercise did not increase the level of brain natriuretic peptide level in those patients with the classical Fontan procedure, nor those with a total cavopulmonary connection, findings which may indicate that systolic ventricular dysfunction is not the major cause of the decreased working capacity observed in patients with well functioning palliated functionally univentricular hearts.

Furosemide (FUR) and the equine nasal strip (NS) decrease exercise-induced pulmonary haemorrhage (EIPH) compared with control (CON) conditions in the Thoroughbred horse during near-maximal running trials. As FUR and NS have potential performance-enhancing properties, we studied Thoroughbreds running to fatigue to test the hypothesis that time-to-fatigue (TTF) would be increased, yet EIPH reduced, in FUR and NS compared with CON. Thoroughbred geldings (n=6) were run to volitional fatigue on a level treadmill (1 m s−1 increment per minute from an initial trot) every two weeks (order randomized) under CON, NS, FUR (1 mg kg−1; 4 h prior) and FUR+NS conditions. Pulmonary arterial pressure (Ppa) and pulmonary gas exchange were measured throughout exercise, while arterial blood gases were sampled at the end of each 1-min stage. EIPH severity was quantified via bronchoalveolar lavage (BAL) at 30 min post-exercise. TTF was increased for all experimental conditions (i.e. an additional 20±13, 28±8 and 40±6 s for NS, FUR and FUR+NS, respectively; P<0.05) compared with CON. Peak mean Ppa was significantly reduced (P<0.05) for FUR (93.6±6.3 mmHg) and FUR+ NS (95.4±5.1 mmHg), yet unchanged with NS (98.0±5.8 mmHg; P>0.05) compared with CON (100.5±4.9 mmHg). All three experimental conditions exhibited a significant reduction in EIPH compared with CON (64.1±36.8× 6 red blood cells (RBCs) ml−1); however, no significant difference was noted between these conditions (×106 RBCs ml−1: 29.1±16.8, 20.9±13.1 and 26.7±19.8 for NS, FUR and FUR+NS, respectively). Furthermore, no differences for either end-exercise cardiorespiratory (i.e. V˙O2 or V˙CO2) or blood-borne metabolic (i.e. blood gases, lactate or pH) variables were observed. These findings demonstrate that both FUR and NS enhance TTF and reduce EIPH to a similar degree during high-speed treadmill running to fatigue.