Consideration of strategies such as the equine nasal strip for reducing negative extravascular pressures is warranted even for exercise at moderate intensities.

Aminocaproic acid (ACA) and Premarin w (PRE) are used to treat exercise-induced pulmonary haemorrhage (EIPH) at the racetrack based upon their putative coagulation effects. We hypothesized that neither ACA nor PRE would reduce EIPH because the literature does not substantiate coagulation deficits being manifested in EIPH. Six Thoroughbreds were run from 4 m s 21 until fatigue (1 m s 21 s £ 1 min increments; 68 inclined treadmill) after being treated with placebo, PRE (25 mg) or ACA (5 g) at 2-week intervals in a randomized crossover design. Coagulation and exercise-related variables were measured at rest and maximal effort. EIPH and inflammation were quantified via bronchoalveolar lavage fluid (BALF) 30-60 min post-exercise. EIPH was not altered by either treatment (3.8^1.7 (placebo), 4.6^3.2 (ACA) and 2.4^1.2 (PRE) £ 10 6 RBC ml 21 BALF; p ¼ 0.12), nor was coagulation. However, inflammation was decreased (5.9^0.9 (placebo), 4.4^0.9 (ACA) and 4.2^0.4 (PRE) £ 10 5 WBC ml 21 BALF; both p , 0.05). There was a trend for decreased time-to-fatigue (720^27 (placebo), 709^24 (ACA) and 726^28 (PRE) s; p ¼ 0.09 for placebo vs. ACA) and a reduction in plasma lactate (19.5^3.0 (placebo), 14.7^1.0 (ACA) and 17.6^2.5 (PRE) mmol l 21 ; p , 0.05 for placebo vs. ACA) following ACA administration. ACA and PRE were not effective in reducing EIPH, and ACA may be detrimental to performance. However, both may mitigate exercise-induced pulmonary inflammation.

Exercise-induced pulmonary haemorrhage (EIPH) is a serious condition that affects the health and possibly the performance of all racehorses. However, only two treatments, furosemide and the Flair™ equine nasal strip, both of which reduce capillary transmural pressure, have been successful in reducing EIPH. Alternatively, transient impairment of platelet function and coagulation during exercise has been considered an additional contributor to EIPH. Consequently, herbal formulations designed to enhance platelet function, and hence coagulation, are hypothesized to reduce EIPH. To investigate the validity of this hypothesis, five Thoroughbred horses completed three maximal incremental exercise tests on a 10% inclined treadmill in a randomized cross-over design experiment. Treatments included twice daily oral administration (for 3 days) of a placebo (PL; cornstarch) and two herbal formulas, Yunnan Paiyao (YP) or Single Immortal (SI). Blood samples for coagulation profiles, complete blood counts and biochemistry profiles were collected before each exercise test. During each test, pulmonary arterial pressure, oxygen uptake, arterial blood gases, plasma lactate and time-to-fatigue were measured. Severity of EIPH was quantified via bronchoalveolar lavage (BAL) at 30–60 min post-exercise. The herbal formulations were not effective in decreasing EIPH (×106 red blood cells ml−1 BAL fluid: PL, 27.1±11.6; YP, 33.2±23.4; SI, 35.3±15.4, P>0.05) or in changing any of the other variables measured with the exception of time-to-fatigue, which was slightly but significantly prolonged by Single Immortal compared with placebo and Yunnan Paiyao (PL, 670±9.6 s; YP, 665±5.5 s; SI, 685±7.9 s, P<0.05). Thus, these results do not support the use of these herbal formulations in the prevention of EIPH.

No abstract

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 21 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 ¼ 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.