Aminocaproic acid (ACA) and Premarin® 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−1 until fatigue (1 m s−1 × 1 min increments; 6∘ 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) × 106 RBC ml−1 BALF; p = 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) × 105 WBC ml−1 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 = 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−1; 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.
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| All Time | Past 365 days | Past 30 Days | |
|---|---|---|---|
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Aminocaproic acid (ACA) and Premarin® 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−1 until fatigue (1 m s−1 × 1 min increments; 6∘ 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) × 106 RBC ml−1 BALF; p = 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) × 105 WBC ml−1 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 = 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−1; 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.
| All Time | Past 365 days | Past 30 Days | |
|---|---|---|---|
| Abstract Views | 56 | 24 | 12 |
| Full Text Views | 0 | 0 | 0 |
| PDF Views & Downloads | 5 | 0 | 0 |