The Effect of Reversible Left Recurrent Laryngeal Neuropathy on the Metabolic Cost of Locomotion and Peak Aerobic Power in Thoroughbred Racehorses

Authors

  • PAULA J. EHRLICH DVM,

    1. Department of Large Animal Surgery, Tufts University School of Veterinary Medicine, North Grafton, MA. Presented at the ACVS Annual Meeting, San Francisco, CA, 1993.
    Search for more papers by this author
  • HOWARD J. SEEHERMAN PhD, VMD, FACSM,

    Corresponding author
    1. Department of Large Animal Surgery, Tufts University School of Veterinary Medicine, North Grafton, MA. Presented at the ACVS Annual Meeting, San Francisco, CA, 1993.
    Search for more papers by this author
  • ELISABETH MORRIS DVM,

    1. Department of Large Animal Surgery, Tufts University School of Veterinary Medicine, North Grafton, MA. Presented at the ACVS Annual Meeting, San Francisco, CA, 1993.
    Search for more papers by this author
  • CYNTHIA KOLIAS DVM

    1. Department of Large Animal Surgery, Tufts University School of Veterinary Medicine, North Grafton, MA. Presented at the ACVS Annual Meeting, San Francisco, CA, 1993.
    Search for more papers by this author

2 Tufts University School of Veterinary Medicine, Department of Large Animal Surgery, 200 Westboro Rd, North Grafton, MA 01536.

Abstract

W. ROBERT COOK, BVSc, FRCVS

The effect of left recurrent laryngeal neuropathy (LRLN) on the metabolic cost of locomotion (MCL) and peak aerobic power (V̇O2peak) was evaluated in four trained Thoroughbred racehorses. Oxygen consumption (V̇O2), carbon dioxide production (V̇CO2), venous lactate concentrations (LAC), and heart rate (HR) were measured during a treadmill exercise test (TET). Each horse performed the exercise test four times, alternating between normal upper airway function and reversibly induced LRLN. Subcutaneous infusion of 2% mepivicaine, a local anesthetic, into the region where the left recurrent laryngeal nerve passes caudal to the cricoid cartilage was used to induce LRLN. The induction of LRLN did not alter the relationship between V̇O2 and treadmill speed at exercise intensities where V̇O2 was less than V̇O2peak (<9 m/sec). However, a 15.3% reduction in V̇O2peak (Normal = 165.3 ± 3.4, LRLN = 140.0 ± 3.2 mL/kg/min ± SE, P <.001) occurred at higher treadmill speeds in horses with induced LRLN. A significant group (Normal v LRLN) by treadmill speed effect was found for LAC and R only at treadmill speeds where V̇O2=V̇O2peak. Peak lactate (LACpeak) did not change after the induction of LRLN. The relationship between HR and treadmill speed increased in horses with induced LRLN at exercise intensities where V̇O2 < V̇O2peak. Peak heart rate (HRpeak) remained unchanged. Performance as indicated by the maximum number of speed intervals completed (STEPmax) decreased 7% in horses with induced LRLN (Normal = 9.1 ± 0.04, LRLN = 8.5 ± 0.2 minutes ± SE, P <.04). A comparison of paired exercise test measurements showed no evidence of a training effect, or decreased performance caused by a learned response, over the course of the experiment. The results of this study indicate that alterations in ventilation caused by LRLN cause a significant reduction in V̇O2peak, but do not cause an increase in the metabolic cost of locomotion at exercise intensities where V̇O2 is less than V̇O2peak.

Ancillary