Evaluating Physiological Strain In Males During Acute Cold Exposure Following Aspirin Ingestion

Abstract

Research in the area of thermoregulation has previously demonstrated that aspirin is an anti-pyretic and thereby alters thermoregulation by lowering the prostaglandin E2 (PGE2) by directly inhibiting COX enzyme activity. Therefore, since aspirin is widely consumed and an effective analgesic and anti-pyretic agent, it would appear that by varying the dosages of aspirin (ASA) prior to acute cold exposure a differential thermoregulatory response may ensue. A scale that could possibly demonstrate these thermoregulatory differences may therefore prove to be a valuable tool. Moran et al. (1999) have developed a cold strain index (CSI) based on core (Tcore) and mean skin temperatures (Tsk) and is capable of indicating cold strain. The CSI rates cold strain on a universal scale of 0–10 and is derived as follows: CSI =6.67 (Tcore-Tcore0) (35- Tcore0)−1+ 3.33 (Tsk t-Tsk0). (20-Tsk0)−1, where Tcore0 and Tsk0, are initial measurements and Tcore t -Tsk t, are simultaneous measurements taken at any time t; when Tcoret >Tcore0, then Tcore t -Tcore 0 =0. PURPOSE The goal of the present investigation was to evaluate the physiological strain during cold exposure in young (20–40 yr) males using the CSI. METHODS CSI was analyzed employing experimental data on 7 young males that were exposed to 12°C air for 120-min after they were fed a placebo (PL), a low dose of aspirin (ASA-L: 81 mg d−1) or a high dose of aspirin (ASA-H: 650 mg d−1) for one week prior to each experimental trial. RESULTS As expected, CSI demonstrated a main effect for time (p < 0.05) whereby CSI increased with exposure time pooled across treatment during exposure to 12°C. However, CSI did not demonstrate a main effect for treatment (p ≤ 0.05) or a time by treatment interaction (p > 0.05). CONCLUSION Based on these data the CSI index has potential to be widely utilized. However, the present investigation was unable to discern differences between experimental treatments (ASA-L, ASA-H vs. PL) in individuals exposed to 12°C for 120 min. Further research in this area is warranted and may consider altering the dosage of ASA administration prior to acute cold exposure, and extending the duration of the acute cold exposure trial in an effort to more clearly elucidate differences with respect to CSI.