Tumor Necrosis Factor‐alpha, TNFR1, and TNFR2 Responses to Exercise in the Heat
Authors: Arroyo Eliott , Followay Brittany N. , Vaughan Jeremiah A. , Laudato Joseph A. , Gibson Brandon M. , Glickman Ellen L. , Jajtner Adam R. 
Published: June 2021

Plasma levels of Tumor Necrosis Factor‐alpha (TNF‐α) have been shown to increase in response to exercise in hot environments, however, the effects of exercise in the heat on surface expression of TNF receptors (TNFR) 1 and 2 have not been investigated.

OBJECTIVE

To observe the effects of moderate‐ and high‐intensity exercise in the heat on circulating TNF‐α and surface expression of TNFR1 and TNFR2 on human classical monocytes (CD14++CD16–).

METHODS

Eight recreationally active Caucasian men (24.8 ± 3.0 yrs; 179.8 ± 7.4 cm; 84.4 ± 2.9 kg; 46.8 ± 5.9 ml·kg−1·min−1) completed four exercise trials. The first trial consisted of a VO2max assessment, conducted on a cycle ergometer, while the remaining trials were completed in three environmental conditions: high temperature/low humidity (HTLH; 35°C, 20% RH); high temperature/moderate humidity (HTMH; 35°, 45% RH); and moderate temperature/moderate humidity (MTMH; 22°C; 45%RH). The exercise protocol consisted of a 60‐minute cycling trial at 60% of their previously determined VO2max, a 15‐minute rest period, and a time to exhaustion trail at 90% VO2max (TTE). Blood samples were obtained before (T1) and after (T2) the 60‐minute trial; immediately after TTE (T3), and one hour post‐TTE (T4). Plasma concentrations of TNF‐α were measured via commercially available ELISA. TNFR1 and TNFR2 expression was measured on a subset of participants (n= 5) using flow cytometry. Natural log (LN) transformation was used on non‐normally distributed data and area under the curve (AUC) was calculated using the standard trapezoidal technique. Changes were analyzed using a two factor (time × trial) within‐subjects repeated measures ANOVA and one‐way repeated measures ANOVA.

RESULTS

A significant interaction was observed for circulating TNF‐α (F= 3.912, p = 0.034, η2p = 0.358). During HTLH, TNF‐α increased from T1 to T2 (p = 0.026) and T3 (p = 0.036), and decreased from T3 to T4 (p = 0.036). During HTMH, TNF‐α increased from T1 to T2 (p = 0.002), T3 (p = 0.006), and T4 (p = 0.011). No significant time effect was observed during MTMH (p > 0.05). Circulating TNF‐α at T1 was significantly lower during HTMH compared to MTMH (p = 0.040). No significant main effect of trial (F= 1.906, p = 0.185, η2p = 0.214) was observed for TNF‐α AUC. No significant interaction (F= 1.422, p = 0.247, η2p = 0.262), nor main effects of time (F= 0.465, p = 0.712, η2p = 0.104) or trial (F= 1.165, p = 0.360, η2p = 0.226) were observed for TNFR1 expression. Additionally, no significant main effect of trial (F= 1.681, p = 0.246, η2p = 0.296) was observed for TNFR1 AUC. No significant interaction (F= 0.998, p = 0.449, η2p = 0.200), nor main effects of time (F= 0.205, p = 0.681, η2p = 0.049) or trial (F= 1.659, p = 0.250, η2p = 0.293) were observed for TNFR2 expression. Additionally, no significant main effect of trial (F= 1.411, p = 0.299, η2p = 0.261) was observed for TNFR2 AUC.

CONCLUSIONS

Moderate‐ and high‐intensity exercise in hot conditions elicits an increase in plasma TNF‐α concentrations, though moderate temperature does not. Furthermore, the environmental condition during exercise did not affect TNFR1 and TNFR2 expression on classical monocytes.

Support or Funding Information

This study was partially funded by the Kent State University Research Council

This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.