2018The FASEB JournalRequires access

Tumor Necrosis Factor‐alpha, TNFR1, and TNFR2 Responses to Exercise in the Heat

Eliott Arroyo, Brittany N. Followay, Jeremiah A. Vaughan, Joseph A. Laudato, Brandon M. Gibson, Ellen L. Glickman, Adam R. Jajtner

Open publisher page 0 citations

Abstract

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 VO 2 max assessment, conducted on a cycle ergometer, while the remaining trials were completed in three environmental conditions: high temperature/low humidity (HT LH ; 35°C, 20% RH); high temperature/moderate humidity (HT MH ; 35°, 45% RH); and moderate temperature/moderate humidity (MT MH ; 22°C; 45%RH). The exercise protocol consisted of a 60‐minute cycling trial at 60% of their previously determined VO 2 max, a 15‐minute rest period, and a time to exhaustion trail at 90% VO 2 max (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, η 2 p = 0.358). During HT LH, 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 HT MH , 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 MT MH ( p > 0.05). Circulating TNF‐α at T1 was significantly lower during HT MH compared to MT MH ( p = 0.040). No significant main effect of trial (F= 1.906, p = 0.185, η 2 p = 0.214) was observed for TNF‐α AUC. No significant interaction (F= 1.422, p = 0.247, η 2 p = 0.262), nor main effects of time (F= 0.465, p = 0.712, η 2 p = 0.104) or trial (F= 1.165, p = 0.360, η 2 p = 0.226) were observed for TNFR1 expression. Additionally, no significant main effect of trial (F= 1.681, p = 0.246, η 2 p = 0.296) was observed for TNFR1 AUC. No significant interaction (F= 0.998, p = 0.449, η 2 p = 0.200), nor main effects of time (F= 0.205, p = 0.681, η 2 p = 0.049) or trial (F= 1.659, p = 0.250, η 2 p = 0.293) were observed for TNFR2 expression. Additionally, no significant main effect of trial (F= 1.411, p = 0.299, η 2 p = 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 .

About this research paper

What this paper is about

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 VO 2 max assessment, conducted on a cycle ergometer, while the remaining trials were completed in three environmental conditions: high temperature/low humidity (HT LH ; 35°C, 20% RH); high temperature/moderate humidity (HT MH ; 35°, 45% RH); and moderate temperature/moderate humidity (MT MH ; 22°C; 45%RH). The exercise protocol consisted of a 60‐minute cycling trial at 60% of their previously determined VO 2 max, a 15‐minute rest period, and a time to exhaustion trail at 90% VO 2 max (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, η 2 p = 0.358). During HT LH, 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 HT MH , 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 MT MH ( p > 0.05). Circulating TNF‐α at T1 was significantly lower during HT MH compared to MT MH ( p = 0.040). No significant main effect of trial (F= 1.906, p = 0.185, η 2 p = 0.214) was observed for TNF‐α AUC. No significant interaction (F= 1.422, p = 0.247, η 2 p = 0.262), nor main effects of time (F= 0.465, p = 0.712, η 2 p = 0.104) or trial (F= 1.165, p = 0.360, η 2 p = 0.226) were observed for TNFR1 expression. Additionally, no significant main effect of trial (F= 1.681, p = 0.246, η 2 p = 0.296) was observed for TNFR1 AUC. No significant interaction (F= 0.998, p = 0.449, η 2 p = 0.200), nor main effects of time (F= 0.205, p = 0.681, η 2 p = 0.049) or trial (F= 1.659, p = 0.250, η 2 p = 0.293) were observed for TNFR2 expression. Additionally, no significant main effect of trial (F= 1.411, p = 0.299, η 2 p = 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 .

Why it matters

A significance statement is not available in the OpenAlex record.

Key contribution

A contribution statement is not available in the OpenAlex record.

Method / approach

Method details are not available in the OpenAlex metadata.

Main findings

Findings are not separately available in the OpenAlex metadata.

Limitations

Limitations are not available in the OpenAlex metadata.

Applications

Application details are not available in the OpenAlex metadata.

Available abstract

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 VO 2 max assessment, conducted on a cycle ergometer, while the remaining trials were completed in three environmental conditions: high temperature/low humidity (HT LH ; 35°C, 20% RH); high temperature/moderate humidity (HT MH ; 35°, 45% RH); and moderate temperature/moderate humidity (MT MH ; 22°C; 45%RH). The exercise protocol consisted of a 60‐minute cycling trial at 60% of their previously determined VO 2 max, a 15‐minute rest period, and a time to exhaustion trail at 90% VO 2 max (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, η 2 p = 0.358). During HT LH, 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 HT MH , 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 MT MH ( p > 0.05). Circulating TNF‐α at T1 was significantly lower during HT MH compared to MT MH ( p = 0.040). No significant main effect of trial (F= 1.906, p = 0.185, η 2 p = 0.214) was observed for TNF‐α AUC. No significant interaction (F= 1.422, p = 0.247, η 2 p = 0.262), nor main effects of time (F= 0.465, p = 0.712, η 2 p = 0.104) or trial (F= 1.165, p = 0.360, η 2 p = 0.226) were observed for TNFR1 expression. Additionally, no significant main effect of trial (F= 1.681, p = 0.246, η 2 p = 0.296) was observed for TNFR1 AUC. No significant interaction (F= 0.998, p = 0.449, η 2 p = 0.200), nor main effects of time (F= 0.205, p = 0.681, η 2 p = 0.049) or trial (F= 1.659, p = 0.250, η 2 p = 0.293) were observed for TNFR2 expression. Additionally, no significant main effect of trial (F= 1.411, p = 0.299, η 2 p = 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 .

Key concepts: Tumor necrosis factor alpha, Cycle ergometer, CD16, Animal science, CD14, Internal medicine, Chemistry, Medicine

Related papers

Back to paper searchBrowse research topicsOriginal source
Tumor Necrosis Factor‐alpha, TNFR1, and TNFR2 Responses to Exercise in the Heat — Research Paper | ScholarLens