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Effects of an Acute High-Volume Isokinetic Intervention on Circulating Levels of TNF-? and STNFR: Influence of Age
- Date Issued:
- 2017
- Abstract/Description:
- The immune system has been implicated in recovery and muscle regeneration following exercise. In response to muscle damage, the immune system responds with an increase in circulating pro-inflammatory cytokines with the goal of recruiting leukocytes to the damaged area. Tumor Necrosis Factor-alpha (TNF-?), in particular, has been shown to be implicated in both muscle regeneration and muscle wasting. However, it remains unclear whether TNF-? is responsible for the age-related losses in muscle size and function. Also, due to the high clearance rate of TNF-? from circulation, analyzing the circulating levels of soluble TNF-? receptors 1 and 2 (STNFR1 and STNFR2) may provide a better indication of inflammatory events. Therefore, the purpose of this study was to compare changes in circulating levels of TNF-?, STNFR1, and STNFR2 following an acute muscle damaging intervention in young age (YA) and middle-aged (MA) males. Recreationally active young (YA; N=9, 21.8 (&)#177; 2.2 y, 179.5 (&)#177; 4.9 cm, 91.2 (&)#177; 12.2 kg, 21.8 (&)#177; 4.3% BF) and middle-aged (MA; N=10, 47.0 (&)#177; 4.4 y, 176.8 (&)#177; 7.6 cm; 96.0 (&)#177; 21.5 kg, 25.4 (&)#177; 5.3% BF) males completed an acute muscle damaging protocol (MDP). Blood samples were obtained at baseline (BL), immediately (IP), 30 minutes (30P), 60 minutes (60P), 120 minutes (120P), 24 hours (24H), and 48 hours (48H) post-MDP. Lower body performance was analyzed via isokinetic dynamometer at BL, IP, 120P, 24H, and 48H. No significant group x time interactions or main group effects were observed for TNF-?, STNFR1, STNFR2 or any marker of muscle damage. When collapsed across groups, plasma lactate was significantly elevated at IP (p (<) 0.001) and 30P (p = 0.003); serum myoglobin was increased at 30P (p = 0.002), 60P (p = 0.001), and 120P (p = 0.007); creatine kinase was elevated at 24H (p = 0.001) and 48H (p = 0.005). Plasma concentrations of TNF-? were unchanged following MDP. With both groups combined, serum STNFR1 was decreased at 30P (p = 0.001) and increased at 48H (p = 0.028). Serum STNFR2 was decreased at 30P (p = 0.008), 60P (p = 0.003), and 120P (p = 0.002). The results of this study indicate that the TNF-? and STNFRs response to exercise is similar between young and middle-aged males. Measuring STNFRs may be a more appropriate method of assessing the acute inflammatory response to muscle damage. In addition, an acute bout of exercise may attenuate ectodomain shedding of TNFR1 and TNFR2.
Title: | Effects of an Acute High-Volume Isokinetic Intervention on Circulating Levels of TNF-? and STNFR: Influence of Age. |
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Name(s): |
Arroyo Delgado, Eliott, Author Wells, Adam, Committee Chair Hoffman, Jay, Committee Member Stout, Jeffrey, Committee Member Fukuda, David, Committee Member University of Central Florida, Degree Grantor |
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Type of Resource: | text | |
Date Issued: | 2017 | |
Publisher: | University of Central Florida | |
Language(s): | English | |
Abstract/Description: | The immune system has been implicated in recovery and muscle regeneration following exercise. In response to muscle damage, the immune system responds with an increase in circulating pro-inflammatory cytokines with the goal of recruiting leukocytes to the damaged area. Tumor Necrosis Factor-alpha (TNF-?), in particular, has been shown to be implicated in both muscle regeneration and muscle wasting. However, it remains unclear whether TNF-? is responsible for the age-related losses in muscle size and function. Also, due to the high clearance rate of TNF-? from circulation, analyzing the circulating levels of soluble TNF-? receptors 1 and 2 (STNFR1 and STNFR2) may provide a better indication of inflammatory events. Therefore, the purpose of this study was to compare changes in circulating levels of TNF-?, STNFR1, and STNFR2 following an acute muscle damaging intervention in young age (YA) and middle-aged (MA) males. Recreationally active young (YA; N=9, 21.8 (&)#177; 2.2 y, 179.5 (&)#177; 4.9 cm, 91.2 (&)#177; 12.2 kg, 21.8 (&)#177; 4.3% BF) and middle-aged (MA; N=10, 47.0 (&)#177; 4.4 y, 176.8 (&)#177; 7.6 cm; 96.0 (&)#177; 21.5 kg, 25.4 (&)#177; 5.3% BF) males completed an acute muscle damaging protocol (MDP). Blood samples were obtained at baseline (BL), immediately (IP), 30 minutes (30P), 60 minutes (60P), 120 minutes (120P), 24 hours (24H), and 48 hours (48H) post-MDP. Lower body performance was analyzed via isokinetic dynamometer at BL, IP, 120P, 24H, and 48H. No significant group x time interactions or main group effects were observed for TNF-?, STNFR1, STNFR2 or any marker of muscle damage. When collapsed across groups, plasma lactate was significantly elevated at IP (p (<) 0.001) and 30P (p = 0.003); serum myoglobin was increased at 30P (p = 0.002), 60P (p = 0.001), and 120P (p = 0.007); creatine kinase was elevated at 24H (p = 0.001) and 48H (p = 0.005). Plasma concentrations of TNF-? were unchanged following MDP. With both groups combined, serum STNFR1 was decreased at 30P (p = 0.001) and increased at 48H (p = 0.028). Serum STNFR2 was decreased at 30P (p = 0.008), 60P (p = 0.003), and 120P (p = 0.002). The results of this study indicate that the TNF-? and STNFRs response to exercise is similar between young and middle-aged males. Measuring STNFRs may be a more appropriate method of assessing the acute inflammatory response to muscle damage. In addition, an acute bout of exercise may attenuate ectodomain shedding of TNFR1 and TNFR2. | |
Identifier: | CFE0006561 (IID), ucf:51350 (fedora) | |
Note(s): |
2017-05-01 M.S. Education and Human Performance, Educational and Human Sciences Masters This record was generated from author submitted information. |
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Subject(s): | Tumor Necrosis Factor-Alpha (TNF-?) -- Soluble Tumor Necrosis Factor-Alpha Receptor 1 (STNFR1) -- Soluble Tumor Necrosis Factor-Alpha Receptor 2 (STNFR2) -- Middle-aged -- Muscle Damage -- Inflammation | |
Persistent Link to This Record: | http://purl.flvc.org/ucf/fd/CFE0006561 | |
Restrictions on Access: | public 2017-05-15 | |
Host Institution: | UCF |