Acute endurance exercise stimulates circulating levels of mitochondrial-derived peptides in humans
In this manuscript, we report for the first time, to our knowledge, the response of circulating levels of mitochondrial-derived peptides humanin and MOTS-c to acute resistance and endurance exercise. Our data support that acute endurance exercise stimulates MDP levels in plasma, whereas acute resist...
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| Veröffentlicht in: | Journal of applied physiology (1985) 2021-09, Vol.131 (3), p.1035-1042 |
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| creator | von Walden, Ferdinand Fernandez-Gonzalo, Rodrigo Norrbom, Jessica Emanuelsson, Eric B. Figueiredo, Vandré C. Gidlund, Eva-Karin Norrbrand, Lena Liu, Chang Sandström, Philip Hansson, Björn Wan, Junxiang Cohen, Pinchas Alkner, Björn |
| description | In this manuscript, we report for the first time, to our knowledge, the response of circulating levels of mitochondrial-derived peptides humanin and MOTS-c to acute resistance and endurance exercise. Our data support that acute endurance exercise stimulates MDP levels in plasma, whereas acute resistance exercise does not.
Mitochondrial-derived peptides (MDPs) humanin (HN) and mitochondrial open reading frame of the 12S rRNA-c (MOTS-c) are involved in cell survival, suppression of apoptosis, and metabolism. Circulating levels of MDPs are altered in chronic diseases such as diabetes type 2 and chronic kidney disease. Whether acute resistance (RE) or endurance (EE) exercise modulates circulating levels of HN and MOTS-c in humans is unknown. Following familiarization, subjects were randomized to EE ( n = 10, 45 min cycling at 70% of estimated V̇O
2max
), RE ( n = 10, 4 sets × 7RM, leg press and knee extension), or control (CON, n = 10). Skeletal muscle biopsies and blood samples were collected before and at 30 min and 3 h following exercise. Plasma concentration of HN and MOTS-c, skeletal muscle MOTS-c as well as gene expression of exercise-related genes were analyzed. Acute EE and RE promoted changes in skeletal muscle gene expression typically seen in response to each exercise modality (c-Myc, 45S pre-rRNA, PGC-1α-total, and PGC-1α-ex1b). At rest, circulating levels of HN were positively correlated to MOTS-c levels and age. Plasma levels of MDPs were not correlated to fitness outcomes [V̇O
2max
, leg strength, or muscle mitochondrial (mt) DNA copy number]. Circulating levels of HN were significantly elevated by acute EE but not RE. MOTS-C levels showed a trend to increase after EE. These results indicate that plasma MDP levels are not related to fitness status but that acute EE increases circulating levels of MDPs, in particular HN.
NEW & NOTEWORTHY In this manuscript, we report for the first time, to our knowledge, the response of circulating levels of mitochondrial-derived peptides humanin and MOTS-c to acute resistance and endurance exercise. Our data support that acute endurance exercise stimulates MDP levels in plasma, whereas acute resistance exercise does not. |
| doi_str_mv | 10.1152/japplphysiol.00706.2019 |
| format | Article |
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Mitochondrial-derived peptides (MDPs) humanin (HN) and mitochondrial open reading frame of the 12S rRNA-c (MOTS-c) are involved in cell survival, suppression of apoptosis, and metabolism. Circulating levels of MDPs are altered in chronic diseases such as diabetes type 2 and chronic kidney disease. Whether acute resistance (RE) or endurance (EE) exercise modulates circulating levels of HN and MOTS-c in humans is unknown. Following familiarization, subjects were randomized to EE ( n = 10, 45 min cycling at 70% of estimated V̇O
2max
), RE ( n = 10, 4 sets × 7RM, leg press and knee extension), or control (CON, n = 10). Skeletal muscle biopsies and blood samples were collected before and at 30 min and 3 h following exercise. Plasma concentration of HN and MOTS-c, skeletal muscle MOTS-c as well as gene expression of exercise-related genes were analyzed. Acute EE and RE promoted changes in skeletal muscle gene expression typically seen in response to each exercise modality (c-Myc, 45S pre-rRNA, PGC-1α-total, and PGC-1α-ex1b). At rest, circulating levels of HN were positively correlated to MOTS-c levels and age. Plasma levels of MDPs were not correlated to fitness outcomes [V̇O
2max
, leg strength, or muscle mitochondrial (mt) DNA copy number]. Circulating levels of HN were significantly elevated by acute EE but not RE. MOTS-C levels showed a trend to increase after EE. These results indicate that plasma MDP levels are not related to fitness status but that acute EE increases circulating levels of MDPs, in particular HN.
NEW & NOTEWORTHY In this manuscript, we report for the first time, to our knowledge, the response of circulating levels of mitochondrial-derived peptides humanin and MOTS-c to acute resistance and endurance exercise. Our data support that acute endurance exercise stimulates MDP levels in plasma, whereas acute resistance exercise does not.</description><identifier>ISSN: 8750-7587</identifier><identifier>ISSN: 1522-1601</identifier><identifier>EISSN: 1522-1601</identifier><identifier>DOI: 10.1152/japplphysiol.00706.2019</identifier><language>eng</language><ispartof>Journal of applied physiology (1985), 2021-09, Vol.131 (3), p.1035-1042</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c404t-7901ee56a50f908894c217c4011779912d258c6f95d6d599459bc5be60ad10ef3</citedby><cites>FETCH-LOGICAL-c404t-7901ee56a50f908894c217c4011779912d258c6f95d6d599459bc5be60ad10ef3</cites><orcidid>0000-0002-6004-1117 ; 0000-0002-3012-7905 ; 0000-0002-2746-8581 ; 0000-0003-2816-9855 ; 0000-0003-1134-2252</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,550,776,780,881,3026,27901,27902</link.rule.ids><backlink>$$Uhttps://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-299506$$DView record from Swedish Publication Index$$Hfree_for_read</backlink><backlink>$$Uhttps://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-179620$$DView record from Swedish Publication Index$$Hfree_for_read</backlink><backlink>$$Uhttp://kipublications.ki.se/Default.aspx?queryparsed=id:147650878$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>von Walden, Ferdinand</creatorcontrib><creatorcontrib>Fernandez-Gonzalo, Rodrigo</creatorcontrib><creatorcontrib>Norrbom, Jessica</creatorcontrib><creatorcontrib>Emanuelsson, Eric B.</creatorcontrib><creatorcontrib>Figueiredo, Vandré C.</creatorcontrib><creatorcontrib>Gidlund, Eva-Karin</creatorcontrib><creatorcontrib>Norrbrand, Lena</creatorcontrib><creatorcontrib>Liu, Chang</creatorcontrib><creatorcontrib>Sandström, Philip</creatorcontrib><creatorcontrib>Hansson, Björn</creatorcontrib><creatorcontrib>Wan, Junxiang</creatorcontrib><creatorcontrib>Cohen, Pinchas</creatorcontrib><creatorcontrib>Alkner, Björn</creatorcontrib><title>Acute endurance exercise stimulates circulating levels of mitochondrial-derived peptides in humans</title><title>Journal of applied physiology (1985)</title><description>In this manuscript, we report for the first time, to our knowledge, the response of circulating levels of mitochondrial-derived peptides humanin and MOTS-c to acute resistance and endurance exercise. Our data support that acute endurance exercise stimulates MDP levels in plasma, whereas acute resistance exercise does not.
Mitochondrial-derived peptides (MDPs) humanin (HN) and mitochondrial open reading frame of the 12S rRNA-c (MOTS-c) are involved in cell survival, suppression of apoptosis, and metabolism. Circulating levels of MDPs are altered in chronic diseases such as diabetes type 2 and chronic kidney disease. Whether acute resistance (RE) or endurance (EE) exercise modulates circulating levels of HN and MOTS-c in humans is unknown. Following familiarization, subjects were randomized to EE ( n = 10, 45 min cycling at 70% of estimated V̇O
2max
), RE ( n = 10, 4 sets × 7RM, leg press and knee extension), or control (CON, n = 10). Skeletal muscle biopsies and blood samples were collected before and at 30 min and 3 h following exercise. Plasma concentration of HN and MOTS-c, skeletal muscle MOTS-c as well as gene expression of exercise-related genes were analyzed. Acute EE and RE promoted changes in skeletal muscle gene expression typically seen in response to each exercise modality (c-Myc, 45S pre-rRNA, PGC-1α-total, and PGC-1α-ex1b). At rest, circulating levels of HN were positively correlated to MOTS-c levels and age. Plasma levels of MDPs were not correlated to fitness outcomes [V̇O
2max
, leg strength, or muscle mitochondrial (mt) DNA copy number]. Circulating levels of HN were significantly elevated by acute EE but not RE. MOTS-C levels showed a trend to increase after EE. These results indicate that plasma MDP levels are not related to fitness status but that acute EE increases circulating levels of MDPs, in particular HN.
NEW & NOTEWORTHY In this manuscript, we report for the first time, to our knowledge, the response of circulating levels of mitochondrial-derived peptides humanin and MOTS-c to acute resistance and endurance exercise. Our data support that acute endurance exercise stimulates MDP levels in plasma, whereas acute resistance exercise does not.</description><issn>8750-7587</issn><issn>1522-1601</issn><issn>1522-1601</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>D8T</sourceid><recordid>eNqNkc1OwzAQhC0EEqXwDOQFUtZpbMfHqvxKlbgAV8uxN43b_MlOCn17UooQJ8RpRzszK60-Qq4pzChlyc1Gd13Vlfvg2moGIIDPEqDyhExGN4kpB3pKJplgEAuWiXNyEcIGgKYpoxOSL8zQY4SNHbxuzKg-0BsXMAq9q4dK9xgi47w5SNesowp3WIWoLaLa9a0p28Z6p6vYonc7tFGHXe_sWHJNVA61bsIlOSt0FfDqe07J6_3dy_IxXj0_PC0Xq9ikkPaxkEARGdcMCglZJlOTUDF6lAohJU1swjLDC8kst0zKlMncsBw5aEsBi_mUxMe74R27IVedd7X2e9Vqp75X21GhSvn4vvwzf-veFqr1a1W5QVEheQL_y2_7UiVSMuBjXhzzxrcheCx-GhTUAZ36jU59oVMHdPNPb4yT5Q</recordid><startdate>20210901</startdate><enddate>20210901</enddate><creator>von Walden, Ferdinand</creator><creator>Fernandez-Gonzalo, Rodrigo</creator><creator>Norrbom, Jessica</creator><creator>Emanuelsson, Eric B.</creator><creator>Figueiredo, Vandré C.</creator><creator>Gidlund, Eva-Karin</creator><creator>Norrbrand, Lena</creator><creator>Liu, Chang</creator><creator>Sandström, Philip</creator><creator>Hansson, Björn</creator><creator>Wan, Junxiang</creator><creator>Cohen, Pinchas</creator><creator>Alkner, Björn</creator><scope>AAYXX</scope><scope>CITATION</scope><scope>ADTPV</scope><scope>AFDQA</scope><scope>AOWAS</scope><scope>D8T</scope><scope>D8V</scope><scope>ZZAVC</scope><scope>DG8</scope><orcidid>https://orcid.org/0000-0002-6004-1117</orcidid><orcidid>https://orcid.org/0000-0002-3012-7905</orcidid><orcidid>https://orcid.org/0000-0002-2746-8581</orcidid><orcidid>https://orcid.org/0000-0003-2816-9855</orcidid><orcidid>https://orcid.org/0000-0003-1134-2252</orcidid></search><sort><creationdate>20210901</creationdate><title>Acute endurance exercise stimulates circulating levels of mitochondrial-derived peptides in humans</title><author>von Walden, Ferdinand ; Fernandez-Gonzalo, Rodrigo ; Norrbom, Jessica ; Emanuelsson, Eric B. ; Figueiredo, Vandré C. ; Gidlund, Eva-Karin ; Norrbrand, Lena ; Liu, Chang ; Sandström, Philip ; Hansson, Björn ; Wan, Junxiang ; Cohen, Pinchas ; Alkner, Björn</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c404t-7901ee56a50f908894c217c4011779912d258c6f95d6d599459bc5be60ad10ef3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>von Walden, Ferdinand</creatorcontrib><creatorcontrib>Fernandez-Gonzalo, Rodrigo</creatorcontrib><creatorcontrib>Norrbom, Jessica</creatorcontrib><creatorcontrib>Emanuelsson, Eric B.</creatorcontrib><creatorcontrib>Figueiredo, Vandré C.</creatorcontrib><creatorcontrib>Gidlund, Eva-Karin</creatorcontrib><creatorcontrib>Norrbrand, Lena</creatorcontrib><creatorcontrib>Liu, Chang</creatorcontrib><creatorcontrib>Sandström, Philip</creatorcontrib><creatorcontrib>Hansson, Björn</creatorcontrib><creatorcontrib>Wan, Junxiang</creatorcontrib><creatorcontrib>Cohen, Pinchas</creatorcontrib><creatorcontrib>Alkner, Björn</creatorcontrib><collection>CrossRef</collection><collection>SwePub</collection><collection>SWEPUB Kungliga Tekniska Högskolan full text</collection><collection>SwePub Articles</collection><collection>SWEPUB Freely available online</collection><collection>SWEPUB Kungliga Tekniska Högskolan</collection><collection>SwePub Articles full text</collection><collection>SWEPUB Linköpings universitet</collection><jtitle>Journal of applied physiology (1985)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>von Walden, Ferdinand</au><au>Fernandez-Gonzalo, Rodrigo</au><au>Norrbom, Jessica</au><au>Emanuelsson, Eric B.</au><au>Figueiredo, Vandré C.</au><au>Gidlund, Eva-Karin</au><au>Norrbrand, Lena</au><au>Liu, Chang</au><au>Sandström, Philip</au><au>Hansson, Björn</au><au>Wan, Junxiang</au><au>Cohen, Pinchas</au><au>Alkner, Björn</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Acute endurance exercise stimulates circulating levels of mitochondrial-derived peptides in humans</atitle><jtitle>Journal of applied physiology (1985)</jtitle><date>2021-09-01</date><risdate>2021</risdate><volume>131</volume><issue>3</issue><spage>1035</spage><epage>1042</epage><pages>1035-1042</pages><issn>8750-7587</issn><issn>1522-1601</issn><eissn>1522-1601</eissn><abstract>In this manuscript, we report for the first time, to our knowledge, the response of circulating levels of mitochondrial-derived peptides humanin and MOTS-c to acute resistance and endurance exercise. Our data support that acute endurance exercise stimulates MDP levels in plasma, whereas acute resistance exercise does not.
Mitochondrial-derived peptides (MDPs) humanin (HN) and mitochondrial open reading frame of the 12S rRNA-c (MOTS-c) are involved in cell survival, suppression of apoptosis, and metabolism. Circulating levels of MDPs are altered in chronic diseases such as diabetes type 2 and chronic kidney disease. Whether acute resistance (RE) or endurance (EE) exercise modulates circulating levels of HN and MOTS-c in humans is unknown. Following familiarization, subjects were randomized to EE ( n = 10, 45 min cycling at 70% of estimated V̇O
2max
), RE ( n = 10, 4 sets × 7RM, leg press and knee extension), or control (CON, n = 10). Skeletal muscle biopsies and blood samples were collected before and at 30 min and 3 h following exercise. Plasma concentration of HN and MOTS-c, skeletal muscle MOTS-c as well as gene expression of exercise-related genes were analyzed. Acute EE and RE promoted changes in skeletal muscle gene expression typically seen in response to each exercise modality (c-Myc, 45S pre-rRNA, PGC-1α-total, and PGC-1α-ex1b). At rest, circulating levels of HN were positively correlated to MOTS-c levels and age. Plasma levels of MDPs were not correlated to fitness outcomes [V̇O
2max
, leg strength, or muscle mitochondrial (mt) DNA copy number]. Circulating levels of HN were significantly elevated by acute EE but not RE. MOTS-C levels showed a trend to increase after EE. These results indicate that plasma MDP levels are not related to fitness status but that acute EE increases circulating levels of MDPs, in particular HN.
NEW & NOTEWORTHY In this manuscript, we report for the first time, to our knowledge, the response of circulating levels of mitochondrial-derived peptides humanin and MOTS-c to acute resistance and endurance exercise. Our data support that acute endurance exercise stimulates MDP levels in plasma, whereas acute resistance exercise does not.</abstract><doi>10.1152/japplphysiol.00706.2019</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0002-6004-1117</orcidid><orcidid>https://orcid.org/0000-0002-3012-7905</orcidid><orcidid>https://orcid.org/0000-0002-2746-8581</orcidid><orcidid>https://orcid.org/0000-0003-2816-9855</orcidid><orcidid>https://orcid.org/0000-0003-1134-2252</orcidid><oa>free_for_read</oa></addata></record> |
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| title | Acute endurance exercise stimulates circulating levels of mitochondrial-derived peptides in humans |
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