Endothelial nitric oxide synthase mediates the nitric oxide component of reflex cutaneous vasodilatation during dynamic exercise in humans
Key points Increases in skin blood flow and sweating also occur during exercise; however, it is not known if the mechanisms controlling these responses are the same during passive heat stress and exercise. The prevailing thought has been that mechanisms of cutaneous vasodilatation during passive hea...
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| Published in | The Journal of physiology Vol. 592; no. 23; pp. 5317 - 5326 |
|---|---|
| Main Authors | , , , , |
| Format | Journal Article |
| Language | English |
| Published |
England
Wiley Subscription Services, Inc
01.12.2014
BlackWell Publishing Ltd |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0022-3751 1469-7793 1469-7793 |
| DOI | 10.1113/jphysiol.2014.272898 |
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| Abstract | Key points
Increases in skin blood flow and sweating also occur during exercise; however, it is not known if the mechanisms controlling these responses are the same during passive heat stress and exercise.
The prevailing thought has been that mechanisms of cutaneous vasodilatation during passive heat stress and sustained dynamic exercise are the same, or very similar.
Nitric oxide (NO) has been shown to be important for increasing skin blood flow during passive heat stress but it is unknown if this molecule is also involved during sustained dynamic exercise.
The findings from our study suggest NO is involved in increasing skin blood flow during sustained dynamic exercise in humans but the NO is produced from a different enzyme compared to passive heat stress.
These findings may help us better understand and aid individuals who have difficulty regulating their body temperature during sustained dynamic exercise (e.g. ageing).
Recent data suggests neuronal nitric oxide synthase (nNOS) mediates the NO component of reflex cutaneous vasodilatation with passive heat stress. We tested the hypothesis that nNOS inhibition would attenuate reflex cutaneous vasodilatation during sustained dynamic exercise in young healthy humans. All subjects first performed an incremental V̇O2, peak test to exhaustion on a custom‐built supine cycle ergometer. On a separate day, subjects were instrumented with four intradermal microdialysis fibres on the forearm and each randomly assigned as: (1) lactated Ringer's (control); (2) 20 mm Nω‐nitro‐l‐arginine methyl ester hydrochloride (non‐selective NOS inhibitor); (3) 5 mm N‐propyl‐l‐arginine (nNOS inhibitor); and (4) 10 mm N5‐(1‐iminoethyl)‐l‐ornithine dihydrochloride [endothelial NOS (eNOS) inhibitor]. Following microdialysis placement, subjects performed supine cycling with the experimental arm at heart level at 60% V̇O2, peak for a period sufficient to raise core temperature 0.8°C. At the end of cycling, all microdialysis sites were locally heated to 43°C and sodium nitroprusside was perfused to elicit maximal vasodilatation. Mean arterial pressure, skin blood flow via laser‐Doppler flowmetry and core temperature via ingestible telemetric pill were measured continuously; cutaneous vascular conductance (CVC) was calculated as laser‐Doppler flowmetry/mean arterial pressure and normalized to maximum. There was no significant difference between control (58 ± 2%CVCmax) and nNOS‐inhibited (56 ± 3%CVCmax) sites in response to exercise‐induced hyperthermia. The increase in CVC at eNOS‐inhibited (41 ± 3%CVCmax) and non‐selective NOS‐inhibited (40 ± 4%CVCmax) sites were significantly attenuated compared to control and nNOS‐inhibited (P < 0.001 all conditions) but there was no difference between eNOS‐inhibited and non‐selective NOS‐inhibited sites. These data suggest eNOS, not nNOS, mediate NO synthesis during reflex cutaneous vasodilatation with sustained dynamic exercise. |
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| AbstractList | Key points
Increases in skin blood flow and sweating also occur during exercise; however, it is not known if the mechanisms controlling these responses are the same during passive heat stress and exercise.
The prevailing thought has been that mechanisms of cutaneous vasodilatation during passive heat stress and sustained dynamic exercise are the same, or very similar.
Nitric oxide (NO) has been shown to be important for increasing skin blood flow during passive heat stress but it is unknown if this molecule is also involved during sustained dynamic exercise.
The findings from our study suggest NO is involved in increasing skin blood flow during sustained dynamic exercise in humans but the NO is produced from a different enzyme compared to passive heat stress.
These findings may help us better understand and aid individuals who have difficulty regulating their body temperature during sustained dynamic exercise (e.g. ageing).
Recent data suggests neuronal nitric oxide synthase (nNOS) mediates the NO component of reflex cutaneous vasodilatation with passive heat stress. We tested the hypothesis that nNOS inhibition would attenuate reflex cutaneous vasodilatation during sustained dynamic exercise in young healthy humans. All subjects first performed an incremental V̇O2, peak test to exhaustion on a custom‐built supine cycle ergometer. On a separate day, subjects were instrumented with four intradermal microdialysis fibres on the forearm and each randomly assigned as: (1) lactated Ringer's (control); (2) 20 mm Nω‐nitro‐l‐arginine methyl ester hydrochloride (non‐selective NOS inhibitor); (3) 5 mm N‐propyl‐l‐arginine (nNOS inhibitor); and (4) 10 mm N5‐(1‐iminoethyl)‐l‐ornithine dihydrochloride [endothelial NOS (eNOS) inhibitor]. Following microdialysis placement, subjects performed supine cycling with the experimental arm at heart level at 60% V̇O2, peak for a period sufficient to raise core temperature 0.8°C. At the end of cycling, all microdialysis sites were locally heated to 43°C and sodium nitroprusside was perfused to elicit maximal vasodilatation. Mean arterial pressure, skin blood flow via laser‐Doppler flowmetry and core temperature via ingestible telemetric pill were measured continuously; cutaneous vascular conductance (CVC) was calculated as laser‐Doppler flowmetry/mean arterial pressure and normalized to maximum. There was no significant difference between control (58 ± 2%CVCmax) and nNOS‐inhibited (56 ± 3%CVCmax) sites in response to exercise‐induced hyperthermia. The increase in CVC at eNOS‐inhibited (41 ± 3%CVCmax) and non‐selective NOS‐inhibited (40 ± 4%CVCmax) sites were significantly attenuated compared to control and nNOS‐inhibited (P < 0.001 all conditions) but there was no difference between eNOS‐inhibited and non‐selective NOS‐inhibited sites. These data suggest eNOS, not nNOS, mediate NO synthesis during reflex cutaneous vasodilatation with sustained dynamic exercise. Recent data suggests neuronal nitric oxide synthase (nNOS) mediates the NO component of reflex cutaneous vasodilatation with passive heat stress. We tested the hypothesis that nNOS inhibition would attenuate reflex cutaneous vasodilatation during sustained dynamic exercise in young healthy humans. All subjects first performed an incremental test to exhaustion on a custom-built supine cycle ergometer. On a separate day, subjects were instrumented with four intradermal microdialysis fibres on the forearm and each randomly assigned as: (1) lactated Ringer's (control); (2) 20 m m N ω -nitro- l -arginine methyl ester hydrochloride (non-selective NOS inhibitor); (3) 5 m m N -propyl- l -arginine (nNOS inhibitor); and (4) 10 m m N 5 -(1-iminoethyl)- l -ornithine dihydrochloride [endothelial NOS (eNOS) inhibitor]. Following microdialysis placement, subjects performed supine cycling with the experimental arm at heart level at 60% for a period sufficient to raise core temperature 0.8°C. At the end of cycling, all microdialysis sites were locally heated to 43°C and sodium nitroprusside was perfused to elicit maximal vasodilatation. Mean arterial pressure, skin blood flow via laser-Doppler flowmetry and core temperature via ingestible telemetric pill were measured continuously; cutaneous vascular conductance (CVC) was calculated as laser-Doppler flowmetry/mean arterial pressure and normalized to maximum. There was no significant difference between control (58 ± 2%CVC max ) and nNOS-inhibited (56 ± 3%CVC max ) sites in response to exercise-induced hyperthermia. The increase in CVC at eNOS-inhibited (41 ± 3%CVC max ) and non-selective NOS-inhibited (40 ± 4%CVC max ) sites were significantly attenuated compared to control and nNOS-inhibited ( P < 0.001 all conditions) but there was no difference between eNOS-inhibited and non-selective NOS-inhibited sites. These data suggest eNOS, not nNOS, mediate NO synthesis during reflex cutaneous vasodilatation with sustained dynamic exercise. Key points Increases in skin blood flow and sweating also occur during exercise; however, it is not known if the mechanisms controlling these responses are the same during passive heat stress and exercise. The prevailing thought has been that mechanisms of cutaneous vasodilatation during passive heat stress and sustained dynamic exercise are the same, or very similar. Nitric oxide (NO) has been shown to be important for increasing skin blood flow during passive heat stress but it is unknown if this molecule is also involved during sustained dynamic exercise. The findings from our study suggest NO is involved in increasing skin blood flow during sustained dynamic exercise in humans but the NO is produced from a different enzyme compared to passive heat stress. These findings may help us better understand and aid individuals who have difficulty regulating their body temperature during sustained dynamic exercise (e.g. ageing). Recent data suggests neuronal nitric oxide synthase (nNOS) mediates the NO component of reflex cutaneous vasodilatation with passive heat stress. We tested the hypothesis that nNOS inhibition would attenuate reflex cutaneous vasodilatation during sustained dynamic exercise in young healthy humans. All subjects first performed an incremental V O 2 , peak test to exhaustion on a custom-built supine cycle ergometer. On a separate day, subjects were instrumented with four intradermal microdialysis fibres on the forearm and each randomly assigned as: (1) lactated Ringer's (control); (2) 20 mm N[omega]-nitro-l-arginine methyl ester hydrochloride (non-selective NOS inhibitor); (3) 5 mm N-propyl-l-arginine (nNOS inhibitor); and (4) 10 mm N5-(1-iminoethyl)-l-ornithine dihydrochloride [endothelial NOS (eNOS) inhibitor]. Following microdialysis placement, subjects performed supine cycling with the experimental arm at heart level at 60% V O 2 , peak for a period sufficient to raise core temperature 0.8°C. At the end of cycling, all microdialysis sites were locally heated to 43°C and sodium nitroprusside was perfused to elicit maximal vasodilatation. Mean arterial pressure, skin blood flow via laser-Doppler flowmetry and core temperature via ingestible telemetric pill were measured continuously; cutaneous vascular conductance (CVC) was calculated as laser-Doppler flowmetry/mean arterial pressure and normalized to maximum. There was no significant difference between control (58 ± 2%CVCmax) and nNOS-inhibited (56 ± 3%CVCmax) sites in response to exercise-induced hyperthermia. The increase in CVC at eNOS-inhibited (41 ± 3%CVCmax) and non-selective NOS-inhibited (40 ± 4%CVCmax) sites were significantly attenuated compared to control and nNOS-inhibited (P < 0.001 all conditions) but there was no difference between eNOS-inhibited and non-selective NOS-inhibited sites. These data suggest eNOS, not nNOS, mediate NO synthesis during reflex cutaneous vasodilatation with sustained dynamic exercise. Increases in skin blood flow and sweating also occur during exercise; however, it is not known if the mechanisms controlling these responses are the same during passive heat stress and exercise. Recent data suggests neuronal nitric oxide synthase (nNOS) mediates the NO component of reflex cutaneous vasodilatation with passive heat stress. We tested the hypothesis that nNOS inhibition would attenuate reflex cutaneous vasodilatation during sustained dynamic exercise in young healthy humans. All subjects first performed an incremental VO2, peak test to exhaustion on a custom-built supine cycle ergometer. On a separate day, subjects were instrumented with four intradermal microdialysis fibres on the forearm and each randomly assigned as: (1) lactated Ringer's (control); (2) 20 mmN omega -nitro-l-arginine methyl ester hydrochloride (non-selective NOS inhibitor); (3) 5 mmN-propyl-l-arginine (nNOS inhibitor); and (4) 10 mmN5-(1-iminoethyl)-l-ornithine dihydrochloride [endothelial NOS (eNOS) inhibitor]. Following microdialysis placement, subjects performed supine cycling with the experimental arm at heart level at 60% VO2, peak for a period sufficient to raise core temperature 0.8 degree C. At the end of cycling, all microdialysis sites were locally heated to 43 degree C and sodium nitroprusside was perfused to elicit maximal vasodilatation. Mean arterial pressure, skin blood flow via laser-Doppler flowmetry and core temperature via ingestible telemetric pill were measured continuously; cutaneous vascular conductance (CVC) was calculated as laser-Doppler flowmetry/mean arterial pressure and normalized to maximum. There was no significant difference between control (58 plus or minus 2%CVCmax) and nNOS-inhibited (56 plus or minus 3%CVCmax) sites in response to exercise-induced hyperthermia. The increase in CVC at eNOS-inhibited (41 plus or minus 3%CVCmax) and non-selective NOS-inhibited (40 plus or minus 4%CVCmax) sites were significantly attenuated compared to control and nNOS-inhibited (P < 0.001 all conditions) but there was no difference between eNOS-inhibited and non-selective NOS-inhibited sites. These data suggest eNOS, not nNOS, mediate NO synthesis during reflex cutaneous vasodilatation with sustained dynamic exercise. Recent data suggests neuronal nitric oxide synthase (nNOS) mediates the NO component of reflex cutaneous vasodilatation with passive heat stress. We tested the hypothesis that nNOS inhibition would attenuate reflex cutaneous vasodilatation during sustained dynamic exercise in young healthy humans. All subjects first performed an incremental V̇O2, peak test to exhaustion on a custom-built supine cycle ergometer. On a separate day, subjects were instrumented with four intradermal microdialysis fibres on the forearm and each randomly assigned as: (1) lactated Ringer's (control); (2) 20 mm Nω-nitro-l-arginine methyl ester hydrochloride (non-selective NOS inhibitor); (3) 5 mm N-propyl-l-arginine (nNOS inhibitor); and (4) 10 mm N(5)-(1-iminoethyl)-l-ornithine dihydrochloride [endothelial NOS (eNOS) inhibitor]. Following microdialysis placement, subjects performed supine cycling with the experimental arm at heart level at 60% V̇O2, peak for a period sufficient to raise core temperature 0.8°C. At the end of cycling, all microdialysis sites were locally heated to 43°C and sodium nitroprusside was perfused to elicit maximal vasodilatation. Mean arterial pressure, skin blood flow via laser-Doppler flowmetry and core temperature via ingestible telemetric pill were measured continuously; cutaneous vascular conductance (CVC) was calculated as laser-Doppler flowmetry/mean arterial pressure and normalized to maximum. There was no significant difference between control (58 ± 2%CVCmax) and nNOS-inhibited (56 ± 3%CVCmax) sites in response to exercise-induced hyperthermia. The increase in CVC at eNOS-inhibited (41 ± 3%CVCmax) and non-selective NOS-inhibited (40 ± 4%CVCmax) sites were significantly attenuated compared to control and nNOS-inhibited (P < 0.001 all conditions) but there was no difference between eNOS-inhibited and non-selective NOS-inhibited sites. These data suggest eNOS, not nNOS, mediate NO synthesis during reflex cutaneous vasodilatation with sustained dynamic exercise. Recent data suggests neuronal nitric oxide synthase (nNOS) mediates the NO component of reflex cutaneous vasodilatation with passive heat stress. We tested the hypothesis that nNOS inhibition would attenuate reflex cutaneous vasodilatation during sustained dynamic exercise in young healthy humans. All subjects first performed an incremental V̇O2, peak test to exhaustion on a custom-built supine cycle ergometer. On a separate day, subjects were instrumented with four intradermal microdialysis fibres on the forearm and each randomly assigned as: (1) lactated Ringer's (control); (2) 20 mm Nω-nitro-l-arginine methyl ester hydrochloride (non-selective NOS inhibitor); (3) 5 mm N-propyl-l-arginine (nNOS inhibitor); and (4) 10 mm N(5)-(1-iminoethyl)-l-ornithine dihydrochloride [endothelial NOS (eNOS) inhibitor]. Following microdialysis placement, subjects performed supine cycling with the experimental arm at heart level at 60% V̇O2, peak for a period sufficient to raise core temperature 0.8°C. At the end of cycling, all microdialysis sites were locally heated to 43°C and sodium nitroprusside was perfused to elicit maximal vasodilatation. Mean arterial pressure, skin blood flow via laser-Doppler flowmetry and core temperature via ingestible telemetric pill were measured continuously; cutaneous vascular conductance (CVC) was calculated as laser-Doppler flowmetry/mean arterial pressure and normalized to maximum. There was no significant difference between control (58 ± 2%CVCmax) and nNOS-inhibited (56 ± 3%CVCmax) sites in response to exercise-induced hyperthermia. The increase in CVC at eNOS-inhibited (41 ± 3%CVCmax) and non-selective NOS-inhibited (40 ± 4%CVCmax) sites were significantly attenuated compared to control and nNOS-inhibited (P < 0.001 all conditions) but there was no difference between eNOS-inhibited and non-selective NOS-inhibited sites. These data suggest eNOS, not nNOS, mediate NO synthesis during reflex cutaneous vasodilatation with sustained dynamic exercise.Recent data suggests neuronal nitric oxide synthase (nNOS) mediates the NO component of reflex cutaneous vasodilatation with passive heat stress. We tested the hypothesis that nNOS inhibition would attenuate reflex cutaneous vasodilatation during sustained dynamic exercise in young healthy humans. All subjects first performed an incremental V̇O2, peak test to exhaustion on a custom-built supine cycle ergometer. On a separate day, subjects were instrumented with four intradermal microdialysis fibres on the forearm and each randomly assigned as: (1) lactated Ringer's (control); (2) 20 mm Nω-nitro-l-arginine methyl ester hydrochloride (non-selective NOS inhibitor); (3) 5 mm N-propyl-l-arginine (nNOS inhibitor); and (4) 10 mm N(5)-(1-iminoethyl)-l-ornithine dihydrochloride [endothelial NOS (eNOS) inhibitor]. Following microdialysis placement, subjects performed supine cycling with the experimental arm at heart level at 60% V̇O2, peak for a period sufficient to raise core temperature 0.8°C. At the end of cycling, all microdialysis sites were locally heated to 43°C and sodium nitroprusside was perfused to elicit maximal vasodilatation. Mean arterial pressure, skin blood flow via laser-Doppler flowmetry and core temperature via ingestible telemetric pill were measured continuously; cutaneous vascular conductance (CVC) was calculated as laser-Doppler flowmetry/mean arterial pressure and normalized to maximum. There was no significant difference between control (58 ± 2%CVCmax) and nNOS-inhibited (56 ± 3%CVCmax) sites in response to exercise-induced hyperthermia. The increase in CVC at eNOS-inhibited (41 ± 3%CVCmax) and non-selective NOS-inhibited (40 ± 4%CVCmax) sites were significantly attenuated compared to control and nNOS-inhibited (P < 0.001 all conditions) but there was no difference between eNOS-inhibited and non-selective NOS-inhibited sites. These data suggest eNOS, not nNOS, mediate NO synthesis during reflex cutaneous vasodilatation with sustained dynamic exercise. |
| Author | McNamara, Tanner C. Keen, Jeremy T. Alexander, Lacy M. Wong, Brett J. Simmons, Grant H. |
| Author_xml | – sequence: 1 givenname: Tanner C. surname: McNamara fullname: McNamara, Tanner C. organization: Kansas State University – sequence: 2 givenname: Jeremy T. surname: Keen fullname: Keen, Jeremy T. organization: Kansas State University – sequence: 3 givenname: Grant H. surname: Simmons fullname: Simmons, Grant H. organization: Nike – sequence: 4 givenname: Lacy M. surname: Alexander fullname: Alexander, Lacy M. organization: The Pennsylvania State University – sequence: 5 givenname: Brett J. surname: Wong fullname: Wong, Brett J. organization: Georgia State University |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/25260636$$D View this record in MEDLINE/PubMed |
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| ContentType | Journal Article |
| Copyright | 2014 The Authors. The Journal of Physiology © 2014 The Physiological Society 2014 The Authors. The Journal of Physiology © 2014 The Physiological Society. Journal compilation © 2014 The Physiological Society 2014 The Authors. The Journal of Physiology © 2014 The Physiological Society 2014 |
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Increases in skin blood flow and sweating also occur during exercise; however, it is not known if the mechanisms controlling these responses are the... Recent data suggests neuronal nitric oxide synthase (nNOS) mediates the NO component of reflex cutaneous vasodilatation with passive heat stress. We tested the... Key points Increases in skin blood flow and sweating also occur during exercise; however, it is not known if the mechanisms controlling these responses are the... Increases in skin blood flow and sweating also occur during exercise; however, it is not known if the mechanisms controlling these responses are the same... |
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| SubjectTerms | Adult Arginine - analogs & derivatives Arginine - pharmacology Body Temperature Regulation - physiology Enzyme Inhibitors - pharmacology Exercise - physiology Heat Stress Disorders - physiopathology Hemodynamics Hot Temperature - adverse effects Humans Integrative Male Microdialysis NG-Nitroarginine Methyl Ester - pharmacology Nitric Oxide - physiology Nitric Oxide Synthase Type I - antagonists & inhibitors Nitric Oxide Synthase Type I - physiology Nitric Oxide Synthase Type III - antagonists & inhibitors Nitric Oxide Synthase Type III - physiology Ornithine - analogs & derivatives Ornithine - pharmacology Oxygen Consumption Reflex - physiology Skin - blood supply Vasodilation - drug effects Vasodilation - physiology Young Adult |
| Title | Endothelial nitric oxide synthase mediates the nitric oxide component of reflex cutaneous vasodilatation during dynamic exercise in humans |
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