FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2079667098> ?p ?o ?g. }

• W2079667098 endingPage "2330" @default.
• W2079667098 startingPage "2328" @default.
• W2079667098 abstract "Aerobic training improves thermal tolerance (Armstrong and Pandolf, 1988Armstrong L.E. Pandolf K.B. Physical training, cardiorespiratory physical fitness and exercise-heat tolerance.in: Pandolf K.B. Sawka M.N. Gonzalez R.R. Human Performance Physiology and Environmental Medicine at Terrestrial Extremes. Cooper Publishing, Carmel, IN1988: 199-226Google Scholar), which is postulated to result in part from improved evaporative cooling (Taylor, 1986Taylor N.A. Eccrine sweat glands. Adaptations to physical training and heat acclimation.Sports Med. 1986; 3: 387-397Crossref PubMed Scopus (37) Google Scholar; Shibasaki et al., 2006Shibasaki M. Wilson T.E. Crandall C.G. Neural control and mechanisms of eccrine sweating during heat stress and exercise.J Appl Physiol. 2006; 100: 1692-1701Crossref PubMed Scopus (184) Google Scholar). Previous observations indicate that aerobic training either lowers the internal temperature at which sweating begins (sweating threshold) or increases the slopes of the internal temperature-sweat rate (Roberts et al., 1977Roberts M.F. Wenger C.B. Stolwijk J.A. Nadel E.R. Skin blood flow and sweating changes following exercise training and heat acclimation.J Appl Physiol. 1977; 43: 133-137PubMed Google Scholar) or exercise intensity–sweat rate relations (Yanagimoto et al., 2002Yanagimoto S. Aoki K. Horikawa N. Shibasaki M. Inoue Y. Nishiyasu T. et al.Sweating response in physically trained men to sustained handgrip exercise in mildly hyperthermic conditions.Acta Physiol Scand. 2002; 174: 31-39Crossref PubMed Scopus (16) Google Scholar). In contrast, deconditioning or detraining, associated with bedrest, increases the sweating threshold and decreases the slope of internal temperature–sweat rate relation (Lee et al., 2002Lee S.M. Williams W.J. Schneider S.M. Role of skin blood flow and sweating rate in exercise thermoregulation after bed rest.J Appl Physiol. 2002; 92: 2026-2034Crossref PubMed Scopus (32) Google Scholar). Importantly these deconditioning-related responses can be prevented by exercising during bedrest (Shibasaki et al., 2003Shibasaki M. Wilson T.E. Cui J. Levine B.D. Crandall C.G. Exercise throughout 6 degrees head-down tilt bed rest preserves thermoregulatory responses.J Appl Physiol. 2003; 95: 1817-1823Crossref PubMed Scopus (21) Google Scholar). These studies, although informative, do not provide mechanistic insight into whether altered sweating responses to aerobic training are mediated by a central sympathetic component or at the level of the eccrine gland. Application of cholinergic agonists directly in the dermal space without repeated injections or electric current can isolate peripheral sweating responses (Crandall et al., 2003Crandall C.G. Shibasaki M. Wilson T.E. Cui J. Levine B.D. Prolonged head-down tilt exposure reduces maximal cutaneous vasodilator and sweating capacity in humans.J Appl Physiol. 2003; 94: 2330-2336Crossref PubMed Scopus (40) Google Scholar; Morgan et al., 2006Morgan C.J. Friedmann P.S. Church M.K. Clough G.F. Cutaneous microdialysis as a novel means of continuously stimulating eccrine sweat glands in vivo.J Invest Dermatol. 2006; 126: 1220-1225Abstract Full Text Full Text PDF PubMed Scopus (18) Google Scholar; Schlereth et al., 2006Schlereth T. Dittmar J.O. Seewald B. Birklein F. Peripheral amplification of sweating--a role for calcitonin gene-related peptide.J Physiol. 2006; 576: 823-832Crossref PubMed Scopus (59) Google Scholar). Cross-sectional studies (comparing aerobic trained vs. untrained) using electrical current drug delivery (iontophoresis) have observed increased sweating capacity and number of activated sweat glands with aerobic training (Buono and Sjoholm, 1988Buono M.J. Sjoholm N.T. Effect of physical training on peripheral sweat production.J Appl Physiol. 1988; 65: 811-814PubMed Google Scholar; Buono et al., 1992Buono M.J. White C.S. Connolly K.P. Cholinergic sensitivity of the eccrine sweat gland in trained and untrained men.J Dermatol Sci. 1992; 4: 33-37Abstract Full Text PDF PubMed Scopus (20) Google Scholar). However, these studies provided minimal insight into whether these adaptatory responses were mediated by changes in receptor responsiveness and sensitivity, or were simply a function of subject population selected. Accordingly, we tested the hypothesis that 8 weeks of aerobic training increases in vivo cholinergic sensitivity and responsiveness of eccrine sweat glands, without altering the number of exogenous acetylcholine-activated glands. Eleven sedentary, young (age=26±1), healthy, non-obese (BMI<30kgm–2), normotensive (<140/90 mmHg), non-smokers participated in this institutional approved longitudinal training study that adhered to Declaration of Helsinki guidelines. Each subject provided written informed consent and received a medical history and physical exam before participating in the study. Two intradermal microdialysis membranes were placed ∼3cm apart in dorsal forearm skin in a similar location pre- and post-training, which unlike previous studies allows for continuous monitoring of sweat glands at a prescribed agonist concentration (Morgan et al., 2006Morgan C.J. Friedmann P.S. Church M.K. Clough G.F. Cutaneous microdialysis as a novel means of continuously stimulating eccrine sweat glands in vivo.J Invest Dermatol. 2006; 126: 1220-1225Abstract Full Text Full Text PDF PubMed Scopus (18) Google Scholar). This technique involved placing a small (200-μm outer diameter, 10-mm length) semipermeable membrane (20-kDa cutoff) intradermally at a depth of approximately 0.3–1.0mm below the epidermis (Kellogg et al., 1999Kellogg Jr, D.L. Liu Y. Kosiba I.F. O'Donnell D. Role of nitric oxide in the vascular effects of local warming of the skin in humans.J Appl Physiol. 1999; 86: 1185-1190PubMed Google Scholar). Eight doses of acetylcholine (10−7 to 1M acetylcholine) in a lactated Ringer's vehicle were administered for 5minutes at 2μl/minutes via a microdialysis infusion pump. Sweat rate was measured via capacitance hygrometry and the number of activated sweat glands was quantified using a starch–iodine technique during infusion of 1M acetylcholine. Cholinergic dose–response relations were determined by logistic regression modeling. Endurance training consisted of running or cycling 4 times/week for 8 weeks. Subjects wore a heart rate monitor during all exercise sessions to ensure maintenance of target heart rates. Training began with exercising for 20minutes at a work rate sufficient to achieve 80% of maximum heart rate. Exercise times increased to 60minutes as training progressed, and high-intensity interval exercises were added twice/week during the second week to further stimulate training adaptations. Peak oxygen uptake increased from 32.9 to 40.7mlkg−1min−1 or 19±2% (P<0.05) and resting heart rate decreased 9±2b.p.m. (P<0.05) indicative of a training effect. The number of cholinergic-activated glands was unchanged by training (pre-training=40±6 and post-training=39±7 glands per 0.5cm2). This indicates that a similar number of glands were recruited both pre- and post-training and that this type and duration of training does not increase the number of exogenous cholinergic-activated glands. Dose–response relations were established with goodness of fit (R2) relations of 0.67±0.02 for pre-training and 0.72±0.02 for post-training, indicating that the logistic regression modeling adequately modeled the data (Figure 1). Training did not affect the ED50, but increased the maximal responses of the dose–response relation (Figure 2).Figure 2Effect of aerobic training on in vivo cholinergic dose–response relations. ED50 is the effective dose causing 50% of the maximal response and is an indicator of sensitivity. Maximum is the maximal response of the cholinergic dose–response relation and is indicative of responsiveness. The asterisk denotes a significant difference from the previous time point (P<0.05).View Large Image Figure ViewerDownload (PPT) These findings provide important insight into the adaptatory mechanism(s) of eccrine sweat glands to longitudinal aerobic training in humans. First, we did not observe a leftward shift in the ED50 of the cholinergic dose–response curve, strongly suggesting that exercise training does not alter eccrine sweat gland in vivo cholinergic sensitivity as previously suggested (Roberts et al., 1977Roberts M.F. Wenger C.B. Stolwijk J.A. Nadel E.R. Skin blood flow and sweating changes following exercise training and heat acclimation.J Appl Physiol. 1977; 43: 133-137PubMed Google Scholar; Buono et al., 1992Buono M.J. White C.S. Connolly K.P. Cholinergic sensitivity of the eccrine sweat gland in trained and untrained men.J Dermatol Sci. 1992; 4: 33-37Abstract Full Text PDF PubMed Scopus (20) Google Scholar). However, these reports suggesting an increase in cholinergic sensitivity used an iontophoresis drug delivery system to engage muscarinic receptors with pilocarpine or observed an increase in the slope of internal temperature–sweat rate relation. Pilocarpine iontophoresis, although beneficial for determining gross changes in sweating such as occuring with cystic fibrosis (Quinton, 2007Quinton P.M. Cystic fibrosis: lessons from the sweat gland.Physiology (Bethesda). 2007; 22: 212-225Crossref PubMed Scopus (129) Google Scholar), has certain limitations (Hjortskov et al., 1995Hjortskov N. Jepsen L.T. Nielsen B. Juul A. Skakkebaek N.E. Pilocarpine iontophoresis test: an index of physiological sweat secretion?.Clin Physiol. 1995; 15: 409-414Crossref PubMed Scopus (15) Google Scholar). These limitations include possible direct damage to the sweat gland that could result in erythemia and release of inflammatory mediators, and a poor ability to precisely adjust drug doses. Previous reports of increased slope of the internal temperature–sweat rate relation are also methodologically limited (Cheuvront et al., 2009Cheuvront S.N. Bearden S.E. Kenefick R.W. Ely B.R. Degroot D.W. Sawka M.N. et al.A simple and valid method to determine thermoregulatory sweating threshold and sensitivity.J Appl Physiol. 2009; 107: 69-75Crossref PubMed Scopus (82) Google Scholar) and likely gauge the sensitivity of the homeostatic gain rather than the sweat gland per se. Second, the observed increases in in vivo cholinergic responsiveness in the eccrine sweat gland after aerobic training suggests that adaptations are due to changes in peripheral glandular function rather than via a central sympathetic component. Previously, isolated sweat glands from trained or acclimated individuals were reported to possess larger secretory coils that were more responsive to direct application of methylcholine (Sato and Sato, 1983Sato K. Sato F. Individual variations in structure and function of human eccrine sweat gland.Am J Physiol. 1983; 245: R203-R208PubMed Google Scholar). This finding of normal but enlarged ultrastructure is also observed in focal hyperhidrosis patients (Bovell et al., 2001Bovell D.L. Clunes M.T. Elder H.Y. Milsom J. Jenkinson D.M. Ultrastructure of the hyperhidrotic eccrine sweat gland.Br J Dermatol. 2001; 145: 298-301Crossref PubMed Scopus (46) Google Scholar). As adaptations to aerobic exercise training appear to also include larger, more responsive eccrine glands, the possibility exists that exercise training could provide a model for studying alterations in sweat gland structure and function associated with hyperhidrosis. Another dermatological application includes reduced sweating responses, such as that which occurs in skin graft patients, in which sweat gland adaptations may be used to increase their sweating responses (Wingo et al., 2008Wingo J.E. Low D.A. Keller D.M. Davis S.L. Kowalske K.J. Purdue G.F. et al.Heat acclimation of an adult female with a large surface area of grafted skin.J Burn Care Res. 2008; 29: 848-851Crossref PubMed Scopus (8) Google Scholar; Davis et al., 2009Davis S.L. Shibasaki M. Low D.A. Cui J. Keller D.M. Wingo J.E. et al.Sustained impairments in cutaneous vasodilation and sweating in grafted skin following long-term recovery.J Burn Care Res. 2009; 30: 675-685Crossref PubMed Scopus (29) Google Scholar). Combined with Crandall et al., 2003Crandall C.G. Shibasaki M. Wilson T.E. Cui J. Levine B.D. Prolonged head-down tilt exposure reduces maximal cutaneous vasodilator and sweating capacity in humans.J Appl Physiol. 2003; 94: 2330-2336Crossref PubMed Scopus (40) Google Scholar cholinergic dose–response data, our findings allow the formation of a sweating adaptation model, in which bedrest attenuates exercise during bedrest rescues, and exercise training accentuates in vivo cholinergic responsiveness. This study was supported by National Institutes of Health grants HL77670 and AG24420. Additional support was provided by NIH grants M01 RR-10732 and C06 RR-016499." @default.
• W2079667098 created "2016-06-24" @default.
• W2079667098 creator A5033821833 @default.
• W2079667098 creator A5037980905 @default.
• W2079667098 creator A5042846218 @default.
• W2079667098 creator A5052801788 @default.
• W2079667098 creator A5073233446 @default.
• W2079667098 creator A5091090769 @default.
• W2079667098 date "2010-09-01" @default.
• W2079667098 modified "2023-10-15" @default.
• W2079667098 title "Aerobic Training Improves In Vivo Cholinergic Responsiveness but Not Sensitivity of Eccrine Sweat Glands" @default.
• W2079667098 cites W160960326 @default.
• W2079667098 cites W1905556056 @default.
• W2079667098 cites W1972758415 @default.
• W2079667098 cites W1972919954 @default.
• W2079667098 cites W1989475500 @default.
• W2079667098 cites W2039242870 @default.
• W2079667098 cites W2051819643 @default.
• W2079667098 cites W2060048173 @default.
• W2079667098 cites W2068797036 @default.
• W2079667098 cites W2100089027 @default.
• W2079667098 cites W2126124470 @default.
• W2079667098 cites W2134850367 @default.
• W2079667098 cites W2144456074 @default.
• W2079667098 cites W2146111561 @default.
• W2079667098 cites W2157541292 @default.
• W2079667098 cites W2169023090 @default.
• W2079667098 cites W2169987553 @default.
• W2079667098 doi "https://doi.org/10.1038/jid.2010.125" @default.
• W2079667098 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2922435" @default.
• W2079667098 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/20463689" @default.
• W2079667098 hasPublicationYear "2010" @default.
• W2079667098 type Work @default.
• W2079667098 sameAs 2079667098 @default.
• W2079667098 citedByCount "13" @default.
• W2079667098 countsByYear W20796670982013 @default.
• W2079667098 countsByYear W20796670982015 @default.
• W2079667098 countsByYear W20796670982017 @default.
• W2079667098 countsByYear W20796670982018 @default.
• W2079667098 countsByYear W20796670982020 @default.
• W2079667098 countsByYear W20796670982022 @default.
• W2079667098 crossrefType "journal-article" @default.
• W2079667098 hasAuthorship W2079667098A5033821833 @default.
• W2079667098 hasAuthorship W2079667098A5037980905 @default.
• W2079667098 hasAuthorship W2079667098A5042846218 @default.
• W2079667098 hasAuthorship W2079667098A5052801788 @default.
• W2079667098 hasAuthorship W2079667098A5073233446 @default.
• W2079667098 hasAuthorship W2079667098A5091090769 @default.
• W2079667098 hasBestOaLocation W20796670981 @default.
• W2079667098 hasConcept C126322002 @default.
• W2079667098 hasConcept C150903083 @default.
• W2079667098 hasConcept C207001950 @default.
• W2079667098 hasConcept C22885893 @default.
• W2079667098 hasConcept C2776248900 @default.
• W2079667098 hasConcept C2778040839 @default.
• W2079667098 hasConcept C63398376 @default.
• W2079667098 hasConcept C71924100 @default.
• W2079667098 hasConcept C86803240 @default.
• W2079667098 hasConceptScore W2079667098C126322002 @default.
• W2079667098 hasConceptScore W2079667098C150903083 @default.
• W2079667098 hasConceptScore W2079667098C207001950 @default.
• W2079667098 hasConceptScore W2079667098C22885893 @default.
• W2079667098 hasConceptScore W2079667098C2776248900 @default.
• W2079667098 hasConceptScore W2079667098C2778040839 @default.
• W2079667098 hasConceptScore W2079667098C63398376 @default.
• W2079667098 hasConceptScore W2079667098C71924100 @default.
• W2079667098 hasConceptScore W2079667098C86803240 @default.
• W2079667098 hasIssue "9" @default.
• W2079667098 hasLocation W20796670981 @default.
• W2079667098 hasLocation W20796670982 @default.
• W2079667098 hasLocation W20796670983 @default.
• W2079667098 hasLocation W20796670984 @default.
• W2079667098 hasOpenAccess W2079667098 @default.
• W2079667098 hasPrimaryLocation W20796670981 @default.
• W2079667098 hasRelatedWork W1533505969 @default.
• W2079667098 hasRelatedWork W1848515695 @default.
• W2079667098 hasRelatedWork W1967863708 @default.
• W2079667098 hasRelatedWork W1996446568 @default.
• W2079667098 hasRelatedWork W2018181463 @default.
• W2079667098 hasRelatedWork W2119527242 @default.
• W2079667098 hasRelatedWork W2339337964 @default.
• W2079667098 hasRelatedWork W2494246423 @default.
• W2079667098 hasRelatedWork W2773784935 @default.
• W2079667098 hasRelatedWork W3016271487 @default.
• W2079667098 hasVolume "130" @default.
• W2079667098 isParatext "false" @default.
• W2079667098 isRetracted "false" @default.
• W2079667098 magId "2079667098" @default.
• W2079667098 workType "article" @default.