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PERSPECTIVES
Sweating the details: what really drives eccrine output during exercise-heat stress Thad E. Wilson1,2 1 Ohio Musculoskeletal and Neurological Institute, Ohio University, Athens, OH, USA 2 Departments of Biomedical Sciences & Specialty Medicine, Ohio University Heritage College of Osteopathic Medicine, Athens, OH, USA
The Journal of Physiology
Email:
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Copious sweating observed during passive or exercise-induced heat stress (exercise-heat stress) is the primary outcome of the sophisticated eccrine-dependent cooling system that has evolved in humans. One can speculate as to why sweating, with its large ability to liberate heat (580 kcal l−1 ), would be advantageous for a ‘naked ape’ ambulating in a warm savanna environment. Despite this grand role of sweating in human thermoregulation and evolution, it is humbling how little we know of its control and regulation. Recent work is beginning to detect the precise brain areas involved (Shafton & McAllen, 2013), but imprecise systemic factors are reported in the literature to be the primary drivers of eccrine sweating. In this issue of The Journal of Physiology, Gagnon and colleagues (Gagnon et al. 2013) challenge the notion that relative workload (current workload compared to maximum work capacity) is the primary determinant of sweat output during exercise-heat stress. In their experiment, human subjects performed exercise-heat stresses in a direct calorimeter at a fixed workload (290 W) in variable thermal environments (30, 35, 40 and 45◦ C) or at a variable workload (200, 350, or 500 W) in a fixed 30◦ C thermal environment. Using this direct method of measuring heat emitted, the evaporative requirement for heat balance was superior to relative workload in predicting whole-body sweat rate, and when relative workload was combined with the evaporative requirement for heat balance, predictions did not improve. Authors interpret these data as definitive evidence against the use of relative workload in experiments when the primary determinant is sweat rate. Rather,
authors indicate that matching evaporative requirements to what is needed to maintain heat balance in both steady-state and non-steady-state exercise-heat stress is a superior experimental approach. Do these interpretations make sense?
Using Occam’s razor (the most direct hypothesis being most likely correct), it is logical that the evaporative requirement to maintain a regulated internal temperature would be the driving force for eccrine sweat output rather than a less direct measure such as relative workload. As one can see from a traditional heat balance equation (eqn (1)), relative workload is located within the M – W k component vs. the more direct E: S = (M − Wk ) ± (R + C + K ) − E (1) where S is heat storage (balance); M is metabolism and W k is external work; R + C + K is dry heat exchange via radiation, convection, and conduction; and E is evaporative heat loss. Relative workload has an inherent fitness bias. This can be observed with similar whole-body and local sweat rates when comparing high fitness (∼60 ml kg−1 min−1 ) and average fitness (∼40 ml kg−1 min−1 ) groups at fixed workload (100–110 W). In contrast, at a relative workload (60% of maximal), the same high fitness group had greater whole-body and local sweat rates compared to the average fitness group (Jay et al. 2011). What are the potential mechanisms of the fitness-induced increase in sweat output?
Whole-body sweating mechanisms are difficult to determine and remain elusive. However, locally perfusing the sudorific agonist acetylcholine (ACh) via intradermal microdialysis stimulates muscarinic type-3 receptors on eccrine sweat glands, and if water vapour is collected via capacitance hygrometry just above the skin containing the microdialysis membrane, agonist to sweating dose–response relations can be determined in small areas of skin. Using this limited but better controlled approach, increasing maximal work capacity via 8 weeks of aerobic exercise training causes an increase in the in
C 2013 The Author. The Journal of Physiology C 2013 The Physiological Society
vivo maximal sweating responses (Wilson et al. 2010). Inactivity, such as 14 days of bedrest, decreases maximal work and sweating capacity and importantly, aerobic exercise training during bedrest rescues this response (Crandall et al. 2003). However, neither of these changes in work capacity changes the in vivo eccrine sweat gland cholinergic sensitivity. This indicates that for a given amount of ACh release from cholinergic sudomotor nerves there is not more sweating, but if the amount of ACh released increases, more eccrine sweating results. These data combined with this new study (Gagnon et al. 2013) suggest that trained individuals may release more ACh at a given relative workload, which may be responsible for their higher sweat rate. Gagnon et al. (2013) provide a long list of previous studies that compared independent groups at a relative workload rather than the more predictive evaporative requirement for heat balance. Are all these previous studies flawed? Not necessarily. Many, but not all, of these studies were fitness-matched to maximal work capacity and thus relative workloads would be similar. That said, the authors of this new study (Gagnon et al. 2013) give the field pause to consider what actually drives the sweating response during exercise-heat stress. Although more work needs to be completed to determine these precise driving forces and what can be used to compare experimental groups, future studies should be cautioned against using relative workload as a between-groups standardization when eccrine sweating is the main variable of interest.
References Crandall CG, Shibasaki M, Wilson TE, Cui J & Levine BD (2003). J Appl Physiol 94, 2330–2336. Gagnon D, Jay O & Kenny GP (2013). J Physiol 591, 2925–2935. Jay O, Bain AR, Deren TM, Sacheli M & Cramer MN (2011). Am J Physiol Regul Integr Comp Physiol 301, R832–R841. Shafton AD & McAllen RM (2013). Am J Physiol Regul Integr Comp Physiol (in press; DOI: 10.1152/ajpregu.00040.2013). Wilson TE, Monahan KD, Fogelman A, Kearney ML, Sauder CL & Ray CA (2010). J Invest Dermatol 130, 2328–2330. DOI: 10.1113/jphysiol.2013.255430
