Fine tuning your loss of body fluids may be more problematic now that researchers find receptors have an active role in our sweat rate

For most of us, hot weather leads to elevated internal and skin temperatures, which increase sweat rates and skin blood flow. How much we sweat can also depend on nonthermal factors such as exercise, baroreceptor loading status, and body fluid status.

During exercise, heart rate and mean arterial pressure (MAP) are elevated via a combination of central command and muscle mechanoreceptor and metaboreceptor stimulation.

These receptors may be equally important in producing sweat as the most high-tech treadmill. Sensory receptors can occur as part of sense organs or on their own, as a specialized detector for a particular type of stimulus; receptor cells provide the sensor neurons, responsible for responding to the stimulus. Receptors can be grouped according to the kind of energy that they are most sensitive to, whether it is chemical, mechanical, light, thermal, electrical, or magnetic. The mechanoreceptor responds to mechanical energy of physical movement or muscle activity derived from exercise.

Passive limb movement using a tandem ergometer has been employed to investigate the role of muscle mechanoreceptor stimulation, independent of the contribution of “central command” during exercise. A new study used this approach to test the hypothesis that sweat rate is modulated by muscle mechanoreceptor stimulation during the recovery period from exercise.

That study, “Muscle Mechanoreceptor Modulation of Sweat Rate During Recovery from Moderate Exercise,” is authored by Manabu Shibasaki, Mieko Sakai, Mayumi Oda, all from the Faculty of Human Life and Environmental Health, Nara Women’s University, Nara, Japan; and Craig G. Crandall, affiliated with the Institute for Exercise and Environmental Medicine, Presbyterian Hospital of Dallas and the Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX. Their findings appear in the June 2004 edition of the Journal of Applied Physiology.

Study participants were seven healthy men, all approximately 20 years old, of normal weight and height, nonsmokers, and free of any known cardiovascular, neurological, or metabolic diseases. The subjects refrained from alcohol and stimulants such as caffeine for 24 hours before testing.

Each subject performed the following exercise protocol on separate days, with each bout being separated from the prior bout by at least 48 hours: The subjects lay face up (supine) at the rear position of an adapted supine tandem cycle ergometer. Each subject remained in this position for 30 minutes while additional measurement devices were attached. After five minutes of baseline data collection, each subject performed one minute of loadless exercise while remaining in the supine position. This was immediately followed by the subject exercising for 20 minutes at a workload that elicited 65 percent of the individual’s predicted maximal heart rate at a pedaling cadence of 60 rpm. After the exercise bout, the subject either stopped all leg movement or, on a separate day, the subject’s legs were passively moved (at 60 rpm) via a second person cycling the tandem ergometer. The order of postexercise treatment was randomized, and each bout of exercise was performed at the same time of day. Data were obtained throughout exercise and for 20 min of recovery. The recovery period consisted of two phases: (1) during the first 10 min of recovery, the subjects either rested or passively cycled as described above; (2) for the subsequent 10 minutes, subjects rested without any leg movements (inactive recovery) to confirm whether the differences between recovery modes in the first 10 min, if any, resulted from the passive leg movements.

Each subject was instrumented for the measurement of esophageal temperature with a probe (thermistor) swallowed to the level of the left atrium. Skin temperatures were measured at seven sites by thermocouples, and mean skin temperature was calculated. Heart rate was obtained from the electrocardiogram signal. Systolic and diastolic blood pressures were recorded every minute by electrosphygmomanometry of the left upper arm. Mean arterial pressure was calculated as diastolic pressure plus one-third pulse pressure. Electromyography (EMG) was continuously measured from the rectus femoris muscle to confirm the absence of voluntary muscle contracting during recovery modes. Sweat rate was continuously recorded from two sites (right forearm and chest).

The increase in sweat rate during exercise was similar between exercise bouts such that there was no difference in this variable at the end of exercise. Forearm sweat rate was significantly greater throughout passive cycling recovery relative to during no-pedaling recovery. Midway through the recovery period, forearm sweat rate was significantly greater in the passive cycling recovery mode relative to the no-pedaling condition and remained greater through the end of the challenge recovery period.

In contrast, chest sweat rate was significantly greater at the mid-recovery period during passive cycling but not at the end of the challenge recovery period. Pre-exercise chest and forearm skin blood flow (cutaneous vascular conductance; CVC) were not different between the two trials. Both chest and forearm CVC significantly increased during exercise, whereas no differences in either variable were observed at the end of exercise between exercise bouts. In contrast to sweat rate, there were no differences in chest or forearm CVC between recovery modes.

Esophageal temperature at rest, throughout exercise, and throughout recovery was not significantly different between exercise bouts or modes of recovery. Although there was a slight difference in mean skin temperature before exercise, after that time there were no significant differences in mean skin temperature throughout the test protocol.

The primary finding of this study is that, despite no differences in sweat rate at the end of the two exercise bouts, when muscle mechanoreceptors were stimulated during postexercise recovery (i.e., passive cycling), forearm and chest sweat rate were greater during passive cycling recovery relative to no pedaling recovery. Throughout exercise and recovery, there were no significant differences in esophageal or mean skin temperatures between bouts. These data suggest that muscle mechanoreceptor stimulation is capable of modulating sweat rate independent from the contributions of vasometric and thermal factors.