Nonthermoregulatory control of cutaneous vascular conductance and sweating during recovery from dynamic exercise in women

Abstract

The purpose of the study was to examine the effect of 1) active (loadless pedaling), 2) passive (assisted pedaling), and 3) inactive (motionless) recovery modes on mean arterial pressure (MAP), cutaneous vascular conductance (CVC), and sweat rate during recovery after 15 min of dynamic exercise in women. It was hypothesized that an active recovery mode would be most effective in attenuating the fall in MAP, CVC, and sweating during exercise recovery. Ten female subjects performed 15 min of cycle ergometer exercise at 70% of their predetermined peak oxygen consumption followed by 20 min of 1) active, 2) passive, or 3) inactive recovery. Mean skin temperature (Tsk), esophageal temperature (Tes), skin blood flow, sweating, cardiac output (CO), stroke volume (SV), heart rate (HR), total peripheral resistance (TPR), and MAP were recorded at baseline, end exercise, and 2, 5, 8, 12, 15, and 20 min postexercise. Cutaneous vascular conductance (CVC) was calculated as the ratio of laser-Doppler blood flow to MAP. In the active recovery mode, CVC, sweat rate, MAP, CO, and SV remained elevated over inactive values (P < 0.05). The passive mode was equally as effective as the active mode in maintaining MAP. Sweat rate was different among all modes after 12 min of recovery (P < 0.05). TPR during active recovery remained significantly lower than during recovery in the inactive mode (P < 0.05). No differences in either Tes or Tsk were observed among conditions. The results indicate that CVC can be modulated by central command and possibly cardiopulmonary baroreceptors in women. However, differences in sweat rate may be influenced by factors such as central command, mechanoreceptor stimulation, or cardiopulmonary baroreceptors.

Thermometry and calorimetry assessment of sweat response during exercise in the heat

“…We chose this site given that the ventilated capsule technique requires a wide flat surface to avoid air leakage. As such, the upper back is a site often used when the ventilated capsule technique is adopted (Journeay et al 2005). Our evaporative heat loss estimates may have been influenced by nonthermal factors, which are known to play a significant role in heat balance (Journeay et al 2005).…”

“…As such, the upper back is a site often used when the ventilated capsule technique is adopted (Journeay et al 2005). Our evaporative heat loss estimates may have been influenced by nonthermal factors, which are known to play a significant role in heat balance (Journeay et al 2005). Furthermore, as oesophageal temperature is considered a good indicator of blood temperature perfusing the brain (Shiraki et al 1986), it is tenable that this variable could have shown a relationship with sweat rate.…”

Evidence of a greater onset threshold for sweating in females following intense exercise

“…It has been shown that sweat rate during postexercise recovery can be modulated by central command, mechanoreceptors and possibly baroreceptors in males and females (Carter et al 2002;Journeay et al 2004bJourneay et al , 2005Shibasaki et al 2004;Wilson et al 2004). At the cessation of exercise however, dramatic changes in mean arterial pressure occur secondary to changes in input from central command, metaboreceptor and mechanoreceptor feedback.…”

Human heat balance during postexercise recovery: separating metabolic and nonthermal effects

“…Several studies (2,4,16,25,30) have shown that an active (loadless pedaling) and a passive (assisted loadless pedaling) recovery mode, both of which maintain mean arterial pressure (MAP) via the augmentation of venous return through engagement of the skeletal muscle pump, elicit greater levels of skin blood flow (4, 16) and LSR (4,16,25,30) relative to inactive recovery. Since no differences in core temperature have been observed between any of these recovery modes (4,16,25,30), an adjustment (i.e., increased thermal sensitivity and/or shifted onset threshold) of the thermal control of sweating and/or skin blood flow has been ascribed as the underlying nonthermal mechanism (16), primarily because of a reduced postexercise baroreceptor unloading and hypotensive effect typically evident during inactive recovery (13,19).Most studies have not compared measurements of oxygen consumption between active and inactive recovery modes, assuming that any elevations in metabolism during active recovery relative to inactive recovery are insufficient to produce changes in hypothalamic temperature (16,17,30). Consequently, previous studies have ruled out the possibility that elevations in heat production are responsible for the modifications in skin blood flow or sweating response (16,17,30) during an active recovery.…”