Biomedical subjects

W Shane Journeay

Publications and source records attributed to W Shane Journeay.

11 recordsLinked to original sources

PubMed2006

15 degrees head-down tilt attenuates the postexercise reduction in cutaneous vascular conductance and sweating and decreases esophageal temperature recovery time.

The following study examined the effect of 15 degrees head-down tilt (HDT) on postexercise heat loss and hemodynamic responses. We tested the hypothesis that recovery from dynamic exercise in the HDT position would attenuate the reduction in the heat loss responses of cutaneous vascular conductance (CVC) and sweating relative to upright seated (URS) recovery in association with an augmented hemodynamic response and an increased rate of core temperature decay. Seven male subjects performed the following three experimental protocols: 1) 60 min in the URS posture followed by 60 min in the 15 degrees HDT position; 2) 15 min of cycle ergometry at 75% of their predetermined V(O2 peak) followed by 60 min of recovery in the URS posture; or 3) 15 min of cycle ergometry at 75% of their predetermined V(O2 peak) followed by 60 min of recovery in the 15 degrees HDT position. Mean skin temperature, esophageal temperature (T(es)), skin blood flow, sweat rate, cardiac output (CO), stroke volume (SV), heart rate (HR), total peripheral resistance, and mean arterial pressure (MAP) were recorded at baseline, end exercise, 2, 5, 8, 12, 15, and 20 min, and every 5 min until end of recovery (60 min). Without preceding exercise, HDT decreased HR and increased SV (P < or = 0.05). During recovery after exercise, a significantly greater MAP, SV, CVC, and sweat rate and a significantly lower HR were found with HDT compared with URS posture (P < or = 0.05). Subsequently, a significantly lower T(es) was observed with HDT after 15 min of recovery onward (P < or = 0.05). At the end of 60 min of recovery, T(es) remained significantly elevated above baseline with URS (P < or = 0.05); however, T(es) returned to baseline with HDT. In conclusion, extended recovery from dynamic exercise in the 15 degrees HDT position attenuates the reduction in CVC and sweating, thereby significantly increasing the rate of T(es) decay compared with recovery in the URS posture.

Adaptation, Physiological↗

PubMed2006

Postexercise hypotension causes a prolonged perturbation in esophageal and active muscle temperature recovery.

We examined the effect of two levels of exercise-induced hypotension on esophageal (Tes) and active and nonactive muscle temperatures during and following exercise. Seven males performed an incremental isotonic test on a Kin-Com isokinetic apparatus to determine their peak oxygen consumption during bilateral knee extensions (VO2sp). This was followed on separate days by 15-min of isolated bilateral knee extensions at moderate (60% VO2sp) (MEI) and high (80% VO2sp) (HEI) exercise intensities, followed by 90 min of recovery. Muscle temperature was measured with an intramuscular probe inserted in the left vastus medialis (Tvm) and triceps brachii (Ttb) muscles under ultrasound guidance. The deepest sensor (tip) was located approximately 10 mm from the femur and deep femoral artery and from the superior ulnar collateral artery and humerus for the Tvm and Ttb, respectively. Additional sensors were located 15 and 30 mm from the tip with an additional sensor located at 45 mm for the Tvm measurements only. Following exercise, mean arterial pressure (MAP) remained significantly below preexercise rest for the initial 60 min of recovery after MEI and for the duration of the postexercise recovery period after HEI (P< or =0.05). After HEI, significantly greater elevations from preexercise rest were recorded for Tes and all muscle temperatures paralleled a greater decrease in MAP compared with MEI (P< or =0.05). By the end of 90-min postexercise recovery, MAP, Tes, and all muscle temperatures remained significantly greater after HEI than MEI. Furthermore, a significantly shallower muscle temperature profile across Tvm, relative to preexercise rest, was observed at the end of exercise for both HEI and MEI (P< or=0.05), and for 30 min of recovery for MEI and throughout 90 min of recovery for HEI. No significant differences in muscle temperature profile were observed for Ttb. Thus we conclude that the increase in the postexercise hypotensive response, induced by exercise of increasing intensity, was paralleled by an increase in the magnitude and recovery time of the postexercise esophageal and active muscle temperatures.

Adult↗

PubMed2006

Thermoregulatory control following dynamic exercise.

Post-exercise thermoregulatory control in humans has received limited attention. In the post-exercise period skin blood flow and sweating return to pre-exercise levels despite a persistent elevation in esophageal temperature, suggesting an alteration in thermoregulatory control. The esophageal temperature response post-exercise appears to be correlated to the marked cardiovascular changes that occur after dynamic exercise. Recent work has shown that non-thermoregulatory factors associated with hemodynamic changes and hydration status post-exercise may influence the regulation of core temperature during exercise recovery. This review will characterize the thermal response and describe our current understanding of the physiological influences on thermoregulatory control during recovery from dynamic exercise.

Body Temperature Regulation↗

PubMed2005

Differences in the postexercise threshold for cutaneous active vasodilation between men and women.

The purpose of this study was to evaluate the possible differences in the postexercise cutaneous vasodilatory response between men and women. Fourteen subjects (7 men and 7 women) of similar age, body composition, and fitness status remained seated resting for 15 min or cycled for 15 min at 70% of peak oxygen consumption followed by 15 min of seated recovery. Subjects then donned a liquid-conditioned suit. Mean skin temperature was clamped at approximately 34 degrees C for 15 min. Mean skin temperature was then increased at a rate of 4.3 +/- 0.8 degrees C/h while local skin temperature was clamped at 34 degrees C. Skin blood flow was measured continuously at two forearm skin sites, one with (UT) and without (BT) (treated with bretylium tosylate) intact alpha-adrenergic vasoconstrictor activity. The exercise threshold for cutaneous vasodilation in women (37.51 +/- 0.08 degrees C and 37.58 +/- 0.04 degrees C for UT and BT, respectively) was greater than that measured in men (37.33 +/- 0.06 degrees C and 37.35 +/- 0.06 degrees C for UT and BT, respectively) (P < 0.05). Core temperatures were similar to baseline before the start of whole body warming for all conditions. Postexercise heart rate (HR) for the men (77 +/- 4 beats/min) and women (87 +/- 6 beats/min) were elevated above baseline (61 +/- 3 and 68 +/- 4 beats/min for men and women, respectively), whereas mean arterial pressure (MAP) for the men (84 +/- 3 mmHg) and women (79 +/- 3 mmHg) was reduced from baseline (93 +/- 3 and 93 +/- 4 mmHg for men and women, respectively) (P < 0.05). A greater increase in HR and a greater decrease in the MAP postexercise were noted in women (P < 0.05). No differences in core temperature, HR, and MAP were measured in the no-exercise trial. The postexercise threshold for cutaneous vasodilation measured at the UT and BT sites for men (37.15 +/- 0.03 degrees C and 37.16 +/- 0.04 degrees C, respectively) and women (37.36 +/- 0.05 degrees C and 37.42 +/- 0.03 degrees C, respectively) were elevated above no exercise (36.94 +/- 0.07 degrees C and 36.97 +/- 0.05 degrees C for men and 36.99 +/- 0.09 degrees C and 37.03 +/- 0.11 degrees C for women for the UT and BT sites, respectively) (P < 0.05). A difference in the magnitude of the thresholds was measured between women and men (P < 0.05). We conclude that women have a greater postexercise onset threshold for cutaneous vasodilation than do men and that the primary mechanism influencing the difference between men and women in postexercise skin blood flow is likely the result of an altered active vasodilatory response and not an increase in adrenergic vasoconstrictor tone.

Adult↗

PubMed2005

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

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.

Adult↗

PubMed2005

The postexercise increase in the threshold for cutaneous vasodilation and sweating is not observed with extended recovery.

The following study was conducted to evaluate the hypothesis that an increase in the postexercise onset threshold for cutaneous vasodilation (Th(VD)) and sweating (Th(SW)) would not be observed upon the restoration of baseline mean arterial pressure (MAP). Subjects remained either seated resting for 15 min or performed 15 min of treadmill running at 70% VO2peak followed by either 20- (short) or 60-min (extended) recovery. At the end of each recovery protocol (20 and 60 min) a water perfusion suit was then used to increase mean skin temperature until Th(VD) and Th(SW) was noted. Exercise resulted in an increase in Th(VD) and Th(SW) of 0.24 +/- 0.03 and 0.24 +/- 0.02 degrees C, respectively, above no-exercise for the short recovery (p < 0.05). No increase was measured for the extended recovery. Postexercise MAP was significantly reduced prior to whole-body warming for the short recovery whereas no reduction was measured for the extended recovery. The increase in Th(VD) and Th(SW), measured during the early stages of recovery, is reversed with the reestablishment of baseline MAP.

Adult↗

PubMed2004

Control of cutaneous vascular conductance and sweating during recovery from dynamic exercise in humans.

The purpose of the study was to examine the effect of 1) passive (assisted pedaling), 2) active (loadless pedaling), and 3) inactive (motionless) recovery modes on mean arterial pressure (MAP), skin blood flow (SkBF), and sweating during recovery after 15 min of dynamic exercise. It was hypothesized that an active recovery mode would be most effective in attenuating the fall in MAP, SkBF, and sweating during exercise recovery. Six male subjects performed 15 min of cycle ergometer exercise at 70% of their predetermined peak oxygen consumption followed by 15 min of 1) active, 2) passive, or 3) inactive recovery. Mean skin temperature (T(sk)), esophageal temperature (T(es)), SkBF, 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, and 15 min postexercise. Cutaneous vascular conductance (CVC) was calculated as the ratio of laser-Doppler blood flow to MAP. In the active and passive recovery modes, 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 CO, SV, MAP, CVC, and sweat rate above inactive recovery. Sweat rate was different among all modes after 8 min of recovery (P < 0.05). TPR during active recovery remained significantly lower than during recovery in the passive and inactive modes (P < 0.05). No differences in either T(es) or T(sk) were observed among conditions. Given that MAP was higher during passive and active recovery modes than during inactive recovery suggests differences in CVC may be due to differences in baroreceptor unloading and not factors attributed to central command. However, differences in sweat rate may be influenced by factors such as central command and mechanoreceptor stimulation.

Blood Pressure↗

PubMed2004

Lower body positive and negative pressure alter thermal and hemodynamic responses after exercise.

INTRODUCTION: The purpose of this study was to determine the effect of upright lower body positive and negative pressure (LBPP/LBNP) application on the post-exercise thermal response. It was hypothesized that the application of LBPP would decrease core temperature secondary to increases in skin blood flow (SkBF) and sweating, whereas the application of LBNP would maintain core temperature secondary to attenuated SkBF and sweating responses. METHODS: There were six subjects who randomly underwent each of the following treatments in the upright posture, separated by a minimum of 48 h: 1) +45 mmHg LBPP; 2) -20 mmHg LBNP; or 3) no pressure for 45 min after performing 15 min of cycle ergometry exercise at 70% of their VO2peak. Measurements included mean arterial pressure (MAP), heart rate (HR), cardiac output (Q), stroke volume (SV), total peripheral resistance (TPR), mean skin temperature (Tsk), mean heat flux, esophageal temperature (Tes), SkBF, and sweat rate. RESULTS: After the application of LBPP, we observed a significantly greater decrease in core temperature relative to the LBNP and control conditions (p < 0.001). This was accompanied by increases in SkBF, sweating, and heat flux (p < 0.05), all of which were higher than the LBNP and control conditions. Core temperature, SkBF, sweating, and heat flux in the LBNP and control conditions were not different from each other. LBPP promoted the restoration of hemodynamics while LBNP and control prolonged the post-exercise hemodynamic state. CONCLUSION: We conclude that during recovery from exercise in the upright seated posture, core temperature recovery is affected by compromised SkBF and sweating secondary to nonthermal cardiovascular influences.

Adult↗

PubMed2003

Effect of exercise intensity on the postexercise sweating threshold.

The hypothesis that the magnitude of the postexercise onset threshold for sweating is increased by the intensity of exercise was tested in eight subjects. Esophageal temperature was monitored as an index of core temperature while sweat rate was measured by using a ventilated capsule placed on the upper back. Subjects remained seated resting for 15 min (no exercise) or performed 15 min of treadmill running at either 55, 70, or 85% of peak oxygen consumption (V(o2 peak)) followed by a 20-min seated recovery. Subjects then donned a liquid-conditioned suit used to regulate mean skin temperature. The suit was first perfused with 20 degrees C water to control and stabilize skin and core temperature before whole body heating. Subsequently, the skin was heated ( approximately 4.0 degrees C/h) until sweating occurred. Exercise resulted in an increase in the onset threshold for sweating of 0.11 +/- 0.02, 0.23 +/- 0.01, and 0.33 +/- 0.02 degrees C above that measured for the no-exercise resting values (P < 0.05) for the 55, 70, and 85% of V(o2 peak) exercise conditions, respectively. We did note that there was a greater postexercise hypotension as a function of exercise intensity as measured at the end of the 20-min exercise recovery. Thus it is plausible that the increase in postexercise threshold may be related to postexercise hypotension. It is concluded that the sweating response during upright recovery is significantly modified by exercise intensity and may likely be influenced by the nonthermal baroreceptor reflex adjustments postexercise.

Anaerobic Threshold↗

PubMed2003

Cutaneous active vasodilation in humans during passive heating postexercise.

The hypothesis that exercise causes an increase in the postexercise esophageal temperature threshold for onset of cutaneous vasodilation through an alteration of active vasodilator activity was tested in nine subjects. Increases in forearm skin blood flow and arterial blood pressure were measured and used to calculate cutaneous vascular conductance at two superficial forearm sites: one with intact alpha-adrenergic vasoconstrictor activity (untreated) and one infused with bretylium tosylate (bretylium treated). Subjects remained seated resting for 15 min (no-exercise) or performed 15 min of treadmill running at either 55, 70, or 85% of peak oxygen consumption followed by 20 min of seated recovery. A liquid-conditioned suit was used to increase mean skin temperature ( approximately 4.0 degrees C/h), while local forearm temperature was clamped at 34 degrees C, until cutaneous vasodilation. No differences in the postexercise threshold for cutaneous vasodilation between untreated and bretylium-treated sites were observed for either the no-exercise or exercise trials. Exercise resulted in an increase in the postexercise threshold for cutaneous vasodilation of 0.19 +/- 0.01, 0.39 +/- 0.02, and 0.53 +/- 0.02 degrees C above those of the no-exercise resting values for the untreated site (P < 0.05). Similarly, there was an increase of 0.20 +/- 0.01, 0.37 +/- 0.02, and 0.53 +/- 0.02 degrees C for the treated site for the 55, 70, and 85% exercise trials, respectively (P < 0.05). It is concluded that reflex activity associated with the postexercise increase in the onset threshold for cutaneous vasodilation is more likely mediated through an alteration of active vasodilator activity rather than through adrenergic vasoconstrictor activity.

Adrenergic Agents↗

PubMed2003

Cardiovascular responses to apneic facial immersion during altered cardiac filling.

The hypothesis that reduced cardiac filling, as a result of lower body negative pressure (LBNP) and postexercise hypotension (PEH), would attenuate the reflex changes to heart rate (HR), skin blood flow (SkBF), and mean arterial pressure (MAP) normally induced by facial immersion was tested. The purpose of this study was to investigate the cardiovascular control mechanisms associated with apneic facial immersion during different cardiovascular challenges. Six subjects randomly performed 30-s apneic facial immersions in 6.0 +/- 1.2 degrees C water under the following conditions: 1) -20 mmHg LBNP, 2) +40 mmHg lower body positive pressure (LBPP), 3) during a period of PEH, and 4) normal resting (control). Measurements included SkBF at one acral (distal phalanx of the thumb) and one nonacral region of skin (ventral forearm), HR, and MAP. Facial immersion reduced HR and SkBF at both sites and increased MAP under all conditions (P < 0.05). Reduced cardiac filling during LBNP and PEH significantly attenuated the absolute HR nadir observed during the control immersion (P < 0.05). The LBPP condition did not result in a lower HR nadir than control but did result in a nadir significantly lower than that of the LBNP and PEH conditions (P < 0.05). No differences were observed in either SkBF or MAP between conditions; however, the magnitude of SkBF reduction was greater at the acral site than at the nonacral site for all conditions (P < 0.05). These results suggest that the cardiac parasympathetic response during facial immersion can be attenuated when cardiac filling is compromised.

Adult↗