Biomedical subjects

Narihiko Kondo

Publications and source records attributed to Narihiko Kondo.

At least 19 recordsLinked to original sources

PubMed2006

Modulation of the control of muscle sympathetic nerve activity during severe orthostatic stress.

We tested the hypothesis that arterial baroreflex (ABR)-mediated beat-to-beat control over muscle sympathetic nerve activity (MSNA) is progressively modulated as orthostatic stress increases in humans, but that this control becomes impaired just before the onset of orthostatic syncope. In 17 healthy subjects, the ABR control over MSNA (burst incidence, burst strength and total MSNA) was evaluated by analysing the relationship between beat-to-beat spontaneous variations in diastolic blood pressure (DAP) and MSNA during supine rest (control) and during progressive, stepwise increases in lower body negative pressure (LBNP) that were incremented by -10 mmHg every 5 min until presyncope (nine subjects) or -60 mmHg was reached. (1) The linear relationships between DAP and burst strength and between DAP and total MSNA were shifted progressively upward as LBNP increased until the level at which syncope occurred. The relationship between DAP and burst incidence, however, gradually shifted upward from control only to LBNP = -30 mmHg; there was no further upward shift at higher LBNPs. (2) Although the slope of the relationship between DAP and burst strength and between DAP and total MSNA remained constant at all LBNPs tested, except at the level where syncope occurred, the slope of the relationship between DAP and burst incidence was reduced at LBNPs of -40 mmHg and higher (versus control). (3) In syncopal subjects, the slopes of the relationships between DAP and burst incidence, burst strength, and total MSNA were all substantially reduced during the 1-2 min period prior to the onset of syncope. Taken together, these results suggest baroreflex control over MSNA is progressively modulated as orthostatic stress increases, so that its sensitivity is substantially reduced during the period immediately preceding the severe hypotension associated with orthostatic syncope.

Adult↗

PubMed2005

Time-dependent modulation of arterial baroreflex control of muscle sympathetic nerve activity during isometric exercise in humans.

We investigated the time-dependent modulation of arterial baroreflex (ABR) control of muscle sympathetic nerve activity (MSNA) that occurs during isometric handgrip exercise (IHG). Thirteen healthy subjects performed a 3-min IHG at 30% maximal voluntary contraction, which was followed by a period of imposed postexercise muscle ischemia (PEMI). The ABR control of MSNA (burst incidence and strength and total activity) was evaluated by analyzing the relationship between spontaneous variations in diastolic arterial pressure (DAP) and MSNA during supine rest, at each minute of IHG, and during PEMI. We found that 1) the linear relations between DAP and MSNA variables were shifted progressively rightward until the third minute of IHG (IHG3); 2) 2 min into IHG (IHG2), the DAP-MSNA relations were shifted upward and were shifted further upward at IHG3; 3) the sensitivity of the ABR control of total MSNA was increased at IHG2 and increased further at IHG3; and 4) during PEMI, the ABR operating pressure was slightly higher than at IHG2, and the sensitivity of the control of total MSNA was the same as at IHG2. During PEMI, the DAP-burst strength and DAP-total MSNA relations were shifted downward from the IHG3 level to the IHG2 level, whereas the DAP-burst incidence relation remained at the IHG3 level. These results indicate that during IHG, ABR control of MSNA is modulated in a time-dependent manner. We suggest that this modulation of ABR function is one of the mechanisms underlying the progressive increase in blood pressure and MSNA during the course of isometric exercise.

Adaptation, Physiological↗

PubMed2005

Relationship between ventilatory response and body temperature during prolonged submaximal exercise.

We examined whether an increase in skin temperature or the rate of increase in core body temperature influences the relationship between minute ventilation (Ve) and core temperature during prolonged exercise in the heat. Thirteen subjects exercised for 60 min on a cycle ergometer at 50% of peak oxygen uptake while wearing a suit perfused with water at 10 degrees C (T10), 35 degrees C (T35), or 45 degrees C (T45). During the exercise, esophageal temperature (Tes), skin temperature, heart rate (HR), Ve, tidal volume, respiratory frequency (f), respiratory gases, blood pressure (BP), and blood lactate were all measured. We found that oxygen uptake, carbon dioxide output, BP, and blood lactate did not differ among the sessions. Tes, HR, Ve, and f remained nearly constant from minute 10 onward in the T10 session, but all of these parameters progressively increased in the T35 and T45 sessions, and significantly higher levels were seen in the T45 than the T35 session. For all but two subjects in the T35 and T45 sessions, plotting Ve as a function of Tes revealed no threshold for hyperventilation; instead, increases in Ve were linearly related to Tes, and there were no significant differences in the slopes or intercepts between the T35 and T45 sessions. Thus, during prolonged submaximal exercise in the heat, Ve increases with core temperature, and the influences of skin temperature and the rate of increase in Tes on the relationship between Ve and Tes are apparently small.

Adult↗

PubMed2005

Effects of rhythmic muscle compression on cardiovascular responses and muscle oxygenation at rest and during dynamic exercise.

We examined the way in which the duration of rhythmic muscle compressions affects cardiovascular responses and muscle oxygenation at rest and during dynamic exercise. We measured the mean arterial pressure (MAP), heart rate (HR) and oxygenation of the vastus lateralis muscle (by near-infrared spectroscopy) in eight healthy male subjects at rest and during supine bicycle exercise (50 and 100 W at 60 r.p.m.) while applying pulsed muscle compressions at 1000 ms intervals. Compression pressure and durations were 150 mmHg and 300, 600, 900 and 1000 ms (1000 ms being static continuous compression), respectively. During exercise, the pulsed leg compression was synchronized to each thigh extensor muscle contraction. The observed changes in muscle oxygenation were dependent on compression duration (increased at 300 ms, no change at 600 ms and decreased at 900 or 1000 ms) and were different from those seen at rest (increases at < 1000 ms and decrease at 1000 ms). This suggests that the effects of external pulsed muscle compression may have a duration threshold below which muscle pumping counteracts the obstruction to flow caused by the compression, and that the threshold is set at a shorter compression duration during exercise than at rest. Although HR and MAP did not change during pulsed compression at rest, during exercise they both increased progressively as compression duration increased. Thus, while exercising, the increased MAP and HR seen during the compression could be due to the combination and interaction of mechanical effects and the muscle mechanoreflex and/or metaboreflex.

Adult↗

PubMed2005

Modification of internal temperature regulation for cutaneous vasodilation and sweating by bright light exposure at night.

Bright light (BL) exposure at night leads to suppressed secretion of melatonin and an attenuated fall in internal temperature at rest from the night to the early morning. However, it is unknown at the present whether typical diurnal variations in reflex responses to thermal challenges are similarly affected by BL exposure at night. We investigated the control of cutaneous vasodilator and sweating responses to hyperthermia in the early morning after artificial BL exposure at night, compare with dim light (DL) exposure. Six subjects stayed awake in a semi-supine position under DL (120 lx) or BL (2800 lx) conditions between 21.00 and 04.30 h. Urine samples were collected at 04.30 h. Beginning at 05.30 h, the lower legs were immersed for 50 min in 42 degrees C water. The subjects remained awake for 21 h until the end of hot water immersion. Urinary 6-sulphatoxymelatonin levels following BL were significantly lower than after DL. Oesophageal temperature (T es) before heating was significantly higher following BL [36.41+/-0.10 (DL) vs. 36.55+/-0.09 (BL) degrees C]. The T es thresholds for the onset of cutaneous vasodilation and sweating were significantly higher with BL than with DL conditions (approximately 0.15 degrees C, respectively). We found that the internal temperature threshold for thermoregulatory control of cutaneous vasodilation and sweating responses to passive heating in the early morning can be modified by the level of light exposure the prior night. Thus both basal internal temperature and the regulation of internal temperature are modified by BL exposure at night.

Adult↗

PubMed2005

Effects of physical training on heat loss responses of young women to passive heating in relation to menstrual cycle.

To examine the effects of physical training on cutaneous vasodilation and sweating responses of young women in the follicular and luteal phase, 11 physically trained (T group) and 13 untrained (U group) women were passively heated by lower-leg immersion into hot water of 42 degrees C (ambient temperature of 30 degrees C and 45%RH) for 60 min in their mid-follicular and mid-luteal phases of the menstrual cycle. Female hormones increased significantly from the mid-follicular to the mid-luteal phase in T and U groups, but the degree of increase was significantly lower in T group. Mean body temperature (T(B)) thresholds for cutaneous vasodilation and sweating responses were significantly lower in T group than in U group, in both the menstrual phases, and the differences between the groups were greatest during the mid-luteal phase. The slope of the relationship between frequency of sweat expulsion (F(sw)) and (T(B)), and between local sweating rate and F(sw) was significantly greater in T group, although the slope of the relationship between cutaneous blood flow and (T(B)) did not differ between the groups, regardless of body site or menstrual phase. These results suggest that regular physical activity enhanced sweating and cutaneous vasodilation in young women. The enhancement of sweating was due to both central and peripheral mechanisms, and the enhancement of cutaneous vasodilation was possibly due to a central mechanism. Enhancement of heat loss responses via central mechanisms was greater during the mid-luteal phase than in the mid-follicular phase because the elevation of female reproductive hormone levels during the mid-luteal phase was relatively low in T group.

Body Temperature Regulation↗

PubMed2005

Effects of menstrual cycle and physical training on heat loss responses during dynamic exercise at moderate intensity in a temperate environment.

We evaluated the effects of the menstrual cycle and physical training on heat loss (sweating and cutaneous vasodilation) responses during moderate exercise in a temperate environment. Ten untrained (group U) and seven endurance-trained (group T) women (maximal O2 uptake of 36.7+/-1.1 vs. 49.4+/-1.7 ml.kg-1.min-1, respectively; P<0.05) performed a cycling exercise at 50% maximal O2 uptake for 30 min during both the midfollicular and midluteal menstrual phase in a temperate environment (ambient temperature of 25 degrees C, relative humidity of 45%). In group U, plasma levels of estrone, estradiol, and progesterone at rest and esophageal temperature (Tes) during exercise were significantly higher during the midluteal than during the midfollicular phase (P<0.05). Sweating rate and cutaneous blood flow (measured via laser-Doppler flowmetry) on the chest, back, forearm, and thigh were lower during the midluteal than during the midfollicular phase during exercise. Tes threshold for heat loss responses was significantly higher and sensitivity of the heat loss responses was significantly lower in the midluteal than in the midfollicular phase, regardless of body site. These effects of the menstrual cycle in group U were not observed in group T. The sweating rate and cutaneous blood flow were significantly higher in group T than in group U, regardless of menstrual phase or body site. Tes threshold for heat loss responses was significantly lower and sensitivity of heat loss responses was significantly greater in group T than in group U in the midluteal phase; however, sensitivity of the sweating response was significantly greater in the midfollicular phase. These results suggest that heat loss responses in group U were inhibited in the midluteal phase compared with in the midfollicular phase. Menstrual cycle had no remarkable effects in group T. Physical training improved heat loss responses, which was more marked in the midluteal than in the midfollicular phase.

Adult↗

PubMed2004

Comparison of oxygen uptake kinetics during knee extension and cycle exercise.

The knee extension exercise (KE) model engenders different muscle and fiber recruitment patterns, blood flow, and energetic responses compared with conventional cycle ergometry (CE). This investigation had two aims: 1) to test the hypothesis that upright two-leg KE and CE in the same subjects would yield fundamentally different pulmonary O(2) uptake (pVo(2)) kinetics and 2) to characterize the muscle blood flow, muscle Vo(2) (mVo(2)), and pVo(2) kinetics during KE to investigate the rate-limiting factor(s) of pVo(2) on kinetics and muscle energetics and their mechanistic bases after the onset of heavy exercise. Six subjects performed KE and CE transitions from unloaded to moderate [< ventilatory threshold (VT)] and heavy (>VT) exercise. In addition to pVo(2) during CE and KE, simultaneous pulsed and echo Doppler methods, combined with blood sampling from the femoral vein, were used to quantify the precise temporal profiles of femoral artery blood flow (LBF) and mVo(2) at the onset of KE. First, the gain (amplitude/work rate) of the primary component of pVo(2) for both moderate and heavy exercise was higher during KE ( approximately 12 ml.W(-1).min(-1)) compared with CE ( approximately 10), but the time constants for the primary component did not differ. Furthermore, the mean response time (MRT) and the contribution of the slow component to the overall response for heavy KE were significantly greater than for CE. Second, the time constant for the primary component of mVo(2) during heavy KE [25.8 +/- 9.0 s (SD)] was not significantly different from that of the phase II pVo(2). Moreover, the slow component of pVo(2) evident for the heavy KE reflected the gradual increase in mVo(2). The initial LBF kinetics after onset of KE were significantly faster than the phase II pVo(2) kinetics (moderate: time constant LBF = 8.0 +/- 3.5 s, pVo(2) = 32.7 +/- 5.6 s, P < 0.05; heavy: LBF = 9.7 +/- 2.0 s, pVo(2) = 29.9 +/- 7.9 s, P < 0.05). The MRT of LBF was also significantly faster than that of pVo(2). These data demonstrate that the energetics (as gain) for KE are greater than for CE, but the kinetics of adjustment (as time constant for the primary component) are similar. Furthermore, the kinetics of muscle blood flow during KE are faster than those of pVo(2), consistent with an intramuscular limitation to Vo(2) kinetics, i.e., a microvascular O(2) delivery-to-O(2) requirement mismatch or oxidative enzyme inertia.

Adolescent↗

PubMed2004

Effects of brief leg cooling after moderate exercise on cardiorespiratory responses to subsequent exercise in the heat.

We investigated the effects of brief leg cooling after moderate exercise on the cardiorespiratory responses to subsequent exercise in the heat. Following 40 min of ergometer cycling [65% peak oxygen uptake (VO(2peak))] at 35 degrees C (Ex. 1), seven male subjects [21.9 (1.1) years of age; 170.9 (1.9) cm height; 66.0 (2.0) kg body mass; 46.7 (2.0) ml kg(-1) min(-1) VO(2peak)] immersed their legs in 35 degrees C (control condition, CONT) or 20 degrees C (cooling condition, COOL) water for 5 min and then repeated the cycling (as before, but for 10 min) (Ex. 2). Just before Ex. 2, esophageal temperature ( T(es)) was lower in COOL than in CONT [36.9 (0.2) vs 37.5 (0.1) degrees C] ( P<0.01), as also were both mean skin temperature [33.9 (0.2) vs 35.2 (0.2) degrees C] ( P<0.01), and heart rate (HR) [93.2 (6.0) vs 102.7 (4.9) beats min(-1)] ( P<0.05). During Ex. 2, no differences between CONT and COOL were observed in oxygen uptake, arterial blood pressure, blood lactate concentration, or ratings of perceived exertion; however, T(es), skin temperature, and HR were lower in COOL than in CONT. Further, during the first 5 min of Ex. 2, minute ventilation was significantly lower in COOL than in CONT [50.3 (2.0) vs 53.4 (2.6) l min(-1)] ( P<0.01). These results suggest that brief leg cooling during the recovery period may be effective at reducing thermal and cardiorespiratory strain during subsequent exercise in the heat.

Adult↗

PubMed2004

Modulation of arterial baroreflex dynamic response during mild orthostatic stress in humans.

We tested the hypothesis that in humans, carotid-baroreflex dynamic responses (evaluated by examining the time course of the carotid-baroreflex-induced alterations in muscle sympathetic nerve activity (MSNA), mean arterial blood pressure (MAP) and heart rate (HR)) would be altered during mild orthostatic stress in ways that serve to limit orthostatic hypotension. In 12 healthy subjects (10 male, 2 female), 5-s periods of neck pressure (NP) (50 mmHg) and neck suction (NS) (-60 mmHg) were used to evaluate carotid baroreflex function at rest (CON) and during lower body negative pressure (LBNP) (-15 mmHg). During LBNP (as compared with CON) (a) the augmentations in MSNA and MAP elicited by NP were greater, (b) the NS-induced period of MSNA suppression was, if anything, shorter, (c) the peak decrement in MAP elicited by NS, although not different in amplitude, occurred earlier and recovered to its initial level more quickly after NS, and (d) the HR responses to NP and NS were greater. These results suggest that during mild orthostatic stress, carotid-baroreflex dynamic responses are modulated in ways that should help maintain blood pressure and limit orthostatic hypotension.

Adult↗

PubMed2004

Modulation of control of muscle sympathetic nerve activity during orthostatic stress in humans.

We tested the hypothesis that orthostatic stress would modulate the arterial baroreflex (ABR)-mediated beat-by-beat control of muscle sympathetic nerve activity (MSNA) in humans. In 12 healthy subjects, ABR control of MSNA (burst incidence, burst strength, and total activity) was evaluated by analysis of the relation between beat-by-beat spontaneous variations in diastolic blood pressure (DAP) and MSNA during supine rest (CON) and at two levels of lower body negative pressure (LBNP: -15 and -35 mmHg). At -15 mmHg LBNP, the relation between burst incidence (bursts per 100 heartbeats) and DAP showed an upward shift from that observed during CON, but the further shift seen at -35 mmHg LBNP was only marginal. The relation between burst strength and DAP was shifted upward at -15 mmHg LBNP (vs. CON) and further shifted upward at -35 mmHg LBNP. At -15 mmHg LBNP, the relation between total activity and DAP was shifted upward from that obtained during CON and further shifted upward at -35 mmHg LBNP. These results suggest that ABR control of MSNA is modulated during orthostatic stress and that the modulation is different between a mild (nonhypotensive) and a moderate (hypotensive) level of orthostatic stress.

Adult↗

PubMed2004

Modulation of arterial baroreflex control of muscle sympathetic nerve activity by muscle metaboreflex in humans.

We aimed to investigate the interaction [with respect to the regulation of muscle sympathetic nerve activity (MSNA) and blood pressure] between the arterial baroreflex and muscle metaboreflex in humans. In 10 healthy subjects who performed a 1-min sustained handgrip exercise at 50% maximal voluntary contraction followed by forearm occlusion, arterial baroreflex control of MSNA (burst incidence and strength and total activity) was evaluated by analyzing the relationship between beat-by-beat spontaneous variations in diastolic arterial blood pressure (DAP) and MSNA both during supine rest (control) and during postexercise muscle ischemia (PEMI). During PEMI (vs. control), 1) the linear relationship between burst incidence and DAP was shifted rightward with no alteration in sensitivity, 2) the linear relationship between burst strength and DAP was shifted rightward and upward with no change in sensitivity, and 3) the linear relationship between total activity and DAP was shifted to a higher blood pressure and its sensitivity was increased. The modification of the control of total activity that occurs in PEMI could be a consequence of alterations in the baroreflex control of both MSNA burst incidence and burst strength. These results suggest that the arterial baroreflex and muscle metaboreflex interact to control both the occurrence and strength of MSNA bursts.

Adult↗

PubMed2003

Central command is capable of modulating sweating from non-glabrous human skin.

Isometric handgrip exercise (IHG) increases sweating rate without changing core or skin temperatures. The contribution of central command resulting in increases in sweating rate during IHG is unknown. To investigate this question, seven subjects performed IHG (35 % maximum voluntary contraction (MVC) for 2 min) followed by 2-min of post-exercise ischaemia (PEI), with and without partial neuromuscular blockade (PNB). PNB was performed to augment central command during the IHG bout. These trials were conducted while the subject was normothermic, mildly heated, and moderately heated. On the non-exercising arm, forearm sweating rate was monitored over a microdialysis membrane perfused with neostigmine (acetylcholinesterase inhibitor), and at an adjacent untreated site. In normothermia with PNB, despite reduced force production during IHG (17 +/- 9 versus 157 +/- 13 N; P < 0.001), the elevation in sweating rate at the neostigmine-treated site was greater relative to the control IHG bout (P < 0.05). During subsequent PEI, for the PNB trial mean arterial blood pressure (MAP) and sweating rate returned towards pre-IHG levels, while during the control trial these variables remained elevated. During IHG while mildly heated, the elevation in sweating rate was greater during the PNB trial relative to the control trial. In contrast, during moderate heating sweating increased during IHG for both trials, however the elevation in sweating rate during the PNB trial was not greater than during the control trial. These results suggest that central command is capable of modulating sweating rate in all thermal conditions, however its effect is reduced when body temperatures and/or sweating rate are substantially elevated.

Adult↗

PubMed2003

Intensity-dependent thermoregulatory responses at the onset of dynamic exercise in mildly heated humans.

To investigate quantitatively how sweating and cutaneous blood flow responses at the onset of dynamic exercise are affected by increasing exercise intensity in mildly heated humans, 18 healthy male subjects performed cycle exercise at 30, 50, and 70% of maximal O2 uptake (VO2 max) for 60 s in a warm environment. The study was conducted in a climatic chamber with a regulated ambient temperature of 35 degrees C and relative humidity of 50%. The subjects rested in the semisupine position in the chamber for 60 min, and then sweating rate (SR) and skin blood flow were measured during cycle exercise at three different intensities. Changes in the heart rate, rating of perceived exertion, and mean arterial blood pressure were proportional to increasing exercise intensity, whereas esophageal and mean skin temperatures were essentially constant throughout the experiment. The SR on the chest, forearm, and thigh, but not on the palm, increased significantly with increasing exercise intensity (P < 0.05). The mean SR of the chest, forearm, and thigh increased 0.05 mg.cm-2.min-1 with an increase in exercise intensity equivalent to 10% VO2 max. On the other hand, the cutaneous vascular conductance (CVC) on the chest, forearm, and palm decreased significantly with increasing exercise intensity (P < 0.05). The mean CVC of the chest and forearm decreased 5.5% and the CVC on the palm decreased 8.0% with an increase in exercise intensity equivalent to 10% VO2 max. In addition, the reduction in CVC was greater on the palm than on the chest and forearm at all exercise intensities (P < 0.01). We conclude that nonthermal sweating and cutaneous blood flow responses are exercise intensity dependent but directionally opposite at the onset of dynamic exercise in mildly heated humans. Furthermore, cutaneous blood flow responses to increased exercise intensity are greater in glabrous (palm) than in nonglabrous (chest and forearm) skin.

Adult↗

PubMed2003

Effects of muscle metaboreceptor stimulation on cutaneous blood flow from glabrous and nonglabrous skin in mildly heated humans.

Given differences in sympathetic innervation to glabrous and nonglabrous skin, we tested the hypothesis that muscle metaboreceptor regulation of cutaneous vascular conductance (CVC) differs between these skin regions. Subjects (n = 21) performed isometric handgrip exercise (IHG; 50% maximal voluntary contraction for 60 s), followed by 2 min of postexercise ischemia. Throughout IHG and postexercise ischemia, CVC was measured from glabrous (palm) and nonglabrous (forearm and chest) regions contralateral to the exercising arm. These procedures were conducted after the subjects had been exposed to an ambient temperature of 35 degrees C and a relative humidity of 50% for 60 min. These thermal conditions were intended to cause slight increases in cutaneous blood flow via sympathetic withdrawal. Esophageal, sublingual, and mean skin temperatures did not change markedly during IHG or postexercise ischemia. During IHG, forearm CVC did not change, chest CVC increased slightly, and palm CVC decreased substantially (from 100 to 34.8 +/- 3.5%; P = 0.001). During muscle metaboreceptor stimulation due to postexercise ischemia, CVC from nonglabrous regions returned to preexercise baselines, whereas CVC at the palm remained below preexercise baseline (68.2 +/- 4.2%; P = 0.001 relative to preexercise baseline). These results indicate that in mildly heated humans muscle metaboreflex stimulation is capable of modulating CVC in glabrous, but not in nonglabrous, skin.

Adult↗

PubMed2003

Non-thermoregulatory modulation of sweating in humans.

Sweating in humans is critical for appropriate thermoregulation during exercise and/or exposure to warm environmental temperatures. In addition to thermal controllers of sweating, a number of non-thermal factors modulate the sweating response. This review summarizes the primary non-thermal neural modifiers of sweating in humans.

Body Temperature Regulation↗

PubMed2002

Modulation of arterial baroreflex dynamic response during muscle metaboreflex activation in humans.

We aimed to investigate the interaction between the arterial baroreflex and muscle metaboreflexes (as reflected by alterations in the dynamic responses shown by muscle sympathetic nerve activity (MSNA), mean arterial blood pressure (MAP) and heart rate (HR)) in humans. In nine healthy subjects (eight male, one female) who performed a sustained 1 min handgrip exercise at 50 % maximal voluntary contraction followed by forearm occlusion, a 5 s period of neck pressure (NP) (30 and 50 mmHg) or neck suction (NS)(-30 and -60 mmHg) was used to evaluate carotid baroreflex function at rest (CON) and during post-exercise muscle ischaemia (PEMI). In PEMI (as compared with CON): (a) the augmentations in MSNA and MAP elicited by 50 mmHg NP were both greater; (b) MSNA seemed to be suppressed by NS for a shorter period, (c) the decrease in MAP elicited by NS was smaller, and (d) MAP recovered to its initial level more quickly after NS. However, the HR responses to NS and NP were not different between PEMI and CON. These results suggest that during muscle metaboreflex activation, the dynamic arterial baroreflex response is modulated, as exemplified by the augmentation of the MSNA response to arterial baroreflex unloading (i.e. NP) and the reduction in the suppression of MSNA induced by baroreceptor stimulation (i.e. NS).

Adult↗

PubMed2002

Time-of-day effect on nonthermal control of sweating response to maintained static exercise in humans.

To investigate the influence of nonthermal factors in the time-of-day effect on the sweating response to maintained static exercise, eight healthy male subjects performed handgrip exercise at 20%, 35% and 50% maximal voluntary contraction (MVC) for 60 s at 0600 hours (morning) and at 1800 hours (evening). Oesophageal temperature ( T(oes)) before the experiment showed a diurnal rhythm [mean (SEM)] [36.3 (0.1) (morning) compared to 36.8 (0.1) degrees C (evening), P<0.01]. Experiments were conducted with subjects in a state of mild hyperthermia during which the mean skin temperature ( T(sk)) was kept constant at 35.5-36.5 degrees C using a water-perfused suit to activate sudomotor responses. The T(oes) and mean T(sk)remained stable during the pre-exercise, handgrip exercise and recovery periods. The response in sweating rate (DeltaSR) on the chest and forearm to handgrip exercise increased significantly with increasing exercise intensity in both the morning and evening tests ( P<0.05). The DeltaSR on the palm did not change significantly with increasing exercise intensity in the morning test ( P>0.1). During handgrip exercise at 50% MVC only, DeltaSR on the chest, forearm and palm in the evening was significantly higher than in the morning ( P<0.05). On the other hand, mean arterial blood pressure and the rating of perceived exertion during 50% MVC handgrip exercise were not significantly different between the morning and evening ( P>0.1). These results indicate the presence of a time-of-day effect on nonthermal control of the sweating response to isometric handgrip exercise, and that this effect is dependent on exercise intensity.

Adult↗