Biomedical subjects

P T Wall

Publications and source records attributed to P T Wall.

At least 19 recordsLinked to original sources

PubMed2001

Progressive resistance muscle strength training of hospitalized frail elderly.

OBJECTIVE: To determine whether frail elderly patients recuperating from acute illnesses could safely participate in and gain appreciable improvement in muscle strength from progressive resistance muscle strength training. DESIGN: Muscle strength (one repetition maximum), functional abilities (sit-to-stand maneuver and 20-sec maximal safe gait speed), and body composition were measured before and at the conclusion of a 10-wk program of lower limb progressive resistance muscle strength training. The nonrandomized study was conducted in a 30-bed geriatric rehabilitation unit of a university-affiliated Veterans Affairs hospital and a 28-bed transitional care unit of a community nursing home. Participants included 19 recuperating elderly subjects (14 male, 5 female; 13 ambulatory, 6 nonambulatory) >64 yr (mean age, 82.8+/-7.9 yr). RESULTS: The one repetition maximum increased an average of 74%+/-49% (median, 70%; interquartile range, 38%-95%, and an average of 20+/-13 kg (P = 0.0001). Sit-to-stand maneuver times improved in 15 of 19 cases (79%). Maximum safe gait speeds improved in 10 of 19 cases (53%). Four of the six nonambulatory subjects progressed to ambulatory status. No subject experienced a complication. CONCLUSIONS: A carefully monitored program of progressive resistance muscle strength training to regain muscle strength is a safe and possibly effective method for frail elderly recuperating from acute illnesses. A randomized control study is needed to examine the degree to which progressive resistance muscle strength training offers advantages, if any, over routine posthospital care that includes traditional low-intensity physical therapy.

Activities of Daily Living↗

PubMed2000

A sexual dimorphism in hypothalamic arginine vasotocin (AVT) gene expression and AVT plasma levels in the Japanese quail (Coturnix coturnix japonica) in response to water deprivation.

To examine a possible sexual dimorphism in the osmotic control of arginine vasotocin (AVT) release in birds, age-matched male and female Japanese quail were subjected to water deprivation. The observed increased plasma osmolalities were accompanied by increased plasma AVT levels. Plasma mesotocin levels did not change with water deprivation. The sensitivity of the osmotic control of AVT release as determined by the slope of the relationship between plasma AVT levels and plasma osmolalities was significantly (P < 0.05) higher in males than in females. By Northern blot analysis, levels of hypothalamic AVT gene transcripts were increased 2.3 +/- 0.14- and 3.5 +/- 0.13-fold in water-deprived male and female Japanese quail, respectively, compared to normally hydrated birds. Our data suggest gender-related differences in the osmotic control of AVT release and in hypothalamic AVT gene expression in the Japanese quail.

Animals↗

PubMed1996

Divergence of ventilatory responses to isometric contraction in anesthetized cats.

The purpose of this study was to determine if the initial ventilatory and phrenic nerve responses to isometric contraction of the triceps surae muscle of anesthetized cats are influenced by the pattern of the contraction. To address this, three different types of muscle contraction were evoked: (1) a high tension, continuous tetanic (HT-CT) contraction; (2) a moderate tension, continuous tetanic (MT-CT) contraction; and (3) high tension, intermittent tetanic (HT-IT) contractions. The duration of each contraction period was 60 sec. The MT-CT and HT-IT contractions increased minute volume (VE; 19 +/- 4% and 15 +/- 5%, respectively) within the first 15 sec. These increases were the result of rises in breathing frequency and tidal volume. However, only the MT-CT contraction increased phrenic activity (pVE) in the first 15 sec. By contrast, ventilation and phrenic nerve activity failed to increase within the first 15 sec of the HT-CT contraction. If fact, 'tidal' phrenic activity (pVT; -14 +/- 5%) decreased during the first 5 sec, and there was a tendency for tidal volume (VT; -8 +/- 5%), VE (-8 +/- 6%), and pVE (-16 +/- 8%) to fall. These data suggest that stimulation of muscle afferent fibers by static contraction can initially inhibit phrenic nerve activity, provided the activation is sustained and of sufficient intensity.

Anesthesia, General↗

PubMed1995

Differential effects of clonidine on renal sympathetic nerve activity and heart rate at onset of static exercise.

The effects of the alpha 2-adrenergic agonist clonidine on the increase in renal sympathetic nerve activity (RSNA) and heart rate (HR) at the onset of voluntary static exercise were studied using conscious cats. Five cats were trained to press a bar with one forelimb. A total of 60 exercise trials were performed before and after injection of clonidine (5-10 micrograms/kg i.v.). Before clonidine, RSNA and HR increased immediately before or at the onset of exercise, which was followed by a rise in arterial blood pressure (AP). The initial increases in RSNA and HR are likely to be caused by descending input from higher brain centers. After clonidine, baseline RSNA was decreased to 21 +/- 5% of the control before clonidine, probably due to a central action of clonidine. HR and AP were decreased from 221 +/- 4 to 178 +/- 5 bpm and from 108 +/- 2 to 82 +/- 4 mmHg, respectively. The increase in RSNA at the onset of exercise and the rise in AP during exercise were blunted to 56-57% of the responses before clonidine injection. In contrast, the increase in HR at the onset of exercise was not altered by clonidine. Thus, it is suggested that clonidine, administered intravenously, attenuates the centrally-induced increase in RSNA at the onset of static exercise but does not affect the increase in HR.

Adrenergic Fibers↗

PubMed1995

Effect of skeletal muscle fiber type on the pressor response evoked by static contraction in rabbits.

The purpose of this study was to determine whether the reflex hemodynamic responses to static contraction of predominately glycolytic muscle are greater than the changes elicited by primarily oxidative muscle. Low-frequency electrical stimulation (continuous 21 days) of the tibial nerve of one hindlimb of adult rabbits converted the metabolic characteristics of the predominately glycolytic gastrocnemius to a muscle that was primarily oxidative. After 21 days of stimulation, the rabbits were decerebrated, and static contraction of the glycolytic muscle (unstimulated gastrocnemius) initially decreased heart rate (HR; -16 +/- 3 beats/min) and mean arterial pressure (MAP; -17 +/- 3 mmHg). Thereafter, MAP increased 13 +/- 3 mmHg above baseline. Static contraction of the oxidative muscle (stimulated gastrocnemius) produced similar decreases in HR and MAP (-12 +/- 4 beats/min and -12 +/- 3 mmHg, respectively). However, the subsequent increase in MAP (8 +/- 3 mmHg; above baseline) was less than that evoked by contraction of the glycolytic muscle. The responses evoked by stretch of each muscle and high-intensity electrical stimulation were the same, indicating that the afferents from the muscle were not destroyed by the chronic-stimulation technique. These results support the hypothesis that metabolic by-products play a role in the pressor response to static contraction of skeletal muscle. In addition, these data confirm that contraction of predominately oxidative muscle can evoke a reflex pressor response, albeit smaller than the change elicited from primarily glycolytic muscle.

Analysis of Variance↗

PubMed1995

Attenuation of the reflex responses to muscle contraction by the coadministration of antagonists to substance P and somatostatin into the dorsal horn.

OBJECTIVE: The aim was to determine if the coadministration of antagonists to substance P and somatostatin into the L7 dorsal horn blunts the reflex cardiovascular responses to static contraction to a greater extent than each antagonist alone. The possibility that this attenuation is mediated by blunting the contraction evoked increases in sympathetic outflow was also tested. METHODS: Using alpha chloralose anaesthetised cats (n = 8), static contraction and stretch of the triceps surae muscle were performed before and after microinjecting (1 microliter) 250 ng of the substance P antagonist, D-Pro2-D-Phe7-D-Trp9-substance P, and the somatostatin antagonist, cyclo(7-amino-heptanoyl-phenylalanyl-D-tryptophyl-lysyl-threonyl-[ benzyl]). The muscle was contracted by electrically stimulating the peripheral end of the cut L7 ventral root. RESULTS: Before injecting the antagonists, static muscle contraction increased mean arterial blood pressure by 40(SEM 6) mm Hg, heart rate by 13(2) beats.min-1, and renal sympathetic nerve activity (RSNA) by 41(7)%. These changes were blunted by the antagonists since the increases in blood pressure, heart rate, and RSNA were reduced to 21(3) mm Hg, 8(1) beats.min-1, and 23(5)%, respectively. In contrast, antagonist administration did not affect the pressor [33(5) v 31(5) mm Hg], heart rate [9(2) v 10(2) beats.min-1], or RSNA [23(4)% v 25(5)%] responses to muscle stretch. Microinjection of 2% lignocaine into the dorsal horn virtually abolished the reflex changes elicited by muscle stretch. CONCLUSIONS: The release of substance P and somatostatin in the spinal cord plays a role in mediating the cardiovascular changes caused by static contraction, but the release of other neurotransmitters/neuromodulators is also involved. The attenuation produced by these antagonists is mediated, at least in part, by reducing sympathetic outflow.

Animals↗

PubMed1995

The range of PaO2 variation determines the severity of oxygen-induced retinopathy in newborn rats.

PURPOSE: This study was conducted to determine the potential influence of PaO2 fluctuation on the retinal neovascular response known to occur in newborn rats exposed to hyperoxic conditions. As an inherent corollary, the authors also defined the relationship between the fraction of inspired oxygen (FiO2) and the arterial blood oxygen tension (PaO2) in newborn rats. METHODS: Experiment 1 was composed of several oxygen-exposure protocols in which atmospheres of 10% oxygen concentration were alternated with different higher levels of ambient oxygen (50%, 40%, 30%, and room air). In experiment 2, two alternating oxygen concentrations were made to converge toward room air (20.9% oxygen) with each successive group of four treatment groups. These included another group exposed to alternating 50% and 10% oxygen, a group exposed to alternating 45% and 12.5% oxygen concentrations, one exposed to alternating concentrations of 40% and 15% oxygen, and a final group exposed to 35% and room air oxygen concentrations. In each case, oxygen was alternated between the two exposure concentrations every 24 hours. The term delta FiO2 is used to designate the difference in the two oxygen concentrations to which a treatment group was subjected, applying the units of fraction of inspired oxygen (i.e., delta FiO2 = 0.4 for the exposure to alternating 50% and 10% oxygen). At birth, litters of albino rats were placed in each of these environments for 13 or 14 days, after which PaO2 and retinal vascular development were assessed in some rats. The remainder were removed to room air for 4 days before the incidence and severity of abnormal neovascularization were measured. RESULTS: PaO2 and FiO2 were directly and linearly correlated (r2 = 0.998). In experiment 1, the extent of retinal vascular development on removal from oxygen was a linear function of delta FiO2. Retinal neovascularization subsequently occurred in all rats exposed to alternating 50% and 10% or 40% and 10% oxygen concentrations, but only a third of the 30% and 10% exposure group, indicating a minimum threshold for proliferative disease at delta FiO2 = 0.2. In experiment 2, retinal avascularity also increased linearly with increasing delta FiO2. There was a threshold for neovascularization between the exposure to alternating 45% and 12.5% oxygen and the 40% and 15% oxygen exposure (100% versus 4.8% incidence of neovascularization), indicating a requirement of < or = 12.5% oxygen episodes to stimulate a consistent proliferative response. CONCLUSIONS: These results suggest that PaO2 fluctuation and degree of hypoxia may have more influence on proliferative retinal disease in newborn rats than the extended hyperoxia that has historically received greater attention. Experimental designs that address the inherent differences in pulmonary function between intrinsically healthy animals and compromised premature infants are of substantial value to our understanding of the pathogenesis of retinopathy of prematurity.

Animals↗

PubMed1994

Chemokine-induced fever: intracerebroventricular actions of MIP-1 and MIP-1 alpha in rats.

The central pyrogenic actions in the rat of doublet macrophage inflammatory protein-1 (MIP-1) and MIP-1 alpha were determined by their intracerebroventricular infusion. Doses of 560 pg and 11.2 ng of MIP-1 or 10.0 ng MIP-1 alpha infused into the third cerebral ventricle induced a long lasting fever. However, MIP-1 alpha was much less potent than MIP-1 in terms of intensity and longer latency. Overall, these cytokines are pyrogenic when acting on the walls of the third ventricle; however, a dose 10 times greater than that injected directly into the anterior hypothalamus is required to evoke fever, as based on earlier experiments. Finally, circulating MIP-1 could act centrally by its entry through the choroid plexus into the ventricular system of the brain.

Animals↗

PubMed1994

Reflex stimulation of cardiac sympathetic nerve activity during static muscle contraction in cats.

Reflex response of cardiac sympathetic nerve activity (CSNA) during static contraction of the triceps surae muscle was studied using anesthetized cats. A 1-min contraction was evoked by stimulating the peripheral ends of the cut L7 and S1 ventral roots. CSNA increased 48 +/- 13% immediately after the onset of contraction, which was abolished by cutting the L4-S1 dorsal roots. This rapid increase in CSNA preceded rises in heart rate (13 +/- 1 beats/min) and arterial blood pressure (33 +/- 6 mmHg). When tension development was altered by changing the frequency of ventral root stimulation or the initial muscle length, the CSNA increase depended on the tension developed. Passive stretch of the muscle, which primarily activates mechanoreceptors, increased CSNA by 41 +/- 22%. When the contraction was sustained for 5 min, CSNA remained elevated throughout the contraction despite a fall in tension, suggesting that the later increase in CSNA is caused by factors other than a mechanical event of contraction (e.g., metabolic products). Thus it is suggested that cardiac sympathetic outflow is stimulated due to a reflex arising from the contracting muscle. The increase in CSNA at the initiation of contraction is likely to be caused by a reflex from muscle mechanoreceptors, which is followed by a subsequent increase due to a reflex from muscle metaboreceptors.

Animals↗

PubMed1994

Cardiovascular and renal nerve responses to static muscle contraction of decerebrate rabbits.

The purpose of this study was to determine whether the biphasic arterial blood pressure responses elicited by static muscle contraction of decerebrate rabbits are mediated, at least in part, by an initial decrease and a subsequent increase in sympathetic outflow. Renal sympathetic nerve activity (RSNA) was used as an index of sympathetic outflow. Static contraction of the triceps surae muscle (n = 14) initially decreased mean arterial blood pressure (MAP) -20 +/- 3 mmHg and heart rate (HR) -15 +/- 5 beats/min (nadir values). After this initial decrease, MAP increased 12 +/- 2 mmHg (peak increase) above baseline and there was a tendency for HR to be elevated (6 +/- 3 beats/min). The changes in RSNA during muscle contraction (n = 6) mirrored the nadir and peak responses of MAP (-50 +/- 9 and 32 +/- 11%). Muscle stretch (n = 11) also evoked similar nadir and peak responses of MAP (-20 +/- 5 and 9 +/- 1 mmHg), HR (-17 +/- 7 and 3 +/- 3 beats/min), and RSNA (-43 +/- 9 and 46 +/- 15%). These data suggest that the initial depressor and subsequent pressor responses elicited by skeletal muscle contraction and stretch are mediated, at least in part, by biphasic changes in sympathetic outflow.

Animals↗

PubMed1993

Substance P release in the spinal cord during the exercise pressor reflex in anaesthetized cats.

1. The purpose of this study was to determine if static skeletal muscle contraction causes the release of substance P(SP) in the L7-dorsal horn region of the spinal cord. A laminectomy was performed to expose the spinal cord of alpha-chloralose anaesthetized cats. The L6 spinal root was cut. A microdialysis probe was inserted into the L7 dorsal horn region ipsilateral to the contracting triceps surae muscle. The probe was perfused with a buffer solution at 3 microliters/min. Substance P-like immunoreactivity (SP-LI) was measured, from the microdialysis samples, by radioimmunoassay. 2. A 5-9 min contraction of the triceps surae muscle was evoked by alternate electrical stimulation of the peripheral ends of the cut L7 and S1 ventral roots. Basal SP-LI release was 0.20 +/- 0.03 fmol/100 microliters and was increased to 0.54 +/- 0.05 fmol/100 microliters (mean +/- S.D.) by static muscle contraction. This increase was greatly attenuated after cutting the L7 and S1 dorsal roots (0.23 +/- 0.03 to 0.39 +/- 0.08 fmol/100 microliters) or completely abolished by muscle paralysis (0.27 +/- 0.03 to 0.31 +/- 0.01 fmol/100 microliters). Muscle contraction also increased mean arterial blood pressure (MAP) 29 +/- 20 mmHg and heart rate (HR) 11 +/- 5 beats/min (mean +/- S.D.). These cardiovascular changes to muscle contraction were abolished by sectioning the dorsal roots or when the ventral roots were electrically stimulated after the cats were paralysed. 3. These results demonstrate that static contraction of skeletal muscle increases the release of SP-LI in the dorsal horn of the spinal cord. Furthermore, these data support the hypothesis that SP plays a role in mediating the cardiovascular responses evoked during static exercise.

Animals↗

PubMed1992

Neurally mediated renal vasoconstriction during isometric muscle contraction in cats.

The aim of this study was to determine if the reflex increase in renal sympathetic nerve activity (RSNA) during static (isometric) muscle contraction evokes renal vasoconstriction and decreases renal blood flow. RSNA, renal blood flow velocity, and arterial pressure were measured simultaneously during isometric contraction of the hindlimb triceps surae muscle in eight chloralose-anesthetized cats. A 1-min contraction was evoked by stimulating the peripheral ends of the cut L7 and S1 ventral roots. RSNA and mean arterial pressure (MAP) increased 41 +/- 14% (SE) and 50 +/- 10 mmHg during static contraction, whereas mean renal blood flow velocity (MRBV) decreased 14 +/- 5%. Calculated renal vascular resistance increased 73 +/- 20% during the contraction. The increase in RSNA preceded the decrease in MRBV by 20 s. Passive mechanical stretch of the muscle increased RSNA 21 +/- 12% but did not alter MRBV. Renal denervation abolished the decrease in MRBV during isometric contraction but only attenuated the rise in MAP. Cutting the L4-S1 dorsal roots or muscle paralysis abolished the MRBV and MAP responses. Thus reflex stimulation of RSNA from the contracting muscle can induce renal vasoconstriction and decrease renal blood flow.

Animals↗

PubMed1992

Effect of spinal microinjections of an antagonist to substance P or somatostatin on the exercise pressor reflex.

The purpose of this study was to determine the heart rate and arterial blood pressure changes to isometric skeletal muscle contraction and muscle stretch before and after microinjecting an antagonist to substance P (SP) or somatostatin (SOM) into the L-7 dorsal horn region of the spinal cord of anesthetized cats. Anesthesia was induced by administering an anesthetic gas mixture and was subsequently maintained with alpha-chloralose. Triceps surae contraction was induced by electrically stimulating the L-7 ventral root. Three muscle manipulations (all 1 minute in duration) were performed: 1) continuous tetanic contraction, 2) intermittent tetanic contractions (1 second of contraction, 1 second of relaxation), and 3) passive muscle stretch. Saline microinjections had no effect on the cardiovascular responses to these muscle manipulations. However, both peptide antagonists blunted the pressor response to a continuous tetanic contraction as mean arterial pressure increased 47 +/- 4 and 44 +/- 4 mm Hg before and 28 +/- 3 and 28 +/- 4 mm Hg after microinjecting the SP or SOM antagonist, respectively. In contrast, neither antagonist influenced the increase in mean arterial pressure produced by passive stretch; values were 43 +/- 6 versus 41 +/- 6 mm Hg (SP antagonist) and 39 +/- 7 versus 42 +/- 7 mm Hg (SOM antagonist) before and after injections, respectively. Microinjecting the SOM antagonist attenuated the pressor response to intermittent tetanic contractions (44 +/- 4 mm Hg before SOM antagonist versus 26 +/- 4 mm Hg after SOM antagonist), whereas the SP antagonist had no effect (35 +/- 3 mm Hg before SP antagonist versus 32 +/- 4 mm Hg after SP antagonist).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1991

Stimulation-induced setting of postural muscle tone in the decerebrate rat.

These studies demonstrate the presence of pontomedullary areas in the rat brainstem which, when stimulated electrically, serve to set postural muscle tone in the hindlimbs. Low amplitude stimulation of the dorsal tegmental field (DTF) was found to inhibit postural muscle tone and, in some rats, was found to decrease mean arterial pressure. Low amplitude stimulation of the ventral tegmental field (VTF) was found to increase postural muscle tone and, in all cases tested, was found to increase mean arterial pressure.

Animals↗

PubMed1991

Multiplicity of the afferent pathways mediating the exercise pressor reflex.

The cardiovascular responses to isometric contraction of the triceps surae muscle of one leg were determined before and after transecting the ipsilateral L7 or L6 and S1 spinal roots. Sectioning only the L7 spinal root slightly attenuated the pressor, but not the heart rate response induced by skeletal muscle contraction, while cutting the L6 and S1 spinal roots (L7 intact) had no effect on the cardiovascular changes. This indicates that there is multiplicity in neural afferent pathways that mediate the exercise pressor reflex.

Animals↗

PubMed1991

The effect of static exercise on renal sympathetic nerve activity in conscious cats.

1. Renal sympathetic nerve activity (RNA), heart rate (HR), arterial blood pressure (AP), and force development were measured simultaneously during voluntary static (isometric) exercise performed by conscious cats. The cats were operantly trained to press a bar with one forelimb. When the force applied to the bar exceeded a predetermined value (threshold), a sound was emitted by a buzzer for audio-feedback. If the cat continued to produce the appropriate force for a period of 26-55 s, food was given as a reward. 2. A total of eighty-nine exercise trials were performed by seven cats. The peak force applied to the bar was 468 +/- 28 g (mean +/- S.E.M.). RNA, HR, and AP increased significantly from the control value during static exercise by 102 +/- 14%, 23 +/- 2 beats/min, and 11 +/- 1 mmHg, respectively. 3. The increase in RNA had both an initial and a late component. The initial component occurred at or immediately before the onset of force development and lasted for 10 s, while the late component gradually increased 14 s after the onset of static exercise and was sustained until the exercise was terminated. 4. HR also increased at the beginning of static exercise with a similar time course as RNA. Then, HR returned to the control value and remained at that level during the remainder of exercise. The increase in AP was delayed by 10 s from the initial increase in RNA and then continued to rise throughout the period of exercise. 5. The sound of the buzzer was emitted during rest to determine any influence of anticipation or conditioning on the response. RNA and AP increased slightly, but HR did not change. The increases in RNA and AP were much smaller than the increases obtained during static exercise. Thus, the increases in RNA, HR and AP during static exercise appeared to be associated with the exercise itself and not due to anticipation and/or conditioning. 6. When AP was elevated by a bolus injection of noradrenaline, RNA during rest was almost abolished and the increase of RNA during static exercise was markedly inhibited. Thus the arterial baroreflex significantly influences RNA both during rest and during static exercise. 7. This study suggests that the initial increases in RNA and HR at the beginning of static exercise in conscious cats are caused by descending input from higher brain centres and not by afferent feedback signals from muscle receptors or by arterial baroreceptors.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1990

Reflex responses of renal nerve activity during isometric muscle contraction in cats.

Renal sympathetic nerve activity (RSNA), arterial blood pressure (AP), and heart rate (HR) were measured during isometric muscle contraction of a hindlimb in chloralose-anesthetized cats. In 14 cats RSNA, AP, and HR increased during a 1-min contraction by 45%, 39 mmHg, and 11 beats/min, respectively; however, in three cats there was a brief initial decrease in RSNA followed by an increase. In 11 cats isometric contraction was maintained for 5 min by alternate stimulation of the L7 and S1 ventral roots. In the first 1 min of sustained contraction, there was a positive correlation (gamma = 0.58, P less than 0.005) between RSNA and tension development. Thereafter RSNA remained elevated despite a tension decrease, and there was no significant correlation between these changes. The RSNA response to contraction of both hindlimbs was greater than that to contraction of either hindlimb alone. Passive stretch of the hindlimb muscle significantly increased RSNA. Thus the initial increase in RSNA during sustained contraction is likely due to activation of muscle mechanoreceptors, whereas the later increase is probably caused by activation of the muscle metaboreceptors.

Animals↗

PubMed1988

Effects of changing hypothalamic temperature on eccrine sweating in the patas monkey.

Two male (10-13 kg) patas monkeys (Erythrocebus patas) were implanted with bilateral thermodes to control hypothalamic temperature. Animals were restrained in primate chairs and instrumented to yield hypothalamic (THYPO), colonic (Tc), and mean skin (Tsk) temperatures, chest sweat rate (mSW), and heart rate (HR). THYPO was monitored using a thermocouple inserted to the tip of a non-perfused thermode; mSW was measured using resistance hygrometry. After the monkey equilibrated to a selected ambient temperature, four thermodes were perfused with water from a temperature-controlled bath. Increasing THYPO from 37 to 41 degrees C increased mSW from 0.05 to 0.30 mg.cm-2.min-1. Reducing Tsk shifted the THYPO:mSW relationship to the right (p less than 0.05) without significantly altering its slope. Activity-induced changes in HR, when THYPO was constant, caused fluctuations in ongoing sweating that closely tracked HR. We conclude that mSW in the patas monkey is controlled by both peripheral and central thermal inputs and nonthermal factors.

Animals↗