Biomedical subjects

S G Rhind

Publications and source records attributed to S G Rhind.

15 recordsLinked to original sources

PubMed2004

Cytokine induction during exertional hyperthermia is abolished by core temperature clamping: neuroendocrine regulatory mechanisms.

The immunomodulatory effects of physiological temperature change remain poorly understood and inter-relationships between changes in core temperature, stress hormones and cytokines during exertional hyperthermia are not well established. This experimental study was designed to examine how cytokine (tumour necrosis factor (TNF)-alpha, interleukin (IL)-6, IL-12 and IL-1ra (receptor antagonist)) and hormone (epinephrine (Epi), norepinephrine (NE), growth hormone (GH) and cortisol (CORT)) responses are modified when the exercise-induced rise in core temperature is attenuated or exacerbated by immersion in a water bath. Ten men ((mean +/- SD) age: 26.9 +/- 5.7 years; height 1.75 +/- 0.07 m; body mass 76.0 +/- 10.9 kg; O(2 peak): 48.0 +/- 12.4 mL kg(-1) min(-1)) completed two 40-min cycle ergometer exercise trials at 65% O(2 peak) while immersed to mid-chest. Rectal temperature (T(re)) peaked at 39.1 +/- 0.03 and 37.5 +/- 0.13 degrees C during the hot (39 degrees C) and cold (18 degrees C) conditions, respectively. Blood samples were collected before, during (20- and 40-min) and after (30- and 120-min) exercise. Increases in circulating NE (>350%), Epi (>500%), GH (>900%), IL-12 (>150%) and TNF-alpha (>90%) were greatest after 40-min exercise in the heat. Substantial elevations of CORT (80%), IL-1ra (150%) and IL-6 (>400%) did not occur until after exercise was complete. Core temperature clamping decreased the rise in circulating stress hormone concentrations and abolished increases in plasma cytokine concentrations. These findings suggest that exercise-associated elevations of T(re) mediate increases of circulating stress hormones, which subsequently contribute to induction of circulating cytokine release.

Adult↗

PubMed2002

Body temperature in sedentary adults during moderate exercise: no effect from exercise the day before.

BACKGROUND: Epidemiological findings show a continued presence of exertional heat injury during military basic recruit training. Current guidelines do not consider the carry-over effects of prior exercise or exposure to high ambient temperatures on the risk of succumbing to heat illness. HYPOTHESIS: From the epidemiological evidence we hypothesized that both prior exercise and exposure to hot environments on the day before would increase the core temperature response during exercise the next day. METHODS: Seven sedentary and non heat-acclimated men and women each performed eight randomized exposures involving treadmill walking for a maximum of 2 h every 2 wk. Two separate control trials at a wet bulb globe temperature (WBGT) of 22.5 degrees C and 26.5 degrees C consisted of exercise during the morning only. Six experimental trials involved successive days of exercise with trials on the second day at either a WBGT of 22.5 degrees C or 26.5 degrees C. All of the experimental trials involved walking during the first morning at a WBGT of 22.5 degrees C. Further, four of these trials included additional exercise in the afternoon at either a WBGT of 22.5 degrees C (two trials) or 29.5 degrees C (two trials). RESULTS: There was no impact of prior exercise on the day preceding the tests at either WBGT for any of the dependent measures. Rectal temperatures increased to 38.0 degrees C at the WBGT of 22.5 degrees C and to 38.5 degrees C for trials at 26.5 degrees C. There were also no carry-over effects from exercise conducted during the preceding afternoon. CONCLUSIONS: Under situations where individuals are well hydrated, rested, and free of injury, illness, and drug use, repeated exercise bouts on successive days do not alter the thermoregulatory response to exercise.

Adult↗

PubMed2001

Differential cell adhesion molecule expression and lymphocyte mobilisation during prolonged aerobic exercise.

This study was undertaken to determine the cell adhesion molecule profile of CD4+, CD8hi and CD56+ lymphocytes, which are mobilised to and from the peripheral blood during and after prolonged aerobic exercise. Ten healthy males (21-35 years old) were tested on two occasions, separated by at least 14 days. On the first occasion, subjects were examined in a rested state but did not exercise. On the second occasion, the same subjects were examined at the same time of day before, during and after 2 h of exercise at 65% of peak oxygen consumption. Blood samples obtained at rest (t0), during (at 0.5, 1, 1.5 and 2 h, t0.5, t1, t1.5 and t2, respectively) and after (at 4 and 24 h, t4 and t24, respectively) exercise were analysed by two-colour flow cytometry for CD4+, CD8hi and CD56+ cell surface expression, and density of CD62L, CD49d and CD11a. At t2, circulating concentrations of CD56+, CD8hi and CD4+ lymphocytes had increased (P < 0.05) by 330%, 105% and 30%, respectively. The majority of CD4+, CD8hi and CD56+ lymphocytes mobilised to the blood at t2 were CD62L- and CD11ahi, although populations of CD4+ and CD56+ cells that expressed CD62L+ and CD11alo were also mobilised. Changes in subset concentrations at t0.5 were positively associated (r = 0.63; P < 0.01) with their corresponding mean surface density of CD11a at t0. Our findings suggest that the differential mobilisation of lymphocytes during prolonged aerobic exercise is linked to the surface expression of CD11a (i.e. lymphocyte-function-associated antigen-1). However, mechanisms unrelated to CD11a expression also appear to be involved.

Adult↗

PubMed2001

Intracellular monocyte and serum cytokine expression is modulated by exhausting exercise and cold exposure.

This study tested the hypothesis that exercise elicits monocytic cytokine expression and that prolonged cold exposure modulates such responses. Nine men (age, 24.6 +/- 3.8 y; VO(2 peak), 56.8 +/- 5.6 ml. kg(-1). min(-1)) completed 7 days of exhausting exercise (aerobic, anaerobic, resistive) and underwent three cold, wet exposures (CW). CW trials comprised </=6 h (six 1-h rest-work cycles) exposure to cold (5 degrees C, 20 km/h wind) and wet (5 cm/h rain) conditions. Blood samples for the determination of intracellular and serum cytokine levels and circulating hormone concentrations were drawn at rest (0700), after exercise (approximately 1130), and after CW (~2000). Whole blood was incubated with (stimulated) or without (spontaneous) lipopolysaccharide (LPS; 1 microgram/ml) and stained for CD14 monocyte surface antigens. Cell suspensions were stained for intracellular cytokine expression and analyzed by flow cytometry. The proportion of CD14(+) monocytes exhibiting spontaneous and stimulated intracellular expression of interleukin (IL)-1beta, IL-6, and tumor necrosis factor (TNF)-alpha increased after exercise, but these cells produced less IL-1beta and TNF-alpha after CW when CW was preceded by exhausting exercise. Serum cytokine concentrations followed a parallel trend. These findings suggest that blood monocytes contribute to exercise-induced cytokinemia and that cold exposure can differentially modulate cytokine production, upregulating expression of IL-6 and IL-1 receptor antagonist but downregulating IL-1beta and TNF-alpha. The cold-induced changes in cytokine expression appear to be linked to enhanced catecholamine secretion associated with cold exposure.

Adult↗

PubMed2001

Thermoregulation during cold exposure after several days of exhaustive exercise.

This study examined the hypothesis that several days of exhaustive exercise would impair thermoregulatory effector responses to cold exposure, leading to an accentuated core temperature reduction compared with exposure of the same individual to cold in a rested condition. Thirteen men (10 experimental and 3 control) performed a cold-wet walk (CW) for up to 6 h (6 rest-work cycles, each 1 h in duration) in 5 degrees C air on three occasions. One cycle of CW consisted of 10 min of standing in the rain (5.4 cm/h) followed by 45 min of walking (1.34 m/s, 5.4 m/s wind). Clothing was water saturated at the start of each walking period (0.75 clo vs. 1.1 clo when dry). The initial CW trial (day 0) was performed (afternoon) with subjects rested before initiation of exercise-cold exposure. During the next 7 days, exhaustive exercise (aerobic, anaerobic, resistive) was performed for 4 h each morning. Two subsequent CW trials were performed on the afternoon of days 3 and 7, approximately 2.5 h after cessation of fatiguing exercise. For controls, no exhaustive exercise was performed on any day. Thermoregulatory responses and body temperature during CW were not different on days 0, 3, and 7 in the controls. In the experimental group, mean skin temperature was higher (P < 0.05) during CW on days 3 and 7 than on day 0. Rectal temperature was lower (P < 0.05) and the change in rectal temperature was greater (P < 0.05) during the 6th h of CW on day 3. Metabolic heat production during CW was similar among trials. Warmer skin temperatures during CW after days 3 and 7 indicate that vasoconstrictor responses to cold, but not shivering responses, are impaired after multiple days of severe physical exertion. These findings suggest that susceptibility to hypothermia is increased by exertional fatigue.

Acclimatization↗

PubMed2001

Epinephrine causes a reduction in lymph node cell output in sheep.

The lymphatic system has a critical role in the return of fluids, proteins, and cells to the circulatory system. However, the effects of stress, including exercise, on this system have not been adequately studied. We investigated the effect of a physiological dose (1 mg) of epinephrine (Epi) on lymph flow, cell concentration, and lymphocyte subsets in efferent subcutaneous lymph in sheep. Blood leukocyte numbers, differential, lymphocyte subsets, and blood and lymph pools of lymphocytes were determined simultaneously. A significant acute increase in lymph flow was followed by a post-injection decrease in flow and cellular output. No changes in lymphocyte subsets or pools of lymphocytes were seen in either blood or lymph. The timing of elevated plasma and lymph concentrations of Epi and norepinephrine (NE) corresponded with the increased lymph flow. In conclusion, Epi injection caused no change in lymphocyte subset distribution, leukocyte concentration, or pools of lymphocytes. A decrease in lymph flow and cellularity was documented post-injection, indicating that lymphatic tissue has no role in the leukocytosis seen after Epi injection. Lymphocyte retention by lymph nodes, however, may contribute to post-injection lymphopenia.

Adrenergic alpha-Agonists↗

PubMed2000

Immune function and incidence of infection during basic infantry training.

The effect of an 18.5-week infantry training program on health status was studied in 23 male military personnel (aged 22.0 +/- 0.5 years, mean +/- SE). Aerobic power, body composition, and immune function (including natural killer cell activity, mitogen-stimulated lymphocyte proliferation, in vivo cell-mediated immunity, and secretory immunoglobulin A levels) were measured in subjects at the beginning and end of the course. Subjects self-reported their symptoms of sickness in health logs using a precoded checklist. Data from this study indicate that subjects became leaner and maintained, but did not increase, their aerobic fitness by the end of the course. Cell function was enhanced significantly; however, in vivo cell-mediated immunity remained the same, and levels of secretory immunoglobulin A were lower by the end of the course. The incidence of infection remained stable throughout the course. These results indicate that the current pattern of infantry training does not have an adverse effect on the health status of recruits.

Adult↗

PubMed1999

Indomethacin inhibits circulating PGE2 and reverses postexercise suppression of natural killer cell activity.

Natural killer (NK) cells are important in combating viral infections and cancer. NK cytolytic activity (NKCA) is often depressed during recovery from strenuous exercise. Lymphocyte subset redistribution and/or inhibition of NK cells via soluble mediators, such as prostaglandin (PG) E2 and cortisol, are suggested as mechanisms. Ten untrained (peak O2 consumption = 44.0 +/- 3.5 ml. kg-1. min-1) men completed at 2-wk intervals a resting control session and three randomized double-blind exercise trials after the oral administration of a placebo, the PG inhibitor indomethacin (75 mg/day for 5 days), or naltrexone (reported elsewhere). Circulating CD3(-)CD16(+)/56(+) NK cell counts, PGE2, cortisol, and NKCA were measured before, at 0.5-h intervals during, and at 2 and 24 h after a 2-h bout of cycle ergometer exercise (65% peak O2 consumption). During placebo and indomethacin conditions, exercise induced significant (P < 0.0001) elevations of NKCA (>100%) and circulating NK cell counts (>350%) compared with corresponding control values. With placebo treatment, total NKCA was suppressed (28%; P < 0.05) 2 h after exercise, and a postexercise elevation (36%; P = 0.02) of circulating PGE2 was negatively correlated (r = 0.475, P = 0.03) with K-562 tumor cell lysis. NK counts were unchanged in the postexercise period, but at this stage CD14(+) monocyte numbers were elevated (P < 0.0001). Indomethacin treatment eliminated the postexercise increase in PGE2 concentration and completely reversed the suppression of total and per CD16(+)56(+) NKCA 2 h after exercise. These data support the hypothesis that the postexercise reduction in NKCA reflects changes in circulating PGE2 rather than a differential lymphocyte redistribution.

Administration, Oral↗

PubMed1999

Contribution of exertional hyperthermia to sympathoadrenal-mediated lymphocyte subset redistribution.

The contribution of hyperthermia to the differential leukocytosis of exercise remains obscure. This study examined changes in circulating sympathoadrenal hormone concentrations and patterns of leukocyte and lymphocyte subset (CD3(+), CD4(+), CD8(+), CD19(+), CD3(-)16(+)/56(+)) redistribution during exercise, with and without a significant rise of rectal temperature (T(re)). Ten healthy men [age 26.9 +/- 5.7 (SD) yr, body mass 76.0 +/- 10.9 kg, body fat 13.9 +/- 4.6%, peak O(2) consumption: 48.0 +/- 12.4 ml x kg(-1) x min(-1)] exercised for 40 min (65% peak O(2) consumption) during water immersion at 39 or 18 degrees C. T(re) increased from 37.2 to 39.3 degrees C (P < 0.0001) after 40 min of exercise in 39 degrees C water but was held constant to an increment of 0.5 degrees C during exercise in 18 degrees C water. Application of this thermal clamp reduced exercise-associated increments of plasma epinephrine (Epi) and norepinephrine (NE) by >50% (P < 0.05) and abolished the postexercise increase in cortisol. Thermal clamping also reduced the exercise-induced leukocytosis and lymphocytosis. Multiple regression demonstrated that T(re) had no direct association with lymphocyte subset mobilization but was significantly (P < 0.0001) correlated with hormone levels. Epi was an important determinant of total leukocytes, lymphocytes, and CD3(+), CD4(+), CD8(+), and CD3(-)CD16(+)/56(+) subset redistribution. The relationship between NE and lymphocyte subsets was weaker than that with Epi, with the exception of CD3(-)CD16(+)/56(+) counts, which were positively (P < 0.0001) related to NE. Cortisol was negatively associated with leukocytes, CD14(+) monocytes, and CD19(+) B- and CD4(+) T-cell subsets but was positively related to granulocytes. We conclude that hyperthermia mediates exercise-induced immune cell redistribution to the extent that it causes sympathoadrenal activation, with alterations in circulating Epi, NE, and cortisol.

Adrenal Glands↗

PubMed1998

beta-Endorphin and natural killer cell cytolytic activity during prolonged exercise. is there a connection?

This study was designed to test whether a single 50-mg dose of the opioid antagonist naltrexone hydrochloride, ingested 60 min before 2 h of moderate-intensity exercise (i.e., 65% peak O2 consumption), influenced the exercise-induced augmentation of peripheral blood natural killer cell cytolytic activity (NKCA). Ten healthy male subjects were tested on four occasions separated by intervals of at least 14 days. A rested-state control trial was followed by three double-blind exercise trials [placebo (P), naltrexone (N), and indomethacin] arranged according to a random block design. The indomethacin exercise trial is discussed elsewhere (S. G. Rhind, G. A. Gannon, P. N. Shek, and R. J. Shepherd. Med. Sci. Sports Exerc. 30: S20, 1998). For both the P and N trials, plasma levels of beta-endorphin were increased (P < 0.05) at 90 and 120 min of exercise but returned to resting (preexercise) levels 2 h postexercise. CD3(-)CD16(+)CD56(+) NK cell counts and NKCA were significantly (P < 0.05) elevated at each 30-min interval of exercise compared with correspondingly timed resting control values. However, there were no differences in NK cell counts or NKCA between P and N trials at any time point during the two trials. Changes in NKCA reflected mainly changes in NK cell count (r = 0.72; P < 0.001). The results do not support the hypothesis that the enhancement of NKCA during prolonged submaximal aerobic exercise is mediated by beta-endorphin.

Adult↗

PubMed1997

Effect of melarsoprol treatment on circulating IL-10 and TNF-alpha levels in human African trypanosomiasis.

The pathogenesis of human African trypanosomiasis (HAT) has been the object of considerable research interest but has remained incompletely understood. The importance of cytokines in the pathophysiology of this protozoan infection is now widely recognized, but the full spectrum of cytokines involved has yet to be determined. In the present investigation we compared the plasma concentrations of TNF-alpha and IL-10 in normal African controls and patients suffering from advanced meningocephalic (late-stage) Trypanosomiasis brucei (T.b.) gambiense infections, before and after treatment with the arsenical trypanocide melarsoprol. We found that patients with late-stage T. b. gambiense exhibit chronically elevated circulating levels of both of these cytokines, and that these levels quickly decline following melarsoprol treatment. These findings confirm that TNF-alpha is involved in the immunopathogenesis of late-stage African trypanosomiasis and suggest that IL-10 may also play an important regulatory role in this disease.

Adolescent↗

PubMed1997

Circulating levels of peripheral blood leucocytes and cytokines following competitive cycling.

The objective of the study was to determine if prolonged and strenuous cycling leads to a polarized cytokine response, and/or unique mobilization of circulating leucocyte populations. Resting venous blood samples were collected from 6 amateur cyclists, 24 hr before, and at 10-25 min and 150 min after completion of a 250-km road race (race time: 404 +/- 3.5 min). Total leucocyte counts were significantly elevated following competition. Cell counts of CD3+CD8bright+ lymphocytes were depressed by 50% 150 min after competition. A significant increase in CD4+ cells expressing the IL-2R alpha chain was evident 150 min after competition. IL-6 concentrations were greatly increased, both at 10-25 min and 150 min after competition. Resting TNF-a concentrations were approximately doubled at both time points after competition. Plasma levels of IFN-gamma, IL-10 and IL-12 were below detection thresholds at all time points. These results suggest that performance of a 6.5 h competitive cycle-race does not induce a Type-1 or Type-2-dominated cytokine response, but one that is typical of a proinflammatory cytokine response.

Adult↗

PubMed1996

Effects of moderate endurance exercise and training on in vitro lymphocyte proliferation, interleukin-2 (IL-2) production, and IL-2 receptor expression.

This study was designed to examine immunological responses to an acute bout of cycle ergometry exercise before and after moderate endurance training. Previously sedentary males were randomly assigned to matched training (n = 9) or control (n = 6) groups. Training comprised 12 weeks during which supervised cycle ergometer exercise took place [30 min at 65-70% of maximal oxygen intake (VO2max), 4-5 days .week-1]. An acute bout of exercise (60 min; 60% VO2max) was performed initially and after the 12-week interval. Samples of peripheral venous blood were taken at rest, after 30 and 60 min of exercise, and at 30 and 120 min post-exercise. Training improved VO2max by an average of 20% (40.6 to 49.2 ml.kg-1.min-1). Relative to baseline and control measures, the resting concentration of (CD3-CD16+/CD56+) natural killer (NK) cells increased by 22% (P < 0.05). The resting count of total CD25+ [interleukin-2 receptor (IL-2R) alpha chain] lymphocytes did not change following training, but dual staining analysis showed a 100% increase in the fraction of CD16+ CD25+ NK cells (P < 0.05). Likewise the resting CD122+ (IL-2R beta chain) lymphocyte count increased 35% after training, the greatest increases (44%) being in CD16+ CD122+ NK cells (P < 0.05). Soluble IL-2R levels also increased 33% (P < 0.05) after training. Following acute exercise at the same relative intensity, trained individuals exhibited a larger increase in the NK cell count, reduced lymphocytopenia, and attenuation of exercise-induced suppression of lymphocyte proliferation and IL-2 production (P < 0.05). In addition, smaller increases in CD4 and CD8 counts during exercise were noted, but with faster recovery post-exercise (P < 0.05). Addition of recombinant IL-2 (rIL-2) to phytohemagglutinin-stimulated peripheral blood mononuclear cell cultures did not reverse exercise-induced suppression of cell proliferation, either before or after training. However, rIL-2 did augment the spontaneous blastogenesis of exercise and post-training samples relative to baseline (P < 0.05). We conclude that moderate endurance training is associated with sustained alterations in immune function, both at rest and when exercising. Further investigations are necessary to determine the impact on overall health and susceptibility to disease.

Adult↗

PubMed1996

Endurance exercise with and without a thermal clamp: effects on leukocytes and leukocyte subsets.

To test how leukocyte responses to endurance exercise were modified by clamping body temperature, nine men (27.3 +/- 6.0 yr) completed four 80-min immersions to midchest at water temperatures of 23 or 39 degrees C; two tests included 40-min of cycle ergometer exercise at 65% of aerobic power. When the subjects were exercising, rectal temperature peaked at 39.1 +/- 0.4 degrees C in the warm water and 37.8 +/- 0.3 degrees C in the cool water. When the subjects were sitting in warm water, rectal temperature closely matched the core temperature during exercise in cool water, whereas when they were sitting in cool water, rectal temperatures decreased to 36.4 +/- 0.6 degrees C. Total and differential white cell counts were determined by using a Coulter counter, and cortisol and growth hormone concentrations were determined by radioimmunoassay; all data were adjusted for changes of blood and plasma volumes. Heat clamping during exercise substantially reduced the rise in white cell, lymphocyte, and granulocyte counts but not the increase in monocyte count. Clamping also abolished previously observed associations between cell counts and cortisol and weakened associations with growth hormone concentrations (D. A. McCarthy and M. M. Dale. Sports Med. 6: 333-363, 1988). We conclude that both exercise and a rise of core temperature contribute to the changes in white cell and subset counts during and immediately after moderate exercise. Both cortisol and growth hormone concentrations appear to be mediators of these responses.

Adult↗

PubMed1994

Differential expression of interleukin-2 receptor alpha and beta chains in relation to natural killer cell subsets and aerobic fitness.

Immunophenotyping by dual parameter flow cytometry was used to compare the expression of interleukin-2 receptor alpha and beta chains on lymphocyte subsets in the peripheral blood of 7 trained and 6 untrained volunteers (respective VO2max 57.0 +/- 6.1 and 39.0 +/- 4.5 ml.kg-1.min-1). Venous blood samples were collected at least 36 h after the most recent exercise session. The trained subjects had higher circulating counts (10(9).l-1) of total leukocytes (5.80 +/- 0.83 vs. 4.63 +/- 0.21, p < 0.05), granulocytes (3.14 +/- 0.72 vs. 1.90 +/- 0.30, p < 0.05), and NK cells (CD16+, 0.32 +/- 0.14 vs. 0.16 +/- 0.05, p < 0.05; CD56+, 0.41 +/- 0.14 vs. 0.21 +/- 0.03, p < 0.01), but lower lymphocyte counts than their sedentary peers (1.90 +/- 0.22 vs. 2.26 +/- 0.25, p < 0.05). Counts for T cells (CD3+) and B cells (CD19+), and the CD4+/CD8+ ratio did not differ between the two subject groups. The p55-IL-2 receptor alpha expression (CD25+: 0.63 +/- 0.11 vs. 0.69 +/- 0.17) was unrelated to training, but the p70-75-IL-2 receptor beta expression was higher in the active group (p70/Mik-beta 1+: 0.42 +/- 0.09 vs. 0.20 +/- 0.06, p < 0.001; p75/TU27+: 0.36 +/- 0.08 vs. 0.17 +/- 0.07, p < 0.005). Beta chain co-expression was also higher on NK cell subsets (p < 0.001) in trained than in sedentary subjects. Aerobic power was strongly correlated with IL-2R beta expression (r = 0.914, p < 0.001 for Mik-beta 1; r = 0.884, p < 0.005 for TU27).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗