Influence of menstrual cycle and oral contraceptives on tolerance to uncompensable heat stress

In this study we examined the influence of menstrual cycle phase and oral contraceptive use on thermoregulation and tolerance during uncompensable heat stress. Eighteen women (18–35 years), who differed only with respect to oral contraceptive use (n?=?9) or non-use (n?=?9), performed light intermittent exercise at 40°C and 30% relative humidity while wearing nuclear, biological and chemical protective clothing. Their responses were compared during the early follicular (EF, days 2–5) and mid-luteal (ML, days 19–22) phases of the menstrual cycle. Since oral contraceptives are presumed to inhibit ovulation, a quasi-early follicular (q-EF) and quasi-mid-luteal (q-ML) phase was assumed for the users. Estradiol and progesterone measurements verified that all subjects were tested during the desired phases of the menstrual cycle. Results demonstrated that rectal temperature (T _re) was elevated in ML compared with EF among the non-users at the beginning and throughout the heat-stress trial. For the users, T _re was higher in q-ML compared with q-EF at the beginning, and for 75?min of the heat-stress exposure. Tolerance times were significantly longer during EF [128.1 (13.4)?min, mean (SD)] compared with ML [107.4 (8.6)?min] for the non-users, indicating that these women are at a thermoregulatory advantage during the EF phase of their menstrual cycle. For the users, tolerance times were similar in both the q-EF [113.0 (5.8)?min] and q-ML [116.8 (11.2)?min] phases and did not differ from those of the non-users. It was concluded that oral contraceptive use had little or no influence on tolerance to uncompensable heat stress, whereas tolerance was increased during EF for non-users of oral contraceptives.     

Effects of dehydration, hypohydration, and hyperhydration on tolerance during uncompensable heat stress.

The present study examined the effects of dehydration from prior exercise on subsequent exercise tolerance time (TT) that involved wearing nuclear, biological, and chemical (NBC) protective clothing. It was hypothesised that TT would be reduced in the dehydrated state. Ten men undertook continuous treadmill walking at 4.8 km.h-1 at 35 degrees C and 50% relative humidity, wearing NBC clothing while euhydrated (EU) or dehydrated (D) by 2.3% of body weight. Hydration status had no impact on thermoregulatory or cardiovascular responses during exercise. Also rectal temperature at exhaustion did not differ between EU (38.52 +/- 0.39 degrees C) and D (38.43 +/- 0.45 degrees C). Exercise TT during this uncompensable heat stress was reduced significantly for D (47.7 +/- 15.3 min) compared with EU (59.0 +/- 13.6 min). It was concluded that prior exercise leading to levels of dehydration to 2.3% of body weight, together with subsequent fluid restriction during exposure to uncompensable heat stress, impaired TT while wearing the NBC protective clothing. The integration of these findings together with other comparable studies that have examined the influence of hypo- and hyperhydration on TT while wearing NBC protective clothing revealed that hydration status has less effect on TT as the severity of uncompensable heat stress increases.     

Influence of nonthermal baroreceptor modulation of heat loss responses during uncompensable heat stress

We evaluated the hypothesis that with increasing levels of hyperthermia, thermal influences would predominate over nonthermal baroreceptor control of cutaneous vascular conductance (CVC) and local sweat rate (LSR). On separate days, eight male participants were positioned in either an upright seated posture (URS) or a 15° head-down tilt (HDT) posture in a thermoneutral condition and during passive heating, until mean body temperature (T _body) increased by 1.5°C. Hemodynamic [heart rate (HR), cardiac output, mean arterial pressure (MAP)] and thermal responses [T _re, CVC, LSR] were measured continuously. MAP showed a gradual decrease in the early- to mid-stages of heating for both HDT and URS. At a T _body > 0.6°C, MAP achieved a stable, albeit reduced level from baseline resting for the duration of the heating, whereas MAP decreased significantly throughout the heating period in the URS position (p < 0.001). CVC increased rapidly in the early stages of heating and achieved a stable elevated level in both HDT and URS at the mid-stage of heating (T _body increase ≤ 0.45°C) for the duration of the heating period (i.e., to a T _body increase of 1.5°C). A similar pattern of response was observed in LSR. A rapid increase in LSR was observed in the early- to mid-stages of heating (T _body increase ≤ 0.75°C), followed by a slower increase until the end of heating. Responses were similar between conditions. We conclude that despite a significant nonthermal drive, as evidenced by a significant difference in MAP between conditions in the late stages of heating, the thermoeffector activity governing CVC and LSR responses are primarily modulated by thermal input.     

Melatonin has no effect on tolerance to uncompensable heat stress in man

This study examined whether a 5 mg dose of melatonin induced a lower rectal temperature (T _re) response at rest in both a cool and hot environment while wearing normal military combat clothing, and then examined the influence of this response on tolerance to exercise in the heat while wearing protective clothing. Nine men performed four randomly ordered trials involving 2 h of rest at ambient temperatures of either 23 °C or 40 °C followed by exercise at an ambient temperature of 40 °C. The double-blind ingestion of placebo or melatonin occurred after 30 min of rest. The mean T _re during rest at 23 °C had decreased significantly from 36.8 (SD 0.1) °C to 36.7 (SD 0.2) °C at 90 min following the ingestion of the drug, whereas values during the placebo trial did not change. The lower T _re response during the melatonin trial remained during the first 50 min of exercise in the heat while wearing the protective clothing. Since the final mean T _re at the end of exercise also was significantly reduced for the melatonin [39.0 (SD 0.4) °C] compared with the placebo [mean 39.1 (SD 0.3) °C] trial, tolerance times approximated 95 min in both conditions. During rest at 40 °C, melatonin did not affect the mean T _re response which increased significantly during the last 90 min from 36.9 (SD 0.1) °C to 37.3 (SD 0.1) °C. This increase in T _re during the rest period prior to donning the protective clothing decreased tolerance time approximately 30 min compared with the trials that had involved rest at 23 °C. Total heat storage summated over the rest and exercise periods was not different among the trials at 15 kJ · kg⁻¹. It was concluded that the small decrease in T _re following the ingestion of 5 mg of melatonin at rest in a cool environment had no influence on subsequent tolerance during uncompensable heat stress. Accepted: 26 June 2000     

Melatonin has no effect on tolerance to uncompensable heat stress in man

This study examined whether a 5 mg dose of melatonin induced a lower rectal temperature (Tre) response at rest in both a cool and hot environment while wearing normal military combat clothing, and then examined the influence of this response on tolerance to exercise in the heat while wearing protective clothing. Nine men performed four randomly ordered trials involving 2 h of rest at ambient temperatures of either 23 degrees C or 40 degrees C followed by exercise at an ambient temperature of 40 degrees C. The double-blind ingestion of placebo or melatonin occurred after 30 min of rest. The mean Tre during rest at 23 degrees C had decreased significantly from 36.8 (SD 0.1) degrees C to 36.7 (SD 0.2) degrees C at 90 min following the ingestion of the drug, whereas values during the placebo trial did not change. The lower Tre response during the melatonin trial remained during the first 50 min of exercise in the heat while wearing the protective clothing. Since the final mean Tre at the end of exercise also was significantly reduced for the melatonin [39.0 (SD 0.4) degrees C] compared with the placebo [mean 39.1 (SD 0.3) degrees C] trial, tolerance times approximated 95 min in both conditions. During rest at 40 degrees C, melatonin did not affect the mean Tre response which increased significantly during the last 90 min from 36.9 (SD 0.1) degrees C to 37.3 (SD 0.1) degrees C. This increase in Tre during the rest period prior to donning the protective clothing decreased tolerance time approximately 30 min compared with the trials that had involved rest at 23 degrees C. Total heat storage summated over the rest and exercise periods was not different among the trials at 15 kJ x kg(-1). It was concluded that the small decrease in Tre following the ingestion of 5 mg of melatonin at rest in a cool environment had no influence on subsequent tolerance during uncompensable heat stress.     

The role of aerobic fitness and exercise intensity on endurance performance in uncompensable heat stress conditions

The aim of this study was to examine the influence of aerobic fitness and exercise intensity on the development of thermal and cardiovascular strain in uncompensable heat stress conditions. In three separate trials, eight aerobically trained and eight untrained subjects cycled to exhaustion at 60% (H60%) and 75% (H75%) of maximal oxygen uptake [Formula: see text] in 40°C conditions, and for 60 min at 60% [Formula: see text] in 18°C conditions (CON). Training status had no influence on time to exhaustion between trained (61 ± 10 and 31 ± 9 min) and untrained (58 ± 12 and 26 ± 10 min) subjects (H60% and H75%, respectively). Rectal temperature at exhaustion was also not significantly different between trained (39.8 ± 0.3, 39.3 ± 0.6 and 38.2 ± 0.3°C) and untrained (39.4 ± 0.5, 38.8 ± 0.5 and 38.2 ± 0.4°C) subjects, but was different between trials (H60%, H75% and CON, respectively; P < 0.01). However, because exercise was terminated on reaching the ethics approved rectal temperature limit in four trained subjects in the H60% trial and two in the H75% trial, it is speculated that increased rectal temperature may have further occurred in this cohort. Nonetheless, exhaustion occurred >96% of maximum heart rate in both cohorts and was accompanied by significant declines in stroke volume (15-26%), cardiac output (5-10%) and mean arterial pressure (9-13%) (P < 0.05). The increase in cardiovascular strain appears to represent the foremost factor precipitating fatigue during moderate and high intensity aerobic exercise in the heat in both trained and untrained subjects.     

Influence of hydration status and fluid replacement on heat tolerance while wearing NBC protective clothing

The purpose of the present study was to investigate the influence of hypohydration and fluid replacement on tolerance to an uncompensable heat stress. Eight healthy young males completed a matrix of six trials in an environmental chamber, set at 40°C and 30% relative humidity, while wearing nuclear, biological, and chemical protective clothing. Subjects performed either light (3.5 km · h⁻¹, 0% grade, no wind) or heavy (4.8 km · h⁻¹, 4% grade, no wind) treadmill exercise combined with three hydration states [euhydration with fluid replacement (EU/F), euhydration without fluid replacement (EU/NF), and hypohydration with fluid replacement (H/F)]. Hypohydration of 2.2% body mass was achieved by exercise and fluid restriction on the day preceding the trials. No differences in the endpoint mean skin temperature (Tˉ_sk), sweat rate, or rectal temperature (T _re) were observed among the hydration conditions for either work rate. During light exercise, the change in T _re (ΔT _re) was significantly higher with H/F than EU/F after 40 min, and heart rate was greater after 25 min. The heart rate was greater during EU/NF than during EU/F after 60 min. Tolerance times were significantly greater for EU/F than for either EU/NF or H/F. With heavy exercise, no differences in ΔT _re were observed across hydration conditions. Compared to EU/F, heart rates were higher after 10 and 30 min for H/F and EU/NF, respectively. Tolerance times were significantly less during H/F than with either of the EU conditions. Stroke volume was significantly decreased in H/F trials compared to EU/F trials for both light and heavy work rates, but no differences in cardiac output were observed. It was concluded that even minor levels of hypohydration significantly impaired exercise tolerance in a severely uncompensable heat stress environment at both light and heavy exercise intensities. Accepted: 17 June 1997     

Exercise modality modulates body temperature regulation during exercise in uncompensable heat stress

This study evaluated exercise modality [i.e. self-paced (SP) or fixed-intensity (FI) exercise] as a modulator of body temperature regulation under uncompensable heat stress. Eight well-trained male cyclists completed (work-matched) FI and SP cycling exercise bouts in a hot (40.6 ± 0.2°C) and dry (relative humidity 23 ± 3%) environment estimated to elicit 70% of [(V)\dot] \dot{V} O₂max. Exercise intensity (i.e. power output) decreased over time in SP, which resulted in longer exercise duration (FI 20.3 ± 3.4 min, SP 23.2 ± 4.1 min). According to the heat strain index, the modification of exercise intensity in SP improved the compensability of the thermal environment which, relative to FI, was likely a result of the reductions in metabolic heat production (i.e. [(V)\dot] \dot{V} O₂). Consequently, the rate of rise in core body temperature was higher in FI (0.108 ± 0.020°C/min) than in SP (0.082 ± 0.016°C/min). Interestingly, cardiac output, stroke volume, and heart rate during exercise were independent of exercise modality. However, core body temperature (FI 39.4 ± 0.3°C, SP 39.1 ± 0.4°C), blood lactate (FI 2.9 ± 0.8 mmol/L, SP 2.3 ± 0.7 mmol/L), perceived exertion (FI 18 ± 2, SP 16 ± 2), and physiological strain (FI 9.1 ± 0.9, SP 8.3 ± 1.1) were all higher in FI compared to SP at exhaustion/completion. These findings indicate that, when exercise is SP, behavioral modification of metabolic heat production improves the compensability of the thermal environment and reduces thermoregulatory strain. Therefore, under uncompensable heat stress, exercise modality modulates body temperature regulation.     

Hand immersion in cold water alleviating physiological strain and increasing tolerance to uncompensable heat stress

The current study examines the use of hand immersion in cold water to alleviate physiological strain caused by exercising in a hot climate while wearing NBC protective garments. Seventeen heat acclimated subjects wearing a semi-permeable NBC protective garment and a light bulletproof vest were exposed to a 125 min exercise-heat stress (35 degrees C, 50% RH; 5 km/h, 5% incline). The heat stress exposure routine included 5 min rest in the chamber followed by two 50:10 min work-rest cycles. During the control trial (CO), there was no intervention, whilst in the intervention condition the subjects immersed their hands and forearms in a 10 degrees C water bath (HI). The results demonstrated that hand immersion in cold water significantly reduced physiological strain. In the CO exposure during the first and second resting periods, the average rectal temperature (T (re)) practically did not decrease. With hand immersion, the mean (SD) T (re) decreased by 0.45 (0.05 degrees C) and 0.48 degrees C (0.06 degrees C) during the first and second rest periods respectively (P < 0.005). Significant decreases in skin temperature, sweat rate, heart rate, and heat storage was also noted in the HI vs. the CO trials. Tolerance time in the HI exposure were longer than in the CO exposure (only 12 subjects in the CO trial endured the entire heat exposure session, as opposed to all 17 subjects in the HI group). It is concluded that hand immersion in cold water for 10 min is an effective method for decreasing the physiological strain caused by exercising under heat stress while wearing NBC protective garments. The method is convenient, simple, and allows longer working periods in hot or contaminated areas with shorter resting periods.     

Peripheral markers of central fatigue in trained and untrained during uncompensable heat stress

The development of fatigue is more pronounced in the heat than thermoneutral environments; however, it is unclear whether biomarkers of central fatigue are consistent with the higher core temperature (T _c) tolerated by endurance trained (TR) versus untrained (UT) during exertional heat stress (EHS). The purpose of this study was to examine the indicators of central fatigue during EHS in TR versus UT. Twelve TR and 11 UT males (mean ± SE [(V)\dot]\textO _{2 \textpeak} \dot{V}{\text{O}}_{{ 2 {\text{peak}}}}  = 70 ± 2 and 50 ± 1 mL kg LBM⁻¹ min⁻¹, respectively) walked on a treadmill to exhaustion (EXH) in 40°C (dry) wearing protective clothing. Venous blood was obtained at PRE and 0.5°C T _c increments from 38 to 40°C/EXH. Free tryptophan (f-TRP) decreased dramatically at 39.5°C for the TR. Branch chain amino acids decreased with T _c and were greater for UT than TR at EXH. Tyrosine and phenylalanine remained unchanged. Serum S100β was undetectable (<5 pg mL⁻¹). Albumin was greater for the UT from PRE to 39.0°C and at EXH. Prolactin (PRL) responded to relative thermal strain with similar EXH values despite higher T _c tolerated for TR (39.7 ± 0.09°C) than UT (39.0 ± 0.09°C). The high EXH PRL values for both groups support its use as a biomarker of the serotonin and dopamine interplay within the brain during the development of central fatigue.     

Influence of heat stress and acclimation on maximal aerobic power

Summary Thirteen male volunteers performed cycle ergometer maximal oxygen uptake ( tests) in moderate (21 C, 30% rh) and hot (49 C, 20% rh) environments, before and after a 9-day heat acclimation program. This program resulted in significantly decreased (P<0.01) final heart rate (24 bt·min^–1) and rectal temperature (0.4 C) from the first to last day of acclimation. The was lower (P<0.01) in the hot environment relative to the moderate environment both before (8%) and after (7%) acclimation with no significant difference (P>0.05) shown for maximal power output (PO max, watts) between environments either before or after acclimation. The was higher (P<0.01) by 4% after acclimation in both environments. Also, PO max was higher (P<0.05) after acclimation in both the moderate (4%) and hot (2%) environments. The reduction in in the hot compared to moderate environment was not related to the difference in core temperature at between moderate and hot trials, nor was it strongly related with aerobic fitness level. These findings indicate that heat stress, per se, reduced the . Further, the reduction in due to heat was not affect be state of heat acclimation, the degree of elevation in core temperature, or level of aerobic fitness.     

HPA and SAS responses to increasing core temperature during uncompensable exertional heat stress in trained and untrained males

Increases in core temperature (T _c) augment stress hormones and neurotransmitters; however, the effect of different T _c tolerated with varying fitness levels during uncompensable exertional heat stress (EHS) is unclear. The purpose was to examine the hypothalamic–pituitary–adrenal (HPA) axis and sympathetic-adrenomedullary system (SAS) responses during uncompensable EHS in trained (TR) versus untrained (UT) males. Twelve TR and 11 UT ( [(V)dot]textO_2textpeak = 70 ±2 dot{V}{text{O}}_{{2{text{peak}}}} = 70 pm 2 and 50 ± 1 mL kg of lean body mass⁻¹ min⁻¹) walked on a treadmill to exhaustion (EXH) in 40°C (dry), dressed in protective clothing. PRE and 0.5°C T _c increments from 38.0–40.0°C/EXH venous blood was obtained. Cortisol responded to absolute thermal strain, increasing throughout EHS and independent of fitness. Adrenocorticotropic Hormone, Norepinephrine, and Dehydroepiandrosterone–Sulphate responded to relative thermal strain with similar EXH values, despite higher T _c tolerated for TR (39.7°C) than UT (39.0°C). Epinephrine, Growth Hormone (GH), and Aldosterone increased initially, with a plateau above 38.5°C T _c. Findings demonstrate the complexity of the HPA axis, SAS, and T _c relationship, with the stress pathways responding largely to relative thermal strain, although some hormones exhibited a clamping response likely as a protective mechanism. For the TR, evidence existed for a reduced pituitary sensitivity to glucocorticoids and the amplified GH may have contributed to their greater T _c tolerated.     

Effects of aerobic endurance training status and specificity on oxygen uptake kinetics during maximal exercise

The main purpose of this study was to analyze the effects of exercise mode, training status and specificity on the oxygen uptake (O₂) kinetics during maximal exercise performed in treadmill running and cycle ergometry. Seven runners (R), nine cyclists (C), nine triathletes (T) and eleven untrained subjects (U), performed the following tests on different days on a motorized treadmill and on a cycle ergometer: (1) incremental tests in order to determine the maximal oxygen uptake (O_2max) and the intensity associated with the achievement of O_2max (IO_2max); and (2) constant work-rate running and cycling exercises to exhaustion at IO_2max to determine the effective time constant of the O₂ response (O₂). Values for O_2max obtained on the treadmill and cycle ergometer [R=68.8 (6.3) and 62.0 (5.0); C=60.5 (8.0) and 67.6 (7.6); T=64.5 (4.8) and 61.0 (4.1); U=43.5 (7.0) and 36.7 (5.6); respectively] were higher for the group with specific training in the modality. The U group showed the lowest values for O_2max, regardless of exercise mode. Differences in O₂ (seconds) were found only for the U group in relation to the trained groups [R=31.6 (10.5) and 40.9 (13.6); C=28.5 (5.8) and 32.7 (5.7); T=32.5 (5.6) and 40.7 (7.5); U=52.7 (8.5) and 62.2 (15.3); for the treadmill and cycle ergometer, respectively]; no effects of exercise mode were found in any of the groups. It is concluded that O₂ during the exercise performed at IO_2max is dependent on the training status, but not dependent on the exercise mode and specificity of training. Moreover, the transfer of the training effects on O₂ between both exercise modes may be higher compared with O_2max.     

Acute volume expansion preserves orthostatic tolerance during whole-body heat stress in humans

Whole-body heat stress reduces orthostatic tolerance via a yet to be identified mechanism(s). The reduction in central blood volume that accompanies heat stress may contribute to this phenomenon. The purpose of this study was to test the hypothesis that acute volume expansion prior to the application of an orthostatic challenge attenuates heat stress-induced reductions in orthostatic tolerance. In seven normotensive subjects (age, 40 ± 10 years: mean ± s.d. ), orthostatic tolerance was assessed using graded lower-body negative pressure (LBNP) until the onset of symptoms associated with ensuing syncope. Orthostatic tolerance (expressed in cumulative stress index units, CSI) was determined on each of 3 days, with each day having a unique experimental condition: normothermia, whole-body heating, and whole-body heating + acute volume expansion. For the whole-body heating + acute volume expansion experimental day, dextran 40 was rapidly infused prior to LBNP sufficient to return central venous pressure to pre-heat stress values. Whole-body heat stress alone reduced orthostatic tolerance by ∼80% compared to normothermia (938 ± 152 versus 182 ± 57 CSI; mean ± s.e.m. , P < 0.001). Acute volume expansion during whole-body heating completely ameliorated the heat stress-induced reduction in orthostatic tolerance (1110 ± 69 CSI, P < 0.001). Although heat stress results in many cardiovascular and neural responses that directionally challenge blood pressure regulation, reduced central blood volume appears to be an underlying mechanism responsible for impaired orthostatic tolerance in the heat-stressed human.     

Influence of training status on maximal accumulated oxygen deficit during all-out cycle exercise

The influence of training status on the maximal accumulated oxygen deficit (MAOD) was used to assess the validity of the MAOD method during supramaximal all-out cycle exercise. Sprint trained (ST; n = 6), endurance trained (ET; n = 8), and active untrained controls (UT; n = 8) completed a 90 s all-out variable resistance test on a modified Monark cycle ergometer. Pretests included the determination of peak oxygen uptake ( O_2peak) and a series (5–8) of 5-min discontinuous rides at submaximal exercise intensities. The regression of steady-state oxygen uptake on power output to establish individual efficiency relationships was extrapolated to determine the theoretical oxygen cost of the supramaximal power output achieved in the 90 s all-out test. Total work output in 90 s was significantly greater in the trained groups (P<0.05), although no differences existed between ET and ST. Anaerobic capacity, as assessed by MAOD, was larger in ST compared to ET and UT. While the relative contributions of the aerobic and anaerobic energy systems were not significantly different among the groups, ET were able to achieve significantly more aerobic work than the other two groups, while ST were able to achieve significantly more anaerobic work. Peak power and peak pedalling rate were significantly higher in ST. The results suggested that MAOD determined during all-out exercise was sensitive to training status and provided a useful assessment of anaerobic capacity. In our study sprint training, compared with endurance training, appeared to enhance significantly power output and high intensity performance over brief periods (up to 60 s), yet few overall differences in performance (i.e. total work) existed during 90 s of all-out exercise.     

Hydration status and cardiovascular function: effects of hydration enhancement on cardiovascular function at rest and during psychological stress.

This study examined the effects of a 3-day enhanced hydration regimen on resting cardiac function and reactivity to acute stress. Healthy volunteers (14 male, 14 female) were assigned to one of two groups: Enhanced Hydration and Normal Hydration Group. Participants in the Enhanced Group were given six 1-l bottles of water and instructed to drink two bottles a day in addition to normal fluid intake for 3 days preceding their laboratory session; no extra water was given to the Normal Group. Heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), cardiac output (CO), stroke volume (SV), and total peripheral resistance (TPR) were recorded during a 10-min baseline, 6-min Paced Auditory Serial Addition Test (PASAT), 5-min recovery, 5-min intermediate baseline, and 3-min Cold Pressor Test. Repeated-measures ANOVA revealed a significant Hydration GroupxTask interaction for DBP during the cold pressor (p<0.01) with the Enhanced Group exhibiting greater DBP reactivity to cold stress relative to the Normal Group. Analysis revealed significant Hydration GroupxGender interactions for SV and TPR (p<0.05) at rest and during both the PASAT and Cold Pressor Test. Females in the Enhanced Group displayed higher SV and lower TPR relative to Enhanced Group males, whereas females in the Normal Group displayed lower SV and greater TPR relative to Normal Group males. These results suggest that 3-day hydration enhancement influences blood pressure reactivity in both men and women, and that long-term hydration enhancement is related to resting gender differences in cardiac function.     

The effect of short-term aerobic training on coagulation and fibrinolytic factors in sedentary healthy postmenopausal women

Objective

The purpose of this study was to assess the effect of short-term aerobic training on the fibrinolytic and coagulative factors in postmenopausal women.

Study design

Twenty volunteer sedentary healthy postmenopausal women (48–53 years), who entered the menopause naturally, were divided randomly into two groups: training (n = 10) and control (n = 10).

Methods and main outcome measures

Training consisted of 10 sessions of submaximal aerobic cycling, 35 min for each session (5 min warm-up, 25 min aerobic training with 70% HRmax, 5 min active and 15 min passive recovery), 3 times a week. Coagulation and fibrinolytic factors were assessed both before and after aerobic program in both groups.

Results

Fibrinogen, von Willbrand factor (vWF-Ag) antigen, plasminogen activator inhibitor-1 activity (PAI-1:Ac) and antigen (PAI-1:Ag) showed significant reduction after 10 sessions in the training group (P < 0.05). Also after training, prothrombin time (PT), partial thromboplastin time (PTT), tissue plasminogen activator activity (tPA:Ac) and antigen (tPA:Ag) increased (P < 0.05).

Conclusion

It was concluded that fibrinolytic activity on postmenopausal women could be improved by a 3-week regular submaximal training program. These changes on the hemostatic factors suggest that short-term aerobic training may prevent the decline in fibrinolytic function observed in sedentary postmenopausal women.     

Influence of aerobic exercise training and relaxation training on physical and psychologic health following stressful life events

An experiment was conducted to determine whether aerobic exercise training or relaxation training would be effective for reducing the deleterious effects of life stress on physical and psychologic health. Over 1000 college students were surveyed, and 55 of those who reported experiencing a high number of negative life events over the preceding year were assigned to an aerobic exercise training condition, a relaxation training condition, or a no-treatment control condition. Physical and psychologic health were assessed with self-report measures before, halfway through, immediately following, and 8 weeks after the 11-week training (and control) period. Heart rate data collected during a treadmill test indicated that the aerobic exercise training was effective for improving cardiovascular fitness. Psychologic measures indicated that the exercise training condition was more effective than the other two conditions for reducing depression during the first 5 weeks of training. No differences were found among the conditions on self-report measures of physical health. These findings suggest that aerobic exercise training may be useful for reducing the severity and duration of depressive reactions following stressful life change.     

Age and aerobic training status effects on plasma and skeletal muscle tPA and PAI-1

Introduction

Reductions in fibrinolytic potential occur with both aging and physical inactivity and are associated with an increased cardiovascular disease risk. Plasmin, the enzyme responsible for the enzymatic degradation of fibrin clots, is activated by tissue plasminogen activator (tPA), while plasminogen activator inhibitor-1 (PAI-1) inhibits its activation. Currently, fibrinolysis research focuses almost exclusively on changes within the plasma. However, tPA and PAI-1 are expressed by human skeletal muscle (SM). Currently, no studies have focused on changes in SM fibrinolytic activity with regard to aging and aerobic fitness.

Purpose

The purpose of this study was to cross-sectionally evaluate effects of age and aerobic fitness on tPA and PAI-1 expressions and activity in SM.

Methods

Twenty-six male subjects were categorized into the following groups: (1) young aerobically trained (n = 8); (2) older aerobically trained (n = 6); (3) young aerobically untrained (n = 7); and (4) older aerobically untrained (n = 5). Muscle biopsies were obtained from each subject. SM tPA activity was assessed using gel zymography and SM tPA and PAI-1 expressions were assessed using RT-PCR.

Results

Trained subjects had higher SM tPA activity compared to untrained (25.3 ± 2.4 × 10³ vs. 21.5 ± 5.6 × 10³ pixels, respectively; p = 0.03) with no effect observed for age. VO_{2 max} and SM tPA activity were also significantly correlated (r = 0.42; p < 0.04). SM tPA expression was higher in older participants, but no effect of fitness level was observed. No differences were observed for PAI-1 expression in SM.

Conclusions

Higher levels of aerobic fitness are associated with increased fibrinolytic activity in SM.