Physiological responses to cold in relation to the phase of the menstrual cycle and oral contraceptives.
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Biomedical subjects
Publications and source records attributed to R Grucza.
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A group of 14-healthy men performed anisotonic isometric contractions (AIC), for 60 s, at an intensity of 100% maximal voluntary contraction force (MVC) during handgrip (HG) and leg extension (LE). Heart rate (fc), stroke volume index (SVI) and cardiac output index (QcI) were measured during the last 10 s of both AIC by an impedance reography method. Force (F) exerted by the subjects was recorded continuously and reported as a relative force (Fr) (% MVC). The F generated during MVC was greater for LE than for HG (502.1 N compared to 374.6 N, P < 0.001). The rate of decrease in Fr was significantly slower for LE than HG for the first 25 s of the exercise (phase 1 of AIC). The Fr developed by the subjects at the end of AIC was 40% MVC for both LE and HG. The increase in fc was greater for LE (63 beats.min-1) than for HG (52 beats.min-1), P < 0.01. The SVI decreased significantly from the resting level by 17.0 ml.m-2 and by 18.2 ml.m-2 for LE and HG, respectively. The QcI increased insignificantly for HG by 0.09 l.min-1.m-2 and significantly for LE by 0.56 l.min-1.m-2 (P < 0.001). It was concluded that although both AIC caused a significant decrease in SVI, greater increases in fc and Qc were observed for LE than for HG. The greater fc and Qc reported during LE was probably related to the greater relative force exerted by LE during phase 1 of AIC. It seems, therefore that central command might have dominated for phase 1 of AIC but that the muscle reflex also contributed significantly to the control of the cardiac response to the high intensity AIC.
Influence of work rate (30 and 30 rpm) on exercise hyperpnoea, respiratory entrainment and cardiovascular system was studied in 9 healthy men performing rhythmic-static exercise (RSE). Respiratory frequency (f), tidal volume (VT), minute ventilation (VE), heart rate (HR), stroke volume (SV), and cardiac output (Q) were continuously measured. RSE was performed in upright position on a special motor-driven cycloergometer with an intensity of 40% VO2max for 5 min. The subjects opposed the flywheel movement by pressing the pedal alternately with left and right leg. It was found that in both work rates respiratory frequency followed the rhythm of exercise. The increases in f (28v35 breaths/min. p < 0.05) were associated with decreased VT (1.3v1.0L, p < 0.05) but they did not influence VE which was 33 and 36 1/min (NS). Accelerations of f and VE were faster for 30 than 60 rpm reaching respective values of 2.70v0.75 breaths/min/s (p < 0.05), and 0.59v0.31 1/min/s (p < 0.05). Cardiac response and its kinetics were found to be similar for both exercise rhythms. It is concluded that breathing entrainment does not affect either ventilation or the cardiac response during the RSE exercise. Since changes in acceleration of ventilation were not accompanied by appropriate changes in cardiac output acceleration the cardiodynamic hypothesis of exercise hyperpnoea does not seem to be valid for rhythmic-static exercise.
Nine men [24.6 (SEM 1.1) years] carried out isometric contractions (IC) of the right elbow flexors at 50% and 100% of the maximal voluntary contraction (MVC). At 50% MVC they had to maintain IC until the limit time (isotonic IC: IIC50) and beyond for as long as possible (anisotonic IC: AIC50). At 100% MVC, IC was anisotonic since the decrease in force was immediate (AIC100). Measurements of the force, the integrated electromyogram (iEMG) and the heart rate (fc) were made during the entire period of contraction. There was a linear relationship between the iEMG increase and the fc increase for IIC50 and AIC100. This relationship was not found for AIC50. The role played by the peripheral information would seem to have become more important in fc regulation when the isotonic IC preceding the anisotonic IC was sufficiently long (submaximal IIC). It would seem that the idea of muscle exhaustion at the limit time was only relative, and depended greatly on the subject's motivation and his capacity to endure a certain degree of pain.
Thermoregulatory responses to exercise in relation to the phase of the menstrual cycle were studied in ten women taking oral contraceptives (P) and in ten women not taking oral contraceptives (NP). Each subject was tested for maximal aerobic capacity (VO2max) and for 50% VO2max exercise in the follicular (F) and luteal (L) phases of the menstrual cycle. Since the oral contraceptives would have prevented ovulation a quasi-follicular phase (q-F) and a quasi-luteal phase (q-L) of the menstrual cycle were assumed for P subjects. Exercise was performed on a cycle ergometer at an ambient temperature of 24 degrees C and relative air humidity of 50%. Rectal (Tre), mean skin (Tsk), mean body (Tb) temperatures and heart rate (fc) were measured. Sweat rate was estimated by the continuous measurement of relative humidity of air in a ventilated capsule placed on the chest, converted to absolute pressure (PH2Ochest). Gain for sweating was calculated as a ratio of increase in PH2Ochest to the appropriate increase in Tre for the whole period of sweating (G) and for unsteady-state (Gu) separately. The VO2max did not differ either between the groups of subjects or between the phases of the menstrual cycle. In P, rectal temperature threshold for sweating (Tre,td) was 37.85 degrees C in q-L and 37.60 degrees C in q-F (P < 0.01) and corresponded to a significant difference from Tre at rest. The Tre, Tsk, Tb and fc increased similarly during exercise in q-F and q-L. No menstrual phase-related differences were observed either in the dynamics of sweating or in G.(ABSTRACT TRUNCATED AT 250 WORDS)
The influence of aerobic capacity on the cardiovascular response to handgrip exercise, in relation to the muscle mass involved in the effort, was tested in 8 trained men (T) and 17 untrained men (U). The subjects performed handgrip exercises with the right-hand (RH), left-hand (LH) and both hands simultaneously (RLH) at an intensity of 25% of maximal voluntary contraction force. Maximal aerobic capacity was 4.3 l.min-1 in T and 3.21 l.min-1 in U (P less than 0.01). The endurance time for handgrip was longer in T than in U by 29% (P less than 0.05) for RH, 38% (P less than 0.001) for LH and 24% (P less than 0.001) for RLH. Heart rate (fc) was significantly lower in T than in U before handgrip exercise, and showed smaller increases (P less than 0.01) at the point of exhaustion: 89 vs 106 beats.min-1 for RH, 93 vs 100 beats.min-1 for LH and 92 vs 108 beats.min-1 for RLH. Stroke volume (SV) at rest was greater in T than in U and decreased significantly (P less than 0.05) during handgrip exercise in both groups of subjects. At the point of exhaustion SV was still greater in T than in U: 75 vs 57 ml for RH, 76 vs 54 ml for LH and 76 vs 56 ml for RLH. During the last seconds of handgrip exercise, the left ventricular ejection time was longer in T than in U. Increases in cardiac output (Qc) and systolic blood pressure did not differ substantially between T and U, nor between the handgrip exercise tests.(ABSTRACT TRUNCATED AT 250 WORDS)
Kinetics of cardiorespiratory response to dynamic (DE) and then to rhythmic-static exercise (RSE) was compared in nine male subjects exercising in an upright position on a cycle ergometer at an intensity of about 50% VO2max and a mean pedalling frequency of 60 rpm over 5 min. Respiratory frequency (fR), tidal volume (VT), minute ventilation (VE), heart rate (fc), stroke volume (SV), and cardiac output (Qt) were measured continuously. The RSE caused a greater increase in fR than DE, whereas VT increased more during DE. The effect of reciprocal changes in fR and VT was that VE and its kinetics, expressed as a time constant (tau), did not differ between experimental situations. The ventilatory equivalent for O2 (VE: VO2) was greater for RSE (31.3) than for DE (23.0, P less than 0.01). Elevation of fc was similar for both types of exercise. The SV increased suddenly at the beginning of DE from 54 ml to 74 ml and then decreased to the end of exercise. At the onset of RSE only a moderate increase in SV was observed, from 56 ml to 62 ml, and then SV remained stable. The DE caused a greater and faster increase in Qt (4.20 l.min-1, for tau equal to 16.1 s) than RSE (3.25 l.min-1, for tau equal to 57.0 s, P less than 0.05 and P less than 0.002, respectively). Total peripheral resistance was almost 40% greater for RSE than for DE. No relationship was found between Qt and VE at the first 15 s of both types of exercise.(ABSTRACT TRUNCATED AT 250 WORDS)
The aim of the present work was to estimate the dynamics and efficiency (eta sw) of sweating, and thermoregulatory index (TI) defined as a ratio of heat loaded the body to the heat removed to the environment. In the first part of this work 22 men exercised with an intensity of 50% VO2 max. in 22 degrees C, 16 men were exposed to 40 degrees C at rest, and 9 men exercised at the level of 50% VO2 max. at 30 degrees C. In the second part, 8 men and 8 women were exposed to 40 degrees C before and after dehydration (1% of body mass, approximately), 8 men exercised at 23 degrees C before and after hyperhydration (35 ml/kg of body mass) and 22 men exercised before and after 3 months of endurance training. Body heat balance, rectal (Tre), tympanic (Tty) and mean skin (Tsk) temperatures were measured in all subjects. TI was greater during simultaneous (0.84) than during separate endo- (0.76, p less than 0.01) or exogenous (0.67, p less than 0.001) heat loads. The respective values of eta sw were 0.82; 0.57 (p less than 0.001) and 0.78 (p less than 0.001). No difference in TI was found between men and women. Dynamics of sweating was greater in men but efficiency of sweating was greater in women. Dehydration before heat exposure decreased both dynamics of sweating and TI but it increased eta sw in men. As a result Tre was greater in dehydrated (0.45 degrees C) than in normally hydrated men (0.31 degrees C, p less than 0.002). Dehydration did not affect the measured variables in women. Hyperhydration of exercising men caused an increase in TI from 0.72 to 0.82 (p less than 0.05) and in eta sw from 0.57 to 0.81 (p less than 0.01). In men exercising after endurance training the onset of sweating was shortened from 4.0 to 0.9 min (p less than 0.002). TI increased from 0.76 to 0.89 (p less than 0.001), eta sw increased from 0.57 to 0.74 (p less than 0.02) whereas Tty was lower (1.10 and 0.58 degrees C, p less than 0.001, respectively). It is concluded that dynamics and efficiency of sweating, as well as the thermoregulatory index depend on the type of heat load. Men and women tolerate dry heat equally well. Dehydration changes thermoregulatory function in men but not in women. Hyperhydration before exercise and particularly endurance training increase tolerance of endogenous heat.(ABSTRACT TRUNCATED AT 400 WORDS)
12 healthy men aged 21-25 years performed, in the sitting position, a sustained handgrip at 25% of their maximum voluntary contraction, first with each hand separately and then with both hands simultaneously. Heart rate (HR), systolic blood pressure (SBP), stroke volume (determined reographically) and plasma catecholamine concentration were measured during each handgrip test. The HR and SBP increased consistently during each handgrip test while stroke volume decreased by approximately 20% of the initial value. Cardiac output did not change significantly. There were no significant differences in the magnitude and dynamics of the cardiovascular responses between the tests with one and with both hands. Plasma noradrenaline and adrenaline levels showed similar elevations in response to handgrip performed with the right hand and with both hands, while during the exercise performed with the left hand the increase in the plasma catecholamine concentration was less pronounced. It was concluded that: (1) during sustained handgrip, performed in the sitting position by young healthy subjects, the stroke volume markedly decreases and cardiac output does not change significantly in spite of the increased HR; (2) the cardiovascular and sympatho-adrenal responses to static handgrip do not depend on the mass of contracting muscle when the same relative tension is developed.
Twenty young, untrained men performed two tests on cycle ergometer in order to verify whether the kinetics of the cardiorespiratory reactions exhibit any relation to maximal oxygen uptake (VO2max) in the untrained state. On the 1st day, the subjects exercised at work intensities of 50 and 100 W, the increase as a step function, for periods of 10 min each. The next day, they performed exercise at a relative intensity of 50% VO2max for 10 min. Respiratory frequency, tidal volume, minute ventilation (VE), heart rate (HR), stroke volume (SV), and cardiac output (Q) were measured continuously. The SV was measured by impedance plethysmography. All the cardiorespiratory variables increased rapidly at the onset of both absolute and relative intensity of work, with a faster response for Q than for VE. The increase in absolute intensity of work from 50 to 100 W caused a significantly slower cardiorespiratory reaction than at the beginning of exercise. The SV increased by 20 ml during first 20 s of both absolute and relative intensities of work and then began to decrease after 6 and 4 min of the exercise, respectively. The decrease in SV was associated with an increase in HR and a stable value of Q. Acceleration at the beginning of, and deceleration during recovery from, the relative intensity of work for VE, HR, and Q were well correlated with individual levels of VO2max in the tested men. It is concluded that the kinetics of cardiorespiratory reaction to a constant, relative intensity of work is related to VO2max in untrained men, and that the kinetics probably constitute a physiological feature of an individual.
Cardiorespiratory dynamics was tested in 10 men exercising with a relative intensity of 50% VO2max for 10 min. Time constants for cardiac response (SV 21.7 sec, HR 45.8 sec, Q 21.7 sec) were shorter than those for the ventilatory response (of 27.4 sec, VT 70 sec, VE 69.5 sec). Respiratory dynamics was significantly related to the level of VO2max exhibited by the subjects: (f) r = 0.79, p less than 0.02; (VT) r = 0.63, p less than 0.05; (VE) r = 0.78, p less than 0.01. It is concluded that in man the dynamics of the ventilatory response to exercise depend on the actual level of VO2max in the individual.
Ventilation and cardiac output in response to four different exercises, namely, volitional pedalling using a bicycle ergometer with a very mild (7 Watt) load, passive pedalling, electrically-induced isometric twitches of one leg, and voluntary twitches simulating the previous electrical twitches, were measured simultaneously during the transient phase from rest. Cardiac output was determined by automated impedance cardiography. A sudden increase in ventilation was observed immediately after the onset of the volitional and passive pedalling whereas cardiac output increased only gradually. Only a slight difference was observed between the cardio-ventilatory responses to volitional and passive exercises. Neither ventilation nor cardiac output changed significantly in response to volitional and electrical twitches of one leg. Conclusions were then drawn that the cardio-dynamic process could be ruled out as the origin of the initial ventilatory response, and instead, other neurogenic mechanisms mediated either centrally or peripherally, should be considered.
The influence of hyperhydration on thermoregulatory function was tested in 8 male volunteers. The subjects performed cycle exercise in the upright position at 52% Vo2max for 45 min in a thermoneutral (Ta = 23 degrees C) environment. The day after the control exercise the subjects were hyperhydrated with tap water (35 ml X kg-1 of body weight) and then performed the same physical exercise as before. Total body weight loss was lower after hyperhydration (329 +/- 85 g) than during the control exercise (442 +/- 132 g), p less than 0.05. The decrease in weight loss after hyperhydration was probably due to a decrease in dripped sweat (58 +/- 64 and 157 +/- 101 g, p less than 0.05). With hyperhydration delay in onset of sweating was reduced from 5.8 +/- 3.2 to 3.7 +/- 2.0 min (p less than 0.05), and rectal temperature increased less (0.80 +/- 0.20 and 0.60 +/- 0.10 degrees C, p less than 0.01). The efficiency of sweating was higher in hyperhydrated (81.4%) than in euhydrated subjects (57.1%), p less than 0.01. It is concluded that hyperhydration influences thermoregulatory function in exercising men by shortening the delay in onset of sweating and by decreasing the quantity of dripped sweat. As a result, the increases in body temperature in hyperhydrated exercising men are lower than in normally hydrated individuals.
The effects of dehydration prior to heat exposure on sweating and body temperature were tested in 8 men and 8 women, dehydration being 1.3 and 1.0% of body weight, respectively. The subjects were exposed to 40 degrees C for 60 min. Compared with controls (C), in the dehydrated men (D) there was a longer delay in the onset of sweating (C, 7.8, D, 11.6 min, p less than 0.05), a lower total sweat loss (C, 153, D, 127 g X m-2 X h-1, p less than 0.001), and a greater increase in Tre (C, 0.31, D, 0.43 degree C, p less than 0.002). In women, dehydration did not influence the control time course of sweating significantly, nor were these significant body temperature increases during heat exposure. Delay in the onset of sweating in women (C, 18.1, D, 18.7 min) was generally longer than in men (C, 7.8, D, 11.6 min), [F(1,14) = 7.41, p less than 0.05]. A significant correlation was found between the inertia time of sweating and delta Tre in both control and dehydration conditions in the men (r = 0.81, p less than 0.01). The rectal temperature increases in men were also related to the inertia time of electrical skin resistance (r = 0.83, p less than 0.01). It is concluded that dehydration affects sweating and body temperature in men more severely than in women.
The dynamics of sweating was investigated at rest in 8 men and 8 women. Electrical skin resistance (ESR), rectal temperature (Tre) and mean skin temperature (Tsk) were measured in subjects exposed to 40 degrees C environmental temperature, 30% relative air humidity, and 1 m X s-1 air flow. Sweat rate was computed from continuous measurement of the whole body weight loss. It was found that increases in Tre, Tsk and mean body temperature (Tb) were higher in women than in men by 0.16, 0.38 and 0.21 degrees C, but only the difference in delta Tb was significant (p less than 0.05). The dynamics of sweating in men and women respectively, was as follows: delay (td) 7.8 and 18.1 min (p less than 0.01), time constant (tau) 7.5 and 8.8 min (N.S.), inertia time (ti) 15.3 and 26.9 min (p less than 0.002), and total body weight loss 153 and 111 g X m-2 X h-1 (p less than 0.001). Dynamic parameters of ESR did not differ significantly between men and women. Inertia times of ESR and sweat rate correlated in men (r = 0.93, p less than 0.001), and in women (r = 0.76, p less than 0.02). In men, delta Tre correlated with inertia time of sweat rate (r = 0.81, p less than 0.01) as well as with the inertia time of ESR (r = 0.83, p less than 0.001). No relation was found between delta Tre and the dynamics of sweating in women. It is concluded that the dynamics of sweating plays a decisive role in limiting delta Tre in men under dry heat exposure. The later onset of sweating in women does not influence the rectal temperature increase significantly. In women, delta Tre is probably limited by a complex interaction of sweating, skin blood flow increase, and metabolic rate decrease.
The body heat balance, measured by a thermometric method, was investigated in humans subjected to endogenous and exogenous heat load. The purpose of the present study was to test the concept of heat exchange by a servomechanism in human thermoregulation. Two series of experiments were performed on male volunteers. In series I 15 subjects performed physical exercise (50% VO2 max) for 60 min at a constant ambient temperature of 25 degrees C. In series II 16 subjects rested in a climatic chamber where the ambient temperature was elevated over 30 min from 22 to 42 degrees C and kept stable at this level during the subsequent 60 min. It was found that in both series of experiments the sweating rate followed an exponential curve exhibiting an inertial course. Heat was stored in the body mainly at the beginning of experiment. In series I the net body heat load of 125 W/m2 was equalized by sweat evaporation, beginning after 40 min of the exercise. In series II the net body heat load of 80 W/m2 was equalized in the same way, starting after 35 min of the constant high ambient temperature. In both series of experiments the amount of heat stored in the body calculated from the body heat balance was quite close to the amount of heat calculated from the calorimetric equation. It is concluded, that under the present experimental conditions, heat loss from the body by sweat evaporation seems to be a regulated variable in the human thermoregulatory system. The observed increase in rectal temperature may result from an inertial course of the sweating reaction.
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Influence of dynamics of sweating on rectal temperature increase was tested in 3 groups of men performing cycle exercise with intensity of 65, 90 and 120 W, respectively, in 22 degrees C chamber temperature and 30% of relative air humidity. During exercise at 65 and 90 W the subjects wore suits while exercising with intensity of 120 W they wore only shorts. The dynamics of sweating was described by delay in onset of sweating and time constant of the reaction. Wearing caused significant increase in skin humidity and decreased evaporative rate of sweating. Sweat rate during steady state was related to the metabolic rate in naked (r = 0.89, p less than 0.002) as well as in wearing subjects (r = 0.93, p less than 0.01). Delay in onset of sweating was, in average, 5 min with a time constant of 7 min. Both factors showed a tendency to be shorter with increasing work intensity. Mean increase in rectal temperature was proportional to the intensity of exercise although the individual delta Tre correlated well with the dynamics of sweating in naked (r = 0.83, p less than 0.01) and wearing subjects (r = 0.84, p less than 0.01). Since delta Tre was smaller in subjects with shorter inertia time of sweating in response to beginning of exercise at the same intensity it is concluded that the dynamics of sweating can play an important role in limiting body temperature increase in working men.