Effects of a 6-mo endurance-training program on venous compliance and maximal lower body negative pressure in older men and women.

Aging and chronic exercise training influence leg venous compliance. Venous compliance affects responses to an orthostatic stress. The extent to which exercise training in a previously sedentary older population will affect venous compliance and tolerance to the simulated orthostatic stress of maximal lower body negative pressure (LBNP) is unknown. The purpose of this investigation is to determine the influence of a 6-mo endurance-training program on calf venous compliance and responses and tolerance to maximal LBNP in older men and women. Twenty participants (exercise group: n = 10, 5 men, 5 women; control group: n = 10, 6 men, 4 women; all >60 yr) underwent graded LBNP to presyncope or 4 min at -100 mmHg before and after a 6-mo endurance-training program. Utilizing venous occlusion plethysmography, calf venous compliance was determined in both groups using the first derivative of the pressure-volume relation during cuff pressure reduction before training, at 3 mo, and at the end of the training program. The exercise group improved their fitness with the 6-mo endurance-training program, whereas the control group did not change (14 +/- 3 vs. <1 +/- 2%; P < 0.05). LBNP tolerance did not differ between groups or across trials (P = 0.47). Venous compliance was not different between groups or trials, either initially or after 3 mo of endurance training, but tended to be greater in the exercise group after 6 mo of training (P = 0.08). These data suggest that a 6-mo endurance-training program may improve venous compliance without affecting tolerance to maximal LBNP in older participants.     

Blood flow in the carotid artery during breath-holding in relation to diving bradycardia

The present study investigated the mechanism of diving bradycardia. A group of 14 healthy untrained male subjects were examined during breath-holding either out of the water (30–33°C), in head-out immersion, or in whole-body submersion (27–29°C) in a diving pool. Blood velocity, blood volume flow in the carotid artery, diastolic blood pressure and electrocardiogram were measured and recorded during the experiments. The peak blood velocity increased by 13.6% (P < 0.01) and R-wave amplitude increased by 57.1% (P < 0.005) when the subjects entered water from air. End-diastolic blood velocity in the carotid artery increased significantly during breath-holding, e.g. increased from 0.20 (SD 0.02) m · s⁻¹ at rest to 0.33 (SD 0.04) m · s⁻¹ (P < 0.001) at 50.0 s in breath-hold submersion to a 2.0-m depth. Blood volume flow in the carotid artery increased by 26.6% (P < 0.05) at 30 s and 36.6% (P < 0.001) at 40 s in breath-hold submersion to a 2.0-m depth. Diastolic blood pressure increased by 15.4% (P < 0.01) at 60 s during breath-holding in head-out immersion. Blood volume flow, and diastolic blood pressure increased significantly more and faster during breath-holding in submersion than out of the water. There was a good negative correlation with the heart rate: the root mean square correlation coefficient r was 0.73 (P < 0.001). It was concluded that an increased accumulation of blood in the aorta and arteries at end-diastole and decreased venous return, caused by an increase in systemic peripheral resistance during breath-holding, underlies diving bradycardia. Accepted: 22 November 1996     

Age- and fitness-related differences in limb venous compliance do not affect tolerance to maximal lower body negative pressure in men and women.

Aging and chronic exercise training influence leg venous compliance. Venous compliance affects responses to an orthostatic stress; its effect on tolerance to maximal lower body negative pressure (LBNP) in the elderly is unknown. The purpose of this study was to determine the influence of age and fitness, a surrogate measure of exercise training, on calf venous compliance and tolerance to maximal LBNP in men and women. Forty participants, 10 young fit (YF; age = 22.6 +/- 0.5 yr, peak oxygen uptake = 57.1 +/- 2.0 ml.kg(-1).min(-1)), 10 young unfit (YU; 23.1 +/- 1.0 yr, 41.1 +/- 2.0 ml.kg(-1).min(-1)), 10 older fit (OF; 73.9 +/- 2.0 yr, 39.0 +/- 2.0 ml.kg(-1).min(-1)), and 10 older unfit (OU; 70.9 +/- 1.6 yr, 27.1 +/- 2.0 ml.kg(-1).min(-1)), underwent graded LBNP to presyncope or 4 min at -100 mmHg. By utilizing venous occlusion plethysmography, calf venous compliance was determined by using the first derivative of the pressure-volume relation during cuff pressure reduction. We found that the more fit groups had greater venous compliance than their unfit peers (P < 0.05) as did the young groups compared with their older peers (P < 0.05) such that OU < YU = OF < YF. LBNP tolerance did not differ between groups. In conclusion, these data suggest that aging reduces, and chronic exercise increases, venous compliance. However, these data do not support a significant influence of venous compliance on LBNP tolerance.     

Exercise plus volume loading prevents orthostatic intolerance but not reduction in cerebral blood flow velocity after bed rest

This study tested the hypothesis that reduction in cerebral blood flow (CBF) during orthostatic stress after bed rest can be ameliorated with volume loading, exercise, or both. Transcranial Doppler was used to measure changes in CBF velocity during lower body negative pressure (LBNP) before and after an 18-day bed rest in 33 healthy subjects. Subjects were assigned into four groups with similar age and sex: 1) supine cycling during bed rest (Exercise group; n = 7), 2) volume loading with Dextran infusion after bed rest to restore reduced left ventricular filling pressure (Dextran group; n = 7), 3) exercise combined with volume loading to prevent orthostatic intolerance (Ex-Dex group; n = 7), and 4) a control group (n = 12). LBNP tolerance was measured using a cumulative stress index (CSI). After bed rest, CBF velocity was reduced at a lower level of LBNP in the Control group, and the magnitude of reduction was greater in the Ex-Dex group. However, reduction in orthostatic tolerance was prevented in the Ex-Dex group. Notably, volume loading alone prevented greater reductions in CBF velocity after bed rest, but CSI was reduced still by 25%. Finally, decreases in CBF velocity during LBNP were correlated with reduction in cardiac output under all conditions (r(2) = 0.86; P = < 0.001). Taken together, these findings demonstrate that volume loading alone can ameliorate reductions in CBF during LBNP. However, the lack of associations between changes in CBF velocity and orthostatic tolerance suggests that reductions in CBF during LBNP under steady-state conditions by itself are unlikely to be a primary factor leading to orthostatic intolerance.     

Reduced cardiac stiffness following exercise is associated with preserved myocardial collagen characteristics in the rat

We determined whether the increment in cardiac end-diastolic compliance (a reduced diastolic stiffness constant) following endurance training is related to alterations in myocardial collagen characteristics. Sixteen weeks of habitual exercise (Ex) in rats, which produced left ventricular (LV) hypertrophy (LVH) [LV weight in g: Ex=1.01 (0.04), sedentary control = 0.89 (0.04); P<0.05], resulted in a reduced LV end-diastolic (LVED) chamber stiffness [slope of the linearised LVED pressure versus LVED internal diameter relation in kPa · mm⁻¹: Ex=0.67 (0.03), control=0.80 (0.03); P<0.05]. The increased LVED chamber distensibility was associated with an attenuated myocardial stiffness [slope of the linearised LVED stress versus strain relation in g · cm⁻²; Ex=15 (3), control=25 (2); P<0.05]. Although LV total collagen content (mg) was increased in the exercised rats [Ex=5.0 (0.3), control=4.1 (0.2); P<0.05], this was a reflection of the presence of LVH, as the myocardial collagen concentration (μg · mg⁻¹ LV wet weight) was unaltered [Ex=4.9 (0.2), control=4.6 (0.2)]. Furthermore, habitual exercise did not influence the percentage of myocardial collagen extracted following cyanogen bromide digestion (an index of collagen cross-linking), [i.e. Ex=38 (3), control=38 (3)], nor the proportion of myocardial collagen phenotypes I and III [I/III; Ex=3.04 (0.20), control=2.85 (0.22)]. In conclusion, exercise-induced increments in end-diastolic myocardial distensibility are unlikely to be a consequence of alterations in the properties of myocardial collagen. Accepted: 17 December 1997     

The effect of gender on left ventricular function immediately after the wingate test

The effect of gender on left ventricular systolic function and exercise haemodynamics in healthy young subjects was studied during 30-s all-out sudden strenuous dynamic exercise. A group of 22 men [19.3 (SD 1) years] 20 women [19.1 (SD 1) years] volunteered to participate in this study. Two-dimensional direct M-mode and Doppler echocardiograph studies were performed with the subject in the sitting position. The Doppler examination of flow was located with continuous-wave, interrogating ascending aorta measurements. The subjects completed the study without showing any electrocardiograph abnormalities. An interaction effect with stroke volume (P < 0.05) was characterized by a decrease in the men and an increase of stroke volume in the women. Cardiac output rose significantly (P < 0.05) up to 14.5 (SD 6) l · min⁻¹) for the men and 12.1 (SD 4) l · min⁻¹ for the women compared to the rest values [5.8 (SD 0.4) and 4.7 (SD 0.5) l · min⁻¹, respectively]. Flow velocity integral and acceleration time differed significantly between the two groups at rest (P < 0.05). During exercise these differences showed an interaction effect (P < 0.05). These results would indicate that normal men and women respond to sudden strenuous exercise by reducing their left ventricular systolic function, with a significantly greater decrease in women (P < 0.05). The gender differences in the haemodynamic responses during the present study, may, as suggested by others, be attributable to differences in energy metabolism. In addition, changes in Doppler parameters of aortic flow, haemodynamics and blood pressure responses during sudden strenuous exercise differed markedly from those seen before with endurance exercise. Accepted: 8 January 1997     

The effect of exercise intensity on hematuria in healthy male runners

The purpose of this study were: (1) to establish the prevalence of exercise-induced hematuria in a group of otherwise healthy male runners (n = 70), and (2) to investigate the role of exercise intensity in those runners who exhibited exercise-related hematuria (n = 10) by evaluating the effect of running and cycling at high and low intensities. The identified and recruited subjects participated in four different exercise protocols: (1) a 60-min treadmill run (RUN) at 90% of anaerobic threshold (Th_ae), (2) a 60-min leg cycle ergometer ride (BIKE) at 90% of Th_ae, (3) a 3×400-m sprint (SPRINT), each followed by 4 min of rest or light walking, and (4) 3×60-Wingate leg cycle ergometry tests, each followed by 4 min of rest or light cycling. The study employed a 3×4 (time by protocol) within-subjects design and dependent variables were measured before exercise, 4 min after, and 1 h after exercise, and included measurements of hematuria, proteinuria, urinary pH, serum haptoglobin concentration, serum creatine phosphokinase activity, plasma lactate concentration, and hemoglobin. The 400-m sprint at maximal effort significantly increased both hematuria and proteinuria (P < 0.01). Post-exercise hematuria for the SPRINT protocol was significantly different than that for the BIKE (P < 0.01) and RUN (P < 0.01) protocols. Due to the significant increase in hematuria and proteinuria following the SPRINT protocol, it was concluded that exercise-related changes in renal function were associated with weight-bearing exercise intensity rather than non-weight-bearing exercise duration. Accepted: 30 April 1998     

Femoral to cerebral arterial blood flow redistribution and femoral vein distension during orthostatic tests after 4 days in the head-down tilt position or confinement

The first objective of this study was to confirm that 4 days of head-down tilt (HDT) were sufficient to induce orthostatic intolerance, and to check if 4 days of physical confinement may also induce orthostatic intolerance. Evidence of orthostatic intolerance during tilt-up tests was obtained from blood pressure and clinical criteria. The second objective was to quantify the arterial and venous changes associated with orthostatic intolerance and to check whether abnormal responses to the tilt test and lower body negative pressure (LBNP) may occur in the absence of blood pressure or clinical signs of orthostatic intolerance. The cerebral and lower limb arterial blood flow and vascular resistance, the flow redistribution between these two areas, and the femoral vein distension were assessed during tilt-up and LBNP by ultrasound. Eight subjects were given 4 days of HDT and, 1 month later, 4 days of physical confinement. Tilt and LBNP test were performed pre- and post-HDT and confinement. Orthostatic intolerance was significantly more frequent after HDT (63%) than after confinement (25%, P<0.001). Cerebral haemodynamic responses to tilt-up and LBNP tests were similar pre- and post-HDT or confinement. Conversely, during both tilt and LBNP tests the femoral vascular resistances increased less (P<0.002), and the femoral blood flow reduced less (P<0.001) after HDT than before HDT or after confinement. The cerebral to femoral blood flow ratio increased less after HDT than before (P<0.002) but remained unchanged before and after confinement. This ratio was significantly more disturbed in the subjects who did not complete the tilt test. The femoral superficial vein was more distended during post-HDT LBNP than pre-HDT or after confinement (P<0.01). In conclusion, 4 days of HDT were enough to alter the lower limb arterial vasoconstriction and venous distensibility during tilt-up and LBNP, which reduced the flow redistribution in favour of the brain in all HDT subjects. Confinement did not alter significantly the haemodynamic responses to orthostatic tests. The cerebral to femoral blood flow ratio measured during LBNP was the best predictor of orthostatic intolerance. Accepted: 12 December 1997     

Effect of exercise-induced muscle damage on the blood lactate response to incremental exercise in humans

Eccentric muscle actions are known to induce temporary muscle damage, delayed onset muscle soreness (DOMS) and muscle weakness that may persist for several days. The purpose of the present study was to determine whether DOMS-inducing exercise affects blood lactate responses to subsequent incremental dynamic exercise. Physiological and metabolic responses to a standardised incremental exercise task were measured two days after the performance of an eccentric exercise bout or in a control (no prior exercise) condition. Ten healthy recreationally active subjects (9 male, 1 female), aged 20 (SD 1) years performed repeated eccentric muscle actions during 40 min of bench stepping (knee high step; 15 steps · min⁻¹). Two days after the eccentric exercise, while the subjects experienced DOMS, they cycled on a basket loaded cycle ergometer at a starting work rate of 150 W, with increments of 50 W every 2 min until fatigue. The order of the preceding treatments (eccentric exercise or control) was randomised and the treatments were carried out 2 weeks apart. Two days after the eccentric exercise, all subjects reported leg muscle soreness and exhibited elevated levels of plasma creatine kinase activity (P < 0.05). Endurance time and peak V˙O₂ during cycling were unaffected by the prior eccentric exercise. Minute volume, respiratory exchange ratio and heart rate responses were similar but venous blood lactate concentration was higher (P < 0.05) during cycling after eccentric exercise compared with the control condition. Peak blood lactate concentration, observed at 2 min post-exercise was also higher [12.6 (SD 1.4) vs 10.9 SD (1.3) mM; P < 0.01]. The higher blood lactate concentration during cycling exercise after prior eccentric exercise may be attributable to an increased rate of glycogenolysis possibly arising from an increased recruitment of Type II muscle fibres. It follows that determination of lactate thresholds for the purpose of fitness assessment in subjects experiencing DOMS is not appropriate. Accepted: 27 September 1997     

Indices of skeletal muscle damage and connective tissue breakdown following eccentric muscle contractions

 Indirect indices of exercise-induced human skeletal muscle damage and connective tissue breakdown were studied following a single bout of voluntary eccentric muscle contractions. Subjects (six female, two male), mean (SD) age 22 (2) years performed a bout of 50 maximum voluntary eccentric contractions of the knee extensors of a single leg. The eccentric exercise protocol induced muscle soreness (P < 0.05 Wilcoxon test), chronic force loss, and a decline in the 20:100 Hz percutaneous electrical myostimulation force ratio [P < 0.01, repeated measures analysis of variance (ANOVA)]. Serum creatine kinase (CK) and lactate dehydrogenase (LDH) activities were elevated (P < 0.01, repeated measures ANOVA) following the bout. The mean (SD) CK and LDH levels recorded 3 days post-exercise were 2815 (4144) IU · l^–1 and 375 (198) IU · l^–1, respectively. Serum alkaline phosphatase activity showed no changes throughout the study, and a non-significant increase (P = 0.058, repeated measures ANOVA) in pyridinoline was recorded following the bout. Urinary hydroxyproline (HP) and hydroxylysine (HL) excretion, expressed in terms of creatinine (Cr) concentration, increased after exercise (P < 0.05 and P < 0.01, respectively, repeated measures ANOVA). An increased HP:Cr was recorded 2 days post-exercise and HL:Cr was increased above baseline on days 2, 5, and 9 post-exercise. This indirect evidence of exercise-induced muscle damage suggests that myofibre disruption was caused by the eccentric muscle contractions. Elevated urine concentrations of indirect indices of collagen breakdown following eccentric muscle contractions suggests an increased breakdown of connective tissue, possibly due to a localised inflammatory response. Accepted: 9 October 1996     

The effect of a low-carbohydrate diet on performance, hormonal and metabolic responses to a 30-s bout of supramaximal exercise

The aim of this study was to find out whether a low-carbohydrate diet (L-CHO) affects: (1) the capacity for all-out anaerobic exercise, and (2) hormonal and metabolic responses to this type of exercise. To this purpose, eight healthy subjects underwent a 30-s bicycle Wingate test preceded by either 3 days of a controlled mixed diet (130 kJ/kg of body mass daily, 50% carbohydrate, 30% fat, 20% protein) or 3 days of an isoenergetic L-CHO diet (up to 5% carbohydrate, 50% fat, 45% protein) in a randomized order. Before and during 1 h after the exercise venous blood samples were taken for measurement of blood lactate (LA), β-hydroxybutyrate (β-HB), glucose, adrenaline (A), noradrenaline (NA) and insulin levels. Oxygen consumption (V˙O₂) was also determined. It was found that the L-CHO diet diminished the mean power output during the 30-s exercise bout [533 (7) W vs 581 (7) W, P < 0.05] without changing the maximal power attained during the first or second 5-s interval of the exercise. In comparison with the data obtained after the consumption of a mixed diet, after the consumption of a L-CHO diet resting plasma concentrations of β-HB [2.38 (0.18) vs 0.23 (0.01) mmol · l⁻¹, P < 0.001] and NA [4.81 (0.68) vs 2.2 (0.31) nmol · l⁻¹, P < 0.05] were higher, while glucose [4.6 (0.1) vs 5.7 (0.2) mmol · l⁻¹, P < 0.05] and insulin concentrations [11.9 (0.9) vs 21.8 (1.8) mU · l⁻¹] were lower. The 1-h post-exercise excess of V˙O₂ [9.1 (0.25) vs 10.6 (0.25) l, P < 0.05], and blood LA measured 3 min after the exercise [9.5 (0.4) vs 10.6 (0.5) mmol · l⁻¹, P < 0.05] were lower following the L-CHO treatment, whilst plasma NA and A concentrations reached higher values [2.24 (0.40) vs 1.21 (0.13) nmol · l⁻¹ and 14.30 (1.41) vs 8.20 (1.31) nmol · l⁻¹, P < 0.01, respectively]. In subjects on the L-CHO diet, the plasma β-HB concentration decreased quickly after exercise, attaining ≈30% of the pre-exercise value within 60 min, while insulin and glucose levels were elevated. The main conclusions of this study are: (1) a L-CHO diet is detrimental to anaerobic work capacity, possibly because of a reduced muscle glycogen store and decreased rate of glycolysis; (2) reduced carbohydrate intake for 3 days enhances activity of the sympathoadrenal system at rest and after exercise. Accepted: 31 January 1997     

Salt gland blood flow in the hatchling green turtle, Chelonia mydas

Microsphere and morphometric techniques were used to investigate any circulatory changes that accompany secretion by the salt glands of hatchling Chelonia mydas. Salt glands were activated by a salt load of 27.0 mmol NaCl kg body mass (BM)⁻¹, resulting in a mean sodium secretion rate of 4.14 ± 0.11 mmol Na kg BM⁻¹ h⁻¹ for a single gland. Microsphere entrapment was approximately 160–180 times greater in the active salt gland than the inactive gland, inferring a similar change in blood flow through salt gland capillaries. The concentration of microspheres trapped in the salt gland was significantly correlated with the rate of tear production (ml kg BM⁻¹ h⁻¹) and the total rate of sodium secretion (mmol Na kg BM⁻¹ h⁻¹) but not with tear sodium concentration (mmol Na l⁻¹). Adrenaline (500 μg kg BM⁻¹) inhibited tear production within 2 min and reduced microsphere entrapment by approximately 95% compared with active glands. The volume of filled blood vessels increased from 0.03 ± 0.01% of secretory lobe volume in inactive salt gland sections to 0.70 ± 0.11% in active gland sections. The results demonstrate that capillary blood flow in the salt gland of C. mydas can regulate the activity of the gland as a whole. Accepted: 12 July 2000     

Response of plasma IL-6 and its soluble receptors during submaximal exercise to fatigue in sedentary middle-aged men

The pleiotropic cytokine interleukin-6 (IL-6) has been demonstrated to increase during exercise. Little is known regarding the response of the soluble IL-6 receptors (sIL-6R and sgp130) during such exercise. The aim of the current study was to investigate the response of plasma IL-6, sIL-6R and sgp130 during fatiguing submaximal exercise in humans. Twelve participants underwent an incremental exercise test to exhaustion and one week later performed a submaximal exercise bout (96 ± 6% lactate threshold) to volitional exhaustion. Blood samples taken at rest and immediately post exercise were analyzed for IL-6, sIL-6R and sgp130. IL-6 increased (P < 0.01) by 8.4 ± 8.9 pg ml⁻¹ (75.7%) during the exercise period. sIL-6R and sgp130 also increased (P < 0.05) by 2.7 ± 3.9 ng ml⁻¹ (9.6%) and 37.7 ± 55.6 ng ml⁻¹ (9.6%), respectively. The current study is the first investigation to demonstrate that alongside IL-6, acute exercise stress results in an increase in both sIL-6R and sgp130.     

Body fluid homeostasis and cardiovascular adjustments during submaximal exercise: influence of chewing coca leaves

 The present study was undertaken to determine the haematological and cardiovascular status, at rest and during prolonged (1 h) submaximal exercise (approximately 70% of peak oxygen uptake) in a group (n = 12) of chronic coca users after chewing approximately 50 g of coca leaves. The results were compared to those obtained in a group (n = 12) of nonchewers. At rest, coca chewing was accompanied by a significant increase in heart rate [from 60 (SEM 4) TO 76 (SEM 3) beats · min⁻¹], in haematocrit [from 53.2 (SEM 1.2) to 55.6 (SEM 1.1)%] in haemoglobin concentration, and plasma noradrenaline concentration [from 2.8 (SEM 0.4) to 5.0 (SEM 0.5) μmol · l⁻¹]. It was calculated that coca chewing for 1 h resulted in a significant decrease in blood [−4.3 (SEM 2.2)%] and plasma [−8.7 (SEM 1.2)%] volume. During submaximal exercise, coca chewers displayed a significantly higher heart rate and mean arterial blood pressure. The exercise-induced haemoconcentration was blunted in coca chewers compared to nonchewers. It was concluded that the coca-induced fluid shift observed at rest in these coca chewers was not cumulative with that of exercise, and that the hypovolaemia induced by coca chewing at rest compromised circulatory adjustments during exercise. Accepted: 29 October 1996     

Specificity of resistance training responses in neck muscle size and strength

This study examined hypertrophy after head extension resistance training to assess which muscles of the complicated cervical neuromuscular system were used in this activity. We also determined if conventional resistance exercises, which are likely to evoke isometric action of the neck, induce generalized hypertrophy of the cervical muscle. Twenty-two active college students were studied. [mean (SE) age, weight and height: 21 (1) years, 71 (4) kg and 173 (3) cm, respectively]. Subjects were assigned to one of three groups: RESX (head extension exercise and other resistance exercises), RES (resistance exercises without specific neck exercise), or CON (no training). Groups RESX (n = 8) and RES (n = 6) trained 3 days/week for 12 weeks with large-muscle mass exercises (squat, deadlift, push press, bent row and mid-thigh pull). Group RESX also performed three sets of ten repetitions of a head extension exercise 3 days/week with a load equal to the 3 × 10 repetition maximum (RM). Group CON (n = 8) was a control group. The cross-sectional area (CSA) of nine individual muscles or muscle groups was determined by magnetic resonance imaging (MRI) of the cervical region. The CSA data were averaged over four contiguous transaxial slices in which all muscles of interest were visible. The 3 × 10 RM for the head extension exercise increased for RESX after training [from 17.9 (1.0) to 23.9 (1.4) kg, P < 0.05] but not for RES [from 17.6 (1.4) to 17.7 (1.9)␣kg] or CON [from 10.1 (2.2) to 10.3 (2.1) kg]. RESX showed an increase in total neck muscle CSA after training [from 19.5 (3.0) to 22.0 (3.6) cm², P < 0.05], but RES and CON did not [from 19.6 (2.9) to 19.7 (2.9)␣cm² and 17.0 (2.5) to 17.0 (2.4) cm², respectively]. This hypertrophy for RESX was due mainly to increases in CSA of 23.9 (3.2), 24.0 (5.8), and 24.9 (5.3)% for the splenius capitis, and semispinalis capitis and cervicis muscles, respectively. The lack of generalized neck muscle hypertrophy in RES was not due to insufficient training. For example, the CSA of their quadriceps femoris muscle group, as assessed by MRI, increased by 7 (1)% after this short-term training (P < 0.05). The results suggest that: (1) the splenius capitis, and semispinalis capitis and cervicis muscles are mainly responsible for head extension; (2) short-term resistance training does not provide a sufficient stimulus to evoke neck muscle hypertrophy unless specific neck exercises are performed; and (3) the postural role of head extensors provides modest loading in bipeds. Accepted: 15 October 1996     

Thermoregulatory responses of paraplegic and able-bodied athletes at rest and during prolonged upper body exercise and passive recovery

The thermoregulatory responses of ten paraplegic (PA; T3/4-L4) and nine able-bodied (AB) upper body trained athletes were examined at rest and during prolonged arm-cranking exercise and passive recovery. Exercise was performed for 90 min at 80% peak heart rate, and at 21.5 (1.7)°C and 47.0 (7.8)% relative humidity on a Monark cycle ergometer (Ergomedic 814E) adapted for arm exercise. Mean peak oxygen uptake values for the PA and AB athlete groups were 2.12 (0.41) min⁻¹ and 3.19 (0.38) l · min⁻¹, respectively (P<0.05). At rest, there was no difference in aural temperature between groups [36.2 (0.4)°C for both groups]. However, upper body skin temperatures for the PA athletes were approximately 1.0 °C warmer than for the AB athletes, whereas lower body skin temperatures were cooler than those for the AB athletes (1.3 °C and 2.7 °C for the thigh and calf, respectively). Upper and lower body skin temperatures for the AB athletes were similar. During exercise, blood lactate peaked after 15 min of exercise for both groups [3.33 (1.26) mmol · l⁻¹ and 4.30 (1.03) mmol · l⁻¹ for the PA and AB athletes, respectively, P<0.05] and decreased throughout the remainder of the exercise period. Aural temperature increased by 0.7 (0.5)°C and 0.6 (0.4)°C for the AB and PA athletes, respectively. Calf skin temperature for the PA athletes increased during exercise by 1.4 (2.8)°C (P<0.05), whereas a decrease of 0.8 (2.0)°C (P<0.05) was observed for the AB athletes. During the first 20 min of recovery from exercise, the calf skin temperature of the AB athletes decreased further [−2.6 (1.3)°C; P<0.05]. Weight losses and changes in plasma volume were similar for both groups [0.7 (0.5) kg and 0.7 (0.4) kg; 5.4 (4.9)% and 9.7 (6.2)% for the PA and AB athletes, respectively]. In conclusion, the results of this study suggest that the PA athletes exhibit different thermoregulatory responses at rest and during exercise and passive recovery to those of upper body trained AB athletes. Despite this, during 90 min of arm-crank exercise in a cool environment, the PA athletes appeared to be at no greater thermal risk than the AB athletes. Accepted: 7 May 1997     

Lower body negative pressure exercise plus brief postexercise lower body negative pressure improve post-bed rest orthostatic tolerance.

Orthostatic intolerance follows actual weightlessness and weightlessness simulated by bed rest. Orthostasis immediately after acute exercise imposes greater cardiovascular stress than orthostasis without prior exercise. We hypothesized that 5 min/day of simulated orthostasis [supine lower body negative pressure (LBNP)] immediately following LBNP exercise maintains orthostatic tolerance during bed rest. Identical twins (14 women, 16 men) underwent 30 days of 6 degrees head-down tilt bed rest. One of each pair was randomly selected as a control, and their sibling performed 40 min/day of treadmill exercise while supine in 53 mmHg (SD 4) [7.05 kPa (SD 0.50)] LBNP. LBNP continued for 5 min after exercise stopped. Head-up tilt at 60 degrees plus graded LBNP assessed orthostatic tolerance before and after bed rest. Hemodynamic measurements accompanied these tests. Bed rest decreased orthostatic tolerance time to a greater extent in control [34% (SD 10)] than in countermeasure subjects [13% (SD 20); P < 0.004]. Controls exhibited cardiac stroke volume reduction and relative cardioacceleration typically seen after bed rest, yet no such changes occurred in the countermeasure group. These findings demonstrate that 40 min/day of supine LBNP treadmill exercise followed immediately by 5 min of resting LBNP attenuates, but does not fully prevent, the orthostatic intolerance associated with 30 days of bed rest. We speculate that longer postexercise LBNP may improve results. Together with our earlier related studies, these ground-based results support spaceflight evaluation of postexercise orthostatic stress as a time-efficient countermeasure against postflight orthostatic intolerance.     

The relationship between plasma potassium concentration and muscle torque during recovery following intense exercise

The present study investigated the relationship between plasma potassium ion concentration ([K⁺]) and skeletal muscle torque during three different 15-min recovery periods after fatigue induced by four 30-s sprints. Four males and one female completed the multiple sprint exercise on three separate days; recovery was passive, i.e. no cycling exercise (PRec), active cycling at 30% peak oxygen consumption O_2peak (30% Rec) and active cycling at 60% O_2peak (60% Rec). Plasma [K⁺] was measured from blood sampled from an antecubital vein of subjects at rest and at 0, 3, 5, 10 and 15 min into each recovery. Isokinetic leg strength was measured at rest and at 1, 6, 11 and 16 min during each recovery. Following the exhaustive sprints, [K⁺] increased significantly from an average mean (SEM) resting value of 3.81 (0.07) mmol · l⁻¹ to 4.48 (0.19) mmol · l⁻¹ (P < 0.01). In all recovery conditions, plasma [K⁺] returned to resting levels within 3 min following the fourth sprint. However, in the two active recovery conditions plasma [K⁺] increased over the remainder of the recovery periods to 4.36 (0.12) mmol · l⁻¹ in the 30% Rec condition and 4.62 (0.12) mmol · l⁻¹ in the 60% Rec condition, the latter being significantly higher than the former (P < 0.01). The maximum torque measured following the sprints decreased significantly, on average, to 61.1 (8.36)% of peak levels (P < 0.01). After 15 min of recovery, maximum torque was highest in the 30% Rec condition at 92.13 (3.06)% of peak levels (P < 0.01), compared to 85.23 (3.64)% and 85.71 (0.82)% for the PRec and 60% Rec conditions, respectively. In contrast to the significant differences in plasma [K⁺] across all three recovery conditions, muscle torque recovery was significantly different in only the 30% Rec condition. In summary, recovery of peak levels of muscle torque following fatiguing exercise does not appear to follow changes in plasma [K⁺]. Accepted: 18 October 1996     

Haemodynamic response to exercise in healthy young and elderly subjects

Whereas with advancing age, peak heart rate (HR) and cardiac index (CI) are clearly reduced, peak stroke index (SI) may decrease, remain constant or even increase. The aim of this study was to describe the patterns of HR, SI, CI, arteriovenous difference in oxygen concentration (C _a-vO₂), mean arterial pressure (MAP), systemic vascular resistance index (SVRI), stroke work index (SWI) and mean systolic ejection rate index (MSERI) in two age groups (A: 20–30 years, n = 20; B: 50–60 years n = 20. After determination of pulmonary function, an incremental bicycle exercise test was performed, with standard gas-exchange measurements and SI assessment using electrical impedance cardiography. The following age-related changes were found: similar submaximal HR response to exercise in both groups and a higher peak HR in A than in B[185 (SD 9) vs 167 (SD 14) beats · min⁻¹, P < 0.0005]; increase in SI with exercise up to 60–90 W and subsequent stabilization in both groups. As SI decreased towards the end of exercise in B, a higher peak SI was found in A [57.5 (SD 14.0) vs 43.6 (SD 7.7) ml · m⁻², P < 0.0005]; similar submaximal CI response to exercise, higher peak CI in A [10.6 (SD 2.5) vs 7.2 (SD 1.3) l · min⁻¹ · m⁻², P < 0.0005]; no differences in C _a-vO₂ during exercise; higher MAP at all levels of exercise in B; higher SVRI at all levels of exercise in B; lower SWI in B after recovery; higher MSERI at all levels of exercise in A. The decrease in SI with advancing age would seem to be related to a decrease in myocardial contractility, which can no longer be compensated for by an increase in preload (as during submaximal exercise). Increases in systemic blood pressure may also compromise ventricular function but would seem to be of minor importance. Accepted: 24 September 1996     

Insulin and glucagon immunoreactivity during high-intensity exercise under opiate blockade

Eight fit men [maximum oxygen consumption (O_2max) 64.6 (1.9) ml · kg⁻¹ · min⁻¹, aged 28.3 (1.7) years (SE in parentheses) were studied during two treadmill exercise trials to determine the effect of endogenous opioids on insulin and glucagon immunoreactivity during intense exercise (80% O_2max). A double-blind experimental design was used with subjects undertaking the two exercise trials in counterbalanced order. Exercise trials were 20 min in duration and were conducted 7 days apart. One exercise trial was undertaken following administration of naloxone (N; 1.2 mg; 3 ml) and the other after receiving a placebo (P; 0.9% NaCl saline; 3 ml). Prior to each experimental trial a flexible catheter was placed into an antecubital vein and baseline blood samples were collected. Immediately after, each subject received either a N or P bolus injection. Blood samples were also collected after 20 min of continuous exercise (running). Glucagon was higher (P < 0.05), while insulin was lower (P < 0.05), during exercise compared with pre-exercise values in both trials. However, glucagon was higher (P < 0.05) in the P than in the N exercise trial [141.4 (8.3) ng · l⁻¹ vs 127.2 (7.6) ng · l⁻¹]. There were no differences in insulin during exercise between the P and N trials [50.2 (4.3) pmol · l⁻¹ vs 43.8 (5) pmol · l⁻¹]. These data suggest that endogenous opioids may augment the glucagon response during intense exercise. Accepted: 15 June 1996