Cardiovascular response to static handgrip in trained and untrained men

Summary 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·min^–1 in U (P<0.01). The endurance time for handgrip was longer in T than in U by 29% (P<0.05) for RH, 38% (P<0.001) for LH and 24% (P<0.001) for RLH. Heart rate (f _c) was significantly lower in T than in U before handgrip exercise, and showed smaller increases (P<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<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 (Q _c) and systolic blood pressure did not differ substantially between T and U, nor between the handgrip exercise tests. It was concluded that handgrip exercise caused similar increases inQ _c in both T and U but in T the increased level ofQ _c was an effect of greater SV and lowerf _c than in U. Doubling the muscle mass did not alter the cardiovascular response to handgrip exercise in either T or U.     

Skin vascular response in the hand during sinusoidal exercise in physically trained subjects

The effect of physical training on the cutaneous vascular response during transient exercise load is unclear. We determined the phase response and amplitude response of cutaneous vascular conductance (CVC) in the hand during sinusoidal exercise in endurance exercise-trained and untrained subjects. Subjects exercised on a cycle ergometer with a sinusoidal load for 32 min. The load variation ranged from 10% [23 (1) W in the trained group, 19 (1) W in the untrained group] to 60% [137 (4) W, 114 (6) W] of peak O₂ uptake, and five different time periods (1, 2, 4, 8, and 16 min) were selected. Skin blood flow in the dorsal hand and palm were monitored by laser-Doppler flowmetry. CVC was evaluated from the ratio of blood flow to mean arterial pressure. During sinusoidal exercise, the amplitude of CVC was smaller in the dorsal hand than palm for shorter periods (1, 2, and 4 min) (P<0.05). The phase lag of CVC was smaller in the dorsal hand than palm for longer periods (8 and 16 min) (P<0.05). The amplitude response did not differ significantly between the two groups. The phase lag of CVC in the dorsal hand (P<0.05) and palm (P=0.06) was larger in the trained group than untrained group. These findings suggest that glabrous and nonglabrous skin vascular responses in the hand differ during transient exercise load, and physically trained subjects show a slower vascular response in the two skin areas to exercise stimulation than do untrained subjects.     

The exercise pressor response to sustained handgrip does not augment blood flow in the contracting forearm skeletal muscle

Previous studies have advanced the concept that during sustained handgrip (SHG) reflex increases in blood pressure are able to partially offset increases in tissue pressure and thus effectively maintain increases in muscle blood flow during mild to moderate levels of sustained handgrip. However, this concept is based upon measurements of blood flow to the entire forearm. The aim of this study was to evaluate this concept by simultaneously measuring time-dependent changes in systemic arterial pressure and blood flow in an active muscle during the actual period of exercise. To accomplish this aim, we measured ¹³³Xenon washout from the extensor carpi radialis longus muscle over 3 min of SHG at 15, 30 and 45% of maximal voluntary contraction (MVC). During sustained handgrip at 15% MVC, muscle blood flow increased more than 20 fold from rest to exercise (P < 0.05), even though mean arterial pressure increased by only 12 ± 4 mmHg. This large exercise-induced hyperaemia was abolished during SHG at both 30 and 45% MVC, despite large and progressive increases in mean arterial pressure of 29 ± 3 and 54 ± 5 mmHg, respectively. We conclude that at levels of handgrip above 15% MVC blood pressure ceases to be an important determinant of blood flow in the active skeletal muscle. Importantly, the increases in forearm blood flow that have been reported previously with such levels of static handgrip do not appear to be directed to the most active muscle.     

Plasma noradrenaline response to sustained handgrip in patients with essential hypertension

Summary The responses of plasma noradrenaline, arterial blood pressure, and heart rate to sustained handgrip at 30% maximal voluntary contraction were studied in untreated patients with essential hypertension and in healthy subjects of comparable age.There were no significant differences between these two groups in the intensity and duration of handgrip. Increases in heart rate and blood pressure induced by the effort were similar in hypertensive patients and normotensive control subjects, whereas the absolute levels of blood pressure were considerably higher in the patients.In the first 1–2 min of exercise the increases in plasma noradrenaline concentration were similar in both groups. Subsequently, plasma noradrenaline concentration tended to plateau in hypertensive patients while in control subjects it continued to increase. The elevation of plasma noradrenaline in the last minute of effort was, therefore, significantly smaller in hypertensive patients than in the control group.     

Glucose kinetics during exercise in trained men

Six trained men were studied to examine the relative increases in hepatic glucose output and peripheral glucose uptake during 40 min of exercise at 75%Vo_2max. Rates of appearance (Ra) and disappearance (Rd) were measured using a primed, continuous intravenous infusion of D-[3-³H]glucose. Plasma glucose increased (P < 0.05) from 4.8 ± 0.2 mmol I^-1 at rest to 6.2 ± 0.5 mmol l^-1 after 40 min of exercise. Both Ra and Rd increased (P < 0.05) during exercise, however, during the early phase of exercise, Ra exceeded Rd (P < 0.05). Ra peaked at 42.0 ±3.2/tmol kgf¹ min^-1 after approximately 15 min of exercise. In contrast, the highest Rd of 33.9 ± 4.3 μmol kg^-1 min^-1 was measured at the end of exercise. In additional experiments, five men were studied during 40 min of exercise at 70–75%Vo_2max, 2 h after ingestion of the non-selective β-adrenergic antagonist timolol or a placebo capsule. Subjects were unable to complete the exercise bout following timolol, fatiguing after 28.0 ± 4.0 min (P < 0.05). The increase in blood glucose from 4.3 ±0.1 to 4.7 ± 0.3 mmol l^-1 (P < 0.05) following 20 min of exercise under control conditions was completely abolished by prior timolol ingestion (4.2 ± 0.2 to 4.1±0.2 mmol l^-1). These results demonstrate that during exercise at 75%Vo_2max in trained men, hepatic glucose output is not always closely matched to peripheral muscle glucose uptake and may be subject to feed-forward regulation. The abolition of the hyperglycaemia with non-selective β-adrenergic blockade implicates adrenaline in this response.     

Effect of activated sweat glands on the intensity-dependent sweating response to sustained static exercise in mildly heated humans

Changes in the number of activated sweat glands (ASGs) and sweat output per gland (SGO) with increased exercise intensity during sustained static exercise were investigated. Fourteen male subjects performed 20, 35, and 50% maximal voluntary contraction (MVC) for 60 s with the right hand (exercised arm) at an ambient temperature of 35 degrees C and 50% relative humidity. Although sublingual, local skin, and mean skin temperatures remained essentially constant throughout the exercise at each intensity, the sweating rate (SR) of nonglabrous skin on the nonexercised left forearm increased significantly with a rise in exercise intensity (p<0.05). Changes in the number of ASGs with rising exercise intensity paralleled changes in the SR, but the SGO did not change markedly with altered exercise intensity. These results suggest that in mildly heated humans, at less than 50% MVC, the increase in the SR from nonglabrous skin with rising exercise intensity during sustained static exercise is dependent on changes in the number of ASGs and not on SGO.     

Sweating responses to a sustained static exercise is dependent on thermal load in humans

The purpose of this project was to test the hypothesis that internal temperature modulates the sweating response to sustained handgrip exercise. Ten healthy male subjects immersed their legs in 43 degrees C water for 30-40 min at an ambient temperatures of 30 degrees C and a relative humidity of 50%. Sweating responses to 50% maximal voluntary contraction isometric handgrip exercise (IH) were measured following the onset of sweating (i.e. following slight increases in internal temperature), and after more pronounced increases in internal temperature. Oesophageal temperature (Tes) was significantly lower during the first bout of exercise (37.54 +/- 0.07 degrees C) relative to the second bout (37.84 +/- 0.12 degrees C; P < 0.05). However, the increase in mean sweating rate (SR) from both the chest and forearm (non-glabrous skin) was significantly greater during the first IH bout relative to the second bout (P < 0.05). Increases in mean arterial blood pressure and palm SR (glabrous skin) did not differ significantly between exercise bouts, while heart rate and rating of perceived effort were significantly greater during the second bout of IH. As Tes and mean skin temperature did not change during either bout of exercise, the changes in SR from non-glabrous skin between the bouts of IH were likely because of non-thermal factors. These data suggest that sweating responses from non-glabrous skin during IH vary depending on the magnitude of thermal input as indicated by differing internal temperatures between bouts of IH. Moreover, these data suggest that the contribution of non-thermal factors in governing sweating from non-glabrous skin may be greatest when internal temperature is moderate (37.54 degrees C), but has less of an effect after greater elevations in internal temperature (i.e. 37.84 degrees C).     

Heart rate recovery normality data recorded in response to a maximal exercise test in physically active men

Background

Despite a growing clinical interest in determining the heart rate recovery (HRR) response to exercise, the limits of a normal HRR have not yet been well established.

Purpose

This study was designed to examine HRR following a controlled maximal exercise test in healthy, physically active adult men.

Methods

The subjects recruited (n = 789) performed a maximal stress test on a treadmill. HRR indices were calculated by subtracting the first and third minute heart rates (HRs) during recovery from the maximal HR obtained during stress testing and designated these as HRR-1 and HRR-3, respectively. The relative change in HRR was determined as the decrease in HR produced at the time points 1 and 3 min after exercise as a percentage of the peak HR (%HRR-1/HR_peak and %HRR-3/HR_peak, respectively). Percentile values of HRR-1 and HRR-3 were generated for the study population.

Results

Mean HHR-1 and HHR-3 were 15.24 ± 8.36 and 64.58 ± 12.17 bpm, respectively, and %HRR-1/HR_peak and %HRR-3/HR_peak were 8.60 ± 4.70 and 36.35 ± 6.79 %, respectively. Significant correlation was detected between Peak VO₂ and HRR-3 (r = 0.36; p < 0.001) or %HRR-3/HR_peak (r = 0.23; p < 0.001).

Conclusions

Our study provides normality data for HRR following a maximal Ergometry test obtained in a large population of physically active men.     

Stroke volume response to incremental submaximal exercise in aerobically trained, active, and sedentary men.

Stroke volume response of trained cyclists (n = 10; Trained), active but untrained men (n = 10; Active), and sedentary men (n = 10; Sedentary) was determined by impedance cardiography during cycle ergometer exercise. For the Trained, at a heart rate of 90 beats. min(-1), stroke volume increased by 27% compared to baseline levels, whereas stroke volume of Active and Sedentary groups did not significantly increase. Throughout exercise indices of ventricular emptying and filling of Trained were significantly greater than that of the other two groups whereas ventricular rates of the Active were significantly greater than those of the Sedentary. Throughout exercise cardiac contractility of the Trained was significantly greater than the other two groups. Results indicate that despite similar resting heart rate, stroke volume, and body mass, Trained compared to Active men significantly enhanced stroke volume, ventricular filling, and cardiac contractility during incremental ergometry exercise. Active compared to Sedentary men, however, displayed significantly larger stroke volume and ventricular filling rates during ergometry. We conclude that impedance cardiography indices of ventricular performance of aerobically trained men were superior to those of active, untrained men possessing similar resting stroke volume and heart rate. Furthermore, the ventricular performance of the active men possessing large resting stroke volume was superior to that of sedentary men.     

Active forearm blood flow adjustments to handgrip exercise in young and older healthy men.

1. Our purpose was to test the hypothesis that ageing impairs the active muscle hyperaemia consequent to dynamic exercise in humans. 2. Eleven young (19-29 years) and eleven older (60-74 years) healthy, non-obese men with similar chronic physical activity levels and forearm size performed two protocols of dynamic handgrip exercise: (a) brief (1 min), incremental loads to exhaustion, and (b) sustained (8 min), submaximal loads. Active forearm blood flow (FBF) was measured at rest and during a brief period of relaxation at the end of each minute of exercise. Arterial blood pressure was recorded to calculate active forearm vascular conductance (FVC). Sustained forearm ischaemia plus handgrip was used to elicit a peak forearm vasodilatatory response. 3. There were no differences in pre-exercise levels of any variable between the young and older men. During exercise, ratings of perceived effort, the peak workload attained, and the ability to sustain submaximal workloads were all similar for the two groups. 4. During brief exercise, both submaximal and peak levels of FBF were similar in the two groups; however, the peak increases in FVC were greater in the older men. During sustained exercise, FBF and FVC were not different in the two groups at the lowest loads, but the increases became relatively greater in the older men with increasing workloads. 5. Peak levels of FBF and FVC in response to the peak vasodilatatory stimulus were similar in the young and older men. 6. These findings fail to support the postulate that ageing results in impaired active muscle hyperaemia and vasodilatation during small-muscle dynamic exercise.(ABSTRACT TRUNCATED AT 250 WORDS)     

Stroke volume response to cycle ergometry in trained and untrained older men

The aims of this study were threefold: (1) to investigate the stroke volume (SV) response of trained older male cyclists [Cyclists: 65 (2.1) years; n?=?10] during incremental cycle ergometry (20 W?·?min^?1); (2) to determine the SV dynamics and total peripheral resistance response of untrained, but healthy and active older male controls [Controls: 66 (1.1) years; n?=?10]; (3) to compare the maximum oxygen consumption (˙VO_2max) and SV response of trained older male runners [Runners: 65 (3.4) years; n?=?11] with that of age-matched Cyclists. Impedance cardiography was used to assess the response of cardiac output (CO), SV and total peripheral resistance to exercise involving cycle ergometry. The mean ˙VO_2max of the trained Cyclists [54 (1.6) ml?·?kg^?1?·?min^?1] was significantly higher (P??1?·?min^?1], whereas both groups possessed a significantly higher ˙VO_2max than the Controls [28 (1.3) ml?·?kg^?1?·?min^?1]. During exercise, at a heart rate of 90 beats?·?min^?1, the SV of the Cyclists increased by 41%, that of the Runners increased by 47%, and that of the Controls increased by 31%. However, the Cyclists' and Runners' SV response was significantly greater than that of the Controls. The SV for cyclists and controls peaked at 30% of ˙VO_2max. This early increase in SV was a major factor underlying the increase in CO during exercise in both the trained and the untrained subjects. In addition, all three groups showed a significant decrease in total peripheral resistance throughout exercise. The finding that older male runners possessed a large exercise SV and high ˙VO_2max suggests that run training results in enhanced cardiovascular performance during cycle ergometry.     

Ubiquinone supplementation and exercise capacity in trained young and older men

It has been suggested that ubiquinone improves exercise performance and antioxidant capacity. We studied the effects of ubiquinone supplementation (120 mg · day^–1 for 6 weeks) on aerobic capacity and lipid peroxidation during exercise in 11 young (aged 22–38 years) and 8 older (aged 60–74 years), trained men. The cross-over study was double-blind and placebo-controlled. Serum ubiquinone concentration increased after supplementation (P < 0.0001 for treatment) in both age groups. The maximal oxygen uptake ( ) was measured using a direct incremental ergometer test. In the young subjects, the after placebo and ubiquinone treatment was 58.5 (95% confidence interval: 53.0–64.0) and 59.0 ml · min^–1 · kg^–1 (52.2–66.8), respectively. The corresponding results in the older subjects were: 37.2 (31.7–42.7) and 33.7 ml · min^–1 · kg^–1 (26.2–41.7) (P < 0.0001 for age group,P > 0.05 for treatment). In a prolonged test (60-min submaximal, then incremental load until exhaustion) time to exhaustion was longer after the placebo [young men: 85.7 (82.4–89.0), older men: 82.9 min (75.8–89.9)] than after ubiquinone [young men: 82.1 (78.5–85.8), older men: 77.2 min (70.1–83.7);P = 0.0003 for treatment]. Neither ubiquinone supplementation nor exercise affected serum malondialdehyde concentration. Oral ubiquinone was ineffective as an ergogenic aid in both the young and older, trained men.     

Salivary IgA response to prolonged exercise in a hot environment in trained cyclists

The aim of this study was to determine the effects of prolonged exercise in hot conditions on saliva IgA (s-IgA) responses in trained cyclists. On two occasions, in random order and separated by 1 week, 12 male cyclists cycled for 2 h on a stationary ergometer at 62 (3)% O_{2 max} [194 (4) W; mean (SEM)], on one occasion (HOT: 30.3°C, 76% RH) and on another occasion (CONTROL: 20.4°C, 60% RH). Water was available ad-libitum. Venous blood samples and 2-min whole unstimulated saliva samples were collected at pre, post and 2 h post-exercise. The s-IgA concentration was determined using a sandwich-type ELISA. Exercising heart rate, rating of perceived exertion, rectal temperature, corrected body mass loss (P<0.01) and plasma cortisol (P<0.05) were greater during HOT. The decrease in plasma volume post-exercise was similar on both trials [HOT: –6.7 (1.1) and CONTROL: –6.6 (1.3)%; P<0.01]. Saliva flow rate decreased post-exercise by 43% returning to pre-exercise levels by 2 h post-exercise (P<0.05) with no difference between trials. Saliva IgA concentration increased post-exercise (P<0.05) with no difference between trials. Saliva IgA secretion rate decreased post-exercise by 34% returning to pre-exercise levels by 2 h post-exercise (P<0.05) with no difference between trials. These data show that a prolonged bout of exercise results in a reduction in s-IgA secretion rate. Additionally, these data demonstrate that performing prolonged exercise in the heat, with ad libitum water intake, does not influence s-IgA responses to prolonged exercise.     

Beta-endorphin and adrenocorticotropin response to supramaximal treadmill exercise in trained and untrained males

The response of plasma beta-endorphin (beta-EP) and adrenocorticotropin (ACTH) was studied in seven well-trained (T) young endurance athletes and seven untrained (UT) age- and weight-matched males during treadmill exercise. Subjects ran continuously for 7 min at 60% VO2max, 3 min at 100% VO2max and 2 min at 110% VO2max. Arterialized blood was obtained periodically from a cannulated heated (41 degrees C) hand vein. Plasma beta-EP was measured by radio-immunoassay (RIA) which incorporated an antibody that did not cross-react (less than 1.5%) with beta-lipotropin. Plasma beta-EP was similar between groups at rest (T = 4.3 +/- 0.8 fmol ml-1, mean +/- SE, UT = 3.3 +/- 0.6 fmol ml-1) and did not change at the 60% VO2max stage. Beta-endorphin significantly increased at 100% VO2max with both groups responding similarly. A further increase occurred at 110% VO2max (T = 10.8 + 2.0 and UT = 6.6 + 1.0 fmol ml-1, P less than 0.05 for between group differences). This between group difference persisted 1 min after exercise when the highest beta-EP levels were reached (T = 18.7 +/- 4.7 and UT = 12.8 +/- 3.1 fmol ml-1, P less than 0.05). Plasma ACTH responses were similar to beta-EP with the highest values (T = 61.5 +/- 7.2, UT = 45.7 +/- 6.8 fmol ml-1, P less than 0.05 for between group differences) occurring at 1 min post-exercise. A positive correlation, r = 0.85, P less than 0.05, was found between beta-EP and ACTH using the 1 min post-exercise values. The enhanced response of beta-EP and ACTH in T may indicate a training-induced adaptation which increases the response capacity to extreme levels of stress.     

Commentary on the reduced urinary noradrenaline excretion following cold stress and exercise in physically trained rats

Urinary catecholamine excretions of rats trained by swimming or running were compared with those of cold-acclimated rats and controls i.e. sedentary warm-acclimated rats. During cold stress the trained rats excreted less noradrenaline (NA) than did controls. In fact rats trained by swimming excreted less NA than did cold-acclimated rats. while rats trained by running excreted about the same amount as did cold-acclimated rats. 2 h of swimming increased the urinary catecholamine (CA) exretions of all groups but trained rats excreted less NA than did controls and cold-acclimated rats. which had excretions of similar magnitude. The NA excretions of the two trained groups never deviated statistically from each other. It is concluded that concerning NA requirement in order to maintain homeostasis, training produces “cross tolerance” to cold stress but cold-acclimation does not produce “cross tolerance” to acute exercise. Furthermore the positive effect of training on NA excretion during the stress of cold or that of acute exercise seems essentially to be an effect of increased locomotor activity as such regardless of the type of training. It is also suggested that increased levels of locomotor activity of the rat may be of importance for seasonal acclimation of the species by increasing its tolerance to cold.     

Circulating angiogenic and inflammatory cytokine responses to acute aerobic exercise in trained and sedentary young men

Purpose

Endurance exercise training can ameliorate many cardiovascular and metabolic disorders and attenuate responses to inflammatory stimuli. The purpose of this study was to determine whether the angiogenic and pro-inflammatory cytokine response to acute endurance exercise differs between endurance-trained and sedentary young men.

Methods

Ten endurance-trained and ten sedentary healthy young men performed 30 min of treadmill running at 75 % VO_2max with blood sampling before and after exercise. Plasma concentrations of tumor necrosis factor (TNF)-alpha, interleukin (IL)-8, IL-6, vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), placental growth factor (PlGF), and soluble VEGF receptor-1 (sFlt-1) were measured by multiplex ELISA.

Results

Acute exercise increased IL-6 by 165 % (P < 0.05), IL-8 by 32 % (P < 0.05), PlGF by ~16 % (P < 0.05), sFlt-1 by 36 % (P < 0.001), and tended to increase bFGF by ~25 % (P = 0.06) in main effects analyses. TNF-α and VEGF did not change significantly with exercise in either group. Contrary to our hypothesis, there were no significant differences in TNF-α, IL-6, VEGF, bFGF, PlGF, or sFlt-1 between groups before or after acute exercise; however, there was a tendency for IL-8 concentrations to be higher in endurance-trained subjects compared to sedentary subjects (P = 0.06).

Conclusions

These results indicate that 30 min of treadmill running at 75 % VO_2max produces a systemic angiogenic and inflammatory reaction, but endurance exercise training does not appear to significantly alter these responses in healthy young men.     

Changes in lipid profile variables in response to submaximal and maximal exercise in trained cyclists

This study examined the effect of prolonged submaximal exercise followed by a self-paced maximal performance test on cholesterol (T-Chol), triglycerides (TG), and high-density lipoprotein cholesterol (HDLC). Nine trained male athletes cycled at 70% of maximal oxygen consumption for 60 min, followed by a selfpaced maximal ride for 10 min. Venous blood samples were obtained at rest, at 30 and 60 min during submaximal exercise, and immediately after the performance test. Lactic acid, haematocrit (Hct), haemoglobin (Hb), T-Chol and TG were measured in the blood, while plasma was assayed for HDL-C. Plasma volume changes in response to exercise were calculated from Hct and Hb values and all lipid measurements were corrected accordingly. In order to ascertain the repeatability of lipid responses to exercise, all subjects were re-tested under identical testing conditions and experimental protocols. When data obtained during the two exercise trials were analysed by two-way ANOVA no significant differences (P > 0.05) between tests were observed. Consequently the data obtained during the two testing trials were pooled and analysed by one-way ANOVA. Blood lactic acid increased non-significantly (P > 0.05) during the prolonged submaximal test, but rose markedly (P < 0.05) following the performance ride. Lipid variables ascertained at rest were within the normal range for healthy subjects. ANOVA showed that blood T-Chol and TG were unchanged (P > 0.05), whereas HDL-C rose significantly (P < 0.05) in response to exercise. Post hoc analyses indicated that the latter change was due to a significant rise in HDL-C after the performance ride. It is concluded that apparent favourable changes in lipid profile variables occur in response to prolonged submaximal exercise followed by maximal effort, and these changes showed a good level of agreement over the two testing occasions.