Passive and active wrist joint stiffness following eccentric exercise

The purpose of this study was to investigate the effects of exercise-induced muscle injury on passive and active wrist joint stiffness. Ten male subjects were repeatedly tested over a period of 11 days, once prior to, and four times following a bout of eccentric exercise with the wrist extensor muscles. Static wrist stiffness was measured by applying a 3° ramp and hold displacement of the manipulandum, which stretched the wrist extensor muscles. Wrist extension maximum voluntary contraction (MVC) declined by 24.5% from pre-exercise to 24 h after the exercise bout (P < 0.001). There was a reduced passive range of motion (ROM) from 82.8° pre-exercise to 70.2° on day 1 (P < 0.01), but no change in the passive joint stiffness at the neutral joint position, suggesting mechanical changes in the non-contractile tissues, or swelling that only resisted movement at the extremes of the ROM. Active joint stiffness at 50% pre-exercise MVC declined from 0.299 Nm deg⁻¹ pre-exercise to 0.254 Nm deg⁻¹ on day 1 (P < 0.025). Active joint stiffness at 10% pre-exercise MVC did not change on any of the days of testing compared to pre-exercise. These findings may indicate that large muscle fibers were more affected by the injury than small muscle fibers. Accepted: 7 February 2000     

Carbohydrate supplementation during prolonged cycling exercise spares muscle glycogen but does not affect intramyocellular lipid use

Using contemporary stable-isotope methodology and fluorescence microscopy, we assessed the impact of carbohydrate supplementation on whole-body and fiber-type-specific intramyocellular triacylglycerol (IMTG) and glycogen use during prolonged endurance exercise. Ten endurance-trained male subjects were studied twice during 3 h of cycling at 63 ± 4% of maximal O₂ uptake with either glucose ingestion (CHO trial; 0.7 g CHO kg⁻¹ h⁻¹) or without (CON placebo trial; water only). Continuous infusions with [U-¹³C] palmitate and [6,6-²H₂] glucose were applied to quantify plasma free fatty acids (FFA) and glucose oxidation rates and to estimate intramyocellular lipid and glycogen use. Before and after exercise, muscle biopsy samples were taken to quantify fiber-type-specific IMTG and glycogen content. Plasma glucose rate of appearance (R _a) and carbohydrate oxidation rates were substantially greater in the CHO vs CON trial. Carbohydrate supplementation resulted in a lower muscle glycogen use during the first hour of exercise in the CHO vs CON trial, resulting in a 38 ± 19 and 57 ± 22% decreased utilization in type I and II muscle-fiber glycogen content, respectively. In the CHO trial, both plasma FFA R _a and subsequent plasma FFA concentrations were lower, resulting in a 34 ± 12% reduction in plasma FFA oxidation rates during exercise (P < 0.05). Carbohydrate intake did not augment IMTG utilization, as fluorescence microscopy revealed a 76 ± 21 and 78 ± 22% reduction in type I muscle-fiber lipid content in the CHO and CON trial, respectively. We conclude that carbohydrate supplementation during prolonged cycling exercise does not modulate IMTG use but spares muscle glycogen use during the initial stages of exercise in endurance-trained men.     

The effect of severe eccentric exercise-induced muscle damage on plasma elastase, glutamine and zinc concentrations

The aim of this study was to determine if severe exercise-induced muscle damage alters the plasma concentrations of glutamine and zinc. Changes in plasma concentrations of glutamine, zinc and polymorphonuclear elastase (an index of phagocytic cell activation) were examined for up to 10 days following eccentric exercise of the knee extensors of one leg in eight untrained subjects. The exercise bout consisted of 20 repetitions of electrically stimulated eccentric muscle actions on an isokinetic dynamometer. Subjects experienced severe muscle soreness and large increases in plasma creatine kinase activity indicative of muscle fibre damage. Peak soreness occurred at 2 days post-exercise and peak creatine kinase activity [21714 (6416) U · l⁻¹, mean (SEM)] occurred at 3 days post-exercise (P < 0.01 compared with pre-exercise). Plasma elastase concentration was increased at 3 days post-exercise compared with pre-exercise (P < 0.05), and is presumably indicative of ongoing phagocytic leucocyte infiltration and activation in the damaged muscles. There were no significant changes in plasma zinc and glutamine concentrations in the days following eccentric exercise. We conclude that exercise-induced muscle damage does not produce changes in plasma glutamine or zinc concentrations despite evidence of phagocytic neutrophil activation. Accepted: 3 November 1997     

<Emphasis Type="Italic">V</Emphasis>O<Subscript>2</Subscript>max during successive maximal efforts

The concept of VO₂max has been a defining paradigm in exercise physiology for >75 years. Within the last decade, this concept has been both challenged and defended. The purpose of this study was to test the concept of VO₂max by comparing VO₂ during a second exercise bout following a preliminary maximal effort exercise bout. The study had two parts. In Study #1, physically active non-athletes performed incremental cycle exercise. After 1-min recovery, a second bout was performed at a higher power output. In Study #2, competitive runners performed incremental treadmill exercise and, after 3-min recovery, a second bout at a higher speed. In Study #1 the highest VO₂ (bout 1 vs. bout 2) was not significantly different (3.95 ± 0.75 vs. 4.06 ± 0.75 l min⁻¹). Maximal heart rate was not different (179 ± 14 vs. 180 ± 13 bpm) although maximal V _E was higher in the second bout (141 ± 36 vs. 151 ± 34 l min⁻¹). In Study #2 the highest VO₂ (bout 1 vs. bout 2) was not significantly different (4.09 ± 0.97 vs. 4.03 ± 1.16 l min⁻¹), nor was maximal heart rate (184 + 6 vs. 181 ± 10 bpm) or maximal V _E (126 ± 29 vs. 126 ± 34 l min⁻¹). The results support the concept that the highest VO₂ during a maximal incremental exercise bout is unlikely to change during a subsequent exercise bout, despite higher muscular power output. As such, the results support the “classical” view of VO₂max.     

Short-term recovery from prolonged constant pace running in a warm environment: the effectiveness of a carbohydrate-electrolyte solution

Recovery from prolonged exercise involves both rehydration and replenishment of endogenous carbohydrate stores. This study examined the influence of drinking a carbohydrate-electrolyte solution on short-term recovery and subsequent exercise capacity in a warm environment. Thirteen healthy male volunteers completed two trials, at least 7 days apart. On each occasion subjects performed an initial treadmill run at 60% of maximal oxygen uptake (VO_2max), for 90 min or until volitional fatigue (T1), in a warm environment (35 °C, 40% relative humidity, RH). Volitional ingestion of water was permitted during each of the exercise trials. During a subsequent 4-h recovery period (REC) subjects consumed either a 6.9% carbohydrate-electrolyte solution (CES) or a sweetened placebo (P), in a volume equivalent to 140% of body mass loss. Following REC, subjects ran to exhaustion at the same %VO_2max in order to assess their endurance capacity (T2). Mean (SEM) run times during T1 did not differ between the CES [74.8 (4.6) min] and P [72.5 (5.2) min] trials. Body mass was reduced (P < 0.01) by 1.9 (0.2)% (CES) and 1.7 (0.2)% (P), and plasma volume (P < 0.01) by 6.0 (0.9)% (CES) and 5.4 (1.0)% (P) during the T1 trials. During REC 2006 (176) ml and 1830 (165) ml of fluid was ingested, providing 138 (12) g and 0 g of carbohydrate in the CES and P trials, respectively. Prior to T2, plasma volume and net fluid balance were similarly restored [CES +58 (26) g; P −4 (68) g] in both trials. During T2 the exercise duration was longer (P < 0.01) in the CES compared to the P trial [CES 60.9 (5.5) min; P 44.9 (3.0) min]. Thus, provided that an adequate hydration status is maintained, inclusion of carbohydrate within an oral rehydration solution will delay the onset of fatigue during a subsequent bout of prolonged submaximal running in a warm environment. Accepted: 25 February 2000     

Difference in human cardiovascular response between upright and supine recovery from upright cycle exercise

Cardiovascular responses were examined in seven healthy male subjects during 10 min of recovery in the upright or supine position following 5 min of upright cycle exercise at 80% peak oxygen uptake. An initial rapid decrease in heart rate (f _c) during the early phase of recovery followed by much slower decrease was observed for both the upright and supine positions. The average f _c at the 10th min of recovery was significantly lower (P < 0.05) in the supine position than in the upright position, while they were both significantly greater than the corresponding pre-exercise levels (each P < 0.05). Accordingly, the amplitude of the high frequency (HF) component of R-R interval variability (by spectrum analysis) in both positions was reduced with a decrease in mean R-R interval, the relationship being expressed by a regression line – mean R-R interval = 0.006 × HF amplitude + 0.570 (r = 0.905, n = 28, P < 0.001). These results would suggest that the slower reduction in f _c following the initial rapid reduction in both positions is partly attributable to a retardation in the restoration of the activity of the cardiac parasympathetic nervous system. Post-exercise upright stroke volume (SV, by impedance cardiography) decreased gradually to just below the pre-exercise level, whereas post-exercise supine SV increased markedly to a level similar to that at rest before exercise. The resultant cardiac output (Q˙ _c) and the total peripheral vascular resistance (TPR) in the upright and supine positions returned gradually to their respective pre-exercise levels in the corresponding positions. At the 10th min of recovery, both average SV and Q˙ _c were significantly greater (each P < 0.005) in the supine than in the upright position, while average TPR was significantly lower (P < 0.05) in the supine than in the upright position. In contrast, immediately after exercise, mean blood pressure dropped markedly in both the supine and upright positions, and their levels at the 10th min of recovery were similar. Therefore we concluded that arterial blood pressure is maintained relatively constant through various compensatory mechanisms associated with f _c, SV, Q˙ _c, and TPR during rest and recovery in different body positions. Accepted: 4 September 1999     

Decreased lung capillary blood volume post-exercise is compensated by increased membrane diffusing capacity

The diffusing capacity of the lung for carbon monoxide (DLCO) decreases to below the pre-exercise value in the hours following a bout of intense exercise. Two mechanisms have been proposed: (1) development of pulmonary oedema and (2) redistribution of central blood volume to peripheral muscles causing a reduction in pulmonary capillary blood volume (V_c). In the present study DLCO, V_c and the membrane diffusing capacity (D_m) were measured in nine healthy females using a rebreathing method, in contrast to the single breath technique employed in previous studies. DLCO, V_c and D_m were measured before and at 1, 2, 3, 16 and 24 h following maximal treadmill exercise. Compared with pre-exercise values, DLCO was depressed by up to 8.9 (3.0)% (P<0.05) for the first 3 h following exercise, but had returned to pre-exercise values by 16 h post-exercise. V_c fell by 21.2 (4.1)% (P<0.05) at 3 h post-exercise, but at the same time D_m increased by 14.7 (9.1)%. It was concluded that: (1) the increase in D_m made it unlikely that the fall in DLCO was due to interstitial oedema and injury to the blood gas barrier; (2) on the other hand, the reduction in DLCO following exercise was consistent with a redistribution of blood away from the lungs; and (3) the trend for D_m and V_c to reciprocate one another indicates a situation in which a fall in V_c nevertheless promotes gas transfer at the respiratory membrane. It is suggested that this effect is brought about by the reorientation of red blood cells within the pulmonary capillaries following exercise.     

Influence of acute submaximal exercise on T-lymphocyte suppressor cell function in healthy young men

A defect in T-lymphocyte suppressor cell function has been reported to occur in a number of autoimmune diseases. The influence of exercise on suppressor cell function has not been determined in individuals with autoimmune diseases, nor has it been determined in healthy individuals. The purpose of this investigation was to determine the effect of an acute bout of submaximal exercise on suppressor cell function in healthy males. Each subject (n=10) completed an exercise trial (E; 1 h of cycle ergometry at 70.6% of maximal oxygen uptake, followed by 2 h of recovery) and a resting trial (R; 3 h of seated rest), separated by at least 1 week. Treatment (E or R) order was counterbalanced. Venous blood samples were obtained pre-exercise (PRE), immediately after exercise (POST), and 2 h post-exercise (2HPOST), and at the same time points in the R trial. Lymphocyte phenotype percentages were determined by flow cytometry, while concanavalin- A-induced suppressor cell function was determined on peripheral blood mononuclear cells. No change was observed in the percentage of T-cytotoxic/suppressor cells. Suppressor cell function was significantly different between treatments, with the POST E value [mean (SD) 56.8 (1.6)%] being higher than the POST R value [41.7 (1.9)%]. No significant difference was observed 2HPOST. In conclusion, acute submaximal exercise resulted in a transient increase in suppressor cell function in healthy males. Accepted: 17 January 2000     

The effects of dietary manipulation on blood acid-base status and the performance of high intensity exercise

Summary The effect of a pattern of exercise and dietary modification, which is normally used to alter muscle glycogen content, upon the acid-base status of the blood and the ability to perform high intensity exercise was studied. Eleven healthy male subjects cycled to exhaustion on an electrically braked cycle ergometer at a workload equivalent to 100% of their maximal oxygen uptake ( ) on three separate occasions. The first exercise test took place after a normal diet (46.2±6.7% carbohydrate (CHO)), and was followed by prolonged exercise to exhaustion to deplete muscle glycogen stores. The second test was performed after three days of a low carbohydrate diet (10.1±6.8% CHO) and subsequently after three days of a high CHO diet (65.5±9.8% CHO) the final test took place. Acid-base status and selected metabolites were measured on arterialised venous blood at rest prior to exercise and during the post-exercise period. Exercise time to exhaustion was longer after the normal (p<0.05) and high (p<0.05) CHO dietary phases compared with the low CHO phase. Resting pre-exercise pH was higher after the high CHO diet (p<0.05) compared with the low CHO diet. Pre-exercise bicarbonate, PCO₂ and base excess measurements were higher after the high CHO treatment compared with both the normal (p<0.01,p<0.05,p<0.01 respectively) and low CHO phases (p<0.001,p<0.01,p<0.001 respectively). Daily dietary acid intake, estimated from food composition tables, was higher than normal during the low CHO diet and lower than normal during the high CHO diet. The present investigation suggests that a predetermined regimen of dietary and exercise variation can significantly affect blood acid-base status and may thereby influence high intensity exercise performance.     

Effects of glucose ingestion at the onset of moderate-intensity, prolonged exercise in women as compared to men

To test glucose tolerance during exercise, the effects of oral glucose ingestion (0.5 g · kg⁻¹) on plasma glucose and hormonal responses (insulin, catecholamines) were investigated in 11 women [mean (SEM) age 21.6 (1.3) years] and 10 men [22.0 (0.3) years] during cycle ergometer exercise (30 min at 60% maximum oxygen consumption, V˙O_2max). The two groups exhibited similar V˙O_2max values, when expressed per kg of lean body mass. Venous blood samples (5 ml) were withdrawn immediately before the exercise, during the exercise (at 3, 5, 10, 15 and 30 min) and at the 30th min of the recovery period. Glucose was ingested orally between the 2nd and the 3rd min of the exercise. As compared to men, plasma glucose concentrations were lower in women during exercise (P < 0.05 at 3, 15 and 30 min) and at the 30th min of the recovery period (P < 0.001), while plasma insulin concentrations were higher in women during exercise (P < 0.05 at 3, 15 and 30 min). The ratio of the area under the curve for glucose over the area under the curve for insulin was lower in women during exercise (P < 0.0002). A linear relationship between glucose and insulin concentrations was found only for women during exercise (r = 0.615, P < 0.0001). No gender difference was observed for the catecholamine concentration during exercise. In conclusion, this study postulates that an oral glucose load given at the onset of a prolonged and moderate exercise bout induced lesser plasma glucose and greater insulin concentrations in women as compared to men. These data argue in favour of a greater glucose tolerance in women during exercise. Accepted: 5 June 1999     

Hypotension following mild bouts of resistance exercise and submaximal dynamic exercise

Our purposes were (1) to examine resting arterial blood pressure following an acute bout of resistance exercise and submaximal dynamic exercise, (2) to examine the effects of these exercises on the plasma concentrations of atrial natriuretic peptide ([ANP]), and (3) to evaluate the potential relationship between [ANP] and post-exercise blood pressure. Thirteen males [24.3 ± (2.4) years] performed 15 min of unilateral leg press exercise (65% of their one-repetition maximum) and, 1 week later, ≈15 min of cycle ergometry (at 65% of their maximum oxygen consumption). Intra-arterial pressure was monitored during exercise and for 1 h post-exercise. Arterial blood was drawn at rest, during exercise and at intervals up to 60 min post-exercise for analysis of haematocrit and [αANP]. No differences occurred in blood pressure between trials, but significant decrements occurred following exercise in both trials. Systolic pressure was ≈20 mmHg lower than before exercise after 10 min, and mean pressure was ≈7 mmHg lower from 30 min onwards. Only slight (non-significant) elevations in [αANP] were detected immediately following exercise, with the concentrations declining to pre-exercise values by 5 min post-exercise. We conclude that post-exercise hypotension occurs following acute bouts of either resistance or submaximal dynamic exercise and, in this investigation, that this decreased blood pressure was not directly related to the release of αANP. Accepted: 29 July 1998     

The acute reversal of a diet-induced metabolic acidosis does not restore endurance capacity during high-intensity exercise in man

The present experiment was designed to investigate whether a diet-induced metabolic acidosis was a major factor in the earlier onset of fatigue during high-intensity exercise. Six healthy males cycled to exhaustion at a workload equivalent to 95% of maximum oxygen uptake on four separate occasions. Exercise tests were performed after an overnight fast and each test was preceded by one of four experimental conditions. Two experimental diets were designed, either to replicate each subject's own normal diet [N diet, mean (SD) daily energy intake (E) = 13 (0.7) MJ, 14.5 (0.8)% protein (Pro), 37.5 (2.2)% fat (Fat) and 47.5 (2.1)% carbohydrate (CHO)], or a low-carbohydrate diet [E = 12.6 (0.8) MJ, 33.6 (1.3)% Pro, 64.4 (1.5)% Fat and 2.2 (0.4)% CHO]. These diets were prepared and consumed within the department over a 3-day period. Over a 3-period prior to the exercise trial subjects ingested either NaHCO₃ or CaCO₃ (3.6 and 3.0 mmol · kg body mass), thus giving four experimental conditions: N diet and treatment, N diet and placebo, low-CHO diet and treatment and low-CHO diet and placebo. Treatments were assigned using a randomised protocol. Arterialised venous blood samples were taken for the determination of acid-base status and metabolite concentrations at rest prior to exercise and at intervals for 30 min following exhaustion. Consumption of the low-CHO diet induced a mild metabolic acidosis which was reversed by the ingestion of NaHCO₃. Blood pH, bicarbonate (HCO₃ ^– ) and base excess (BE) were higher following NaHCO₃ ingestion after the normal diet than all of the other experimental conditions (P < 0.01). Exercise time following the low-CHO diet was less than on the normal diet conditions (P < 0.05): bicarbonate ingestion had no effect on exercise time on either of the diet conditions. Post-exercise blood pH, HCO₃ ^– and BE were higher following the ingestion of NaHCO₃ irrespective of the pre-exercise diet (P < 0.05). Blood lactate concentration was higher 2 min after exercise following the N diet with NaHCO₃ when compared to the low-CHO diets with either NaHCO₃ or placebo (P < 0.05). Plasma ammonia accumulation was not significantly different between experimental conditions. These data confirm previous data showing that the ingestion of a low-CHO diet reduces the capacity to perform high-intensity exercise, but it appears that the metabolic acidosis induced by the low-CHO diet is not the cause of the reduced exercise capacity observed during high-intensity exercise under these conditions.     

The influence of dietary manipulation on plasma ammonia accumulation during incremental exercise in man

Summary The influence of a pattern of exercise and dietary manipulation, intended to alter carbohydrate (CHO) availability, on pre-exercise acid-base status and plasma ammonia and blood lactate accumulation during incremental exercise was investigated. On three separate occasions, five healthy male subjects underwent a pre-determined incremental exercise test (IET) on an electrically braked cycle ergometer. Each IET involved subjects exercising for 5 min at 30%, 50%, 70% and 95% of their maximal oxygen uptake ( ) and workloads were separated by 5 min rest. The first IET took place after 3 days of normal dietary CHO intake. The second and third tests followed 3 days of low or high CHO intake, which was preceded by prolonged exercise to exhaustion in an attempt to deplete muscle and liver glycogen stores. Acid-base status and plasma ammonia and blood lactate levels were measured on arterialised venous blood samples immediately prior to and during the final 15 s of exercise at each workload and for 40 min following the completion of each IET. Three days of low CHO intake resulted in the development of a mild metabolic acidosis in all subjects. Plasma ammonia (NH₃) accumulation on the low-CHO diet tended to be greater than normal at each exercise workload. Values returned towards resting levels during each recovery period. After the normal and high-CHO diets plasma NH₃ levels did not markedly increase above resting values until after exercise at 95% . Plasma NH₃ levels after the high-CHO diet were similar to those after the normal CHO diet. Blood lactate levels did not markedly increase with each treatment until after exercise at 70% . There was a trend for blood lactate accumulation after the low-CHO diet to be lower than that after the normal and high-CHO diets during the IET and for the majority of the recovery period. Levels after the high-CHO diet tended to be similar to those after the normal diet. The present experiment demonstrates that an alteration in pre-exercise substrate availability will influence the accumulation of plasma NH₃ during exercise. In this situation, the use of plasma NH₃ as an index of exercise intensity and the onset of fatigue should be viewed with some caution.     

Effects of exercise on vasodilatory capacity in endurance- and resistance-trained men

To determine vasodilatory responsiveness we measured forearm blood flow (FBF) following reactive hyperemia (RH), prior to and following a bout of maximal aerobic exercise in endurance- (n=14) and resistance-trained men (n=10). Both groups were similar in height, body mass, and percentage body fat. Using strain-gauge plethysmography, resting FBF was higher in the resistance-trained group [4.82 (0.84) vs 3.33 (1.17) ml min⁻¹ 100 ml⁻¹ of tissue; P<0.05]. However, the resistance-trained group had a 17%–29% lower pre-exercise FBF response to RH for the first 45 s (P<0.05). Following the maximal exercise bout there were no group differences in FBF. Post-exercise FBF was higher compared to pre-exercise values in both the endurance- (P<0.001) and resistance- (P<0.01) trained groups. Endurance-trained men appear to have a greater peak vasodilatory capacity compared to resistance-trained men, and acute maximal exercise increased the vasodilatory capacity in both groups. Acute exercise also equalized the peak vasodilatory response between the endurance- and resistance-trained groups, suggesting the potential for flow-mediated vasodilatation was similar for both groups. Electronic Publication     

Post-exercise thermal homeostasis as a function of changes in pre-exercise core temperature

We have previously reported that, following continuous exercise, a prolonged elevated plateau of esophageal temperature (T _es) was directly related to the T _es at the time of cutaneous vasodilation (Th_dil) during exercise. In order to investigate the hypothesis that the factors which result in an increase of the post-exercise Thdil and define the post-exercise T _es elevation are related to pre-exercise T _es, nine healthy, young [24.0 (1.9) years], non-training males rested at 29°C, 50% humidity for > 1 h (control). They then completed three successive cycles of 15 min treadmill running at 70% maximal oxygen consumption ( ) followed by 30 min rest. Esophageal, rectal (T _re) and skin (T _sk) temperatures and forearm cutaneous blood flow were recorded at 5-s intervals throughout. Laser-Doppler flowmetry of forearm skin blood flow was used to identify the Thdil during exercise. Pre-exercise T _es was 36.74 (0.25)°C and post-exercise Tes fell to stable and significant (P < 0.05) elevations above pre-exercise values at 37.22(0.27)°C, 37.37(0.27)°C and 37.48(0.26)°C following each successive work bout respectively. Correspondingly, Th_dil during each work bout rose in proportion to, and was not different than, the post-exercise T _es in the following recovery [37.20(0.23)°C, 37.41(0.24)°C and 37.58(0.24)°C]. Although the increases were less with each successive exercise bout, the differences between each exercise bout, in terms of post-exercise Tes and Th_dil values, were significant (P < 0.05). These results reinforce our previous observations of elevations in Th_dil and post-exercise Tes after a single exercise bout and lead to the tentative conclusions that (1) pre-exercise Test has a direct influence on Thdil and post-exercise Test and (2) the exercise-induced increase of Th_dil persists into recovery, influencing post-exercise thermal recovery.     

Minor changes in blood lipids after 6 weeks of high-volume low- intensity physical activity with strict energy balance control

Physical activity has been shown to favorably affect metabolic risk markers, including blood lipids. The impact of high-energy turnover, without influencing the traditionally used markers of exercise training effects, on blood lipids is still unclear. The aim was to study the effect of high-volume low-intensity physical activity on the blood lipid pattern, with a tight control of diet and energy balance. Eight untrained men [42.5 (12.1) years, body mass index 24.2 (2.8) kg m⁻²] were tested in two different 6-week protocols. In the sedentary protocol, the subjects were instructed to limit their everyday physical activity. In the activity protocol, a 2-h physical activity bout was performed 5 days week⁻¹ (~40% of VO_2max; equivalent of an additional 21 MJ week⁻¹ in energy expenditure). The diet for both protocols comprised ~40 energy percent (E%) fat, ~50 E% carbohydrates (CHO). The polyunsaturated fatty acids to saturated fatty acids ratio of the diet was ~0.12. There were no changes during each 6-week period or differences between the two protocols in body weight, body composition or aerobic capacity. Low-intensity physical activity did not affect lipid parameters substantially, except for a slightly lower Apo-B/Apo-A1 ratio with the activity protocol (P<0.05). Total and low-density lipoprotein cholesterol, as well as Apo-B and Apo-A1, were increased during the beginning of each 6-week period (P<0.05), but returned to basal levels by the sixth week. In conclusion, 6 weeks of high-volume low-intensity physical activity did not affect blood lipids substantially.     

Cutaneous vasomotor adjustments during arm-cranking in individuals with paraplegia

Skin blood flow (SKBF) was evaluated during arm-cranking exercise in able-bodied control subjects (AB; n=6) and in individuals with low- (LP; T10–T12 lesions; n=6) and high-level paraplegia (HP; T5–T9 lesions; n=6), using laser Doppler flowmetry (LDF). During moderate exercise SKBF decreased to [mean (SD)] 82 (15)% of the pre-exercise resting level in AB, whereas it increased to 158 (52)% in LP and to 112 (51)% in HP (the LP:AB difference, P < 0.05). During intense exercise SKBF increased to 366 (180)% of the resting level in AB, whereas it increased only moderately [147 (68)%] in both paraplegic groups (the paraplegic:AB difference, P < 0.05). The paraplegics developed a higher esophageal and leg skin temperature, which was attributed to the lack of active vasodilation and evaporative cooling over the legs. The results indicate that individuals with paraplegia suffer from impaired cutaneous vasoconstriction at the onset of arm exercise, and possess only a limited vasodilatory capability in the paralyzed regions. During intense exercise, thermoregulation depends critically on active cutaneous vasodilation and skin cooling. Accepted: 25 August 2000     

The effect of dietary carbohydrate intake on the metabolic response to prolonged walking on consecutive days

Summary Six healthy subjects walked 37 km per day for four consecutive days on two occasions one month apart; on one walk, subjects consumed a high carbohydrate (CHO) diet (85±1% CHO, Mean±SE) and on the other walk an isocaloric low CHO diet (2±0% CHO) was consumed. Subjects were fasted each day until after the completion of the walk. Blood samples were obtained at rest prior to exercise and after completion of each of three laps of 12.3 km. Exercise intensity corresponded to approximately 17% ofV _{O 2max}. The first day of each walk demonstrated that the pattern of substrate mobilisation in response to this type of exercise is highly reproducible, there being no difference in any of the parameters measured between the two walks. Circulating glucose, lactate, insulin and triglyceride levels remained essentially unchanged; alanine fell progressively and glycerol, free fatty acid (FFA) and 3-hydroxybutyrate (BHB) rose progressively. After the first day there was a general tendency for the blood glucose concentration to decline as exercise progressed; by the end of the walk on Day 2, blood glucose was lower on the low CHO diet than on the high CHO diet. On Day 4 plasma insulin was higher (p<0.05) on the high CHO diet than on the low CHO diet and declined progressively on both diets. Blood lactate and alanine concentrations were generally higher at rest on the high CHO diet, but fell so that no differences existed by the end of exercise. Glycerol, FFA and BHB levels rose progressively on the low CHO diet and were generally higher than on the high CHO diet where no increase was seen until the later stages of exercise. Plasma triglycerides were higher on the high CHO diet than on the low CHO diet. These results indicate that even in the overnight fasted state, substrate mobilisation during prolonged low intensity exercise is markedly influenced by the composition of the preceding diet. A high CHO diet results in suppression of lipid mobilisation, and hence utilisation, and this effect may be mediated in part by increased circulating insulin levels on the high CHO diet.     

Systemic oxygen extraction during incremental exercise in patients with severe chronic obstructive pulmonary disease

To determine if decreased systemic oxygen (O₂) extraction contributes to the exercise limit in severe chronic obstructive pulmonary disease (COPD), 40 consecutive incremental cycle ergometer exercise tests performed by such patients, from which a “log-log” lactate threshold (LT) was identified, were compared to those of 8 patients with left ventricular failure (LVF) and 10 normal controls. Pulmonary gas exchange and minute ventilation were measured continuously and arterial blood gas tensions, pH, and lactate concentrations were sampled each minute. Cardiac output (Q˙ _c) was measured by first-pass radionuclide ventriculography. The systemic O₂ extraction ratio (O₂ER) was calculated as arterial − mixed venous O₂ content difference (C _aO₂ − C _vO₂)/C _aO₂. Peak exercise O₂ uptake (V˙O_2peak) was markedly reduced in both COPD and LVF [41 (3) and 42 (3)% predicted, respectively], compared to controls [89 (2)% predicted, P < 0.0001 for each]. Similarly, the LT occurred at a low percentage of predicted maximal oxygen consumption in both COPD and LVF [25 (2) and 27 (3)%] compared to normals [46 (3)%, P < 0.0001 for each]. The systemic O₂ER at peak exercise was severely reduced in COPD [0.36 (0.02)] compared to the other groups [P < 0.0001 for each], for whom it was nearly identical [0.58 (0.03) vs 0.63 (0.04), LVF vs control, P > 0.05]. In the COPD group, an early LT correlated with reduced systemic O₂ER at peak exercise (r = 0.64, P < 0.0001), but not with any index of systemic O₂ delivery. These data suggest that lactic acidemia during exercise in patients with severe COPD is better related to abnormal systemic O₂ extraction than to its delivery and contributes to the exercise limit. Accepted: 10 March 1998     

Metabolic and cardiorespiratory responses to maximal intermittent knee isokinetic exercise in young healthy humans

There have been many studies on the effects of isokinetic exercise on muscle performance in training and rehabilitative programmes. On the other hand, the cardiovascular and metabolic responses elicited by this type of exercise have been poorly investigated. This study was specifically designed to describe the relationships, if any, between metabolic and cardiorespiratory responses and power output during maximal intermittent knee isokinetic exercise when a steady state is reached. A group of 18 healthy subjects (10 men and 8 women, age range 25–30 years) were requested to perform at maximal concentric isokinetic knee extensions/flexions 60° · s⁻¹ and 180° · s⁻¹ for 5 min, with a 5-s pause interposed between consecutive repetitions. The power output (W˙) was calculated; before and during the tasks heart rate (f _c) and arterial blood pressure (AP_a) were continuously monitored. Pulmonary ventilation (V˙ _E) and oxygen uptake (V˙O₂) were measured at the 4th and at the 5th min of exercise and blood lactate concentration at rest and at the 3rd min of recovery. From the 4th to the 5th min only a slight decrease in W˙ was observed, both at 60° · s⁻¹ and 180° · s⁻¹. The V˙O₂, V˙ _E, f _c and AP_a showed similar values in the last 2 min of exercise, suggesting that a steady state had been reached. The V˙O₂ increased linearly as a function of W˙, showing a significantly steeper slope at 60° · s⁻¹ than at 180° · s⁻¹. The f _c, in spite of a large interindividual variation, was linearly related to metabolic demand, and was not affected by angular velocity. Systolic and diastolic AP_a were not related either to V˙O₂ or to angular velocity. In conclusion it would appear that the metabolic response to maximal intermittent knee isokinetic exercise resembles that of dynamic exercise. Conversely, the cardiocirculatory responses would seem to reflect a relevant role of the isometric postural component, the importance of which should be carefully evaluated in each subject. Accepted: 21 September 1999