Effects of Sex, Season and Time of Day upon Glycemic Recovery after Exercise in the Subarctic

The replenishment of blood glucose after exercise was studied in 62 healthy subjects performing a standardized exercise at 2 different times of the day in 5 different months of the year. Blood samples (fingertip) for glucose determination were drawn at the start of exercise and at 1, 5, 10 and 30 min after exercise. The total area under the glucose-time curves during the 30 min of recovery was calculated in either absolute units or as percent of the starting value. ANOVAs, with and without glucose variables from the exercise span as covariates, tested the integrated glucose-time areas for the effect of sex, time of day, and season. Exercise in the morning showed best recovery at all times of the year and females showed best recovery at each test time. In spite of significant time effects, a correlation between glucose recovery and amount of daylight could not be established. Significant differences in recovery between months, times of day and sexes were greatly influenced by glucose levels at start of the exercise, which showed a yearly rhythm.     

Glycemic Response to Exercise in the Subarctic Depends on Time of Day,Season and Sex

Between December 1992 and September 1996, a total of 62 healthy athletes (32 males and 30 females) exercised for 30 minutes, with an intensity of 60% VO 2, in one or more morning and afternoon sessions in the months December, February, April, June and September. Blood samples obtained for determinations of glucose were drawn at 0, 1, 5, 10 and 30 minutes of each exercise span. The total area under the glucose-time curves was calculated both in original units (mmol/l) and after normalization to percent of starting value for 263 exercise spans. These calculated areas, representing the glucose “response” during exercise, were tested for the effect of sex, time of day and season by ANOVA and by the least-squares fit of a 1-year cosine. During exercise a significant effect was found by ANOVA for sex (p < 0.001), time of exercise (p =0.006) and month (p =0.007). No significant interactions were found. Exercise in the morning beginning at 11:30h produced a smaller glucose response for both sexes, when compared with exercise in the afternoon beginning at 16:30h. With regard to sex, a smaller integrated glucose response to exercise occurred in females. The response was lowest for both sexes in Dec (winter) compared to other months, while the response was greatest for females in September, and for males in April and June. A circannual rhythm was found both for baseline glucose (p =0.005, acrophase= Feb 20) and glucose–time response areas in mmol/l (p <0.001, acrophase=Feb 4), and normalized values (p =0.05, acrophase=Dec 19). This finding is in accordance with previous reports that, at least in the subarctic area, the glycemic response to a standardized exercise is influenced by season and timing of exercise. This observation may be of importance for athletes involved in vigorous training and patients with Diabetes Mellitus, among others.     

Influence of oral glucose load upon blood glucose level in relation to the time of day

Blood glucose levels were estimated at different times of day in fasted rats and after 30, 60,90 and 120 min, since oral glucose load. Circadian variations in basal glucose levels and in the levels after glucose load were observed with the highest values noted between 11 a.m. and 7 p.m., and the lowest ones about midnight. These variations were most prominent when the measurements were performed 60 min after glucose load. Circadian variation in glucose tolerance was also revealed with the best tolerance at about midnight while the worst one was noted at noon and in the afternoon.     

Effect of BCAA intake during endurance exercises on fatigue substances,muscle damage substances,and energy metabolism substances

The increase rate of utilization of branched-chain amino acids (BCAA) by muscle is reduced to its plasma concentration during prolonged exercise leading to glycogen. BCAA supplementation would reduce the serum activities of intramuscular enzymes associated with muscle damage. To examine the effects of BCAA administration on fatigue substances (serotonin, ammonia and lactate), muscle damage substances (CK and LDH) and energy metabolism substances (FFA and glucose) after endurance exercise. Subjects (n = 26, college-aged males) were randomly divided into an experimental (n = 13, EXP) and a placebo (n = 13, CON) group. Subjects both EXP and CON performed a bout of cycle training (70% VO₂max intensity) to exhaustion. Subject in the EXP were administrated BCAA (78ml/kg·w) prior to the bout of cycle exercise. Fatigue substances, muscle damage substances and energy metabolism substances were measured before ingesting BCAAs and placebos, 10 min before exercise, 30 min into exercise, immediately after exercise, and 30 min after exercise. Data were analyzed by two-way repeated measure ANCOVA, correlation and statistical significance was set at p < 0.05. The following results were obtained from this study; 1. In the change of fatigue substances : Serotonin in the EXP tended to decreased at the 10 min before exercise, 30 min into exercise, post exercise, and recovery 30 min. Serotonin in the CON was significantly greater than the EXP at the10 min before exercise and recovery 30. Ammonia in the EXP was increased at the 10 min before exercise, 30 min into exercise, and post exercise, but significantly decreased at the recovery 30min (p < 0.05). Ammonia in the CON was significantly lower than the EXP at the 10 min before exercise, 30 min into exercise, and post exercise (p < 0.05). Lactate in the EXP was significantly increased at the 30 min into exercise and significantly decreased at the post exercise and recovery 30 min. Lactate in the CON was significantly lower than the EXP at the post exercise (p < 0.05). 2. In the change of muscle damage substances : CK in the EXP was decreased at the 10 min before exercise and increased at the 30 min into exercise and then decreased at the post exercise and recovery 30 min. CK in the CON was greater than the EXP. LDH in the EXP was decreased at the 10 min before exercise and increased at the 30 min into exercise and then decreased at the post exercise and recovery 30 min. LDH in the CON was higher than the EXP. 3. In the change of energy metabolism substances :Glucose in the EXP tended to decrease at the 10 min before exercise, 30 min into exercise, post exercise and recovery 30 min. Glucose in the CON was significantly greater than the EXP at the recovery 30 min (p < .05). FFA in both EXP and CON was increased at the post exercise and recovery 30 min. % increase for FFA in the EXP was greater than the CON at the post exercise and recovery 30 min. 4. The relationship of the fatigue substances, muscle damage substances and energy metabolism substances after endurance exercise indicated strongly a positive relationship between LDH and ammonia and a negative relationship between LDH and FFA in the EXP. Also, there were a strong negative relationship between glucose and FFA and a positive relationship between glucose and serotonin in the EXP. There was a strong positive relationship between CK and LDH and a strong negative relationship between FFA and glucose in the CON. These results indicate that supplementary BCAA decreased serum concentrations of the intramuscular enzymes as CK and LDH following exhaustive exercise. This observation suggests that BCAA supplementation may reduce the muscle damage associated with endurance exercise.     

Different times of day do not change heart rate variability recovery after light exercise in sedentary subjects: 24 hours Holter monitoring

Incidence of cardiovascular events follows a circadian rhythm with peak occurrence during morning. Disturbance of autonomic control caused by exercise had raised the question of the safety in morning exercise and its recovery. Furthermore, we sought to investigate whether light aerobic exercise performed at night would increase HR and decrease HRV during sleep. Therefore, the aim of this study was to test the hypothesis that morning exercise would delay HR and HRV recovery after light aerobic exercise, additionally, we tested the impact of late night light aerobic exercise on HR and HRV during sleep in sedentary subjects. Nine sedentary healthy men (age 24 ± 3 yr; height 180 ± 5 cm; weight 79 ± 8 kg; fat 12 ± 3%; mean±SD) performed 35 min of cycling exercise, at an intensity of first anaerobic threshold, at three times of day (7 a.m., 2 p.m. and 11 p.m.). R-R intervals were recorded during exercise and during short-time (60 min) and long-time recovery (24 hours) after cycling exercise. Exercise evoked increase in HR and decrease in HRV, and different times of day did not change the magnitude (p < 0.05 for time). Morning exercise did not delay exercise recovery, HR was similar to rest after 15 minutes recovery and HRV was similar to rest after 30 minutes recovery at morning, afternoon, and night. Low frequency power (LF) in normalized unites (n.u.) decreased during recovery when compared to exercise, but was still above resting values after 60 minutes of recovery. High frequency power (HF-n.u.) increased after exercise cessation (p < 0.05 for time) and was still below resting values after 60 minutes of recovery. The LF/HF ratio decreased after exercise cessation (p < 0.05 for time), but was still different to baseline levels after 60 minutes of recovery. In conclusion, morning exercise did not delay HR and HRV recovery after light aerobic cycling exercise in sedentary subjects. Additionally, exercise performed in the night did change autonomic control during the sleep. So, it seems that sedentary subjects can engage physical activity at any time of day without higher risk.     

运动后补充肉碱可提升骨骼肌糖原合成代谢

本研究旨在探讨单次口服肉碱是否有利于促进人体运动后骨骼肌糖原恢复。本研究为交叉实验设计,选取20名受试者,随机分为肉碱试验(实验组)和安慰剂试验(安慰剂组),两次实验间隔至少7 d。所有受试者接受单次60 min 70%VO_2max功率车测试,运动后立即给予高碳水化合物饮食补充和肉碱胶囊或安慰剂淀粉胶囊口服补充,同时观察运动后3 h恢复期内的生理反应。功率车运动后第0、第3小时从股外侧肌采集肌肉样本,同期间隔每30 min收集血液样本,每60 min收集10 min气体样本。研究发现,实验组肌糖原含量增加率显著增加,在血液生化值方面,两组的血糖浓度在各时间点均无显著差异,但实验组的胰岛素反应显著低于安慰剂组。同时在运动恢复期间,实验组呼吸交换率明显低于安慰剂组,这代表运动恢复期口服肉碱后,身体以脂肪为主要能量来源。研究表明,运动后立即补充肉碱能显著提升人体运动后肌糖原恢复,具备临床进一步推广应用的价值。     

Rectal temperature,distal sweat rate,and forearm blood flow following mild exercise at two phases of the circadian cycle

Changes in rectal temperature during mild exercise in the middle of the rising (11:00 h) and falling (23:00 h) phases of the circadian rhythm of resting core temperature have been compared. Seven healthy males were studied at rest, while exercising on a cycle ergometer (60 min at 80 W), and during the first 30 min of recovery. Rectal temperature, forearm blood flow, and forearm sweat rate were measured at 1 min intervals throughout. During exercise, there were significant time‐of‐day differences in the profiles of all three variables, and in the thresholds for increases in forearm blood flow and sweating. Forearm blood flow and sweat rate were recruited more rapidly and to a greater extent with evening exercise, and rectal temperature rose less. Analysis of covariance, with rectal temperature as the covariate, indicated the associations between it and forearm blood flow or sweating were significantly different (p<0.05) between the two times of day. There were also significant (p<0.05) time‐of‐day effects for forearm blood flow and sweating that were independent of rectal temperature. During recovery, rectal temperature fell more quickly in the late evening than late morning. Forearm blood flow and sweating also showed time‐of‐day differences, but these did not co‐vary with rectal temperature. Control of rectal temperature during exercise and recovery appears to be more effective in the late evening than late morning, and differences in forearm blood flow and sweating, as well as factors independent of these two variables, contribute to this difference. The results support our “heat‐gain/heat‐loss modes” hypothesis.     

多次短时间快走能提高机体脂肪和能量的消耗

为探讨多次短时间及单次长时间的快走对脂肪代谢与激素反应的影响,以提高鼓励运动的说服力,本研究选择15名健康大学男生为研究对象,进行单次长时间快走运动(SL)(1次×30 min),或多次短时间快走运动(MS)(6次×5 min,每次中间休息30 min)。数据收集后以独立样本t检验和双因素方差分析进行统计检验。研究结果发现:MS在运动后超额摄氧量(EPOC)和恢复期能量消耗显著高于SL,且MS的总摄氧量和总能量消耗(运动期+恢复期)也显著高于SL;而SL在运动结束后甘油浓度显著高于运动前,同时显著高于同期的MS。本研究认为,多次短时间的运动在恢复期的能量消耗显著大于单次长时间的运动,且在恢复期脂肪的消耗也较高,建议不易开展长时间运动的人,可采用多次短时间的运动方式,以增加能量和脂肪的消耗。     

Effect of carbohydrate ingestion on glycogen resynthesis in human liver and skeletal muscle, measured by (13)C MRS

This study investigated the effect of carbohydrate (CHO) ingestion on postexercise glycogen resynthesis, measured simultaneously in liver and muscle (n = 6) by (13)C magnetic resonance spectroscopy, and subsequent exercise capacity (n = 10). Subjects cycled at 70% maximal oxygen uptake for 83 +/- 8 min on six separate occasions. At the end of exercise, subjects ingested 1 g/kg body mass (BM) glucose, sucrose, or placebo (control). Resynthesis of glycogen over a 4-h period after treatment ingestion was measured on the first three occasions, and subsequent exercise capacity was measured on occasions four through six. No glycogen was resynthesized during the control trial. Liver glycogen resynthesis was evident after glucose (13 +/- 8 g) and sucrose (25 +/- 5 g) ingestion, both of which were different from control (P < 0.01). No significant differences in muscle glycogen resynthesis were found among trials. A relationship between the CHO load (g) and change in liver glycogen content (g) was evident after 30, 90, 150, and 210 min of recovery (r = 0.59-0. 79, P < 0.05). Furthermore, a modest relationship existed between change in liver glycogen content (g) and subsequent exercise capacity (r = 0.53, P < 0.05). However, no significant difference in mean exercise time was found (control: 35 +/- 5, glucose: 40 +/- 5, and sucrose: 46 +/- 6 min). Therefore, 1 g/kg BM glucose or sucrose is sufficient to initiate postexercise liver glycogen resynthesis, which contributes to subsequent exercise capacity, but not muscle glycogen resynthesis.     

Aerobic conditioning effects on substrate responses during graded cycling in pregnancy

This study was conducted to test the hypothesis that aerobic conditioning prevents exercise-induced hypoglycemia and preserves the capacity to utilize carbohydrates and to produce lactate during heavy exercise in late gestation. The effects of closely monitored cycle ergometer conditioning (heart rate = 143 +/- 2 beats/min, 25 min/day, 3 days/week) during the second and third trimesters were studied in 18 previously sedentary women (exercised group, EG). A nonexercising pregnant control group (CG, n = 9) was also studied. Data collection times for both groups were as follows: start of the second trimester (Entry), ends of the second (TM2) and third (TM3) trimesters (post-training), and 4-6 months postpartum (nonpregnant control). Respiratory gas exchange was studied and venous blood samples were obtained before, during, and after a graded cycle ergometer test that was terminated at a peak heart rate of 170 beats/min. Measurements included plasma glucose, insulin, free fatty acids, the respiratory exchange ratio at peak exercise, and peak postexercise lactate concentration. A significant aerobic conditioning effect in the EG was confirmed by a 17% increase in O2 pulse at peak exercise between Entry and TM3. As expected, values for free fatty acids in the CG rose with advancing gestational age. The CG showed a clear trend for a rise in plasma insulin with advancing gestational age, under all experimental conditions. Also, peak exercise respiratory exchange ratio and peak postexercise lactate concentration were significantly reduced in late gestation, and plasma glucose decreased significantly during and following the end of TM3 testing. Effects of pregnancy to reduce peak postexercise lactate and to reduce plasma glucose during and after exercise at the end of the third trimester were significantly attenuated in the EG. These effects were attributed to attenuation of pregnancy-induced insulin resistance (as reflected by insulin/glucose ratio) by physical conditioning. These findings support our original experimental hypothesis that aerobic conditioning prevents exercise-induced hypoglycemia and preserves the ability to utilize carbohydrate and produce lactate during heavy exercise in late gestation.     

Is sprint exercise a leptin signaling mimetic in human skeletal muscle?

This study was designed to determine whether sprint exercise activates signaling cascades linked to leptin actions in human skeletal muscle and how this pattern of activation may be interfered by glucose ingestion. Muscle biopsies were obtained in 15 young healthy men in response to a 30-s sprint exercise (Wingate test) randomly distributed into two groups: the fasting (n = 7, C) and the glucose group (n = 8, G), who ingested 75 g of glucose 1 h before the Wingate test. Exercise elicited different patterns of JAK2, STAT3, STAT5, ERK1/2, p38 MAPK phosphorylation, and SOCS3 protein expression during the recovery period after glucose ingestion. Thirty minutes after the control sprint, STAT3 and ERK1/2 phosphorylation levels were augmented (both, P < 0.05). SOCS3 protein expression was increased 120 min after the control sprint but PTP1B protein expression was unaffected. Thirty and 120 min after the control sprint, STAT5 phosphorylation was augmented (P < 0.05). Glucose abolished the 30 min STAT3 and ERK1/2 phosphorylation and the 120 min SOCS3 protein expression increase while retarding the STAT5 phosphorylation response to sprint. Activation of these signaling cascades occurred despite a reduction of circulating leptin concentration after the sprint. Basal JAK2 and p38 MAPK phosphorylation levels were reduced and increased (both P < 0.05), respectively, by glucose ingestion prior to exercise. During recovery, JAK2 phosphorylation was unchanged and p38 MAPK phosphorylation was transiently reduced when the exercise was preceded by glucose ingestion. In conclusion, sprint exercise performed under fasting conditions is a leptin signaling mimetic in human skeletal muscle.     

Exercise induces isoform-specific increase in 5'AMP-activated protein kinase activity in human skeletal muscle

The 5'AMP-activated protein kinase (AMPK) is stimulated by contractile activity in rat skeletal muscle. AMPK has emerged as an important signaling intermediary in the regulation of cell metabolism being linked to exercise-induced changes in muscle glucose and fatty acid metabolism. In the present study, we determined the effects of exercise on isoform-specific AMPK activity (alpha1 and alpha2) in human skeletal muscle. Needle biopsies of vastus lateralis muscle were obtained from seven healthy subjects at rest, after 20 and 60 min of cycle ergometer exercise at 70% of VO(2)max, and 30 min following the 60 min exercise bout. In comparison to the resting state, AMPK alpha2 activity significantly increased at 20 and 60 min of exercise, and remained at a higher level with 30 min of recovery. AMPK alpha1 activity tended to slightly decrease with 20 min of exercise at 70%VO(2)max; however, the change was not statistically significant. AMPK alpha1 activities were at basal levels at 60 min of exercise and 30 min of recovery. On a separate day, the same subjects exercised for 20 min at 50% of VO(2)max. Exercise at this intensity did not change alpha2 activity, and similar to exercise at 70% of VO(2)max, there was no significant change in alpha1 activity. In conclusion, exercise at a higher intensity for only 20 min leads to increases in AMPK alpha2 activity but not alpha1 activity. These results suggest that the alpha2-containing AMPK complex, rather than alpha1, may be involved in the metabolic responses to exercise in human skeletal muscle.     

Heart rate recovery after exercise: a predictor of ventricular fibrillation susceptibility after myocardial infarction

Heart rate recovery after exercise, thought to be related to cardiac parasympathetic tone, has been shown to be a prognostic tool for all-cause mortality. However, the relationship between this variable and confirmed susceptibility to ventricular fibrillation (VF) has not been established. Therefore, myocardial ischemia was induced with a 2-min occlusion of the left circumflex artery during the last minute of exercise in mongrel dogs with myocardial infarction (n = 105 dogs). VF was induced in 66 animals (susceptible), whereas the remaining 39 dogs had no arrhythmias (resistant). On a previous day, ECG was recorded and a time-series analysis of heart rate variability was measured 30, 60, and 120 s after submaximal exercise (treadmill running). The heart rate recovery was significantly greater in resistant dogs than in susceptible dogs at all three times, with the most dramatic difference at the 30-s mark (change from maximum: 48.1 +/- 3.6 beats/min, resistant dogs; 31.0 +/- 2.2 beats/min, susceptible dogs). Correspondingly, indexes of parasympathetic tone increased to a significantly greater extent in resistant dogs at 30 and 60 s after exercise. These differences were eliminated by atropine pretreatment. When considered together, these data suggest that resistant animals exhibit a more rapid recovery of vagal activity after exercise than those susceptible to VF. As such, postexercise heart rate recovery may help identify patients with a high risk for VF following myocardial infarction.     

Influence of endogenous opioids on the response of selected hormones to exercise in humans

To examine the influence of endogenous opioids on the hormonal response to isotonic exercise, eight males were studied 2 h after oral administration of placebo or 50 mg naltrexone, a long-lasting opioid antagonist. Venous blood samples were obtained before, during, and after 30 min of bicycle exercise at 70% VO2max. Naltrexone had no effect on resting cardiovascular, endocrine, or serum variables. During exercise epinephrine was higher [mean 433 +/- 100 (SE) pg/ml] at 30 min with naltrexone than during placebo (207 +/- 26 pg/ml, P less than 0.05). Plasma norepinephrine showed the same trend but the difference (2,012 +/- 340 pg/ml with naltrexone and 1,562 +/- 241 pg/ml with placebo) was not significant. Plasma glucose was higher at all times with naltrexone. However, the difference was significant only 10 min into recovery from exercise (104.7 +/- 4.7 vs. 94.5 +/- 2.8 mg/dl). Plasma growth hormone and cortisol increased during recovery and these elevations were significantly (P less than 0.05) augmented by naltrexone. Plasma vasopressin and prolactin increased with exercise as did heart rate, blood pressure, lactic acid, and several serum components; these increases were not affected by naltrexone. Psychological tension or anxiety was lower after exercise compared with before and this improved psychological state was not influenced by the naltrexone treatment. These data suggest that exercise-induced activation of the endogenous opioid system may serve to regulate the secretion of several important hormones (i.e., epinephrine) during and after exercise.     

Recovery from insulin-induced hypoglycemia after saccharose or glucose administration

This study compared the effects of saccharose and glucose on the recovery from insulin hypoglycemia. 17 normal volunteers (12 men, 5 women, 25-40 years old) received the same dose (0.1 IU i.v.) of semisynthetic rapid-acting human insulin on two different days after an overnight fast. Blood glucose and C peptide were measured in venous blood samples before as well as at regular time intervals after insulin administration. 30 min after the injection, 20 g saccharose or 20 g glucose p.o. (diluted in water) were given. The mean glucose values were at most time intervals higher after glucose than after saccharose administration. In addition, glucose ingestion resulted in an earlier and steeper blood glucose rise (mean recovery rates during the first 5 min 3.10 and 1.38 mg/dl/min for glucose and saccharose, respectively). The C peptide values decreased progressively and did not achieve baseline levels even at 120 min in spite of blood sugar normalization. It is concluded that glucose acts faster than saccharose in insulin-induced hypoglycemia. Exogenous insulin results in a prolonged depression of C peptide which lasts longer than the hypoglycemic effect.     

Acute exposure to GH during exercise stimulates the turnover of free fatty acids in GH-deficient men.

The secretion of growth hormone (GH) increases acutely during exercise, but whether this is associated with the concomitant alterations in substrate metabolism has not previously been studied. We examined the effects of acute GH administration on palmitate, glucose, and protein metabolism before, during, and after 45 min of moderate-intensity aerobic exercise in eight GH-deficient men (mean age = 40.8 +/- 2.9 yr) on two occasions, with (+GH; 0.4 IU GH) and without GH administered (-GH). A group of healthy controls (n = 8, mean age = 40.4 +/- 4.2 yr) were studied without GH. The GH replacement during exercise on the +GH study mimicked the endogenous GH profile seen in healthy controls. No significant difference in resting free fatty acid (FFA) flux was found between study days, but during exercise a greater FFA flux was found when GH was administered (211 +/- 26 vs. 168 +/- 28 micromol/min, P < 0.05) and remained elevated throughout recovery (P < 0.05). With GH administered, the exercise FFA flux was not significantly different from that observed in control subjects (188 +/- 14 micromol/min), but the recovery flux was greater on the +GH day than in the controls (169 +/- 17 vs. 119 +/- 11 micromol/min, respectively, P < 0.01). A significant time effect (P < 0.01) for glucose rate of appearance from rest to exercise and recovery occurred in the GH-deficient adults and the controls, whereas there were no differences in glucose rate of disappearance. No significant effect across time was found for protein muscle balance. In conclusion, 1) acute exposure to GH during exercise stimulates the FFA release and turnover in GH-deficient adults, 2) GH does not significantly impact glucose or protein metabolism during exercise, and 3) the exercise-induced secretion of GH plays a significant role in the regulation of fatty acid metabolism.     

Effect of exogenous insulin on plasma free carnitine levels during exercise in normal man

Preliminary data from our laboratory have shown that the decrease in plasma free carnitine levels normally found during prolonged exercise is blunted in type 1 diabetic man. This study was designed to test the hypothesis that this might be due to the sustained peripheral hyperinsulinemia seen during exercise in diabetics treated by subcutaneous insulin. Ten male subjects underwent 90 min of cycle ergometry at 60% of their maximal oxygen uptake capacity on two occasions, one with and the other without a constant 0.13 mU.kg-1.min-1 i.v. insulin infusion. Blood samples were taken at rest, during exercise, and after exercise for measurement of plasma glucose, insulin, C-peptide, free fatty acids, and carnitine. Plasma glucose dropped significantly (p less than 0.01) from basal during both infusions, but values at 30, 45, and 60 min of exercise were lower (p less than 0.05) during insulin infusion compared with the saline infusion. Exercise produced a significant (p less than 0.01) fall in plasma insulin in both infusions. However, from 30 to 90 min of exercise, the plateau insulin level was higher during the insulin infusion compared with the saline infusion (91.4 +/- 3.0 vs. 32.9 +/- 3.0 pmol/L; p less than 0.001). Plasma C-peptide decreased significantly (p less than 0.01) during exercise and recovery in both infusions, but values between infusions were not significantly different. Plasma free fatty acids increased significantly (p less than 0.01) at 90 min of exercise during the saline infusion, while during the insulin infusion this was noted during recovery only.(ABSTRACT TRUNCATED AT 250 WORDS)     

Metabolic and circulatory responses to the ingestion of glucose polymer and glucose/electrolyte solutions during exercise in man

Six men exercised on a cycle ergometer for 60 min on two occasions one week apart, at 68 +/- 3% of VO2max. On one occasion, a dilute glucose/electrolyte solution (E: osmolality 310 mosmol X kg-1, glucose content 200 mmol X l-1) was given orally at a rate of 100 ml every 10 min, beginning immediately prior to exercise. On the other occasion, a glucose polymer solution (P: osmolality 630 mosmol X kg-1, glucose content equivalent to 916 mmol X l-1) was given at the same rate. Blood samples were obtained from a superficial forearm vein immediately prior to exercise and at 15-min intervals during exercise; further samples were obtained at 15-min intervals for 60 min at rest following exercise. Heart rate and rectal temperature were measured at 5-min intervals during exercise. Blood glucose concentration was not different between the two tests during exercise, but rose to a peak of 8.7 +/- 1.2 mmol X l-1 (mean +/- SD) at 30-min post-exercise when P was drunk. Blood glucose remained unchanged during and after exercise when E was drunk. Plasma insulin levels were unchanged during exercise and were the same on both trials, but again a sharp rise in plasma insulin concentration was seen after exercise when P was drunk. The rate of carbohydrate oxidation during exercise, as calculated from VO2 and the respiratory exchange ratio, was not different between the two tests.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of humoral factors on ventilation kinetics during recovery after impulse-like exercise

To clarify the ventilatory kinetics during recovery after impulse-like exercise, subjects performed one impulse-like exercise test (one-impulse) and a five-times repeated impulse-like exercises test (five-impulse). Duration and intensity of the impulse-like exercise were 20 sec and 400 watts (80 rpm), respectively. Although blood pH during recovery (until 10 min) was significantly lower in the five-impulse test than in the one-impulse test, ventilation (.VE) in the two tests was similar except during the first 30 sec of recovery, in which it was higher in the five-impulse test. In one-impulse, blood CO2 pressure (PCO2) was significantly increased at 1 min during recovery and then returned to the pre-exercise level at 5 min during recovery. In the five-impulse test, PCO2 at 1 min during recovery was similar to the pre-exercise level, and then it decreased to a level lower than the pre-exercise level at 5 min during recovery. Accordingly, PCO2 during recovery (until 30 min) was significantly lower in the five-impulse than in one-impulse test..VE and pH during recovery showed a curvilinear relationship, and at the same pH, ventilation was higher in the one-impulse test. These results suggest that ventilatory kinetics during recovery after impulse-like exercise is attributed partly to pH, but the stimulatory effect of lower pH is diminished by the inhibitory effect of lower PCO2.     

Exercise-induced muscle glycogen depletion and repletion in diabetic rats.

The purpose of this experiment was to examine glycogen depletion in muscles of chronic diabetic rats during treadmill running of moderate intensity and glycogen repletion following the exercise bouts. Diabetes was induced with a single intravenous injection of streptozotocin (70 mg × kg^?1). Glycogen concentrations in muscles from diabetic and normal animals were determined at rest, after running either 10 or 30 min at 23 m × min^?1 (5% incline), or 2, 4, or 8 hr following 30 min of running at the same speed and incline. With the exception of soleus muscle after 30 min of running, there were no differences in muscle glycogen contents between normal and diabetic rats before exercise, immediately after exercise, or during the recovery period. All muscles showed a significant loss of glycogen during exercise, and most muscles had completely restored their glycogen by 2 hr following exercise. Blood lactate concentrations were also similar for normal and diabetic rats at rest and after exercise. It is concluded that the diabetic condition studied in this experiment did not significantly alter muscle glycogen metabolism during exercise of moderate intensity or during recovery from the activity.