Glucoregulation and hormonal responses to maximal exercise in non-insulin-dependent diabetes

Maximal dynamic exercise results in a postexercise hyperglycemia in healthy young subjects. We investigated the influence of maximal exercise on glucoregulation in non-insulin-dependent diabetic subjects (NIDDM). Seven NIDDM and seven healthy control males bicycled 7 min at 60% of their maximal O2 consumption (VO2max), 3 min at 100% VO2max, and 2 min at 110% VO2max. In both groups, glucose production (Ra) increased more with exercise than did glucose uptake (Rd) and, accordingly, plasma glucose increased. However, in NIDDM subjects the increase in Ra was hastened and Rd inhibited compared with controls, so the increase in glucose occurred earlier and was greater [147 +/- 21 to 169 +/- 19 (30 min postexercise) vs. 90 +/- 4 to 100 +/- 5 (SE) mg/dl (10 min postexercise), P less than 0.05]. Glucose levels remained elevated for greater than 60 min postexercise in both groups. Glucose clearance increased during exercise but decreased postexercise to or below (NIDDM, P less than 0.05) basal levels, despite increased insulin levels (P less than 0.05). Plasma epinephrine and glucagon responses to exercise were higher in NIDDM than in control subjects (P less than 0.05). By use of the insulin clamp technique at 40 microU.m-2.min-1 of insulin with plasma glucose maintained at basal levels, glucose disposal in NIDDM subjects, but not in controls, was enhanced 24 h after exercise. It is concluded that, because of exaggerated counter-regulatory hormonal responses, maximal dynamic exercise results in a 60-min period of postexercise hyperglycemia and hyperinsulinemia in NIDDM. However, this event is followed by a period of increased insulin effect on Rd that is present 24 h after exercise.(ABSTRACT TRUNCATED AT 250 WORDS)     

Human muscle metabolism during sprint running

Biopsy samples were obtained from vastus lateralis of eight female subjects before and after a maximal 30-s sprint on a nonmotorized treadmill and were analyzed for glycogen, phosphagens, and glycolytic intermediates. Peak power output averaged 534.4 +/- 85.0 W and was decreased by 50 +/- 10% at the end of the sprint. Glycogen, phosphocreatine, and ATP were decreased by 25, 64, and 37%, respectively. The glycolytic intermediates above phosphofructokinase increased approximately 13-fold, whereas fructose 1,6-diphosphate and triose phosphates only increased 4- and 2-fold. Muscle pyruvate and lactate were increased 19 and 29 times. After 3 min recovery, blood pH was decreased by 0.24 units and plasma epinephrine and norepinephrine increased from 0.3 +/- 0.2 nmol/l and 2.7 +/- 0.8 nmol/l at rest to 1.3 +/- 0.8 nmol/l and 11.7 +/- 6.6 nmol/l. A significant correlation was found between the changes in plasma catecholamines and estimated ATP production from glycolysis (norepinephrine, glycolysis r = 0.78, P less than 0.05; epinephrine, glycolysis r = 0.75, P less than 0.05) and between postexercise capillary lactate and muscle lactate concentrations (r = 0.82, P less than 0.05). The study demonstrated that a significant reduction in ATP occurs during maximal dynamic exercise in humans. The marked metabolic changes caused by the treadmill sprint and its close simulation of free running makes it a valuable test for examining the factors that limit performance and the etiology of fatigue during brief maximal exercise.     

Neural adaptation to resistance training: changes in evoked V-wave and H-reflex responses.

Combined V-wave and Hoffmann (H) reflex measurements were performed during maximal muscle contraction to examine the neural adaptation mechanisms induced by resistance training. The H-reflex can be used to assess the excitability of spinal alpha-motoneurons, while also reflecting transmission efficiency (i.e., presynaptic inhibition) in Ia afferent synapses. Furthermore, the V-wave reflects the overall magnitude of efferent motor output from the alpha-motoneuron pool because of activation from descending central pathways. Fourteen male subjects participated in 14 wk of resistance training that involved heavy weight-lifting exercises for the muscles of the leg. Evoked V-wave, H-reflex, and maximal M-wave (M(max)) responses were recorded before and after training in the soleus muscle during maximal isometric ramp contractions. Maximal isometric, concentric, and eccentric muscle strength was measured by use of isokinetic dynamometry. V-wave amplitude increased approximately 50% with training (P < 0.01) from 3.19 +/- 0.43 to 4.86 +/- 0.43 mV, or from 0.308 +/- 0.048 to 0.478 +/- 0.034 when expressed relative to M(max) (+/- SE). H-reflex amplitude increased approximately 20% (P < 0.05) from 5.37 +/- 0.41 to 6.24 +/- 0.49 mV, or from 0.514 +/- 0.032 to 0.609 +/- 0.025 when normalized to M(max). In contrast, resting H-reflex amplitude remained unchanged with training (0.503 +/- 0.059 vs. 0.499 +/- 0.063). Likewise, no change occurred in M(max) (10.78 +/- 0.86 vs. 10.21 +/- 0.66 mV). Maximal muscle strength increased 23-30% (P < 0.05). In conclusion, increases in evoked V-wave and H-reflex responses were observed during maximal muscle contraction after resistance training. Collectively, the present data suggest that the increase in motoneuronal output induced by resistance training may comprise both supraspinal and spinal adaptation mechanisms (i.e., increased central motor drive, elevated motoneuron excitability, reduced presynaptic inhibition).     

Effects of treadmill exercise to exhaustion on the insulin response to hyperglycemia in untrained men

The effects of a single bout of exercise to exhaustion on pancreatic insulin secretion were determined in seven untrained men by use of a 3-h hyperglycemic clamp with plasma glucose maintained at 180 mg/100 ml. Clamps were performed either 12 h after an intermittent treadmill run at approximately 77% maximum O2 consumption or without prior exercise. Arterialized blood samples for glucose, insulin, and C-peptide determination were obtained from a heated hand vein. The peak insulin response during the early phase (0-10 min) of the postexercise clamp was higher (81 +/- 8 vs. 59 +/- 9 microU/ml; P less than 0.05) than in the nonexercise clamp. Incremental areas under the insulin (376 +/- 33 vs. 245 +/- 51 microU.ml-1.min) and C-peptide (17 +/- 2 vs. 12 +/- 1 ng.ml-1.min) curves were also greater (P less than 0.05) during the early phase of the postexercise clamp. No differences were observed in either insulin concentrations or whole body glucose disposal during the late phase (15-180 min). Area under the C-peptide curve was greater during the late phase of the postexercise clamp (650 +/- 53 vs. 536 +/- 76 ng.ml-1.min, P less than 0.05). The exercise bout induced muscle soreness and caused an elevation in plasma creatine kinase activity (142 +/- 32 vs. 305 +/- 31 IU/l; P less than 0.05) before the postexercise clamp. We conclude that in untrained men a bout of running to exhaustion increased pancreatic beta-cell insulin secretion during the early phase of the hyperglycemic clamp. Increased insulin secretion during the late phase of the clamp appeared to be compensated by increased insulin clearance.     

Evaluation of physiological responses during recovery following three resistance exercise programs

The present study was conducted to examine (a) whether there is an association between maximal oxygen uptake (Vo(2)max) and reduction in postexercise heart rate (HR) and blood lactate concentrations ([La]) following resistance exercise and (b) how intensity and Volume of resistance exercise affect postexercise Vo(2). Eleven regularly weight-trained males (20.8 +/- 1.3 years; 96.2 +/- 14.4 kg, 182.4 +/- 7.3 cm) underwent 4 sets of squat exercise on 3 separate occasions that differed in both exercise intensity and volume. During each testing session, subjects performed either 15 repetitions.set(-1) at 60% of 1 repetition maximum (1RM) (L), 10 repetitions.set(-1) at 75% of 1RM (M), or 4 repetitions.set(-1) at 90% of 1RM (H). During each exercise, Vo(2) and HR were measured before (PRE), immediately post (IP), and at 10 (10P), 20 (20P) 30 (30P), and 40 (40P) minutes postexercise. The [La] was measured at PRE, IP, 20P, and 40P. Decrease in HR (DeltaHR) was determined by subtracting HR at 10P from that at IP, whereas decrease in [La] (Delta[La]) was computed by subtracting [La] at 20P from that at IP. A significant correlation (p < 0.05) was found between Vo(2)max and DeltaHR in all exercise conditions. A significant correlation (p < 0.05) was also found between Vo(2)max and Delta[La] in L and M but not in H. The Vo(2) was higher (p < 0.05) during M than H at IP and 10P, while no difference was seen between L and M and between L and H. These results indicate that those with greater aerobic capacity tend to have a greater reduction in HR and [La] during recovery from resistance exercise. In addition, an exercise routine performed at low to moderate intensity coupled with a moderate to high exercise volume is most effective in maximizing caloric expenditure following resistance exercise.     

H1 and H2 receptors mediate postexercise hyperemia in sedentary and endurance exercise-trained men and women.

In sedentary individuals, H(1) receptors mediate the early portion of postexercise skeletal muscle hyperemia, whereas H(2) receptors mediate the later portion. It is not known whether postexercise hyperemia also presents in endurance-trained individuals. We hypothesized that the postexercise skeletal muscle hyperemia would also exist in endurance-trained individuals and that combined blockade of H(1) and H(2) receptors would abolish the long-lasting postexercise hyperemia in trained and sedentary individuals. We studied 28 sedentary and endurance trained men and women before and through 90 min after a 60-min bout of cycling at 60% peak O(2) uptake on control and combined H(1)- and H(2)-receptor antagonist days (fexofenadine and ranitidine). We measured arterial pressure (brachial auscultation) and femoral blood flow (Doppler ultrasound). On the control day, femoral vascular conductance (calculated as flow/pressure) was elevated in all groups 60 min after exercise (sedentary men: Delta86 +/- 35%, trained men, Delta65 +/- 18%; sedentary women, Delta61 +/- 19%, trained women: Delta59 +/- 23%, where Delta is change; all P < 0.05 vs. preexercise). In contrast, on the histamine antagonist day, femoral vascular conductance was not elevated in any of the groups after exercise (sedentary men: Delta21 +/- 17%, trained men: Delta9 +/- 5%, sedentary women: Delta19 +/- 4%, trained women: Delta11 +/- 11%; all P > 0.16 vs. preexercise; all P < 0.05 vs. control day). These data suggest postexercise skeletal muscle hyperemia exists in endurance trained men and women. Furthermore, histaminergic mechanisms produce the long-lasting hyperemia in sedentary and endurance-trained individuals.     

Performance and metabolic responses to a high caffeine dose during prolonged exercise.

The present study examined whether a high caffeine dose improved running and cycling performance and altered substrate metabolism in well-trained runners. Seven trained competitive runners [maximal O2 uptake (VO2max) 72.6 +/- 1.5 ml.kg-1.min-1] completed four randomized and double-blind exercise trials at approximately 85% VO2max; two trials running to exhaustion and two trials cycling to exhaustion. Subjects ingested either placebo (PL, 9 mg/kg dextrose) or caffeine (CAF, 9 mg/kg) 1 h before exercise. Endurance times were increased (P less than 0.05) after CAF ingestion during running (PL 49.2 +/- 7.2 min, CAF 71.0 +/- 11.0 min) and cycling (PL 39.2 +/- 6.5 min, CAF 59.3 +/- 9.9 min). Plasma epinephrine concentration [EPI] was increased (P less than 0.05) with CAF before running (0.22 +/- 0.02 vs. 0.44 +/- 0.08 nM) and cycling (0.31 +/- 0.06 vs. 0.45 +/- 0.06 nM). CAF ingestion also increased [EPI] (P less than 0.05) during exercise; PL and CAF values at 15 min were 1.23 +/- 0.13 and 2.51 +/- 0.33 nM for running and 1.24 +/- 0.24 and 2.53 +/- 0.32 nM for cycling. Similar results were obtained at exhaustion. Plasma norepinephrine was unaffected by CAF at rest and during exercise. CAF ingestion also had no effect on respiratory exchange ratio or plasma free fatty acid data at rest or during exercise. Plasma glycerol was elevated (P less than 0.05) by CAF before exercise and at 15 min and exhaustion during running but only at exhaustion during cycling. Urinary [CAF] increased to 8.7 +/- 1.2 and 10.0 +/- 0.8 micrograms/ml after the running and cycling trials.(ABSTRACT TRUNCATED AT 250 WORDS)     

Exercise training prevents decline in stroke volume during exercise in young healthy subjects.

Stroke volume (SV) increases above the resting level during exercise and then declines at higher intensities of exercise in sedentary subjects. The purpose of this study was to determine whether an attenuation of the decline in SV at higher exercise intensities contributes to the increase in maximal cardiac output (Qmax) that occurs in response to endurance training. We studied six men and six women, 25 +/- 1 (SE) yr old, before and after 12 wk of endurance training (3 days/wk running for 40 min, 3 days/wk interval training). Cardiac output was measured at rest and during exercise at 50 and 100% of maximal O2 uptake (Vo2max) by the C2H2-rebreathing method. VO2max was increased by 19% (from 2.7 +/- 0.2 to 3.2 +/- 0.3 l/min, P less than 0.001) in response to the training program. Qmax was increased by 12% (from 18.1 +/- 1 to 20.2 +/- 1 l/min, P less than 0.01), SV at maximal exercise was increased by 16% (from 97 +/- 6 to 113 +/- 8 ml/beat, P less than 0.001) and maximal heart rate was decreased by 3% (from 185 +/- 2 to 180 +/- 2 beats/min, P less than 0.01) after training. The calculated arteriovenous O2 content difference at maximal exercise was increased by 7% (14.4 +/- 0.4 to 15.4 +/- 0.4 ml O2/100 ml blood) after training. Before training, SV at VO2max was 9% lower than during exercise at 50% VO2max (P less than 0.05). In contrast, after training, the decline in SV between 50 and 100% VO2max was only 2% (P = NS). Furthermore, SV was significantly higher (P less than 0.01) at 50% VO2max after training than it was before. Left ventricular hypertrophy was evident, as determined by two-dimensional echocardiography at the completion of training. The results indicate that in young healthy subjects the training-induced increase in Qmax is due in part to attenuation of the decrease in SV as exercise intensity is increased.     

White blood cell response to uphill walking and downhill jogging at similar metabolic loads

The object of this study was to determine whether leukocytosis would occur in response to eccentric exercise, to concentric exercise, and/or to possible increases in serum cortisol levels. Eight men performed 2 bouts of exercise at 46% VO2max for 40 min. Subjects initially walked up a 10% grade (UW); 2 weeks later they jogged down a 10% grade (DJ), a form of eccentric exercise known to induce delayed onset muscle soreness (DOMS). Venous blood samples were drawn before and after each exercise bout (0, 0.5, 1, 1.5, 2, 2.5, 3, 3.5, 4, and 5 h). Total and differential WBCc and serum cortisol levels were assessed. Results were analyzed using repeated measures ANOVA (2 x 11). Subjects experienced severe DOMS after DJ. There was a significant difference in TWBCc (p less than 0.0001) between UW and DJ. Post-hoc testing revealed no significant increase over baseline values for UW; after DJ there was a 46% increase over baseline values (p less than 0.05) initially seen at 1.0 h. These increases in TWBCc were predominantly a reflection of increases in neutrophils which were significant (p less than 0.0001) when compared to baseline values at 1.0, 1.5 and 2.0 h (approximately 60%). No significant neutrophil increases were seen after UW. Cortisol levels were similar for both groups pre-exercise (UW = 367.1 +/- 38.6, DJ = 320.2 +/- 44.16 nmol.L-1 means +/- SE) and decreased similarly for both groups after exercise, and thus were not related to the post-exercise neutrophilia.(ABSTRACT TRUNCATED AT 250 WORDS)     

Increased epinephrine response and inaccurate glucoregulation in exercising athletes

Epinephrine responses to insulin-induced hypoglycemia have indicated that athletes have a higher adrenal medullary secretory capacity than untrained subjects. This view was tested by an exercise protocol aiming at identical stimulation of the adrenal medulla in the two groups. Eight athletes (T) and eight controls (C) ran 7 min at 60% maximal O2 consumption (VO2max), 3 min at 100% VO2max, and 2 min at 110% VO2max. Plasma epinephrine both at rest and at identical relative work loads [110% VO2max: 8.73 +/- 1.51 (T) vs. 3.60 +/- 1.09 mmol X l-1 (C)] was higher [P less than 0.05) in T than in C. Norepinephrine, as well as heart rate, increased identically in the two groups, indicating identical sympathetic nervous activity. Lactate and glycerol were higher in T than in C after running. Glucose production peaked immediately after exercise and was higher in T than in C. Glucose disappearance increased less than glucose production and was identical in T and C. Accordingly plasma glucose increased, more in T than in C (P less than 0.01). In T glucose levels approached the renal threshold greater than 20 min postexercise. Glucose clearance increased less in T than in C during exercise and decreased postexercise to or below (T, P less than 0.05) basal levels, despite increased insulin levels. Long-term endurance training increases responsiveness of the adrenal medulla to exercise, indicating increased secretory capacity. During maximal exercise this may contribute to higher glucose production, lower clearance, more inaccurate glucoregulation, and higher lypolysis in T compared with C.     

Effect of training on muscle metabolism during treadmill sprinting

Sixteen subjects volunteered for the study and were divided into a control (4 males and 4 females) and experimental group (4 males and 4 females, who undertook 8 wk of sprint training). All subjects completed a maximal 30-s sprint on a nonmotorized treadmill and a 2-min run on a motorized treadmill at a speed designed to elicit 110% of maximum oxygen uptake (110% run) before and after the period of training. Muscle biopsies were taken from vastus lateralis at rest and immediately after exercise. The metabolic responses to the 110% run were unchanged over the 8-wk period. However, sprint training resulted in a 12% (P less than 0.05) and 6% (NS) improvement in peak and mean power output, respectively, during the 30-s sprint test. This improvement in sprint performance was accompanied by an increase in the postexercise muscle lactate (86.0 +/- 26.4 vs. 103.6 +/- 24.6 mmol/kg dry wt, P less than 0.05) and plasma norepinephrine concentrations (10.4 +/- 5.4 vs. 12.1 +/- 5.3 nmol/l, P less than 0.05) and by a decrease in the postexercise blood pH (7.17 +/- 0.11 vs. 7.09 +/- 0.11, P less than 0.05). There was, however, no change in skeletal muscle buffering capacity as measured by the homogenate technique (67.6 +/- 6.5 vs. 71.2 +/- 4.5 Slykes, NS).     

Bicarbonate attenuates arterial desaturation during maximal exercise in humans.

The contribution of pH to exercise-induced arterial O2 desaturation was evaluated by intravenous infusion of sodium bicarbonate (Bic, 1 M; 200-350 ml) or an equal volume of saline (Sal; 1 M) at a constant infusion rate during a "2,000-m" maximal ergometer row in five male oarsmen. Blood-gas variables were corrected to the increase in blood temperature from 36.5 +/- 0.3 to 38.9 +/- 0.1 degrees C (P < 0.05; means +/- SE), which was established in a pilot study. During Sal exercise, pH decreased from 7.42 +/- 0.01 at rest to 7.07 +/- 0.02 but only to 7.34 +/- 0.02 (P < 0.05) during the Bic trial. Arterial PO2 was reduced from 103.1 +/- 0.7 to 88.2 +/- 1.3 Torr during exercise with Sal, and this reduction was not significantly affected by Bic. Arterial O2 saturation was 97.5 +/- 0.2% at rest and decreased to 89.0 +/- 0.7% during Sal exercise but only to 94.1 +/- 1% with Bic (P < 0.05). Arterial PCO2 was not significantly changed from resting values in the last minute of Sal exercise, but in the Bic trial it increased from 40.5 +/- 0.5 to 45.9 +/- 2.0 Torr (P < 0.05). Pulmonary ventilation was lowered during exercise with Bic (155 +/- 14 vs. 142 +/- 13 l/min; P < 0.05), but the exercise-induced increase in the difference between the end-tidal O2 pressure and arterial PO2 was similar in the two trials. Also, pulmonary O2 uptake and changes in muscle oxygenation as determined by near-infrared spectrophotometry during exercise were similar. The enlarged blood-buffering capacity after infusion of Bic attenuated acidosis and in turn arterial desaturation during maximal exercise.     

Fructose and glucose ingestion and muscle glycogen use during submaximal exercise

Substrate utilization after fructose, glucose, or water ingestion was examined in four male and four female subjects during three treadmill runs at approximately 75% of maximal O2 uptake. Each test was preceded by three days of a carbohydrate-rich diet. The runs were 30 min long and were spaced at least 1 wk apart. Exercise began 45 min after ingestion of 300 ml of randomly assigned 75 g fructose (F), 75 g glucose (G), or control (C). Muscle glycogen depletion determined by pre- and postexercise biopsies (gastrocnemius muscle) was significantly (P less than 0.05) less during the F trial than during C or G. Venous blood samples revealed a significant increase in serum glucose (P less than 0.05) and insulin (P less than 0.01) within 45 min after the G drink, followed by a decrease (P less than 0.05) in serum glucose during the first 15 min of exercise, changes not observed in the C or F trials. Respiratory exchange ratio was higher (P less than 0.05) during the G than C or F trials for the first 5 min of exercise and lower (P less than 0.05) during the C trial compared with G or F for the last 15 min of exercise. These data suggest that fructose ingested before 30 min of submaximal exercise maintains stable blood glucose and insulin concentrations, which may lead to the observed sparing of muscle glycogen.     

Combined ingestion of protein and free leucine with carbohydrate increases postexercise muscle protein synthesis in vivo in male subjects

The present study was designed to determine postexercise muscle protein synthesis and whole body protein balance following the combined ingestion of carbohydrate with or without protein and/or free leucine. Eight male subjects were randomly assigned to three trials in which they consumed drinks containing either carbohydrate (CHO), carbohydrate and protein (CHO+PRO), or carbohydrate, protein, and free leucine (CHO+PRO+Leu) following 45 min of resistance exercise. A primed, continuous infusion of L-[ring-13C6]phenylalanine was applied, with blood samples and muscle biopsies collected to assess fractional synthetic rate (FSR) in the vastus lateralis muscle as well as whole body protein turnover during 6 h of postexercise recovery. Plasma insulin response was higher in the CHO+PRO+Leu compared with the CHO and CHO+PRO trials (+240 +/- 19% and +77 +/- 11%, respectively, P < 0.05). Whole body protein breakdown rates were lower, and whole body protein synthesis rates were higher, in the CHO+PRO and CHO+PRO+Leu trials compared with the CHO trial (P < 0.05). Addition of leucine in the CHO+PRO+Leu trial resulted in a lower protein oxidation rate compared with the CHO+PRO trial. Protein balance was negative during recovery in the CHO trial but positive in the CHO+PRO and CHO+PRO+Leu trials. In the CHO+PRO+Leu trial, whole body net protein balance was significantly greater compared with values observed in the CHO+PRO and CHO trials (P < 0.05). Mixed muscle FSR, measured over a 6-h period of postexercise recovery, was significantly greater in the CHO+PRO+Leu trial compared with the CHO trial (0.095 +/- 0.006 vs. 0.061 +/- 0.008%/h, respectively, P < 0.05), with intermediate values observed in the CHO+PRO trial (0.0820 +/- 0.0104%/h). We conclude that coingestion of protein and leucine stimulates muscle protein synthesis and optimizes whole body protein balance compared with the intake of carbohydrate only.     

Relationship between fat-to-fat-free mass ratio and decrements in leg strength after downhill running.

The purpose of this study was to determine whether greater body fat mass (FM) relative to lean mass would result in more severe muscle damage and greater decrements in leg strength after downhill running. The relationship between the FM-to-fat-free mass ratio (FM/FFM) and the strength decline resulting from downhill running (-11% grade) was investigated in 24 male runners [age 23.4 +/- 0.7 (SE) yr]. The runners were divided into two groups on the basis of FM/FFM: low fat (FM/FFM = 0.100 +/- 0.008, body mass = 68.4 +/- 1.3 kg) and normal fat (FM/FFM = 0.233 +/- 0.020, body mass = 76.5 +/- 3.3 kg, P < 0.05). Leg strength was reduced less in the low-fat (-0.7 +/- 1.3%) than in the normal-fat individuals (-10.3 +/- 1.5%) 48 h after, compared with before, downhill running (P < 0.01). Multiple linear regression analysis revealed that the decline in strength could be predicted best by FM/FFM (r2 = 0.44, P < 0.05) and FM-to-thigh lean tissue cross-sectional area ratio (r2 = 0.53, P < 0.05), with no additional variables enhancing the prediction equation. There were no differences in muscle glycogen, creatine phosphate, ATP, or total creatine 48 h after, compared with before, downhill running; however, the change in muscle glycogen after downhill running was associated with a higher FM/FFM (r = -0.56, P < 0.05). These data suggest that FM/FFM is a major determinant of losses in muscle strength after downhill running.     

The effects of ibuprofen on delayed muscle soreness and muscular performance after eccentric exercise

The purpose of this study was to examine the effects of ibuprofen on delayed onset muscle soreness (DOMS), indirect markers of muscle damage and muscular performance. Nineteen subjects (their mean [+/- SD] age, height, and weight was 24.6 +/- 3.9 years, 176.2 +/- 11.1 cm, 77.3 +/- 18.7 kg) performed the eccentric leg curl exercise to induce muscle soreness in the hamstrings. Nine subjects took an ibuprofen pill of 400 mg every 8 hours within a period of 48 hours, whereas 10 subjects received a placebo randomly (double blind). White blood cells (WBCs) and creatine kinase (CK) were measured at pre-exercise, 4-6, 24, and 48 hours after exercise and maximal strength (1 repetition maximum). Vertical jump performance and knee flexion range of motion (ROM) were measured at pre-exercise, 24 and 48 hours after exercise. Muscle soreness increased (p < 0.05) in both groups after 24 and 48 hours, although the ibuprofen group yielded a significantly lower value (p < 0.05) after 24 hours. The WBC levels were significantly (p < 0.05) increased 4-6 hours postexercise in both groups with no significant difference (p > 0.05) between the 2 groups. The CK values increased (p < 0.05) in the placebo group at 24 and 48 hours postexercise, whereas no significant differences (p > 0.05) were observed in the ibuprofen group. The CK values of the ibuprofen group were lower (p < 0.05) after 48 hours compared with the placebo group. Maximal strength, vertical jump performance, and knee ROM decreased significantly (p < 0.05) after exercise and at 24 and 48 hours postexercise in both the placebo and the ibuprofen groups with no differences being observed (p > 0.05) between the 2 groups. The results of this study reveal that intake of ibuprofen can decrease muscle soreness induced after eccentric exercise but cannot assist in restoring muscle function.     

Mechanisms contributing to knee extensor strength loss after prolonged running exercise.

The aim of this study was to identify the mechanisms that contribute to the decline in knee extensor (KE) muscles strength after a prolonged running exercise. During the 2 days preceding a 30-km running race [duration 188.7 +/- 27.0 (SD) min] and immediately after the race, maximal percutaneous electrical stimulations (single twitch, 0.5-s tetanus at 20 and 80 Hz) were applied to the femoral nerve of 12 trained runners. Superimposed twitches were also delivered during isometric maximal voluntary contraction (MVC) to determine the level of voluntary activation (%VA). The vastus lateralis electromyogram was recorded. KE MVC decreased from pre- to postexercise (from 188.1 +/- 25.2 to 142.7 +/- 29.7 N x m; P < 0.001) as did %VA (from 98.8 +/- 1.8 to 91.3 +/- 10.7%; P < 0.05). The changes from pre- to postexercise in these two variables were highly correlated (R = 0.88; P < 0.001). The modifications in the mechanical response after the 80-Hz stimulation and M-wave peak-to-peak amplitude were also significant (P < 0.001 and P < 0.05, respectively). It can be concluded that 1) central fatigue, neuromuscular propagation, and muscular factors are involved in the 23.5 +/- 14.9% reduction in MVC after a prolonged running bout at racing pace and 2) runners with the greatest KE strength loss experience large activation deficit.     

V(O2) recovery kinetics in the horse following moderate, heavy, and severe exercise.

At the onset of exercise, horses exhibit O2 uptake (VO2) kinetics that are qualitatively similar to those of humans. In humans, there is a marked dissymmetry between on- and off-kinetics for VO2. This investigation sought to formally characterize the off-transient (recovery) VO2 kinetics in the horse within the moderate (M), heavy (H), and severe (S) exercise domains. Six horses were run on a high-speed treadmill at M, H, and S exercise intensities (i.e., that speed which yielded approximately 50, 85, 100% peak VO2, respectively, on the maximal incremental test). The time courses for the recovery were modeled by using a three-phase model with a single-exponential (fast component) or double-exponential (fast and slow component) phase 2. The single-exponential phase 2 model provided an excellent fit to the off-transient data, with the exception of one horse in the H domain which was best modeled by a double exponential. The time delay elicited no domain dependency (M, 18.0 +/- 1.0; H, 17.6 +/- 1.1; S, 17.8 +/- 2.0 s; P > 0.05), as was the case for the fast-component time constants (M, 16.3 +/- 2.0 s; H, 13.5 +/- 1.0 s; S, 14.6 +/- 0.3 s; P > 0.05). In the H and S (but not M) domains, the VO2 following resolution of the fast component was elevated above the preexercise baseline (H, 3.0 +/- 1.0 l/min; S, 5.7 +/- 1.1 l/min). This additional postexercise VO2 was correlated to the end-exercise increase in lactate (r = 0.94, P < 0.001) but not the end-exercise pulmonary arterial blood temperature (r = 0.45, P > 0.05). These data indicate that the time delay and subsequent kinetic response of the primary (fast-component) phase of exercise VO2 recovery in the horse is independent of the preceding exercise-intensity domain. However, in the H and S domains, the fast component resolves to an elevated baseline.     

Glucose formation in human skeletal muscle. Influence of glycogen content.

Eight men exercised at 66% of their maximal isometric force to fatigue after prior decrease in the glycogen store in one leg (low-glycogen, LG). The exercise was repeated with the contralateral leg (control) at the same relative intensity and for the same duration. Muscle (quadriceps femoris) glycogen content decreased in the LG leg from 199 +/- 17 (mean +/- S.E.M.) to 163 +/- 16 mmol of glucosyl units/kg dry wt. (P less than 0.05), and in the control leg from 311 +/- 23 to 270 +/- 18 mmol/kg (P less than 0.05). The decrease in glycogen corresponded to a similar accumulation of glycolytic intermediates. Muscle glucose increased in the LG leg during the contraction, from 1.8 +/- 0.1 to 4.3 +/- 0.6 mmol/kg dry wt. (P less than 0.01), whereas no significant increase occurred in the control leg (P greater than 0.05). It is concluded that during exercise glucose is formed from glycogen through the debranching enzyme when muscle glycogen is decreased to values below about 200 mmol/kg dry wt.     

Enhanced protein breakdown after eccentric exercise in young and older men

The effects of eccentric exercise on whole body protein metabolism were compared in five young untrained [age 24 +/- 1 yr, maximal O2 uptake (VO2max) = 49 +/- 6 ml.kg-1.min-1] and five older untrained men (age 61 +/- 1 yr, VO2max = 34 +/- 2 ml.kg-1.min-1). They performed 45 min of eccentric exercise on a cycle ergometer at a power output equivalent to 80% VO2max (182 +/- 18 W). Beginning 5 days before exercise and continuing for at least 10 days after exercise, they consumed a eucaloric diet providing 1.5 g.kg-1.day-1 of protein. Leucine metabolism in the fed state was measured before, immediately after, and 10 days after exercise, with intravenous L-[1-13C]leucine as a tracer (0.115 mumol.kg-1.min-1). Leucine flux increased 9% immediately after exercise (P less than 0.011) and remained elevated 10 days later, with no effect of age. Leucine oxidation increased 19% immediately after exercise and remained 15% above baseline 10 days after exercise (P less than 0.0001), with no effect of age. In the young men, urinary excretion of 3-methylhistidine per gram of creatinine did not increase until 10 days postexercise (P less than 0.05), but in the older men, it increased 5 days after exercise and remained high through 10 days postexercise (P less than 0.05), averaging 37% higher than in the young men. These data suggest that eccentric exercise produces a similar increase in whole body protein breakdown in older and young men, but myofibrillar proteolysis may contribute more to whole body protein breakdown in the older group.