Exercise intensity and erythrocyte 2,3-diphosphoglycerate concentration

The present study examines the acute effects of two different exercise intensities on erythrocyte 2,3-diphosphoglycerate (2,3-DPG) concentration. Thirty-one females (X +/- SD age = 23.7 +/- 3.37 yr; VO2max = 44.3 +/- 5.40 ml X kg-1 X min-1) completed 2 separate 15-min constant load cycling tests at exercise intensities representing 35 and 75% of VO2max. Venous blood was obtained pre-exercise (PRE), immediately post-exercise (POST), 15 min post-exercise (POST15), and 30 min post-exercise (POST30) to determine lactic acid, 2,3-DPG, and hemoglobin concentrations and hematocrit. Significant increases (P less than 0.01) in lactic acid concentration (1.1 +/- 0.14 at PRE to 6.2 +/- 0.48 m X mol-1 X l-1 at POST), 2,3-DPG concentration (1.9 +/- 0.06 at PRE to 2.1 +/- 0.06 mumol X ml-1 at POST), and 2,3-DPG corrected for plasma volume shift (PVC 2,3-DPG) (1.9 +/- 0.06 at PRE to 2.4 +/- 0.07 mumol X ml-1 at POST15) were observed only following the 75% submaximal exercise. At POST30 (75% VO2max) PVC 2,3-DPG and lactic acid remained 5.3 and 97% (P less than 0.05) above baseline, respectively. An exercise intensity effect was observed only in lactic acid response (P less than 0.05) but not in 2,3-DPG (mumol X ml-1 and mumol X g-1 hemoglobin or PVC 2,3-DPG. A significant time-intensity interaction (P less than 0.05) for PVC 2,3-DPG suggests that PVC 2,3-DPG response over time was different between the two exercise intensity levels, with the 75% intensity eliciting a greater increase in PVC 2,3-DPG.(ABSTRACT TRUNCATED AT 250 WORDS)     

Muscle metabolism during constant- and alternating-intensity exercise around critical power

Few studies have focused on the metabolic responses to alternating high- and low-intensity exercise and, specifically, compared these responses to those seen during constant-load exercise performed at the same average power output. This study compared muscle metabolic responses between two patterns of exercise during which the intensity was either constant and just below critical power (CP) or that oscillated above and below CP. Six trained males (mean +/- SD age 23.6 +/- 2.6 y) completed two 30-minute bouts of cycling (alternating and constant) at an average intensity equal to 90 % of CP. The intensity during alternating exercise varied between 158 % CP and 73 % CP. Biopsy samples from the vastus lateralis muscle were taken before (PRE), at the midpoint and end (POST) of exercise and analysed for glycogen, lactate, PCr and pH. Although these metabolic variables in muscle changed significantly during both patterns of exercise, there were no significant differences (p > 0.05) between constant and alternating exercise for glycogen (PRE: 418.8 +/- 85 vs. 444.3 +/- 70; POST: 220.5 +/- 59 vs. 259.5 +/- 126 mmol x kg (-1) dw), lactate (PRE: 8.5 +/- 7.7 vs. 8.5 +/- 8.3; POST: 49.9 +/- 19.0 vs. 42.6 +/- 26.6 mmol x kg (-1) dw), phosphocreatine (PRE: 77.9 +/- 11.6 vs. 75.7 +/- 16.9; POST: 65.8 +/- 12.1 vs. 61.2 +/- 12.7 mmol x kg (-1) dw) or pH (PRE: 6.99 +/- 0.12 vs. 6.99 +/- 0.08; POST: 6.86 +/- 0.13 vs. 6.85 +/- 0.06), respectively. There were also no significant differences in blood lactate responses to the two patterns of exercise. These data suggest that, when the average power output is similar, large variations in exercise intensity exert no significant effect on muscle metabolism.     

Excretion of 3-methylhistidine and hydroxyproline following acute weight-training exercise

Changes in urine excretion of 3-methylhistidine (3MH) and hydroxyproline (OHP) were investigated following a single session of weight training that produced delayed onset muscle soreness (DOMS). The subjects (n = 18) maintained meat-free diets for 6 days and collected 24-h urine volume on day 4 (PRE), day 5 (POST1), and day 6 (POST2) for analysis of 3MH, OHP, and creatinine (CRE). At the end of PRE, nine subjects (EX) performed intensive weight-training exercises. The remaining subjects (NE) served as a nonexercised group. All subjects were measured for fat free weight (FFW) and rated DOMS at the end of each urine collection period, i.e., PRE, POST1, and POST2. The results were significant DOMS ratings on POST1 and POST2 compared with PRE2 for EX only. Excretion of 3MH (x +/- SE in mumol/day) by group were, for EX, PRE 271 +/- 18, POST1 243 +/- 16, POST2 259 +/- 23; for NE, PRE 203 +/- 23, POST1 209 +/- 27, POST2 225 +/- 32. Excretion of OHP (x +/- SE in mg/day) were, for EX, PRE 30.0 +/- 5.4, POST1 32.8 +/- 6.4, POST2 29.6 +/- 6.1; for NE, PRE 22.5 +/- 5.2, POST1 21.6 +/- 6.0, POST2 22.7 +/- 6.0. Changes in urine 3MH and OHP were not statistically significant, whether analyzed in absolute terms or relative to CRE and FFW. It was concluded that the acute session of weight training which produced muscle soreness did not effect excretion of 3MH or OHP.     

Effect of carbohydrate feeding frequencies and dosage on muscle glycogen use during exercise

Nine men were studied during three 4-h cycling bouts to determine the effect of frequency and dosage of solid carbohydrate (CHO) feedings (86 g) on muscle glycogen utilization and exercise performance. In the frequency trial (F), the subjects ingested 10.75 g of CHO along with 200 ml of water at 30-min intervals; in the dosage trial (D), the subjects ingested 21.5 g of CHO with 400 ml of water at 60-min intervals. During the control trial (C), the subjects ingested 400 ml of an artificially sweetened placebo at 60-min intervals. Respiratory exchange ratios were significantly elevated in both trials D and F (P less than 0.05). Blood glucose was significantly elevated in trial D 20 min post-feeding but had returned to control levels by 50 min. In trial F, blood glucose was maintained at a constant level throughout the entire 4 h. In trial C, blood glucose declined steadily during the entire 4 h. Despite the differences in blood glucose levels between the three trials, there were no significant differences in the rate of muscle glycogen utilization in any of the trials (D = 82.9 +/- 6.6 [SE] mmol X kg-1 vs C = 80.9 +/- 6.9 mmol X kg-1 vs F = 74.4 +/- 12.2 mmol X kg-1). In a sprint ride (100% VO2max) to exhaustion at the end of each trial, the subjects performed significantly longer in trial F compared to C (120.97 +/- 9.6 vs 81.0 +/- 7.1 s).(ABSTRACT TRUNCATED AT 250 WORDS)     

Weight loss, dietary carbohydrate modifications, and high intensity, physical performance

Well trained subjects (N = 12) were studied before and after losing approximately 6% of body weight to determine whether physical performance could be maintained while consuming a hypocaloric, high percentage carbohydrate diet. During a 4-d period of weight loss, subjects were randomly assigned to a high carbohydrate (HC) or low carbohydrate (LC) diet. A crossover design was used; subjects were measured before (PRE) and after (POST) weight loss on both diets for a 6-min bout of high intensity arm cranking, weight, skinfold thickness, and profile of mood states (POMS). Hemoglobin, hematocrit, and glycerol concentrations were analyzed for resting blood samples, while lactate, pH, and base excess were analyzed for blood samples drawn at rest and 1, 3, and 5 min after arm cranking. A three-way ANOVA of sprint work revealed a weight loss effect, a diet by weight loss interaction, and an order by diet by weight loss interaction (P less than 0.05). Total sprint work (mean +/- SE) PRE and POST HC was 37.7 +/- 2.1 kJ and 37.4 +/- 2.2 kJ, respectively. Sprint work was higher for PRE LC vs POST LC, with mean values of 37.4 +/- 2.1 kJ and 34.4 +/- 2.2 kJ, respectively. Post-arm cranking lactate was significantly higher PRE compared to POST for both HC and LC. Post-exercise blood pH was lower (P less than 0.05) at PRE vs POST, with no diet effect. Regardless of the diet, POMS variables tension, depression, anger, fatigue, and confusion were significantly elevated from PRE to POST; vigor was significantly lower.(ABSTRACT TRUNCATED AT 250 WORDS)     

Influence of sodium bicarbonate on sprint performance: relationship to dosage

The purpose of this investigation was to determine the minimum oral dosage of bicarbonate needed to significantly elevate blood bicarbonate and the influence of induced alkalosis on performance in high-intensity, short-duration exercise. Nine endurance-trained cyclists performed four 2-min sprints on separate occasions using an isokinetic cycle ergometer (Fitron, Cybex, Inc.). One hour before each test, the cyclists consumed either a placebo (A), a solution of 0.10 g NaHCO3.kg-1 body weight (B), a solution of 0.15 g NaHCO3.kg-1 body weight (C), or a solution of 0.20 g NaHCO3.kg-1 body weight (D) in random order. Arterialized venous blood was taken before (PRE) and after (POST) ingestion, and 1, 3, 5, 10, and 15 min following the 2-min bike sprint. The results showed a significant increase in POST blood bicarbonate, and the elevation was incrementally related to the dosage. There was, however, no significant improvement in performance. Total work (mean +/- SE) for each treatment (N.m per 2 min) were: A, 47,267 (+/- 2,472); B, 47,004 (+/- 3,094); C, 46,312 (+/- 2,964); and D, 47,190 (+/- 2,621). The results of this study show that incremental doses of NaHCO3 of 0.20 g.kg-1 and below produce incremental elevations in blood bicarbonate but do not produce improvements in performance for a sprint bout lasting 2 min.     

Effects of resistance training on protein utilization in healthy children

PURPOSE: Public health initiatives promote increased physical activity in children. More specifically, resistance training has recently received attention as an important component of youth fitness programs. The study examined the effect of this mode of exercise on protein utilization in young boys and girls. METHODS: Healthy children (N = 11, 8.6 +/- 1.1 yr, 33.7 +/- 9.4 kg, 131 +/- 9.6 cm, BMI = 19.1 +/- 3.4) participated in a supervised resistance-training program 2 times.wk-1 for 6 wk. 15N glycine methodology was used to assess nitrogen flux (Q), protein synthesis (PS), protein breakdown (PB), and net turnover ([NET] = PS - PB) before (PRE) and after (POST) resistance training. Percent body fat (%BF), fat-free mass (FFM), fat mass (FM), and energy and protein intakes were also determined. PRE/POST measurements of 1RM for the chest press and leg extension were used to examine strength gains. RESULTS: Gains associated with the chest press and leg extension were 10% and 75% (P < 0.001), respectively. Significant increases (P < 0.05) were noted for weight, height, FFM, and FM. Energy and protein intake remained constant. Significant decreases (PRE vs POST) were observed for Q (1.22 +/- 0.1 vs 0.75 +/- 0.05 gN.kg-1.d-1, P < 0.001), PS (6.48 +/- 0.47 vs 3.55 +/- 0.30 g.kg-1.d-1, P < 0.001), and PB (5.24 +/- 0.41 vs 2.96 +/- 0.30 g.kg-1.d-1, P < 0.01) after 6 wk of resistance training. NET was also reduced (P = 0.07, 1.24 +/- 0.31 vs 0.59 +/- 0.20 g.kg-1.d-1). CONCLUSIONS: Resistance training resulted in a downregulation in protein metabolism, which may be energy based. Future studies are needed to clarify energy, as well as protein, needs in young children participating in this form of exercise.     

Effect of carbohydrate feedings on muscle glycogen utilization and exercise performance

Ten men were studied during 4 h of cycling to determine the effect of solid carbohydrate (CHO) feedings on muscle glycogen utilization and exercise performance. In the experimental trial (E) the subjects ingested 43 g of sucrose in solid form along with 400 ml of water at 0, 1, 2 and 3 h of exercise. During the control trial (C) they received 400 ml of an artificially sweetened drink without solid CHO. No differences in VO2, heart rate, or total energy expenditure were observed between trials; however, respiratory exchange ratios were significantly (P less than 0.05) higher during E. Blood glucose was significantly (P less than 0.05) elevated 20 min post-feeding in E; however, by 50 min no differences were observed between trials until 230 min (E = 4.5 +/- 0.2 mmol X l-1 vs C = 3.9 +/- 0.2, means +/- SE; P less than 0.05). Muscle glycogen utilization was significantly (P less than 0.05) lower during E (100.7 +/- 10.2 mmol X kg-1 w.w.) than C (126.2 +/- 5.5). During a sprint (100% VO2max) ride to exhaustion at the end of each trial, subjects performed 45% longer when fed CHO (E = 126.8 +/- 24.7 s vs C = 87.2 +/- 17.5; P less than 0.05). It was concluded that repeated solid CHO feedings maintain blood glucose levels, reduce muscle glycogen depletion during prolonged exercise, and enhance sprint performance at the end of such activity.     

Metabolic and blood catecholamine responses to exercise during alkalosis

The effects of metabolic alkalosis on muscle lactate accumulation and plasma catecholamine concentrations were studied in six highly trained subjects during short-term ergocycle exercises to exhaustion (375 W). The studies were performed after oral administration of NaHCO3 (alkalosis) and CaCO3 (placebo). There was a significant increase in resting blood pH after NaHCO3 ingestion (7.35 +/- 0.02) compared to placebo (7.27 +/- 0.02). A longer endurance time was achieved during alkalosis (75.3 +/- 8 s) than during control (61.5 +/- 2 s), but similar blood pH and HCO3- levels were found at exhaustion in both treatments. Metabolic alkalosis resulted in higher elevation in muscle lactate concentration (31.7 +/- 4.6 mmol.kg-1 wet weight) compared to control (17 +/- 4 mmol.kg-1 wet weight). Despite longer exercise duration in alkalosis, plasma norepinephrine and epinephrine concentrations at exhaustion were reduced by 30 and 34%, respectively. These results indicate that alkalosis increased muscle lactate accumulation during exhaustive exercise. These changes were associated with a reduced blood catecholamine response to exercise.     

Training status (endurance or sprint) and catecholamine response to the Wingate-test in women

The aim of this study was to verify if, as for men, training status induces different catecholamine responses to exercise. To do this, we investigated the effect of training status (sprint or endurance) on plasma catecholamine response to a supramaximal exercise in women. Nineteen subjects took part in our study: six untrained subjects (UT), seven endurance trained subjects (ET) and six sprint trained ones (ST). The trained subjects (ET and ST) were all competing at a high national level. The maximal power (W max ) and the mean power (W) were determined from the Wingate-test. Blood lactate, adrenaline (A) and noradrenaline (NA) were analysed at rest (La 0, A 0 and NA 0 ), immediately at the end of the exercise (A max and NA max ) and after 5 min recovery (La max [3 min in arterialized blood], A 5 and NA 5 ). The disappearance of A and NA was judged by the ratio (A max -A 5 )/A max and (NA max -NA 5 )/NA 5. The ratio A max /NA max was considered as an index of the adrenal medulla responsiveness to the sympathetic nervous activity. As expected, during the Wingate-test ST exhibited significantly higher performances compared to UT and ET. But in contrast to the men's data no difference was observed between the three groups both for La max (13.1 +/- 0.8 mmol x L (-1); 14.8 +/- 1.0 mmol x L (-1) and 11.2 +/- 0.5 mmol x L (-1) respectively for ET, ST and UT), NA max (22.1 +/- 1.2 nmol x L (-1); 13.1 +/- 2.4 nmol x L (-1) and 20.2 +/- 7 nmol x L (-1)respectively for ET, ST and UT) and A max (4.1 +/- 0.8 nmol x L (-1); 2.6 +/- 0.6 nmol x L (-1); 13.1 +/- 0.6 nmol x L (-1) respectively for ET, ST and UT). Consequently the ratio A max /NA max was similar in UT, ET and ST (respectively 0.2 +/- 0.03; 0.2 +/- 0.04; 0.17 +/- 0.04), These results indicated, in contrast to the men's data, that the catecholamine response to the Wingate-test did not differ between female subjects of different status of training. In conclusion this study did not find any significant effect of training status on the catecholamine response to supramaximal exercise and so argues in favour of sex differences in response to training.     

Effect of pre-exercise carbohydrate feedings on endurance cycling performance

Six men were studied to compare the effects of pre-exercise carbohydrate feedings on endurance performance and muscle glycogen utilization during prolonged exercise. Trials consisted of a cycling ride to exhaustion at 75% maximal oxygen uptake preceded by the ingestion of either 75 g of glucose in 350 ml of water (GLU), 75 g of fructose in 350 ml of water (FRU), or 350 ml of an artificially sweetened and flavored placebo (CON). No differences were observed between trials for oxygen uptake, respiratory exchange ratio, heart rate, or exercise time to exhaustion (CON = 92.7 +/- 5.2 min, FRU = 90.6 +/- 12.4, and GLU = 92.8 +/- 11.3, mean +/- SE). Blood glucose was elevated as a result of the GLU feeding, but fell rapidly with the onset of exercise, reaching a low of 4.02 +/- 0.34 mmol X l-1 at 15 min of exercise. Serum insulin also increased following the GLU feeding but had returned to pre-drink levels by 30 min of exercise. No differences in blood glucose and insulin were observed between FRU and CON. Muscle glycogen utilization during the first 30 min of exercise (CON = 46.3 +/- 8.2 mmol X kg-1 wet weight, FRU = 56.3 +/- 3.0 mmol X kg-1 wet weight, GLU = 50.0 +/- 4.9 mmol X kg-1 wet weight) and total glycogen use (CON = 93.4 +/- 11.1, FRU = 118.8 +/- 10.9, and GLU = 99.5 +/- 4.3) were similar in the three trials.(ABSTRACT TRUNCATED AT 250 WORDS)     

Metabolic characteristics of skeletal muscle during detraining from competitive swimming

After 5 months of intense training, eight male swimmers were studied during 4 wk of inactivity. Biopsy specimens from the deltoid muscle revealed that its respiratory capacity (QO2) decreased by 50% (5174 to 2559 microliter X h-1 X g-1) after 1 wk of inactivity. Subsequent weeks of detraining did not change the QO2. Although the trained swimmers' muscle phosphofructokinase and phosphorylase activities were significantly higher (P less than 0.05) than those from a group (N = 8) of untrained men, 4 wk of detraining had no effect on these enzyme activities. Mean (+/-SE) resting muscle glycogen concentrations were significantly higher (P less than 0.05) for the trained swimmers (153 +/- 3 mmol X kg-1) than for the untrained men (85 +/- 7.5 mmol X kg-1). Over the 4 wk of inactivity, the swimmers' muscle glycogen progressively decreased from 153 (+/- 3) to 93 (+/-7) mmol X kg-1. After a standard 183-m swim at 90% of the swimmer's best time for that distance, blood lactate rose from a mean of 4.2 (+/-0.8) at week 0 to 9.7 (+/-0.8) mmol X 1(-1) at week 4. These observations demonstrate dramatic changes in the metabolic characteristics of the swimmer's muscle with a 1-4-wk interruption in training.     

Effects of dietary fat on muscle substrates,metabolism, and performance in athletes

INTRODUCTION: The present investigation aimed at identifying differences in muscle structural composition, substrate selection, and performance capacity in highly trained endurance athletes as a consequence of consuming a high-fat or a low-fat diet. METHODS: Eleven duathletes ingested high-fat (53% fat; HF) or high-carbohydrate diets (17% fat; LF) for 5 wk in a randomized crossover design. RESULTS: In m. vastus lateralis, oxidative capacity estimated as volume of mitochondria per volume of muscle fiber (HF: 9.86 +/- 0.36 vs LF: 9.79 +/- 0.52%, mean +/- SE) was not different after the two diet periods. Intramyocellular lipid (IMCL) was significantly increased after HF compared with LF (1.54 +/- 0.27% vs 0.69 +/- 0.09%, P = 0.0076). Glycogen content was lower after HF than after LF, but this difference was not statistically significant (487.8 +/- 38.2 vs 534.4 +/- 32.6 mmol x kg-1 dry weight, P = 0.2454). Maximal power and [OV0312]O(2max) (63.6 +/- 0.9 vs 63.9 +/- 1.2 mL O(2) x min-1 x kg-1 on HF and LF) during an incremental exercise test to exhaustion were not different between the two diet periods. Total work output during a 20-min all-out time trial (298 +/- 6 vs 297 +/- 7 W) on a bicycle ergometer as well as half-marathon running time (80 min 12 s +/- 86 s vs 80 min 24 s +/- 82 s) were not different between HF and LF. Blood lactate concentrations and respiratory exchange ratios (RER) were significantly lower after HF than after LF at rest and during all submaximal exercise loads. CONCLUSIONS: Muscle glycogen stores were maintained after a 5-wk high-fat diet period whereas IMCL content was more than doubled. Endurance performance capacity was maintained at moderate to high-exercise intensities with a significantly larger contribution of lipids to total energy turnover.     

Left ventricular size following endurance, sprint, and strength training

Left ventricular size following endurance, sprint, and strength training. Med. Sci. Sports Exercise, Vol. 14, No. 5, pp. 344-347, 1982. Left ventricular dimensions in adolescent boys were determined before and after three types of training regimens: endurance (END), N = 8, means = 16.8 yr; sprint (SPR), N = 8, means = 16.3 yr; strength (STR), N = 12, means = 18.7 yr. With training the END group significantly increased VO2max in 1 X min-1 (3.71 +/- 0.27 to 4.16 +/- 0.57, P less than 0.05) and in ml X min-1 X kg-1 (58.4 +/- 5.6 to 64.2 +/- 5.5, P less than 0.05). The SPR group increased VO2max in 1 X min-1 (3.63 +/- 0.63 to 3.98 +/- 0.78, P less than 0.05) but not in ml X min-1 X kg-1 (59.5 +/- 4.1 to 63.2 +/- 5.4) because body weight increased from 61.2 +/- 10.5 to 63.1 +/- 10.7 kg (P less than 0.05) with no change in percent body fat. The STR training group significantly improved upper body strength. Despite these specific training adaptations no significant modifications were found for interventricular and left ventricular posterior wall thickness or for left ventricular internal diameter in either training group. However, calculated left ventricular mass was slightly but significantly higher by 10% and 4% in the END and STR training groups, respectively. These small increases in calculated left ventricular mass with short-term training are probably caused by small but insignificant increases in left ventricular internal diameter secondary to a training bradycardia (END group: 76 +/- 8 to 64 +/- 1 beats X min-1) and to increased diastolic filling time rather than to true cardiac hypertrophy. Significant increases in aerobic capacity and in strength can occur without modification of left ventricular dimensions.     

Leptin, cortisol and distinct concurrent training sequences

In order to investigate the effects of distinct concurrent training sequences on serum leptin and cortisol levels, 10 subjects (27.1±4.8 years, body mass index 25.38±0.09) were submitted to a control session, concurrent training 1 and concurrent training 2. Samples of leptin and cortisol were collected. Concurrent training 1 consisted of indoor cycling followed by strength training and concurrent training 2 of strength training followed by indoor cycling. No exercises were performed at the control session. Blood was collected once again to verify the same variables. Shapiro-Wilk, 2-way ANOVA and Tukey post-hoc tests were used. There was a reduction in leptin levels after concurrent training 1 (Δ%=?-?16.04; p=0.05) and concurrent training 2 (Δ%=?-?8.54; p=0.02). Cortisol decreased after concurrent training 1 (Δ%=?-?26.32; p=0.02) and concurrent training 2 (Δ%=?-?33.57; p=0.05). There was a high and significant correlation between blood variables only in CS (lep PRE X cort PRE and cort POST: r=?-?0.80 and r=?-?0.81; lep POST X cort PRE and cort POST: r=?-?0.62 and r=?-?0.62). Concurrent training promoted a reduction in leptin and cortisol levels irrespective of sequence.     

Resistance exercise reduces muscular substrates in women

The purpose of this investigation was to examine the influence of an acute bout of resistance exercise (RE) on intramuscular triglyceride (IMTG) and muscle glycogen concentrations and intracellular signaling in women with high body fat content. Six overweight women with a high percent body fat (age 29 +/- 3 yr; BMI 28 +/- 3 kg/m (2), body fat 38 +/- 4 %) performed 6 sets of 10 repetitions of knee extension exercise at 70 % 1RM. Muscle biopsies were obtained from the vastus lateralis before, 1 min after (POST1), and 2 h after (POST2) exercise. Acute RE reduced (p < 0.05) IMTG content approximately 40 % at POST1 and POST2 (75 +/- 5; 45 +/- 6; 50 +/- 10 mmol/kg/dry wt). Muscle glycogen was also reduced (p < 0.05) approximately 25 % at POST1 and remained lower at POST2 (317 +/- 14; 241 +/- 30; 235 +/- 26 mmol/kg/dry wt). ERK1/2, SAPK/JNK, and p38 phosphorylation were increased (p < 0.05) approximately 2 - 3-fold at POST1 and ERK1/2 remained elevated and POST2 whereas SAPK/JNK and p38 returned to basal levels. AMPKalpha phosphorylation was unchanged in response to RE. These results show that both IMTG and muscle glycogen stores serve as an important energy source during RE in overweight women and the MAP kinase signaling response to RE is not compromised by high levels of body fat.     

Glycogen synthesis in muscle fibers during active recovery from intense exercise

PURPOSE: There is evidence that active recovery impairs glycogen repletion in skeletal muscles of fasted individuals. Our main goal was to examine the impact of active recovery on the glycogen stores of the different muscle fiber types. METHODS: Eight endurance-trained individuals cycled for 2.5 min at 130% [OV0312]O(2peak) followed by a 30-s all-out cycling sprint. After exercise, the participants were subjected to either a passive recovery or an active recovery protocol that consisted of pedalling for 45 min at 40% [OV0312]O(2peak). RESULTS: During active recovery, blood lactate and pH returned more rapidly toward preexercise levels than during passive recovery. In contrast, average muscle glycogen content remained at stable levels during active recovery (209 +/- 32 and 202 +/- 30 mmol.kg-1 at 0 and 45 min of recovery, respectively) but increased significantly in response to passive recovery (from 185 +/- 27 to 283 +/- 42 mmol.kg-1). The pattern of change in periodic acid-Schiff staining intensity across muscle fibers suggests that the impact of active recovery on average muscle glycogen content is different from that observed at the levels of the individual muscle fibers, with active recovery having no effect on glycogen resynthesis in Type II muscle fibers but causing glycogen breakdown in Type I muscle fibers. Although active recovery was also associated with higher plasma catecholamines and lower insulin levels, such an unfavorable hormonal environment had no effect on glycogen resynthesis in Type II muscle fibers. CONCLUSION: Active recovery in comparison to passive recovery does not affect glycogen resynthesis in Type II muscle fibers despite being associated with an unfavorable hormonal environment but results in a marked glycogen mobilization in Type I muscle fibers.     

31P-MRS characterization of sprint and endurance trained athletes

Muscle metabolism and force production were studied in sprint trained runners, endurance trained runners and in untrained subjects, using 31P-MRS. 31P-spectra were obtained at a time resolution of 5 s during four maximal isometric contractions of 30-sec duration, interspersed by 60-sec recovery intervals. Resting CrP/ATP ratio averaged 3.3 +/- 0.3, with no difference among the three groups. The sprint trained subjects showed about 20 % larger contraction forces in contraction bouts 1 and 2 (p < 0.05). The groups differed with respect to CrP breakdown (p < 0.05), with sprinters demonstrating about 75 % breakdown in each contraction compared to about 60 % and 40 % for untrained and endurance trained subjects, respectively (p < 0.05). The endurance trained runners showed almost twice as fast CrP recovery (t 1/2 = 12.5 +/- 1.5) compared to sprint trained (t 1/2 = 22.5 +/- 2.53) and untrained subjects (t 1/2 = 26.4 +/- 2.8). From the initial rate of CrP resynthesis the rate of maximal aerobic ATP synthesis was estimated to 0.74 +/- 0.07, 0.73 +/- 0.10 and 0.33 +/- 0.07 mmol ATP x kg -1 wet muscle x sec -1 for sprint trained, endurance trained and untrained subjects, respectively. Only the sprint trained and the untrained subjects displayed a significant drop in pH and only during the first of the four contractions, about 0.2 and 0.1 pH units, respectively, indicating that only under those contractions was the glycolytic proton production larger than the proton consumption by the CK reaction. Also, in the first contraction the energy cost of contraction was higher for the sprinters compared to the two other groups. The simple 31P-MRS protocol used in the present study demonstrates marked differences in force production, aerobic as well as anaerobic muscle metabolism, clearly allowing differentiation between endurance trained, sprint trained and untrained subjects.     

Interactions between homocyst(e)ine and nitric oxide during acute submaximal exercise in adult males

Experimental studies investigating the effects of exercise on plasma total homocyst(e)ine (H[e]) levels in humans are almost non-existent. H(e) has been demonstrated to represent an independent risk factor for cardiovascular disease. The exact mechanism through which H(e) exerts its effects on the arteries is unknown but it is thought to involve nitric oxide (NO). The present study was designed to assess the effects of acute submaximal exercise on H(e) while levels of NO inhalation were manipulated using an air-filter mask. The study was completed by seven male volunteers, aged 21.6+/-1.3 yr (X+/-SD), VO2max: 48.6+/-7.6 mL x kg(-1) x min(-1). During two separate occasions the subjects performed a 1-hour bout of submaximal exercise on a stationary cycle ergometer at 60% of their VO2max. The two trials were completed in random order (with and without mask). Data were collected before (PRE) and after (POST) the acute exercise bouts. Plasma H(e) was directly measured by HPLC and NO by quantifying the enzymatic oxidation to nitrite (NO2-) & nitrate (NO3-). Mean H(e) concentrations were 10.89+/-2.05 nmol/mL (PRE) & 11.21+/-1.81 nmol/mL (POST) and were not significantly altered by submaximal exercise. When wearing a mask, the correlation of the PRE/POST H(e) differences with the PRE/ POST differences in NO3- were 0.77 (P=0.07). No correlation was found between either H(e) and NO2- or between NO2- and NO3-. However, a significant correlation (r= - 0.86, P= 0.03) was also observed between H(e) and NO2- but only for the post-exercise values when wearing a mask. The results suggest that: (1) plasma H(e) levels are not affected by acute submaximal exercise; (2) there is insufficient evidence to support the view that plasma H(e) levels are being mediated by NO during either rest or exercise.     

Effects of a 21-day expedition to 6,194 m on human skeletal muscle SR Ca2+-ATPase

We investigated the effects of a 21-day expedition to the summit of Mount Denali, Alaska (6,194 m) on selected Ca2+ sequestration properties of sarcoplasmic reticulum (SR) calcium pump in vastus lateralis muscle. Muscle samples were obtained by biopsy from 5 male climbers (peak oxygen consumption, VO2peak = 52.3 +/- 2.1 mL.kg(-1).min(-1)) approximately 7 days prior to (PRE) and 4 days following (POST) the expedition. A comparison of PRE versus POST measures of maximal Ca2+-ATPase activities (117 +/- 8.5 vs. 97.6 +/- 5.6 nmol.mg protein(-1).min(-1)) and Ca2+-uptake (204 +/- 15 vs. 161 +/- 11 nmol.mg protein(-1).min(-1)) measured in crude homogenates obtained from pre-exercised muscle, indicated only an effect (p < 0.05) of the expedition on Ca2+-uptake. The reduction in Ca2+-ATPase activity, representing 16.6%, was not significant (p = 0.089). The sarco endoplasmic reticulum calcium (SERCA)-ATPase isoforms, measured using Western blotting techniques, revealed a small reduction (p < 0.05) in SERCA 1 (-4.6 +/- 1.9%), but not in SERCA 2a (+2.0 +/- 1.4%). Prior to the expedition, both Ca2+-ATPase activity and Ca2+-uptake were reduced (p < 0.05) by approximately 34 and 18%, respectively, following 40 min of a two-step continuous cycling task (20 min at 59% VO2peak and 20 min at 74% VO2peak). The exercise-induced reduction in Ca2+-ATPase activity was independent of fiber type. Only in the case of Ca2+-uptake was a lower exercise response (p < 0.05) observed following the expedition, an effect that was due to the lower resting value. It is concluded that acclimatization as experienced during a mountaineering expedition induces changes in the properties of the SR Ca2+-pump, and particularly to Ca2+-sequestering function.