Physiological responses to prolonged treadmill walking with external loads

Limited information is available regarding the physiological responses to prolonged load carriage. This study determined the energy cost of prolonged treadmill walking (fixed distance of 12 km) at speeds of 1.10 m.s-1, 1.35 m.s-1, and 1.60 m.s-1, unloaded (clothing mass 5.2 kg) and with external loads of 31.5 and 49.4 kg. Fifteen male subjects performed nine trials in random order over a 6-week period. Oxygen uptake (VO2) was determined at the end of the first 10 min and every 20 min thereafter. A 10-min rest period was allowed following each 50 min of walking. No changes occurred in VO2 over time in the unloaded condition at any speed. The 31.5 and 49.4 kg loads, however, produced significant increases (ranging from 10 to 18%) at the two fastest and at all three speeds, respectively, even at initial exercise intensities less than 30% VO2max. In addition, the 49.4 kg load elicited a significantly higher (P less than 0.05) VO2 than did the 31.5 kg load at all speeds. The measured values of metabolic cost were also compared to those predicted using the formula of Pandolf et al. In trials where VO2 increased significantly over time, predicted values underestimated the actual metabolic cost during the final minute by 10-16%. It is concluded that energy cost during prolonged load carriage is not constant but increases significantly over time even at low relative exercise intensities. It is further concluded that applying the prediction model which estimates energy expenditure from short-term load carriage efforts to prolonged load carriage can result in significant underestimations of the actual energy cost.     

Adaptation of Cardiac Performance to Physical Exercise of Increasing Power in Adolescents

Cardiac performance during bicycle ergometer tests with increasing loads was examined in 12- and 14-year-old boys at different stages of puberty, professionally trained in basketball and swimming, as well as in boys of the same age without regular athletic training. In all these boys, the cardiac chronotropic response grew in intensity with the power and duration of exercise, being maximal in 14-year-old adolescents untrained athletically. During exercise at 0.5 W/kg, the cardiac chronotropic function stabilized within the first ten seconds; at 1.0 and 1.5 W/kg, the heart rate increased more or less monotonically throughout the entire test period. In 12- and 14-year-old swimmers and in untrained boys, the threshold value for an adequate hemodynamic response was found at 0.5 W/kg. The patterns of stroke volume adaptation to increasing loads were shown to be dependent on athletic specialization and independent of age. During the first 30 s of exercise at 0.5 W/kg, cardiac output increased significantly over its basal level. Subsequent load increases to 1.0 and 1.5 W/kg were accompanied by progressive growth of this parameter during the whole period of exercise. Upon transition to a different workload, the increment of cardiac output decreased.     

Endurance training reduces the magnitude of exercise-induced hyperammonemia in humans

The purpose of this study was to determine the influence of endurance-type exercise training on alterations of the ammonia content of blood in exercising humans. Seven females and four males trained 6 days/wk for 7 wk alternating days of continuous cycling (40 min) and interval running (five 5-min bouts). The NH3 content of blood was determined before and during cycle ergometer (CE) exercise (4 min) at power outputs (PO) of 119, 172, and 241 W pretraining and of 163, 230, and 271 W posttraining. These PO for each occasion represent relative work loads of approximately 65, 90, and 115% of peak CE maximum O2 uptake (PCE VO2), respectively. Training increased (P less than 0.05) PCE VO2 approximately 32% (2.72 +/- 0.25 to 3.56 +/- 0.29 l/min or 38.5 +/- 1.9 to 51.2 +/- 2.3 ml X kg-1 X min-1). Both pre- and posttraining the NH3 content of blood increased (P less than 0.05) with increasing intensity of exercise. Training did not influence the measure of these responses during exercise at the same relative intensity. During exercise at the same absolute PO, approximately 168 or 235 W, however, increases in blood NH3 were less (P less than 0.05) after training. The results indicate that the magnitude of increase in blood NH3 during exercise is determined by the energy requirement of the absolute work load, relative to an individual's aerobic power.     

Adaptations in skeletal muscle exercise metabolism to a sustained session of heavy intermittent exercise

The purpose of this study was to investigate the hypothesis that a single, extended session of heavy exercise would be effective in inducing adaptations in energy metabolism during exercise in the absence of increases in oxidative potential. Ten healthy males [maximal aerobic power (VO(2 peak)) = 43.4 +/- 2.2 (SE) ml x kg(-1) x min(-1)] participated in a 16-h training session involving cycling for 6 min each hour at approximately 90% of maximal oxygen consumption. Measurements of metabolic changes were made on tissue extracted from the vastus lateralis during a two-stage standardized submaximal cycle protocol before (Pre) and 36-48 h after (Post) the training session. At Pre, creatine phosphate (PCr) declined (P < 0.05) by 32% from 0 to 3 min and then remained stable until 20 min of exercise at 60% VO(2 peak) before declining (P < 0.05) by a further 35% during 20 min of exercise at 75% VO(2 peak). Muscle lactate (mmol/kg dry wt) progressively increased (P < 0.05) from 4.59 +/- 0.64 at 0 min to 17.8 +/- 2.7 and 30.9 +/- 5.3 at 3 and 40 min, respectively, whereas muscle glycogen (mmol glucosyl units/kg dry wt) declined (P < 0.05) from a rest value of 360 +/- 24 to 276 +/- 31 and 178 +/- 36 at similar time points. During exercise after the training session, PCr and glycogen were not as depressed (P < 0.05), and increases in muscle lactate were blunted (P < 0.05). All of these changes occurred in the absence of increases in oxidative potential as measured by the maximal activities of citrate synthase and malate dehydrogenase. These findings are consistent with other studies, namely, that muscle metabolic adaptations to regular exercise are an early adaptive event that occurs before increases in oxidative potential.     

Short-Term Intensified Cycle Training Alters Acute and Chronic Responses of PGC1α and Cytochrome C Oxidase IV to Exercise in Human Skeletal Muscle

Reduced activation of exercise responsive signalling pathways have been reported in response to acute exercise after training; however little is known about the adaptive responses of the mitochondria. Accordingly, we investigated changes in mitochondrial gene expression and protein abundance in response to the same acute exercise before and after 10-d of intensive cycle training. Nine untrained, healthy participants (mean±SD; VO_2peak 44.1±17.6 ml/kg/min) performed a 60 min bout of cycling exercise at 164±18 W (72% of pre-training VO_2peak). Muscle biopsies were obtained from the vastus lateralis muscle at rest, immediately and 3 h after exercise. The participants then underwent 10-d of cycle training which included four high-intensity interval training sessions (6×5 min; 90–100% VO_2peak) and six prolonged moderate-intensity sessions (45–90 min; 75% VO_2peak). Participants repeated the pre-training exercise trial at the same absolute work load (64% of pre-training VO_2peak). Muscle PGC1-α mRNA expression was attenuated as it increased by 11- and 4- fold (P<0.001) after exercise pre- and post-training, respectively. PGC1-α protein expression increased 1.5 fold (P<0.05) in response to exercise pre-training with no further increases after the post-training exercise bout. RIP140 protein abundance was responsive to acute exercise only (P<0.01). COXIV mRNA (1.6 fold; P<0.01) and COXIV protein expression (1.5 fold; P<0.05) were increased by training but COXIV protein expression was decreased (20%; P<0.01) by acute exercise pre- and post-training. These findings demonstrate that short-term intensified training promotes increased mitochondrial gene expression and protein abundance. Furthermore, acute indicators of exercise-induced mitochondrial adaptation appear to be blunted in response to exercise at the same absolute intensity following short-term training.     

Effects on energy expenditure of facial cooling during exercise.

Estimated energy expenditures for men during Arctic manhauling expeditions were 29-33 MJ day-1, higher than those documented for other hard-working groups and exceeding predicted energy costs for such activities. Although physiological effects from generalised cooling were unlikely, cold exposure of the face could have influenced exercise metabolism via autonomic stimulation. This hypothesis was examined by measuring oxygen consumption, energy expenditure, respiratory exchange ratio (R) and cardiovascular changes during rest and exercise, with and without exposure of the face to air at--20 degrees C. Measurements were made in five subjects during 15 min of rest followed by continuous exercise on a cycle ergometer consisting of 15-min periods at 75, 100, 125 and 150 W external work. The cold air caused a profound fall in facial temperatures and small falls in mean skin and rectal temperatures (P less than 0.001). These changes were associated with a small increase in the mean oxygen consumption over all levels of rest and exercise (0.86 l min-1 vs 0.82 l min-1, P less than 0.001) and a corresponding increase in mean energy expenditure (294 W vs 283 W, P less than 0.05). Cold air also caused an increase in mean resting R values (1.00 vs 0.88, P less than 0.01) but a decrease in the mean R value for all levels of exercise (0.85 vs 0.91, P less than 0.05). Pulse rates were unchanged but systolic and diastolic blood pressures were relatively elevated throughout the cold face experiments (P less than 0.001).     

Twelve Weeks of Sprint Interval Training Improves Indices of Cardiometabolic Health Similar to Traditional Endurance Training despite a Five-Fold Lower Exercise Volume and Time Commitment

AimsWe investigated whether sprint interval training (SIT) was a time-efficient exercise strategy to improve insulin sensitivity and other indices of cardiometabolic health to the same extent as traditional moderate-intensity continuous training (MICT). SIT involved 1 minute of intense exercise within a 10-minute time commitment, whereas MICT involved 50 minutes of continuous exercise per session.MethodsSedentary men (27±8y; BMI = 26±6kg/m²) performed three weekly sessions of SIT (n = 9) or MICT (n = 10) for 12 weeks or served as non-training controls (n = 6). SIT involved 3x20-second ‘all-out’ cycle sprints (~500W) interspersed with 2 minutes of cycling at 50W, whereas MICT involved 45 minutes of continuous cycling at ~70% maximal heart rate (~110W). Both protocols involved a 2-minute warm-up and 3-minute cool-down at 50W.ResultsPeak oxygen uptake increased after training by 19% in both groups (SIT: 32±7 to 38±8; MICT: 34±6 to 40±8ml/kg/min; p<0.001 for both). Insulin sensitivity index (CS_I), determined by intravenous glucose tolerance tests performed before and 72 hours after training, increased similarly after SIT (4.9±2.5 to 7.5±4.7, p = 0.002) and MICT (5.0±3.3 to 6.7±5.0 x 10⁻⁴ min^-1 [μU/mL]^-1, p = 0.013) (p<0.05). Skeletal muscle mitochondrial content also increased similarly after SIT and MICT, as primarily reflected by the maximal activity of citrate synthase (CS; P<0.001). The corresponding changes in the control group were small for VO₂peak (p = 0.99), CS_I (p = 0.63) and CS (p = 0.97).ConclusionsTwelve weeks of brief intense interval exercise improved indices of cardiometabolic health to the same extent as traditional endurance training in sedentary men, despite a five-fold lower exercise volume and time commitment.     

Durability of the reproductive axis in eumenorrheic women during 1 yr of endurance training.

Menstrual cycle (MC) alterations occur in some endurance-training women. We hypothesized that a prospective running program would evoke alterations in MC phase lengths and in the physiological frequency of pulses of luteinizing hormone (LH) and/or diminish 24-h integrated serum LH concentrations in some women. In addition, we postulated that women who train more intensively (above the lactate threshold) would show alterations in gonadotropin release earlier in the training program or to a greater degree. To test these hypotheses, we examined the effects of different exercise intensities on physiological and endocrine responses. Twenty-three healthy eumenorrheic gynecologically mature (postmenarchal age 17.8 +/- 0.9 yr) untrained women undertook a 1-yr training program at one of two exercise intensities, one at a velocity corresponding to the lactate threshold (LT) and the other halfway between that of LT and peak running velocity, or served as controls. Training distance was the same in each exercise group. Physiological measurements were repeated every four MC to track changes in fitness and readjust training velocities. The lengths of the MC and the follicular and luteal phases were determined from hormonal concentrations. Body composition, nutritional intake, and pulsatile release of LH were determined. The women ran approximately 790 miles. Each group improved physiologically, with the greater than LT group improving to a greater degree. A less than 2-day decrease in the luteal phase length was observed only in the greater than LT group. No significant changes for any parameter of pulsatile LH release were noted between exercise groups. No significant changes in nutritional intake and only small changes in body composition were noted in either exercise group despite the added energy expenditure of exercise. We conclude that a progressive exercise program of moderate distance and intensity does not adversely affect the robust reproductive system of gynecologically mature eumenorrheic women.     

Three Minutes of All-Out Intermittent Exercise per Week Increases Skeletal Muscle Oxidative Capacity and Improves Cardiometabolic Health

We investigated whether a training protocol that involved 3 min of intense intermittent exercise per week — within a total training time commitment of 30 min including warm up and cool down — could increase skeletal muscle oxidative capacity and markers of health status. Overweight/obese but otherwise healthy men and women (n = 7 each; age  = 29±9 y; BMI  = 29.8±2.7 kg/m²) performed 18 training sessions over 6 wk on a cycle ergometer. Each session began with a 2 min warm-up at 50 W, followed by 3×20 s “all-out” sprints against 5.0% body mass (mean power output: ∼450–500 W) interspersed with 2 min of recovery at 50 W, followed by a 3 min cool-down at 50 W. Peak oxygen uptake increased by 12% after training (32.6±4.5 vs. 29.1±4.2 ml/kg/min) and resting mean arterial pressure decreased by 7% (78±10 vs. 83±10 mmHg), with no difference between groups (both p<0.01, main effects for time). Skeletal muscle biopsy samples obtained before and 72 h after training revealed increased maximal activity of citrate synthase and protein content of cytochrome oxidase 4 (p<0.01, main effect), while the maximal activity of β-hydroxy acyl CoA dehydrogenase increased in men only (p<0.05). Continuous glucose monitoring measured under standard dietary conditions before and 48–72 h following training revealed lower 24 h average blood glucose concentration in men following training (5.4±0.6 vs. 5.9±0.5 mmol/L, p<0.05), but not women (5.5±0.4 vs. 5.5±0.6 mmol/L). This was associated with a greater increase in GLUT4 protein content in men compared to women (138% vs. 23%, p<0.05). Short-term interval training using a 10 min protocol that involved only 1 min of hard exercise, 3x/wk, stimulated physiological changes linked to improved health in overweight adults. Despite the small sample size, potential sex-specific adaptations were apparent that warrant further investigation.     

The effect of training on endurance and the cardiovascular responses of individuals with paraplegia during dynamic exercise induced by functional electrical stimulation

Endurance for dynamic exercise, cardiac output, blood pressure, heart rate, ventilation, and oxygen consumption was measured in eight individuals with paraplegia at the end of 4-min bouts of exercise on a friction braked cycle ergometer. Movement of the subjects' legs was induced by electrically stimulating the quadriceps, gluteus maximus and hamstring muscles with a computer-controlled biphasic square--wave current at a frequency of 30 Hz. The friction braked cycle ergometer was pedalled at work rates which varied between 0 and 40 W. Measurements were repeated after 3 and 6 months to assess the affect of training. After 3 months of training it was found that endurance increased from 8 min at a work rate of 0 W to 30 min at a work rate of 40 W. Compared to the cardiovascular responses in non-paralyzed subjects, computerized cycle ergometry was found to be associated with higher relative stresses for a given level of absolute work. Mean blood pressure, for example, increased by over 30% during maximal work in individuals with paralysis compared to the typical response obtained for able-bodied subjects. Analysis of the data showed that instead of the 20-30% metabolic efficiency commonly reported for cycle ergometry, the calculated metabolic efficiency during computer-controlled cycle ergometry was only 3.6%.     

Separate and combined effects of exercise training and weight loss on exercise efficiency and substrate oxidation

Perturbations in body weight have been shown to affect energy expenditure and efficiency during physical activity. The separate effects of weight loss and exercise training on exercise efficiency or the proportion of energy derived from fat oxidation during physical activity, however, are not known. The purpose of this study was to determine the separate and combined effects of exercise training and weight loss on metabolic efficiency, economy (EC), and fat oxidation during steady-state moderate submaximal exercise. Sixty-four sedentary older (67 +/- 0.5 yr) overweight to obese (30.7 +/- 0.4 kg/m(2)) volunteers completed 4 mo of either diet-induced weight loss (WL; n = 11), exercise training (EX; n = 36), or the combination of both interventions (WLEX; n = 17). Energy expenditure, gross efficiency (GE), EC, and proportion of energy expended from fat (EF) were determined during a 1-h submaximal (50% of peak aerobic capacity) cycle ergometry exercise before the intervention and at the same absolute work rate after the intervention. We found that EX increased GE by 4.7 +/- 2.2%. EC was similarly increased by 4.2 +/- 2.1% by EX. The addition of concomitant WL to EX (WLEX) resulted in greater increases in GE (9.0 +/- 3.3%) compared with WL alone but not compared with EX alone. These effects remained after adjusting for changes in lean body mass. The proportion of energy derived from fat during the bout of moderate exercise increased with EX and WLEX but not with WL. From these findings, we conclude that exercise training, either alone or in combination with weight loss, increases both exercise efficiency and the utilization of fat during moderate physical activity in previously sedentary, obese older adults. Weight loss alone, however, significantly improves neither efficiency nor utilization of fat during exercise.     

Endurance training slows down the kinetics of heart rate increase in the transition from moderate to heavier submaximal exercise intensities

To find out whether endurance training influences the kinetics of the increases in heart rate (fc) during exercise driven by the sympathetic nervous system, the changes in the rate of fc adjustment to step increments in exercise intensities from 100 to 150 W were followed in seven healthy, previously sedentary men, subjected to 10-week training. The training programme consisted of 30-min cycle exercise at 50%-70% of maximal oxygen uptake (VO2max) three times a week. Every week during the first 5 weeks of training, and then after the 10th week the subjects underwent the submaximal three-stage exercise test (50, 100 and 150 W) with continuous fc recording. At the completion of the training programme, the subjects' VO2max had increased significantly (39.2 ml.min-1.kg-1, SD 4.7 vs 46 ml.min-1.kg-1, SD 5.6) and the steady-state fc at rest and at all submaximal intensities were significantly reduced. The greatest decrease in steady-state fc was found at 150 W (146 beats.min-1, SD 10 vs 169 beats.min-1, SD 9) but the difference between the steady-state fc at 150 W and that at 100 W (delta fc) did not decrease significantly (26 beats.min-1, SD 7 vs 32 beats.min-1, SD 6). The time constant (tau) of the fc increase from the steady-state at 100 W to steady-state at 150 W increased during training from 99.4 s, SD 6.6 to 123.7 s, SD 22.7 (P less than 0.01) and the acceleration index (A = 0.63.delta fc.tau-1) decreased from 0.20 beats.min-1.s-1, SD 0.05 to 0.14 beats.min-1.s-1, SD 0.04 (P less than 0.02). The major part of the changes in tau and A occurred during the first 4 weeks of training. It was concluded that heart acceleration following incremental exercise intensities slowed down in the early phase of endurance training, most probably due to diminished sympathetic activation.     

Influence of physiological changes of glycaemia on VEPs and visual ERPs

Since hypoglycemia is known to influence cognitive functions, we checked whether the physiological changes in glycemia (after fasting or exertion) can explain the rather high intra-individual variability of event-related potentials (ERPs). Besides the ERPs to "change in coherence of a moving pattern" with reaction time (RT) recording, binocular pattern reversal VEPs and motion-onset VEPs (to linear and radial motion) were also examined in 14 healthy subjects prior to and after 24-h fasting that decreased glycemia from 5.3 to 3.9 mmol/l on the average. We only found one significant change in the latencies and amplitudes of VEPs and ERPs (with no change of RT). The N160 peak in the motion-onset VEPs to radial (expansive) motion (EM-VEPs) showed a larger amplitude at lower glycemia. For evaluation of the exertion influence, we tested glycemia prior to and after 90 min long exercise -- bicycle ergometry with the load set to 2 W/kg in women and 2.5 W/kg in men (average age-related values for W170/kg index). The changes of glycemia to exertion were, however, less distinct than those to fasting. We conclude that in healthy subjects the glycemia decrease due to 24-h fasting or intensive time-limited exercise never reaches the critical value to change the VEP, ERPs and RTs.     

Activation or inactivation of cardiac Akt/mTOR signaling diverges physiological from pathological hypertrophy

Cardiomyocyte hypertrophy differs according to the stress exerted on the myocardium. While pressure overload-induced cardiomyocyte hypertrophy is associated with depressed contractile function, physiological hypertrophy after exercise training associates with preserved or increased inotropy. We determined the activation state of myocardial Akt signaling with downstream substrates and fetal gene reactivation in exercise-induced physiological and pressure overload-induced pathological hypertrophies. C57BL/6J mice were either treadmill trained for 6 weeks, 5 days/week, at 85-90% of maximal oxygen uptake (VO(2max)), or underwent transverse aortic constriction (TAC) for 1 or 8 weeks. Total and phosphorylated protein levels were determined with SDS-PAGE, and fetal genes by real-time RT-PCR. In the physiologically hypertrophied heart after exercise training, total Akt protein level was unchanged, but Akt was chronically hyperphosphorylated at serine 473. This was accompanied by activation of the mammalian target of rapamycin (mTOR), measured as phosphorylation of its two substrates: the ribosomal protein S6 kinase-1 (S6K1) and the eukaryotic translation initiation factor-4E binding protein-1 (4E-BP1). Exercise training did not reactivate the fetal gene program (beta-myosin heavy chain, atrial natriuretic factor, skeletal muscle actin). In contrast, pressure overload after TAC reactivated fetal genes already after 1 week, and partially inactivated the Akt/mTOR pathway and downstream substrates after 8 weeks. In conclusion, changes in opposite directions of the myocardial Akt/mTOR signal pathway appears to distinguish between physiological and pathological hypertrophies; exercise training associating with activation and pressure overload associating with inactivation of the Akt/mTOR pathway.     

Metabolic adaptations to training precede changes in muscle mitochondrial capacity.

To determine whether increases in muscle mitochondrial capacity are necessary for the characteristic lower exercise glycogen loss and lactate concentration observed during exercise in the trained state, we have employed a short-term training model involving 2 h of cycling per day at 67% maximal O2 uptake (VO2max) for 5-7 consecutive days. Before and after training, biopsies were extracted from the vastus lateralis of nine male subjects during a continuous exercise challenge consisting of 30 min of work at 67% VO2max followed by 30 min at 76% VO2max. Analysis of samples at 0, 15, 20, and 60 min indicated a pronounced reduction (P less than 0.05) in glycogen utilization after training. Reductions in glycogen utilization were accompanied by reductions (P less than 0.05) in muscle lactate concentration (mmol/kg dry wt) at 15 min [37.4 +/- 9.3 (SE) vs. 20.2 +/- 5.3], 30 min (30.5 +/- 6.9 vs. 17.6 +/- 3.8), and 60 min (26.5 +/- 5.8 vs. 17.8 +/- 3.5) of exercise. Maximal aerobic power, VO2max (l/min) was unaffected by the training (3.99 +/- 0.21 vs. 4.05 +/- 0.26). Measurements of maximal activities of enzymes representative of the citric acid cycle (succinic dehydrogenase and citrate synthase) were similar before and after the training. It is concluded that, in the voluntary exercising human, altered metabolic events are an early adaptive response to training and need not be accompanied by changes in muscle mitochondrial capacity.     

Influence of training status on maximal accumulated oxygen deficit during all-out cycle exercise

The influence of training status on the maximal accumulated oxygen deficit (MAOD) was used to assess the validity of the MAOD method during supramaximal all-out cycle exercise. Sprint trained (ST; n = 6), endurance trained (ET; n = 8), and active untrained controls (UT; n = 8) completed a 90 s all-out variable resistance test on a modified Monark cycle ergometer. Pretests included the determination of peak oxygen uptake ( O_2peak) and a series (5–8) of 5-min discontinuous rides at submaximal exercise intensities. The regression of steady-state oxygen uptake on power output to establish individual efficiency relationships was extrapolated to determine the theoretical oxygen cost of the supramaximal power output achieved in the 90 s all-out test. Total work output in 90 s was significantly greater in the trained groups (P<0.05), although no differences existed between ET and ST. Anaerobic capacity, as assessed by MAOD, was larger in ST compared to ET and UT. While the relative contributions of the aerobic and anaerobic energy systems were not significantly different among the groups, ET were able to achieve significantly more aerobic work than the other two groups, while ST were able to achieve significantly more anaerobic work. Peak power and peak pedalling rate were significantly higher in ST. The results suggested that MAOD determined during all-out exercise was sensitive to training status and provided a useful assessment of anaerobic capacity. In our study sprint training, compared with endurance training, appeared to enhance significantly power output and high intensity performance over brief periods (up to 60 s), yet few overall differences in performance (i.e. total work) existed during 90 s of all-out exercise.     

Effects of iron deficiency and training on mitochondrial enzymes in skeletal muscle

We measured mitochondrial enzyme activities in skeletal muscle under conditions of iron deficiency and endurance training to assess the effects of these interventions on the contents and proportions of non-iron-containing and iron-dependent enzymes and proteins. Male Sprague-Dawley rats, 21 days of age, received a diet containing either 6 (iron deficient) or 50 mg iron/kg diet (iron sufficient). At 35 days of age animals were subdivided into sedentary and endurance training groups (running at 0.7 mph, 0% grade, 45 min/day, 6 days/wk). By 70 days of age, iron deficiency had decreased gastrocnemius muscle cytochrome c by 62% in sedentary animals. In contrast, the activities of tricarboxylic acid cycle enzymes were increased, remained unchanged or were slightly decreased, indicating that iron deficiency markedly altered mitochondrial composition. Endurance training increased cytochrome c (35%), tricarboxylic acid cycle enzymes (approximately 15%), and manganese superoxide dismutase (33%) in iron-deficient rats, whereas the same exercise regimen had no effect on the skeletal muscle of iron-sufficient animals. The interactive effect of dietary iron deficiency and mild exercise on mitochondrial enzymes suggests that adaptation to a training stimulus is, to some extent, geared to the relationship between the energy demand of exercise and the capacity for O2 transport and utilization.     

Effect of prolonged training period on plasma adiponectin in elite male rowers.

Adiponectin is secreted by adipocytes and has been implicated in the regulation of energy homeostasis. Vigorous training program represents a physical stress condition in which heavy changes in energy expenditure might increase adiponectin concentration in athletes. Therefore, the aim of the present study was to investigate if there are changes in fasting adiponectin concentration during preparatory period in elite male rowers. Twelve rowers (mean and SD; age: 20.8+/-3.0 years; height: 192.9+/-4.7 cm; body mass: 91.9+/-5.3 kg; body fat percentage: 11.9+/-1.4%) were tested seven times over a 24-week training season. In addition to adiponectin, leptin, insulin, growth hormone, and glucose values were evaluated. Maximal oxygen consumption (VO (2 max)) and aerobic power (Pa (max)) were determined before and after the training period. Training was mainly organized as low-intensity prolonged training. Significant increases in VO (2 max) (by 3.2+/-1.8%; from 6.2+/-0.5 to 6.4+/-0.4 l/min), VO (2 max/kg) (by 2.2+/-2.0%; from 67.9+/-3.0 to 69.4+/-3.0 ml/min/kg) and Pa (max) (by 4.6+/-6.3%; from 444.6+/-39.1 to 465.8+/-25.0 W) were observed after the 24-week period. All measured body compositional values were similar to pretraining values after the training period. Fasting adiponectin did not change during the preparatory period. Likewise, leptin, insulin, growth hormone, and glucose values were not significantly changed after the training period. Adiponectin concentration was significantly correlated (all p<0.05) with body mass (r=-0.40), body fat mass (r=-0.33), body fat free mass (r=0.38), and leptin (r=-0.31) values. In conclusion, fasting adiponectin does not change throughout the prolonged training period in elite male rowers despite substantial changes in training volume. Further studies are needed to clarify possible mechanisms by which adiponectin might influence energy homeostasis during heavy training in elite athletes.