Concurrent strength and endurance training: the influence of dependent variable selection

Twenty-six active university students were randomly allocated to resistance (R, n = 9), endurance (E, n = 8), and concurrent resistance and endurance (C, n = 9) training conditions. Training was completed 3 times per week in all conditions, with endurance training preceding resistance training in the C group. Resistance training involved 4 sets of upper- and lower-body exercises with loads of 4-8 repetition maximum (RM). Each endurance training session consisted of five 5-minute bouts of incremental cycle exercise at between 40 and 100% of peak oxygen uptake (.VO2peak). Parameters measured prior to and following training included strength (1RM and isometric and isokinetic [1.04, 3.12, 5.20, and 8.67 rad.s(-1)] strength), .VO2peak and Wingate test performance (peak power output [PPO], average power, and relative power decline). Significant improvements in 1RM strength were observed in the R and C groups following training. .VO2peak significantly increased in E and C but was significantly reduced in R after training. Effect size (ES) transformations on the other dependent variables suggested that performance changes in the C group were not always similar to changes in the R or E groups. These ES data suggest that statistical power and dependent variable selection are significant issues in enhancing our insights into concurrent training. It may be necessary to assess a range of performance parameters to monitor the relative effectiveness of a particular concurrent training regimen.     

Biological responses to overload training in endurance sports

Five subjects undertook 10 days of twice daily interval training sessions on a treadmill followed by 5 days of active recovery. On days 1, 6, 11, and 16 the subjects were required to undertake a test of submaximal and maximal work capacity on a treadmill combined with a performance test consisting of a run to exhaustion with the treadmill set at 18 km.h-1 and 1% gradient. Also on these days a pre-exercise blood sample was collected and analysed for a range of haematological, biochemical and immunological parameters. The subjects experienced a significant fall in performance on day 11 which had returned to pretraining levels on day 16. Serum ferritin concentrations were depressed significantly from pretraining concentrations at the conclusion of the recovery period while the expression of lymphocyte activation antigens (CD25+ and HLA-DR+) was increased both after the training phase and the recovery phase. The number of CD56+ cells in the peripheral circulation was depressed at the conclusion of the recovery period. Several parameters previously reported to change in association with overload training failing to reflect the decrease in performance experienced by subjects in this study, suggesting that overtraining may best be diagnosed through a multifactorial approach to the recognition of symptoms. The most important factor to consider may be a decrease in the level of performance following a regeneration period. The magnitude of this decreased performance necessary for the diagnosis of overtraining and the nature of an "appropriate" regeneration period are, however, difficult to define and may vary depending upon the training background of the subjects and the nature of the preceding training. It may or may not be associated with biochemical, haematological, physiological and immunological indicators. Individual cases may present a different range of symptoms and diagnosis of overtraining should not be excluded based on the failure of blood parameters to demonstrate variation. However, blood parameters may be useful to identify possible aetiology in each separate case report of over-training. An outstanding factor to emerge from this study was the difficulty associated with an objective diagnosis of overtraining and this is a possible reason why there have been new accounts of overtraining research in the literature.     

Differential responses to endurance training in subsarcolemmal and intermyofibrillar mitochondria

To examinethe effect of endurance training (6 wk of treadmill running) onregional mitochondrial adaptations within skeletal muscle,subsarcolemmal (SS) and intermyofibrillar (IMF) mitochondria wereisolated from trained and control rat hindlimb muscles.Mitochondrial oxygen consumption(O₂) was measuredpolarographically by using the following substrates: 1 mM pyruvate + 1 mM malate (P+M), 10 mM 2-oxoglutarate, 45 µMpalmitoyl-DL-carnitine + 1 mMmalate, and 10 mM glutamate. Spectrophotometric assays ofcytochrome-c reductase andNAD-specific isocitrate dehydrogenase (IDH) activity were alsoperformed. Maximal (state III) and resting (state IV) O₂ were lower in SS than inIMF mitochondria in both trained and control groups. In SSmitochondria, training elicited significant 36 and 20% increases instate III O₂ with P+M andglutamate, respectively. In IMF mitochondria, training resulted in asmaller (20%), yet significant, increase in state IIIO₂ with P+M as a substrate,whereas state IIIO₂ increased 33 and 27% with 2-oxoglutarate andpalmitoyl-DL-carnitine + malate,respectively. Within groups,cytochrome-c reductase and IDHactivities were lower in SS when compared with IMF mitochondria.Training increased succinate-cytochrome-c reductase inboth SS (30%) and IMF mitochondria (28%). IDH activity increased 32%in the trained IMF but remained unchanged in SS mitochondria. Weconclude that endurance training promotes substantial changes inprotein stoichiometry and composition of both SS and IMF mitochondria.

     

The influence of endurance training on multiple sprint cycling performance

The aims of the present study were to examine the effects of endurance training on multiple sprint cycling performance and to evaluate the influence of recovery duration on the magnitude of those effects. Twenty-one physically active male university students were randomly assigned to either an experimental (n = 12) or a control (n = 9) group. The experimental group cycled for 20 minutes each day, 3 times per week, for 6 weeks at 70% of the power output required to elicit maximal oxygen uptake (VO2max). Multiple sprint performance was assessed using 2 maximal (20 x 5 seconds) sprint cycling tests with contrasting recovery periods (10 or 30 seconds). All tests were conducted on a friction-braked cycle ergometer. Relative to controls, training resulted in a 0.2 L.min(-1) increase in mean VO2max (95% likely range: -0.04 to 0.44 L.min(-1)). Changes in anaerobic capacity (determined by maximal accumulated oxygen deficit) over the same period were trivial (p = 0.96). After training, the experimental group showed significant improvements ( approximately 40 W), relative to controls, in multiple sprint measures of peak and mean power output. In contrast, training-induced reductions in fatigue were trivial (p = 0.63), and there were no significant between-protocol differences in the magnitude of any effects. In summary, 6 weeks of endurance training resulted in substantial improvements in multiple sprint cycling performance, the magnitude of the improvements being largely unaffected by the duration of the intervening recovery periods.     

Potent vasodilator responses to human urotensin-II in human pulmonary and abdominal resistance arteries

The peptide human urotensin-II (hUT-II) and its receptor have recently been cloned. The vascular function of this peptide in humans, however, has yet to be determined. Vasoconstrictor and vasodilator responses to hUT-II were investigated in human small muscular pulmonary arteries [approximately 70 microm internal diameter (ID)] and human abdominal resistance arteries (approximately 200 microm ID). Vasodilator responses were investigated in endothelin-1 (3 nM) precontracted vessels and, in the small pulmonary vessels, compared with the known vasodilators adrenomedullin, sodium nitroprusside, and acetylcholine. In human small pulmonary arteries, hUT-II did not induce vasoconstriction but was a potent vasodilator [-log M concentration causing 50% of the maximum vasodilator effect (pIC(50)) 10.4 +/- 0.5; percentage of reduction in tone (E(max)) 81 +/- 8% (vs. 23 +/- 11% in time controls), n = 5]. The order of potency for vasodilation was human urotensin-II = adrenomedullin (pIC(50) 10.1 +/- 0.4, n = 6) > sodium nitroprusside (pIC(50) 7.4 +/- 0.2, n = 6) = acetylcholine (pIC(50) 6.8 +/- 0.3, n = 6). In human abdominal arteries, hUT-II did not induce vasoconstriction but was a potent vasodilator [pIC(50) 10.3 +/- 0.7; E(max) 96 +/- 8% (vs. 43 +/- 16% in time controls), n = 4]. This is the first report that hUT-II is a potent vasodilator but not a vasoconstrictor of human small pulmonary arteries and systemic resistance arteries.     

Concurrent resistance and endurance training influence basal metabolic rate in nondieting individuals

Thirty physically active healthy men (20.1 ± 1.6 yr) wererandomly assigned to participate for 10 wk in one of the following training groups: endurance trained (ET; 3 days/wk joggingand/or running), resistance trained (RT; 3 days/wkresistance training), or combined endurance and resistance trained(CT). Before and after training, basal metabolic rate (BMR), percentbody fat (BF), maximal aerobic power, and one-repetition maximum forbench press and parallel squat were determined for each subject.Urinary urea nitrogen was determined pre-, mid-, and posttraining. BMRincreased significantly from pre- to posttraining for RT (7,613 ± 968 to 8,090 ± 951 kJ/day) and CT (7,455 ± 964 to 7,802 ± 981 kJ/day) but not for ET (7,231 ± 554 to 7,029 ± 666 kJ/day).BF for CT (12.2 ± 3.5 to 8.7 ± 1.7%) was significantly reducedcompared with RT (15.4 ± 2.7 to 14.0 ± 2.7%) and ET (11.8 ± 2.9 to 9.5 ± 1.7%). Maximal aerobic power increasedsignificantly for ET (13%) but not RT (0.2%) or CT (7%),whereas the improvements in one-repetition maximum bench press andparallel squat were greater in RT (24 and 23%, respectively) comparedwith CT (19 and 12%, respectively). Urinary urea nitrogen loss wasgreater in ET (14.6 ± 0.9 g/24 h) than in RT (11.7 ± 1.0 g/24h) and CT (11.5 ± 1.0 g/24 h) at the end of 10 wk oftraining. These data indicate that, although RT alone will increase BMRand muscular strength, and ET alone will increase aerobic power anddecrease BF, CT will provide all of these benefits but to a lessermagnitude than RT and ET after 10 wk of training.

     

Effect of nicotine on vasoconstrictor and vasodilator responses in human skin vasculature

Our objective was to test the hypothesis that acute exposure of human skin vasculature to nicotine may have deleterious effects on endothelial function. Vasoconstriction and vasorelaxation in isolated perfused human skin flaps (approximately 8 x 18 cm) derived from dermolipectomy specimens were assessed by studying changes in skin perfusion pressure measured by a pressure transducer, and skin perfusion was assessed by a dermofluorometry technique (n = 4 or 5). It was observed that nicotine (10(-7) M) amplified (P < 0.05) the norepinephrine (NE)-induced concentration-dependent (10(-7)-10(-5) M) increase in skin vasoconstriction compared with the control. This amplification effect of nicotine in NE-induced skin vasoconstriction was not blocked by the nicotine-receptor antagonist hexamethonium (10(-6) M) or the cyclooxygenase inhibitor indomethacin (10(-5) M). It was also observed that ACh and nitroglycerin (NTG) elicited a concentration-dependent (10(-8)-10(-5) M) vasorelaxation in skin flaps preconstricted with 8 x 10(-7) M of NE. The vasorelaxation induced by ACh was attenuated (P < 0.05) in the presence of nicotine (10(-7) M) compared with the control. However, skin vasorelaxation induced by NTG was not affected by nicotine (10(-7) M). ACh and NTG are known to induce endothelium-dependent and -independent vasorelaxation, respectively. The present findings were interpreted to indicate that acute exposure of human skin vasculature to nicotine was associated with 1) amplification of NE-induced skin vasoconstriction and 2) impairment of endothelium-dependent skin vasorelaxation. Cyclooxygenase products and nicotine receptors blocked by hexamethonium were not involved in the amplification of NE-induced skin vasoconstriction by nicotine. These findings may provide further insight into the pathogenesis of skin vasospasm in skin flap surgery and skin ischemic disease associated with cigarette smoking or use of smokeless tobacco.     

Effects of endurance training on capillary supply of human skeletal muscle on two age groups (20 and 60 years)

Two groups of human subjects were submitted to a 20-week endurance training program (1 h a day, 4 days a week, 70-80% max VO2). The first group (G20) consisted of eight 22 +/- 3 years male students, the second group (G60) was composed of seven still very physically active elderly male subjects (62 +/- 4 years). Training significantly increased max VO2 by 15% in G20 and 7% in G60. Muscle samples taken from the vastus lateralis muscle before and after training were histochemically stained for fibre-typing (myofibrillar ATPase), capillary supply and fibre area measurements (amylase PAS and NADH-TR). Fibre-type distribution was unchanged with training. Capillary density (cap X mm-2) increased significantly in both groups from 316 +/- 42 to 396 +/- 73 in G20 and from 308 +/- 48 to 409 +/- 55 in G60. This enhancement of capillary supply was linked to the proliferation of capillaries in G20 where the number of capillaries in contact with ST and FTa fibres (CC) significantly increased from 4.6 to 5.9 and from 4.8 to 6.1 respectively. No significant changes in fibre areas were found in G20. On the contrary, G60 did not show any significant sign of capillary growth (CC unchanged) whereas fibre areas significantly decreased in ST (6,410 to 5,520 micron 2) and FTa fibres (5,830 to 5,090 micron 2). A methodological evaluation of fibre-area measurement was described, with confirmation of the data. It was concluded that this study may illustrate the trainability of skeletal muscle of elderly men in a possibly different way to that seen in a younger age group.     

Early effects of short-term endurance training on hormonal responses to graded exercise.

Twelve male, sedentary volunteers (22.0 +/-) were submitted to three weeks of a bicycle ergometer training, consisting of 45 min exercise (at 70% VO2max), 4 times in the first week and 3 times in the next 2 weeks. They performed four incremental exercise tests with the power output increased by 50 W every 3 min until volitional exhaustion: two before training (C1 and C2), and after one (T1) and three (T3) weeks of training. Before and after each load the plasma noradrenaline (NA), adrenaline (A) and blood lactate (LA) concentrations were determined in venous blood samples as well as plasma growth hormone (HGH) and cortisol concentrations before and at the end of exercise. A decrease in NA concentration was found already after 1 week of training at power output of 100 W (p<0.01) and 200 W (p<0.05). Similar decline was maintained after 3 weeks of training. No significant training-induced differences in plasma A concentration were found, however, the thresholds for both catecholamines were significantly shifted towards higher values after 3 weeks of training. One week of training caused a decrease in the pre-exercise (p<0.01), as well as post-exercise (p<0.05) plasma cortisol and HGH concentrations. It was concluded that endurance training induced a decrease in HGH, cortisol and NA concentration already after one week of training. A decline of pre-exercise plasma HGH and cortisol levels with time of experiment may, in part, indicate familiarization to exercise protocol.     

Extreme endurance training: evidence of capillary and mitochondria compartmentalization in human skeletal muscle.

Biopsies from the medial gastrocnemius muscle of three experienced endurance runners who had completed an ultramarathon run (160 km) the previous day were assessed for their oxidative characteristics (fibre types, capillarization and mitochondria content). Also, a regional comparison was made for fibres located centrally (completely surrounded by other fibres) versus fibres located peripherally (next to the interfascicular space) and the capillarization of these peripheral fibres was determined. Subsarcolemmal mitochondria were abundant and 'compartmentalized' close to the capillaries. The number of capillaries around fibres ranged from 5.8 to 8.5 and 5.7 to 8.5, and the number of capillaries.mm-2 ranged from 665 to 810 and 727 to 762, for type I (slow twitch) and type II (fast twitch) fibres, respectively. Central fibres contained a greater number of capillaries and more capillaries.mm-2 than their peripheral counterparts. Peripheral fibres contained more capillaries.micron-1 between fibres than at the interfascicular space. Type I fibres were more distributed (63%-78%) and larger than type II fibres. An abundance of subsarcolemmal mitochondria located close to the capillaries, efficient capillary proliferation between fibres where sharing can occur and greater relative distribution and size of type I fibres are, collectively, efficient characteristics of extreme endurance training.     

Potential for strength and endurance training to amplify endurance performance

The impact of adding heavy-resistance training to increase leg-muscle strength was studied in eight cycling- and running-trained subjects who were already at a steady-state level of performance. Strength training was performed 3 days/wk for 10 wk, whereas endurance training remained constant during this phase. After 10 wk, leg strength was increased by an average of 30%, but thigh girth and biopsied vastus lateralis muscle fiber areas (fast and slow twitch) and citrate synthase activities were unchanged. Maximal O2 uptake (VO2max) was also unchanged by heavy-resistance training during cycling (55 ml.kg-1.min-1) and treadmill running (60 ml.kg-1.min-1); however, short-term endurance (4-8 min) was increased by 11 and 13% (P less than 0.05) during cycling and running, respectively. Long-term cycling to exhaustion at 80% VO2max increased from 71 to 85 min (P less than 0.05) after the addition of strength training, whereas long-term running (10 km times) results were inconclusive. These data do not demonstrate any negative performance effects of adding heavy-resistance training to ongoing endurance-training regimens. They indicate that certain types of endurance performance, particularly those requiring fast-twitch fiber recruitment, can be improved by strength-training supplementation.     

Microvascular and myocardial contractile responses to ischemia: influence of exercise training.

We hypothesized that exercise training preserves endothelium-dependent relaxation, lessens receptor-mediated constriction of coronary resistance arteries, and reduces myocardial contractile dysfunction in response to ischemia. After 10 wk of treadmill running or cage confinement, regional and global indexes of left ventricular contractile function were not different between trained and sedentary animals in response to three 15-min periods of ischemia (long-term; n = 17), one 5-min bout of ischemia (short-term; n = 18), or no ischemia (sham-operated; n = 24). Subsequently, coronary resistance vessels ( approximately 106 +/- 4 microm ID) were isolated and studied using wire myographs. Maximal ACh-evoked relaxation was approximately 25, 40, and 60% of KCl-induced preconstriction after the long-term, short-term, and sham-operated protocols, respectively, and was similar between groups. Maximal sodium nitroprusside-evoked relaxation also was similar between groups among all protocols, and vasoconstrictor responses to endothelin-1 and U-46619 were not different in trained and sedentary rats after short-term ischemia or sham operation. We did observe that, after long-term ischemia, maximal tension development in response to endothelin-1 and U-46619 was blunted (P < 0.05) in trained animals by approximately 70 and approximately 160%, respectively. These results support our hypothesis that exercise training lessens receptor-mediated vasoconstriction of coronary resistance vessels after ischemia and reperfusion. However, training did not preserve endothelial function of coronary resistance vessels, or myocardial contractile function, after ischemia and reperfusion.     

Site-specific adipose tissue LPL responses to endurance training in female lean Zucker rats

The effects of endurance exercise training on adipose tissue have been investigated in female lean Zucker rats. Adult trained rats (TR) were followed throughout a swimming program of 5 wk and were compared with a littermate control sedentary group (SED). Data were collected on days 0, 14, 24, and 36 of the training program. Body weight gain and cumulative food intake were significantly lower in TR than in SED (P less than 0.05). Gastrocnemius citrate synthase activity was increased in TR by day 14 of training (P less than 0.05) and was followed by a second significant increase between days 24 and 36 (P less than 0.05). Although inguinal (ING), parametrial (PAR), and retroperitoneal (RP) cell sizes were decreased by the swimming program (P less than 0.05), adipose tissue lipoprotein lipase (LPL) activity was suppressed (P less than 0.05) by training during the first 24 days in PAR and RP depots only. Thereafter, PAR and RP LPL activities increased in TR animals (P less than 0.05) to reach values similar to SED at the end of the study. These results further establish the regionally specific response of adipose tissue metabolism to endurance training. They also suggest that, when fat cell triacylglycerol depletion reaches a smaller level, LPL activity could be involved in the process of stabilizing fat cell size.     

Skeletal muscle vascular responses in human limbs to isometric handgrip

Studies of whole limb blood flow have shown that static handgrip elicits a vasodilatation in the resting forearm and vasoconstriction in the resting leg. We asked if these responses occur in the skeletal muscle vascular bed, and if so, what is the relative contribution of local metabolic versus other mechanisms to these vascular responses. Blood flow recordings were made simultaneously in the skeletal muscle of the resting arm and leg using the Xenon-washout method in ten subjects during 3 min of isometric handgrip at 30% of maximal voluntary contraction. In the arm, skeletal muscle vascular resistance (SMVR) decreased transiently at the onset of exercise followed by a return to baseline levels at the end of exercise. In the leg SMVR remained unchanged during the 1st min of handgrip, but had increased to exceed baseline levels by the end of exercise. During exercise electromyography (EMG) recordings from nonexercising limbs demonstrated a progressive 20-fold increase in activity in the arm, but remained at baseline in the leg. During EMG-signal modelled exercise performed to mimic the inadvertent muscle activity, decreases in forearm SMVR amounted to 57% of the decrease seen with controlateral handgrip. The present study would seem to indicate that vascular tone in nonexercising skeletal muscle in the arm and leg are controlled differently during the early stages of static handgrip. Metabolic vasodilatation due to involuntary contraction could significantly modulate forearm skeletal muscle vascular responses, but other factors, most likely neural vasodilator mechanisms, must make major contributions. During the later stages of contralateral sustained handgrip, vascular adjustments in resting forearm skeletal muscle would seem to be the final result of reflex sympathetic vasoconstrictor drive, local metabolic vasodilator forces and possibly neurogenic vasodilator mechanisms.