Significant, but limited collateral blood flow increases occur with prolonged training in rats with femoral artery occlusion.

This study examined the capacity of collateral dependent blood flow induced by a prolonged treadmill training program, as compared to a low collateral resistance model created by femoral artery to vein (A-V) shunt. Sprague-Dawley rats, with bilateral femoral artery occlusion were confined to cage activity (Sed, n=9) or trained by daily treadmill exercise (Tr, n=15; up to ≈350 min/d) for 15 weeks. Another set of animals received a femoral A-V anastomosis in one limb and treated with (n=4) or without VEGF(165) (n=9) infusion for 2 weeks. The contralateral side was used as control. Blood flow (BF) was measured with isotope labeled microspheres. Maximal calf muscle BF increased by 15 week training (up to 100±5.0 ml x min(-1) x 100g(-1) (p<0.05); 0.71±0.04 ml x min(-1) x 100g(-1) x mmHg(-1)), a response better (20-25%) than the less demanding training programs used previously. In contrast, femoral A-V shunt with VEGF(165) increased calf muscle conductance to 1.70±0.3 ml x min(-1) x 100 g(-1) x mmHg(-1) that is similar to blood flows observed in non-occluded rats during maximal running. Our data indicate that the collateral circuit development is related to the driving stimulus and that exercise training, does not provide a maximal stimulus for adaptation that is possible. Nonetheless, exercise training results in profound increases in exercise capacity associated with this enhanced collateral blood flow. Our results illustrate that vascular adaptations can be much greater when physiologically induced stimuli are enhanced at the time of therapeutic angiogenesis.

Training-induced vascular adaptations to ischemic muscle.

Peripheral arterial insufficiency is a progressive degenerative disease associated with an increased morbidity and mortality. It decreases exercise tolerance and often presents with symptoms of intermittent claudication. Enhanced physical activity is one of the most effective means of improving the life of affected patients. While this occurs for a variety of reasons, vascular remodeling can be an important means for improved oxygen exchange and blood flow delivery. Relevant exercise-induced signals stimulate angiogenesis, within the active muscle (e.g. hypoxia), and arteriogenesis (enlargement of pre-existing vessels via increased shear stress) to increase oxygen exchange and blood flow capacity, respectively. Evidence from pre-clinical studies shows that the increase in collateral blood flow observed with exercise progresses over time of training, is accompanied by significant enlargement of isolated collateral vessels, and enhances the responses observed with angiogenic growth factors (e.g. VEGF, FGF-2). Thus, enhanced physical activity can be an effective means of enlarging the structure and function of the collateral circuit. Interestingly, disrupting normal NO production (via L-NAME) eliminates this increase in collateral blood flow induced by training, but does not disturb the increase in muscle capillarity within the active muscle. Similarly, inhibiting VEGF receptor kinase activity eliminates the increase in collateral-dependent blood flow, and lessens, but does not eliminate, angiogenesis within the calf muscle. These findings illustrate distinctions between the processes influencing angiogenesis and arteriogenesis. Further, sympathetic modulation of the collateral circuit does not eliminate the increase in collateral circuit conductance induced by exercise training. These findings indicate that structural enlargement of the collateral vessels is essential to realize the increase in collateral-dependent blood flow capacity caused by exercise training. This raises the potential that meaningful vascular remodeling can occur in patients with intermittent claudication who actively participate in exercise training.

MRI evaluation of topical heat and static stretching as therapeutic modalities for the treatment of eccentric exercise-induced muscle damage.

The aim of this study was to monitor the effects of topical heat and/or static stretch treatments on the recovery of muscle damage by eccentric exercise. For this purpose, 32 untrained male subjects performed intense eccentric knee extension exercise, followed by 2 weeks of treatment (heat, stretch, heat plus stretch) or no treatment (control, n=8/group). Isometric strength testing, pain ratings, and multi-echo magnetic resonance imaging of the thigh were performed before and at 2, 3, 4, 8, and 15 days following the exercise. Increased T2 relaxation time, muscle swelling, pain ratings, and strength loss confirmed significant muscle damage during the post-exercise period. Pain ratings and muscle volume recovered to baseline by 15 days, although muscle strength remained lower [77 (4) vs. 95 (3) kg pre-exercise, mean (SE)] and T2 values higher [32.2 (0.8) vs. 28.6 (0.2) ms pre-exercise]. Our results indicate that heat and/or static stretching does not consistently reduce soreness, swelling or muscle damage. The practical implication of our findings is that clinicians should be aware that prescribing heat and/or static stretching following intense eccentric or unaccustomed exercise will not enhance the recovery of damaged muscles.

Arteriogenesis: role of nitric oxide.

Arteriogenesis is an important process for adapting the pre-existing circuit of vessels into functional collateral conduits for delivery of oxygen enriched blood to tissue distal to occlusion of a large, peripheral conduit artery. Recent evidence has shown that arteriogenesis is regulated by nitric oxide (NO), angiogenic factors and shear stress. NO significantly impacts vasomotor tone to enhance conductance of the newly recruited collateral arteries, and this effect is augmented by exercise training prior to arterial occlusion. NO-mediated increases in vascular conductance allows for greater collateral dependent blood flow to the tissue distal to occlusion. NO production is also critical to the efficacy of therapeutic arteriogenesis achieved by delivery of exogenous angiogenic growth factors (VEGF, FGF-2) or by exercise training. The critical role of NO in therapeutic arteriogenesis is independent of NO-mediated changes in vascular conductance and implies a central role in arteriogenic signaling events. Maintenance, or improvement, of NO production and signaling, such as with regular exercise, may improve endothelial cell function and thus may help preserve the arteriogenic potential of preexisting collateral networks.

Relation of bone mineral density and content to mineral content and density of the fat-free mass.

Differences in the mineral fraction of the fat-free mass (M(FFM)) and in the density of the FFM (D(FFM)) are often inferred from measures of bone mineral content (BMC) or bone mineral density (BMD). We studied the relation of BMC and BMD to the M(FFM) and D(FFM) in a heterogeneous sample of 216 young men (n = 115) and women (n = 101), which included whites (n = 155) and blacks (n = 61) and collegiate athletes ( n = 132) and nonathletes (n = 84). Whole body BMC and BMD were determined by dual-energy X-ray absorptiometry (DXA; Hologic QDR-1000W, enhanced whole body analysis software, version 5.71). FFM was estimated using a four-component model from measures of body density by hydrostatic weighing, body water by deuterium dilution, and bone mineral by DXA. There was no significant relation of BMD to M(FFM) (r = 0.01) or D(FFM) (r = -0.06) or of BMC to M(FFM) (r = -0.11) and a significant, weak negative relation of BMC to D(FFM) (r = -0.14, P = 0.04) in all subjects. Significant low to moderate relationships of BMD or BMC to M(FFM) or D(FFM) were found within some gender-race-athletic status subgroups or when the effects of gender, race, and athletic status were held constant using multiple regression, but BMD and BMC explained only 10-17% of the variance in M(FFM) and 0-2% of the variance in D(FFM) in addition to that explained by the demographic variables. We conclude that there is not a significant positive relation of BMD and BMC to M(FFM) or D(FFM) in young adults and that BMC and BMD should not be used to infer differences in M(FFM) or D(FFM).

Biarticular and monoarticular muscle activation and injury in human quadriceps muscle.

We hypothesized that activation of the quadriceps femoris muscle group during eccentric exercise is related to the increase in magnitude of several markers of muscle injury that developed during the next week. Fourteen male subjects performed six to eight sets of five to ten repetitions of single-leg eccentric-only seated knee extension exercise. Magnetic resonance (MR) images were collected before and immediately after exercise and on days 2-4 and 6 after eccentric exercise. Changes in maximal voluntary contraction (MVC), perceived soreness, muscle volume and muscle transverse relaxation of water protons (T2) were determined for the quadriceps femoris muscle group each day. Changes in muscle volume and T2 were determined every day for each muscle [vastus lateralis (VL), vastus medialis (VM), vastus intermedius (VI), rectus femoris (RF)] of the quadriceps femoris group. Post-exercise T2 was greater than pre-exercise T2 (P < 0.05) for all muscles. The acute deltaT2 (Post-Pre) was similar (P>0.05) among VL, VM, VI, and RF [5.5 (0.3) ms], suggesting that the four muscles were equally activated during eccentric exercise. In the week after eccentric exercise, subjects experienced delayed-onset muscle soreness (DOMS) and all muscles demonstrated a delayed increase in T2 above pre-exercise values (P < 0.05), suggesting that muscle injury had occurred. For the quadriceps femoris muscle group, there was no correlation between acute deltaT2 and delayed (peak T2 during days 2, 3, 4, 6 minus pre-exercise T2) deltaT2 (r=0.04, P>0.05). Similar results were obtained when VL, VM, VI and RF were examined separately. Of the four muscles in quadriceps femoris, the biarticular RF experienced greater muscle injury [delayed deltaT2= 15.2 (2.0) ms] compared to the three monoarticular vasti muscles [delayed deltaT2 = 7.7 (1.3) ms; P< 0.05]. We propose that the disproportionate muscle injury to RF resulted from an ineffective transfer of torque from the knee to hip joint during seated eccentric knee extension exercise, thus causing RF to dissipate greater energy than normal. We conclude that in humans, muscle activation is not a unique determinant of muscle injury.

Contraction increases the T(2) of muscle in fresh water but not in marine invertebrates.

Previous studies suggest that the activity-induced increase in (1)H-NMR transverse relaxation time (T(2)) observed in mammalian skeletal muscles is related to an osmotic effect of intracellular metabolite accumulation. This hypothesis was tested by comparing T(2) (measured by (1)H-NMR imaging at 4.7 T) and metabolite changes (measured by (31)P-NMR spectroscopy) after stimulation in the muscles of a freshwater (crayfish, Orconectes virilis) vs two osmoconforming marine invertebrates (lobster, Homarus americanus; scallop, Argopecten concentricus). Intracellular pH significantly decreased after stimulation in the lobster tail muscle, but not in the crayfish tail or scallop phasic adductor muscles. The decrease in phosphoarginine-to-ATP ratio after stimulation was similar in the three muscles. Muscle T(2) increased from 37 to 43 ms (p < 0.02, n = 7) after stimulation in crayfish, but was unchanged in lobster muscle (32 ms, n = 7), and significantly decreased (from 40 to 36 ms, p < 0.02, n = 11) in scallop muscle. The observation that T(2) does not increase after stimulation in muscles of marine invertebrates with high natural osmolarity is consistent with the hypothesis that the T(2) increase in mammalian muscle is related to osmotically driven shifts of fluid between subcellular compartments.

Muscularity and the density of the fat-free mass in athletes.

The purpose of this study was to use estimates of body composition from a four-component model to determine whether the density of the fat-free mass (D(FFM)) is affected by muscularity or musculoskeletal development in a heterogenous group of athletes and nonathletes. Measures of body density by hydrostatic weighing, body water by deuterium dilution, bone mineral by whole body dual-energy X-ray absorptiometry (DXA), total body skeletal muscle estimated from DXA, and musculoskeletal development as measured by the mesomorphy rating from the Heath-Carter anthropometric somatotype were obtained in 111 collegiate athletes (67 men and 44 women) and 61 nonathletes (24 men and 37 women). In the entire group, D(FFM) varied from 1.075 to 1.127 g/cm3 and was strongly related to the water and protein fractions of the fat-free mass (FFM; r = -0.96 and 0.89) and moderately related to the mineral fraction of the FFM (r = 0.65). Skeletal muscle (%FFM) varied from 40 to 68%, and mesomorphy varied from 1.6 to 9.6, but neither was significantly related to D(FFM) (r = 0.11 and -0.14) or to the difference between percent fat estimated from the four-component model and from densitometry (r = 0.09 and -0.16). We conclude that, in a heterogeneous group of young adult athletes and nonathletes, D(FFM) and the accuracy of estimates of body composition from body density using the Siri equation are not related to muscularity or musculoskeletal development. Athletes in selected sports may have systematic deviations in D(FFM) from the value of 1.1 g/cm3 assumed in the Siri equation, resulting in group mean errors in estimation of percent fat from densitometry of 2-5% body mass, but the cause of these deviations is complex and not simply a reflection of differences in muscularity or musculoskeletal development.

Fiber type and metabolic dependence of T2 increases in stimulated rat muscles.

This study examined the relationships between muscle fiber type, metabolism, and blood flow vs. the increase in skeletal muscle (1)H-NMR transverse relaxation time (T2) after stimulation. Triceps surae muscles of anesthetized rats were stimulated in situ at 1-10 Hz for 6 min, and T2 was calculated from (1)H-NMR images acquired at 4.7 T immediately after stimulation. At low-to-intermediate frequencies (1-5 Hz), the stimulation-induced T2 increase was greater in the superficial, fast-twitch white portion of the gastrocnemius muscle compared with the deeper, more aerobic muscles of the triceps surae group. Although whole triceps muscle area changed in parallel with T2 after stimulation when blood flow was intact, clamping of the femoral artery during stimulation prevented an increase in muscle area but not an increase in T2. Partial inhibition of lactic acid production with iodoacetate diminished intracellular acidification (measured by (31)P-NMR spectroscopy) during brief (1.5 min) stimulation but had no significant effect either on estimated osmolite accumulation or on muscle T2 after stimulation. Depletion of muscle phosphocreatine content by feeding rats beta-guanidinopropionate decreased both estimated osmolite accumulation and T2 after 1.5-min stimulation. The results are consistent with the hypothesis that the T2 increase in stimulated muscle is related to osmotically driven shifts of fluid into an intracellular compartment.

Effect of aerobic capacity on the T(2) increase in exercised skeletal muscle.

The increase in nuclear magnetic resonance transverse relaxation time (T(2)) of muscle water measured by magnetic resonance imaging after exercise has been correlated with work rate in human subjects. This study compared the T(2) increase in thigh muscles of trained (cycling VO(2 max) = 54.4 +/- 2.7 ml O(2). kg(-1). min(-1), mean +/- SE, n = 8, 4 female) vs. sedentary (31.7 +/- 0.9 ml O(2). kg(-1). min(-1), n = 8, 4 female) subjects after cycling exercise for 6 min at 50 and 90% of the subjects' individually determined VO(2 max). There was no significant difference between groups in the T(2) increase measured in quadriceps muscles within 3 min after the exercises, despite the fact that the absolute work rates were 60% higher in the trained group (253 +/- 15 vs. 159 +/- 21 W for the 90% exercise). In both groups, the increase in T(2) of vastus muscles was twofold greater after the 90% exercise than after the 50% exercise. The recovery of T(2) after the 90% exercise was significantly faster in vastus muscles of the trained compared with the sedentary group (mean recovery half-time 11.9 +/- 1.2 vs. 23.3 +/- 3.7 min). The results show that the increase in muscle T(2) varies with work rate relative to muscle maximum aerobic power, not with absolute work rate.

Functional magnetic resonance imaging of muscle.

Muscle functional magnetic resonance imaging (MRI) is used to compare the relative involvement of different muscles recruited during exercise. The method relies on the activity-induced increase in the nuclear magnetic resonance transverse relaxation time (T2) of muscle water, which is caused by osmotically driven shifts of fluid into the myofibrillar space. In addition to imaging of whole muscle recruitment, muscle MRI may reveal changes in motor unit organization during disease.

Pixel T2 distribution in functional magnetic resonance images of muscle.

Increases in skeletal muscle (1)H-NMR transverse relaxation time (T2) observed by magnetic resonance imaging have been used to map whole muscle activity during exercise. Some studies further suggest that intramuscular variations in T2 after exercise can be used to map activity on a pixel-by-pixel basis by defining an active T2 threshold and counting pixels that exceed the threshold as "active muscle." This implies that motor units are nonrandomly distributed across the muscle and, therefore, that the distribution of pixel T2 values ought to be substantially broader after moderate exercise than at rest or after more intense exercise, since moderate-intensity exercise should recruit some motor units, and hence some pixels, but not others. This study examined the distribution of pixel T2 values in three muscles (quadriceps, anterior tibialis, and biceps/brachialis) of healthy subjects (5 men and 2 women, 18-46 yr old) at rest, after exercise to fatigue (50% 1 repetition maximum at 20/min to failure = Max), and at 1/2Max (25% 1 repetition maximum, same number of repetitions as Max). Although for each muscle there was a linear relationship between exercise intensity and mean pixel T2, there was no significant difference in the variance of pixel T2 between 1/2Max and Max exercise. There was a modest (10-43%) increase in variance of pixel T2 after both exercises compared with rest, but this was consistent with a Monte Carlo simulation of muscle activity that assumed a random distribution of motor unit territories across the muscle and a random distribution of muscle cells within each motor unit's territory. In addition, 40% of the pixel-to-pixel muscle T2 variations were shown to be due to imaging noise. The results indicate that magnetic resonance imaging T2 cannot reliably map active muscle on a pixel-by-pixel basis in normal subjects.

MR measurements of muscle damage and adaptation after eccentric exercise.

The purposes of this study were, first, to clarify the long-term pattern of T2 relaxation times and muscle volume changes in human skeletal muscle after intense eccentric exercise and, second, to determine whether the T2 response exhibits an adaptation to repeated bouts. Six young adult men performed two bouts of eccentric biceps curls (5 sets of 10 at 110% of the 1-repetition concentric maximum) separated by 8 wk. Blood samples, soreness ratings, and T2-weighted axial fast spin-echo magnetic resonance images of the upper arm were obtained immediately before and after each bout; at 1, 2, 4, 7, 14, 21, and 56 days after bout 1; and at 2, 4, 7 and 14 days after bout 2. Resting muscle T2 [27.6 +/- 0.2 (SE) ms] increased immediately postexercise by 8 +/- 1 ms after both bouts. T2 peaked 7 days after bout 1 at 47 +/- 4 ms and remained elevated by 2.5 ms at 56 days. T2 peaked lower (37 +/- 4 ms) and earlier (2-4 days) after bout 2, suggesting an adaptation of the T2 response. Peak serum creatine kinase values, pain ratings, and flexor muscle swelling were also significantly lower after the second bout (P < 0.05). Total volume of the imaged arm region increased transiently after bout 1 but returned to preexercise values within 2 wk. The exercised flexor compartment swelled by over 40%, but after 2 wk it reverted to a volume 10% smaller than that before exercise and maintained this volume loss through 8 wk, consistent with partial or total destruction of a small subpopulation of muscle fibers.

In vivo validation of whole body composition estimates from dual-energy X-ray absorptiometry.

We validated whole body composition estimates from dual-energy X-ray absorptiometry (DEXA) against estimates from a four-component model to determine whether accuracy is affected by gender, race, athletic status, or musculoskeletal development in young adults. Measurements of body density by hydrostatic weighing, body water by deuterium dilution, and bone mineral by whole body DEXA were obtained in 172 young men (n = 91) and women (n = 81). Estimates of body fat (%Fat) from DEXA (%FatDEXA) were highly correlated with estimates of body fat from the four-component model [body density, total body water, and total body mineral (%Fatd,w,m); r = 0.94, standard error of the estimante (SEE) = 2.8% body mass (BM)] with no significant difference between methods [mean of the difference +/- SD of the difference = -0.4 +/- 2.9 (SD) % BM, P = 0.10] in women and men. On the basis of the comparison with %Fatd,w,m, estimates of %FatDEXA were slightly more accurate than those from body density (r = 0.91, SEE = 3.4%; mean of the difference +/- SD of the difference = -1.2 +/- 3.4% BM). Differences between %FatDEXA and %Fatd,w,m were weakly related to body thickness, as reflected by BMI (r = -0.34), and to the percentage of water in the fat-free mass (r = -0.51), but were not affected by race, athletic status, or musculoskeletal development. We conclude that body composition estimates from DEXA are accurate compared with those from a four-component model in young adults who vary in gender, race, athletic status, body size, musculoskeletal development, and body fatness.

Anaerobic capacity and muscle activation during horizontal and uphill running.

Anaerobic capacity as measured by the maximal or peak oxygen deficit is greater during uphill than during horizontal running. The objective of this study was to determine whether the greater peak oxygen deficit determined during uphill compared with horizontal running is related to greater muscle volume or mass activated in the lower extremity. The peak oxygen deficit in 12 subjects was determined during supramaximal treadmill running at 0 and 10% grade. Exercise-induced contrast shifts in magnetic resonance images were obtained before and after exercise and used to determine the percentage of muscle volume activated. The mean peak oxygen deficit determined for uphill running [2.96 +/- 0.63 (SD) liters or 49 +/- 6 ml/kg] was significantly greater (P < 0.05) than for horizontal running (2.45 +/- 0.51 liters or 41 +/- 7 ml/kg) by 21%. The mean percentage of muscle volume activated for uphill running [73.1 +/- 7. 4% (SD)] was significantly greater (P < 0.05) than for horizontal running (67.0 +/- 8.3%) by 9%. The differences in peak oxygen deficit (liters) between uphill and horizontal running were significantly related (y = 8.05 x 10(-4)x + 0.35; r = 0.63, SE of estimate = 0.29 liter, P < 0.05) to the differences in the active muscle volume (cm3) in the lower extremity. We conclude that the higher peak oxygen deficit during uphill compared with horizontal running is due in part to increased mass of skeletal muscle activated in the lower extremity.

Lower extremity muscle activation during horizontal and uphill running.

To provide more comprehensive information on the extent and pattern of muscle activation during running, we determined lower extremity muscle activation by using exercise-induced contrast shifts in magnetic resonance (MR) images during horizontal and uphill high-intensity (115% of peak oxygen uptake) running to exhaustion (2.0-3.9 min) in 12 young women. The mean percentage of muscle volume activated in the right lower extremity was significantly (P <0.05) greater during uphill (73 +/- 7%) than during horizontal (67 +/- 8%) running. The percentage of 13 individual muscles or groups activated varied from 41 to 90% during horizontal running and from 44 to 83% during uphill running. During horizontal running, the muscles or groups most activated were the adductors (90 +/- 5%), semitendinosus (86 +/- 13%), gracilis (76 +/- 20%), biceps femoris (76 +/- 12%), and semimembranosus (75 +/- 12%). During uphill running, the muscles most activated were the adductors (83 +/- 8%), biceps femoris (79 +/- 7%), gluteal group (79 +/- 11%), gastrocnemius (76 +/- 15%), and vastus group (75 +/- 13%). Compared with horizontal running, uphill running required considerably greater activation of the vastus group (23%) and soleus (14%) and less activation of the rectus femoris (29%), gracilis (18%), and semitendinosus (17%). We conclude that during high-intensity horizontal and uphill running to exhaustion, lasting 2-3 min, muscles of the lower extremity are not maximally activated, suggesting there is a limit to the extent to which additional muscle mass recruitment can be utilized to meet the demand for force and energy. Greater total muscle activation during exhaustive uphill than during horizontal running is achieved through an altered pattern of muscle activation that involves increased use of some muscles and less use of others.

Effects of concentric and eccentric training on muscle strength, cross-sectional area, and neural activation.

We compared the effects of concentric (Con) and eccentric (Ecc) isokinetic training on quadriceps muscle strength, cross-sectional area, and neural activation. Women (age 20.0 +/- 0.5 yr) randomly assigned to Con training (CTG; n = 16), Ecc training (ETG; n = 19), and control (CG; n = 19) groups were tested before and after 10 wk of unilateral Con or Ecc knee-extension training. Average torque measured during Con and Ecc maximal voluntary knee extensions increased 18.4 and 12.8% for CTG, 6.8 and 36.2% for ETG, and 4.7 and -1.7% for CG, respectively. Increases by CTG and ETG were greater than for CG (P < 0.05). For CTG, the increase was greater when measured with Con than with Ecc testing. For ETG, the increase was greater when measured with Ecc than with Con testing. The increase by ETG with Ecc testing was greater than the increase by CTG with Con testing. Corresponding changes in the integrated voltage from an electromyogram measured during strength testing were 21.7 and 20.0% for CTG, 7.1 and 16.7% for ETG, and -8.0 and -9.1% for CG. Quadriceps cross-sectional area measured by magnetic resonance imaging (sum of 7 slices) increased more in ETG (6.6%) than in CTG (5.0%) (P < 0.05). We conclude that Ecc is more effective than Con isokinetic training for developing strength in Ecc isokinetic muscle actions and that Con is more effective than Ecc isokinetic training for developing strength in Con isokinetic muscle actions. Gains in strength consequent to Con and Ecc training are highly dependent on the muscle action used for training and testing. Muscle hypertrophy and neural adaptations contribute to strength increases consequent to both Con and Ecc training.

Density of the fat-free mass and estimates of body composition in male weight trainers.

The purpose of this study was to determine whether the assumed density and composition of the fat-free mass (FFM) and estimates of percent fat (%Fat) from body density by use of the Siri equation (%Fatd) are valid in weight trainers with high musculoskeletal development. Measures of body density by underwater weighing (Db), body water by deuterium dilution, and bone mineral by whole body dual-energy X-ray absorptiometry were obtained in young white men: 14 weight trainers with high musculoskeletal development and 14 non-weight-training controls with average musculoskeletal development. %Fatd was significantly higher (P < or = 0.05) than %Fat estimated from body density, water, and mineral (%Fatd,w,m) by use of a four-component model in weight trainers (17.3 +/- 4.6 vs. 13.2 +/- 5.1%) but not in controls (14.8 +/- 3.1 vs. 14.2 +/- 3.6%). The greater discrepancy between %Fatd and %Fatd,w,m was explained by lower density of fat-free mass (Dffm) in weight trainers (1.089 +/- 0.005 g/ml) than in controls (1.099 +/- 0.007 g/ml). The lower Dffm in the weight trainers was due to higher water (74.8 +/- 1.2 vs. 72.6 +/- 20%) and lower mineral (5.3 +/- 0.6 vs. 5.9 +/- 0.4%) and protein (19.9 +/- 1.4 vs. 21.5 +/- 1.9%) fractions of the FFM. We conclude that, in young white men with high musculoskeletal development, Dffm is lower than the assumed value of 1.1 g/ml and %Fat is overestimated from Db by use of the Siri equation.

Effect of the slow-component rise in oxygen uptake on VO2max.

During constant-rate high-intensity (CRHI) exercise lasting longer than 3 min, VO2 has been reported to exceed VO2max measured with a traditional graded exercise test (GXT). This could be because VO2max was not achieved on the GXT or because the factors responsible for the slow-component rise in VO2 alter VO2max. The objective of this study was to test the hypothesis that the slow-component rise in VO2 measured during CRHI running leads to a total VO2 that exceeds VO2max measured during a running GXT. VO2max was determined in eight highly trained individuals using data collected from five grade-incremented, treadmill-running GXT. Each subject demonstrated a definitive plateau of VO2 as a function of exercise intensity. Three VO2max values based on different approaches for representing the VO2max plateau were obtained. Subjects also completed two exhaustive CRHI bouts of treadmill running lasting 7-13 min at speeds estimated from the ACSM equation to elicit an average of 99 +/- 5% VO2max. The mean (+/- SD) VO2peak determined during the CRHI runs (4.17 +/- 0.9 l.min-1) was not different form or less than the three VO2max values (4.19-4.32 +/- 0.09 l.min-1). We conclude that in highly trained individuals, the slow-component rise in VO2 during CRHI treadmill running does not lead to a total VO2 that exceeds the VO2max measured during a running graded exercise test.

Excitation failure in eccentric contraction-induced injury of mouse soleus muscle.

1. Histological evidence suggests that the force deficit associated with eccentric contraction-induced muscle injury is due to structural damage to contractile elements within the muscle fibre. Alternatively, the force deficit could be explained by an inability to activate the contractile proteins. It was the objective of this study to investigate the latter possibility. 2. Mouse soleus muscles were isolated, placed in an oxygenated Krebs-Ringer buffer at 37 degrees C, and baseline measurements were made. The muscle then performed one of three contraction protocols: (1) twenty eccentric (n = 10 muscles); (2) ten eccentric (n = 12); or (3) twenty isometric (n = 10) contractions. At the end of the injury protocol, measurements were made during performance of a passive stretch, twitch and tetanus. Next, force was recorded during exposure of the muscle to buffer containing 50 mM caffeine. 3. Decrements in maximal isometric tetanic force (P0) observed for muscles in the twenty eccentric, ten eccentric, and twenty isometric contraction protocols were 42.6 +/- 4.2, 20.0 +/- 2.3 and 3.9 +/- 2.4%, respectively. However, the caffeine-elicited forces in muscles from the three protocols were not different when corrected for initial differences in P0 (64.9 +/- 1.3, 64.2 +/- 2.1 and 68.9 +/- 2.5% of pre-injury P0). The peak caffeine-elicited force was 118.4 +/- 8.6% of post-injury P0 for the muscles in the twenty eccentric contraction protocol, which was significantly different from that observed for the other protocols (71.8-80.2% post-injury P0). These findings indicate that the force deficit in this muscle injury model results from a failure of the excitation process at some step prior to calcium (Ca2+) release by the sarcoplasmic reticulum. 4. In an attempt to locate the site of failure, intracellular measurements were made in injured muscles to test whether injury to the sarcolemma might have resulted in a shift of the resting membrane potential of the muscle fibre. However, microelectrode measurements of resting membrane potential for muscles in the twenty eccentric contraction protocol (-74.4 +/- 0.6 mV) were not different from muscles in the twenty isometric contraction protocol (-73.4 +/- 1.0 mV). These data suggest that membrane resting conductances were normal and are compatible with the idea that the ability of the injured fibres to conduct action potentials was probably not impaired.