Intermittent low dose carbon monoxide inhalation does not influence glucose regulation in overweight adults: a randomized controlled crossover trial.

NEW FINDINGS: What is the central question of this study? Low dose carbon monoxide (CO) inhalation plays a role in regulating proteins involved in glucose metabolism; does low dose CO improve glucose and insulin responses to an oral glucose tolerance test in overweight adults? What is the main finding and its importance? Five days of intermittent CO inhalation does not alter the glucose or insulin responses to ingestion of a glucose bolus in overweight adults. Low dose CO is utilized in various physiological assessment procedures; these findings allow researchers and clinicians to utilize these procedures without concern of altering glucose metabolism. ABSTRACT: Low dose carbon monoxide (CO) inhalation upregulates several proteins important for glucose metabolism. Such changes could be clinically significant and may be relevant to those who use CO as a research tool. We hypothesized that low dose CO inhalation would improve glucose and insulin responses to an oral glucose bolus in overweight humans. Eleven young adults (5 men, 6 women; body mass index: 25-35 kg m-2 ) were included in this randomized, placebo-controlled, single-blinded crossover study. Following screening, participants completed two 7-day protocols with a 4-week washout. Twenty-four hours prior to and following five consecutive days of either once daily CO (men: 1.2 ml (kg body mass)-1 ; women: 1.0 ml (kg body mass)-1 ) or placebo (room air) inhalation, participants underwent oral glucose tolerance tests (OGTT). For key outcome variables, there were no significant main effects or interactions across condition or time point (mean ± SD), including fasting glucose (mg dl-1 : pre-placebo: 85.2 ± 10.1; post-placebo: 82.9 ± 10.6; pre-CO: 83.6 ± 7.7; post-CO: 84.0 ± 9.0), 2 h post glucose (mg dl-1 : pre-placebo: 100.9 ± 20.0; post-placebo: 98.7 ± 13.1; pre-CO: 94.2 ± 23.2; post-CO: 94.4 ± 14.9), or the Matsuda index (pre-placebo: 16.1 ± 11.5; post-placebo: 20.3 ± 24.7; pre-CO: 15.6 ± 15.3; post-CO: 17.5 ± 16.8). In conclusion, 5 days of low dose CO administration did not influence glucose and insulin responses to an OGTT in overweight adults. Low dose CO inhalation is utilized in a variety of physiological assessment procedures; these findings allow researchers to utilize these procedures without concern of altering glucose metabolism.

Estimating Energy Expenditure using Individualized, Power-Specific Gross Efficiencies.

Our purpose was to determine if using an individual's power-specific gross efficiency improves the accuracy of estimating energy expenditure from cycling power. 30 subjects performed a graded cycling test to develop 4 gross efficiencies: individual power-specific gross efficiencies, a group mean power-specific gross efficiency, individual fixed gross efficiencies, and a group mean fixed gross efficiency. Energy expenditure was estimated from power using these different gross efficiencies and compared to measured energy expenditure during moderate- and hard-intensity constant-power and 2 variable-power cycling bouts. Estimated energy expenditures using individual or group mean power-specific gross efficiencies were not different from measured energy expenditure across all cycling bouts (p>0.05). To examine the intra-individual variability of the estimates, absolute difference scores (absolute value of estimated minus measured energy expenditure) were compared, where values closer to zero represent more accurate individual estimates. The absolute difference score using individual power-specific gross efficiencies was significantly lower compared to the other gross efficiencies across all cycling bouts (p<0.01). Significant and strong correlations (r≥0.97, p<0.001) were found across all cycling bouts between estimated and measured energy expenditures using individual power-specific gross efficiencies. In conclusion, using an individual's power-specific gross efficiency significantly improves their energy expenditure estimate across different power outputs.

Ten Days of Intermittent, Low-dose Carbon Monoxide Inhalation does not Significantly Alter Hemoglobin Mass, Aerobic Performance Predictors, or Peak-power Exercise Tolerance.

Carbon monoxide (CO) rebreathing procedures are used to assess hemoglobin mass (Hbmass) but recent evidence suggests that CO is a signaling molecule that may alter physiological functions. We examined the effects of 10 days of intermittent, low-dose CO inhalation on Hbmass, aerobic performance predictors, and peak-power exercise tolerance. 18 recreationally-active men were randomized to either CO or placebo inhalation groups in a single-blind, pre-post parallel-groups trial. Primary outcomes were assessed before and after an intervention period during which subjects inhaled a bolus of 1.2 ml kg(-1) CO or placebo (room air) for 30 s, once per day on 10 days over a 12-day period. Cycling tests were performed >16 h following CO inhalation to exclude acute effects of CO exposure. CO inhalation elevated carboxyhemoglobin by 4.4±0.4% (mean±SD) following each exposure. Compared to placebo, chronic CO inhalation did not significantly alter Hbmass (p=0.99), peak oxygen uptake (p=0.59), peak power output (p=0.10), submaximal oxygen uptake (p=0.91), submaximal RER (p=0.22), lactate threshold (p=0.65), or peak-power exercise tolerance (p=0.60). In conclusion, our data support the ability to perform repeated measurements of Hbmass using CO rebreathing over a 12-day period without altering physiological responses.

Acute, Low-dose CO Inhalation does not Alter Energy Expenditure during Submaximal Exercise.

Carbon monoxide, a gas known most widely for its toxic effects at high doses, is receiving increased attention for its role as a physiological signaling molecule and potential therapeutic agent when administered in low doses. We sought to quantify any changes to oxygen consumption and energy expenditure during submaximal exercise after low-dose CO inhalation. 9 active individuals completed 4 graded submaximal exercise tests, with each test occurring during a separate visit. For their first exercise test, subjects inhaled CO or room air (1.2 mL·kg(-1) body mass) in a randomized, subject-blind fashion. A second test was repeated 24 h later when the inhaled gas should have cleared the system. Subjects repeated study procedures with the alternate dose after a washout period of at least 2 days. Low-dose CO administration did not affect oxygen consumption or energy expenditure during submaximal exercise immediately or 24 h following its administration. Increases in heart rate, blood [lactate], and perceived exertion were observed following acute CO inhalation but these effects were absent after 24 h. The results of this study suggest that low-dose CO administration does not influence the energetics of submaximal exercise, but it acutely increases the relative intensity associated with absolute workloads below the lactate threshold.

Plasma matrix metalloproteinase-9 response to downhill running in humans.

Matrix metalloproteinase-9 is a proteolytic enzyme capable of degrading proteins of the muscle extracellular matrix. Systemic levels of MMP-9 or its inhibitor, tissue inhibitor of metalloproteinase-1 (TIMP-1), have the potential to serve as blood markers of exercise-induced muscle damage. The purpose of this study was to determine if an eccentrically-dominated task, downhill running (DHR), produces changes in plasma MMP-9 or TIMP-1 and examine the relationship between MMP-9/TIMP-1 levels and indirect indicators of muscle damage. Subjects were sedentary (SED, n=12) or had a history of concentrically-biased training (CON, n=9). MMP-9 and TIMP-1 were measured before (Pre-Ex), immediately after (Post-Ex), and 1-, 2-, 4-, and 7-days post-DHR (-10°), and compared to discomfort ratings, creatine kinase activity and strength loss. At 1-day Post-Ex, discomfort increased (5.6 ± 7.8 to 45.5 ± 19.9 mm; 0-100 mm scale), strength decreased (-6.9 ± 1.6%) and CK increased (162.9 ± 177.2%). MMP-9 was modestly but significantly increased at Post-Ex in both CONC and SED (32.7 ± 33.6%) and at 4-days in SED (66.9 ± 88.1%), Individual responses were variable, however. There were no correlations between MMPs and discomfort ratings, plasma CK or strength. While plasma MMP-9 changes may be detectable in the systemic circulation after DHR, they are small and do not correspond to other markers of damage.

Exercise efficiency of low power output cycling.

Exercise efficiency at low power outputs, energetically comparable to daily living activities, can be influenced by homeostatic perturbations (e.g., weight gain/loss). However, an appropriate efficiency calculation for low power outputs used in these studies has not been determined. Fifteen active subjects (seven females, eight males) performed 14, 5-min cycling trials: two types of seated rest (cranks vertical and horizontal), passive (motor-driven) cycling, no-chain cycling, no-load cycling, cycling at low (10, 20, 30, 40 W), and moderate (50, 60, 80, 100, 120 W) power outputs. Mean delta efficiency was 57% for low power outputs compared to 41.3% for moderate power outputs. Means for gross (3.6%) and net (5.7%) efficiencies were low at the lowest power output. At low power outputs, delta and work efficiency values exceeded theoretical values. In conclusion, at low power outputs, none of the common exercise efficiency calculations gave values comparable to theoretical muscle efficiency. However, gross efficiency and the slope and intercept of the metabolic power vs mechanical power output regression provide insights that are still valuable when studying homeostatic perturbations.

Plasma volume during weight lifting.

The magnitude and pattern of the hematocrit (Hct), hemoglobin (Hb), and plasma volume (PV) responses during and upon recovery from two resistance training protocols based on either a ten-repetition maximum (10 RM) or five-repetition maximum (5 RM) resistance was examined. Twelve college-aged male resistance exercise trainers were equally divided between the protocols and performed at least four workouts prior to testing to determine the 10 RM or 5 RM for each exercise set. Each protocol included three sets of nine exercises. The 10-RM session used one-minute rest periods between sets, and two minutes between exercises. The 5-RM session employed three-minute rest periods between sets and exercises. A catheter inserted in the forearm allowed for venous blood sampling after twenty minutes supine rest, the last set of each exercise, and at fifteen and thirty minutes of recovery. Control conditions were included for posture (P) and limb motion (U). Loaded exercise (L) was significantly different from U and P controls for Hct, Hb, and PV responses. For 10 RM and 5 RM respectively, the mean change from rest was 6.2 (+/- 0.9) and 3.5 (+/- 0.4) % for Hct, 2.2 (+/- 0.2) and 1.2 (+/- 0.1) gm . dl (-1) for Hb, and - 22.6 (+/- 2.3) and - 13.0 (+/- 1.2) % for PV. The main effect for protocol was significant for Hct (p = 0.0006) and Hb (p = 0.0033), with 10-RM changes being greater than 5 RM. The greatest increase in Hct and Hb occurred after the first set for both protocols. An increase in Hct and Hb during the protocol was observed for the 10 RM, but not the 5 RM. During recovery, Hct and Hb were elevated above rest for 10 RM, but not 5 RM. PV decreases mirrored Hct and Hb in pattern of change and significance. The data demonstrate that magnitude and pattern of Hct, Hb, and PV was dependent on the type of resistance training protocol.

Skeletal muscle adaptations in response to voluntary wheel running in myosin heavy chain null mice.

10.1152/ japplphysiol.00832.2001.-To examine the effects of gene inactivation on the plasticity of skeletal muscle, mice null for a specific myosin heavy chain (MHC) isoform were subjected to a voluntary wheel-running paradigm. Despite reduced running performance compared with nontransgenic C57BL/6 mice (NTG), both MHC IIb and MHC IId/x null animals exhibited increased muscle fiber size and muscle oxidative capacity with wheel running. In the MHC IIb null animals, there was no significant change in the percentage of muscle fibers expressing a particular MHC isoform with voluntary wheel running at any time point. In MHC IId/x null mice, wheel running produced a significant increase in the percentage of fibers expressing MHC IIa and MHC I and a significant decrease in the percentage of fibers expressing MHC IIb. Muscle pathology was not affected by wheel running for either MHC null strain. In summary, despite their phenotypes, MHC null mice do engage in voluntary wheel running. Although this wheel-running activity is lessened compared with NTG, there is evidence of distinct patterns of muscle adaptation in both null strains.

Commercial porters of eastern Nepal: health status, physical work capacity, and energy expenditure.

The purpose of the study was to compare full-time hill porters in eastern Nepal with part-time casual porters engaged primarily in subsistence farming. The 50 porters selected for this study in Kenja (elevation 1,664 m) were young adult males of Tibeto-Nepali origin. Following standardized interviews, anthropometry, and routine physical examinations, the porters were tested in a field laboratory for physiological parameters associated with aerobic performance. Exercise testing, using a step test and indirect calorimetry, included a submaximal assessment of economy and a maximal-effort graded exercise test. Energy expenditure was measured in the field during actual tumpline load carriage. No statistically significant differences were found between full-time and part-time porters with respect to age, anthropometric characteristics, health, nutritional status, or aerobic power. Mean VO2 peak was 2.38 +/- 0.27 L/min (47.1 +/- 5.3 ml/kg/min). Load-carrying economy did not differ significantly between porter groups. The relationship between VO2 and load was linear over the range of 10-30 kg with a slope of 9 +/- 4 ml O2/min per kg of load. During the field test of actual work performance, porters expended, on average, 348 +/- 68 kcal/hr in carrying loads on the level and 408 +/- 60 kcal/hr in carrying loads uphill. Most porters stopped every 2 min, on average, to rest their loads briefly on T-headed resting sticks (tokmas). The technique of self-paced, intermittent exercise together with the modest increase in energy demands for carrying increasingly heavier loads allows these individuals to regulate work intensity and carry extremely heavy loads without creating persistent medical problems.

Cardiac and skeletal muscle adaptations to voluntary wheel running in the mouse.

In this paper, we describe the effects of voluntary cage wheel exercise on mouse cardiac and skeletal muscle. Inbred male C57/Bl6 mice (age 6-8 wk; n = 12) [corrected] ran an average of 4.3 h/24 h, for an average distance of 6.8 km/24 h, and at an average speed of 26.4 m/min. A significant increase in the ratio of heart mass to body mass (mg/g) was evident after 2 wk of voluntary exercise, and cardiac atrial natriuretic factor and brain natriuretic peptide mRNA levels were significantly increased in the ventricles after 4 wk of voluntary exercise. A significant increase in the percentage of fibers expressing myosin heavy chain (MHC) IIa was observed in both the gastrocnemius and the tibialis anterior (TA) by 2 wk, and a significant decrease in the percentage of fibers expressing IIb MHC was evident in both muscles after 4 wk of voluntary exercise. The TA muscle showed a greater increase in the percentage of IIa MHC-expressing fibers than did the gastrocnemius muscle (40 and 20%, respectively, compared with 10% for nonexercised). Finally, the number of oxidative fibers as revealed by NADH-tetrazolium reductase histochemical staining was increased in the TA but not the gastrocnemius after 4 wk of voluntary exercise. All results are relative to age-matched mice housed without access to running wheels. Together these data demonstrate that voluntary exercise in mice results in cardiac and skeletal muscle adaptations consistent with endurance exercise.

Treatment of exercise-induced muscle injury via hyperbaric oxygen therapy.

PURPOSE: This study examined the role of hyperbaric oxygen therapy (HBO) in the treatment of exercise-induced muscle injury. METHODS: 21 college-aged male volunteers were assigned to three groups: control, immediate HBO (iHBO), and delayed HBO (dHBO). All subjects performed 6 sets (10 repetitions per set) of eccentric repetitions with a load equivalent to 120% of their concentric maximum. HBO treatments consisted of 100-min exposure to 2.5 ATA and 100% oxygen with intermittent breathing of ambient air (30 min at 100% O2, 5 min at 20.93% O2). HBO treatments began either 2 (iHBO) or 24 h (dHBO) postexercise and were administered daily through day 4 postexercise. Forearm flexor cross-sectional area (CSA) and T2 relaxation time via magnetic resonance imaging (MRI) were assessed at baseline, 2, 7, and 15 d postinjury. Isometric strength and rating of perceived soreness of the forearm flexors were assessed at baseline, 1, 2, 3, 4, 7, and 15 d postinjury. Serum creatine kinase (CK) was assessed on day 0 and on days 1, 2, 7, and 15 postinjury. RESULTS: Mean baseline CSA values were: 2016.3, 1888.5, and 1972.2 mm2 for control, iHBO, and dHBO, respectively. All groups showed significant increases in CSA in response to injury (21% at 2 d, 18% at 7 d) (P < 0.0001), but there were no significant differences between groups (P = 0.438). Mean baseline T2 relaxation times were: 26.18, 26.28, and 27.43 msec for control, iHBO, and dHBO, respectively. Significant increases in T2 relaxation time were observed for all groups (64% at 2 d, 66% at 7 d, and 28% at 15 d) (P < 0.0001), but there were no significant differences between groups (P = 0.692). Isometric strength (P < 0.0001), serum CK levels (P = 0.0007), and rating of perceived soreness (P < 0.0001) also indicated significant muscle injury for all groups, but there were no differences between groups (P = 0.459, P = 0.943, and P = 0.448, respectively). CONCLUSION: These results suggest that hyperbaric oxygen therapy was not effective in the treatment of exercise-induced muscle injury as indicated by the markers evaluated.

Mutation of the IIB myosin heavy chain gene results in muscle fiber loss and compensatory hypertrophy.

The fast skeletal IIb gene is the source of most myosin heavy chain (MyHC) in adult mouse skeletal muscle. We have examined the effects of a null mutation in the IIb MyHC gene on the growth and morphology of mouse skeletal muscle. Loss in muscle mass of several head and hindlimb muscles correlated with amounts of IIb MyHC expressed in that muscle in wild types. Decreased mass was accompanied by decreases in mean fiber number, and immunological and ultrastructural studies revealed fiber pathology. However, mean cross-sectional area was increased in all fiber types, suggesting compensatory hypertrophy. Loss of muscle and body mass was not attributable to impaired chewing, and decreased food intake as a softer diet did not prevent the decrease in body mass. Thus loss of the major MyHC isoform produces fiber loss and fiber pathology reminiscent of muscle disease.

Acute and chronic hormonal responses to resistance training designed to promote muscle hypertrophy.

Acute and chronic hormonal responses to resistance training were evaluated in 11 college men who completed 12 weeks (33 sessions) of high volume resistance training. No differences in resting concentrations of growth hormone (GH), insulin-like growth factor-I, testosterone, or sex hormone-binding globulin occurred from pre- and posttraining in the trained vs. nontrained control group. However, cortisol (c) decreased 17% for both groups (p < 0.05). There were no differences in exercise-induced responses between Sessions 10 and 20, with all hormone concentrations increasing (p < 0.05) from pre- at mid- and post exercise session. However, after correction for plasma volume decreases, only C and GH showed differences, with C increased from mid- to postsession (48% 10th; 49% 20th), and GH increased from pre- at mid- and postsession for both sessions 10 (0.16 +/- 0.42 pre; 4.77 +/- 6.24 mid; 6.26 +/- 5.19 post; microg x L-1) and 20 (0.33 +/- 0.85 pre; 5.42 +/- 9.08 mid; 8.24 +/- 7.61 post; microg x L-1). Significant correlations (p< 0.05) existed only between absolute mean GH increases from presession and the degree of muscle fiber hypertrophy for type I (r = 0.70 mid, 0.74 post) and type II (r = 0.71 post) fibers. In conclusion, resistance training had no effect on resting serum hormone concentrations, whereas similar acute exercise responses occurred between the 10th and 20th training sessions.

Bone mineral density and body composition of the United States Olympic women's field hockey team.

OBJECTIVE: To evaluate total bone mineral density (BMD) and body composition (% fat) in world class women field hockey players, members of the 1996 United States Olympic team. METHODS: Whole body BMD (g/cm2) and relative body fatness (% fat) were assessed by dual energy x ray absorptiometry using a Lunar DPX-L unit with software version 1.3z. Body composition was also estimated by hydrostatic weighing and the sum of seven skinfolds. RESULTS: Mean (SD) BMD was 1.253 (0.048) g/cm2 which is 113.2 (4.0)% of age and weight adjusted norms. Estimates of body composition from the three methods were similar (statistically non-significant): 16.1 (4.4)% fat from dual energy x ray absorptiometry, 17.6 (3.2)% from hydrostatic weighing, and 16.9 (2.6)% from the sum of seven skinfolds. Mean fat free mass was approximately 50 kg. CONCLUSIONS: The mean whole body BMD value for members of the 1996 United States Olympic women's field hockey team is one of the highest reported for any women's sports team. Moreover, the mean fat free mass per unit height was quite high and % fat was low. In this group of world class sportswomen, low % fat was not associated with low BMD.

Sample size required for the accurate determination of fiber area and capillarity of human skeletal muscle.

This study aimed to determine the skeletal muscle fiber sample size required for a reliable, valid representation of an individual's average fiber area and capillary contacts (CC) per fiber. Biopsies were obtained from the biceps brachii of 11 college-age, recreational resistance-trained men in conjunction with a study investigating how muscle morphology changed after 12 weeks of resistance training. The effect of additional measurements on the rolling cumulative means for fiber area and CC per fiber was evaluated using sequential estimation analysis. Results showed that group cumulative mean and standard deviation had stabilized by 50 fiber measurements per individual for type I and II fibers and CC per fiber. Significant correlations (.96-.99; p < .05) existed between the 50th and 95th/100th cumulative individual means. These results indicate that a typical skeletal muscle needle biopsy would be sufficient to characterize type I and II fiber areas and CC per fiber of an individual in most subject populations, although the required sample size for characterizing fiber subtypes might be different.

Myosin heavy chains IIa and IId are functionally distinct in the mouse.

Myosin in adult murine skeletal muscle is composed primarily of three adult fast myosin heavy chain (MyHC) isoforms. These isoforms, MyHC-IIa, -IId, and -IIb, are >93% identical at the amino acid level and are broadly expressed in numerous muscles, and their genes are tightly linked. Mice with a null mutation in the MyHC-IId gene have phenotypes that include growth inhibition, muscle weakness, histological abnormalities, kyphosis (spinal curvature), and aberrant kinetics of muscle contraction and relaxation. Despite the lack of MyHC-IId, IId null mice have normal amounts of myosin in their muscles because of compensation by the MyHC-IIa gene. In each muscle examined from IId null mice, there was an increase in MyHC-IIa- containing fibers. MyHC-IIb content was unaffected in all muscles except the masseter, where its expression was extinguished in the IId null mice. Cross-sectional fiber areas, total muscle cross-sectional area, and total fiber number were affected in ways particular to each muscle. Developmental expression of adult MyHC genes remained unchanged in IId null mice. Despite this universal compensation of MyHC-IIa expression, IId null mice have severe phenotypes. We conclude that despite the similarity in sequence, MyHC-IIa and -IId have unique roles in the development and function of skeletal muscle.

Energy expenditure estimates of the Caltrac accelerometer for running, race walking, and stepping.

OBJECTIVE: To examine the accuracy of the Caltrac accelerometer for estimating energy expenditure (EE) during three exercise modes. METHODS: A subset of 31 women (mean (SEM) age 22.6 (5) years) as selected from a training study comparing various physiological parameters during race walking, running, and stepping. Subjects each performed mode specific graded exercise tests to peak VO2. Regression equations for VO2 v heart rate (HR) were generated from each individual's test data. EE (kcal and kJ) was estimated for each VO2 value based on the respiratory exchange ratio, and kcal v HR regression equations were generated to predict EE from each subject's HR data (EE-HR). HR in the field was monitored by telemetry, and two Caltrac monitors, one set for EE and one to give counts, were attached to a belt over opposite hips. RESULTS: EE-HR was not significantly different across exercise modes. Caltrac overestimated EE (P < 0.01) in runners (14%) and walkers (19%) but underestimated EE in steppers by about 10% (P = 0.12). CONCLUSIONS: The Caltrac is a reliable instrument but it did not accurately distinguish EE in running, race walking, or stepping in a group of young women.

Muscle fiber hypertrophy, hyperplasia, and capillary density in college men after resistance training.

Twelve male subjects with recreational resistance training backgrounds completed 12 wk of intensified resistance training (3 sessions/wk; 8 exercises/session; 3 sets/exercise; 10 repetitions maximum/set). All major muscle groups were trained, with four exercises emphasizing the forearm flexors. After training, strength (1-repetition maximum preacher curl) increased by 25% (P < 0.05). Magnetic resonance imaging scans revealed an increase in the biceps brachii muscle cross-sectional area (CSA) (from 11.8 +/- 2.7 to 13.3 +/- 2.6 cm2; n = 8; P < 0.05). Muscle biopsies of the biceps brachii revealed increases (P < 0.05) in fiber areas for type I (from 4,196 +/- 859 to 4,617 +/- 1,116 microns2; n = 11) and II fibers (from 6,378 +/- 1,552 to 7,474 +/- 2,017 microns2; n = 11). Fiber number estimated from the above measurements did not change after training (293.2 +/- 61.5 x 10(3) pretraining; 297.5 +/- 69.5 x 10(3) posttraining; n = 8). However, the magnitude of muscle fiber hypertrophy may influence this response because those subjects with less relative muscle fiber hypertrophy, but similar increases in muscle CSA, showed evidence of an increase in fiber number. Capillaries per fiber increased significantly (P < 0.05) for both type I (from 4.9 +/- 0.6 to 5.5 +/- 0.7; n = 10) and II fibers (from 5.1 +/- 0.8 to 6.2 +/- 0.7; n = 10). No changes occurred in capillaries per fiber area or muscle area. In conclusion, resistance training resulted in hypertrophy of the total muscle CSA and fiber areas with no change in estimated fiber number, whereas capillary changes were proportional to muscle fiber growth.

Alterations in oxygen consumption during and between bouts of level and downhill running.

Since the etiology of the drift in VO2 during downhill running is unclear, this study was designed to assess the contribution of heart rate (HR), ventilation (VE), blood lactate, rectal temperature (RT), muscle damage, and several variables that have not previously been included in VO2 drift research: muscle temperature (MT), and stride rate (SR) and length (SL), to the drift in VO2. Six subjects participated in a 45-min level run (LEVEL) and two 45-min downhill runs (DOWN1 and DOWN2) at 50% VO2max. Although VO2 increased significantly over time for all bouts, the magnitude [4.3% (LEVEL), 5.4% (DOWN1), and 8.1% (DOWN2)] did not differ between bouts (P > 0.05). VO2 was significantly lower during DOWN2 than during LEVEL and DOWN1 (P < 0.05). MT increased during the three bouts (P < 0.05) but the change over time was not different between bouts. SR and SL did not change over time within each bout nor between the two downhill runs. Muscle damage, as indicated by serum creatine kinase levels and perceived soreness, was less following LEVEL and DOWN2 than DOWN1 (P < 0.05). HR and RT increased over time (P < 0.05) but did not differ between bouts. VE and blood lactate did not differ over time or between bouts. VO2 drift during the three bouts paralleled changes in RT, MT, and HR but appears unrelated to muscle damage or biomechanical factors.

Walking and running energy expenditure estimated by Caltrac and indirect calorimetry.

The purpose of this study was to examine the accuracy of the Caltrac personal activity computer during walking and running. Ten women and 10 men walked at speeds of 2-5 mph and ran at speeds of 4-8 mph on a horizontal treadmill. Two Caltrac monitors were attached over opposite hips: one programed to give caloric expenditure and the other to give Caltrac counts. Oxygen uptake was measured simultaneously. Significant correlations were found during walking between Caltrac estimated and actual energy expenditure (r = 0.91) and between activity counts and net exercise VO2.kg-1 (r = 0.87). However, the Caltrac significantly overestimated energy cost during horizontal walking at speeds above 2 mph. Although there was a significant correlation between Caltrac estimated and actual energy expenditure during running (r = 0.71), the correlation between Caltrac counts and net exercise VO2.kg-1 was not significant (r = 0.29). There was no significant increase in Caltrac kcal or counts with increased running speed between 5 and 8 mph. It is concluded that the Caltrac is a valid indicator of physical activity during walking but does not adequately discriminate between running speeds of 5-8 mph.