Access to abstract permanently restricted to Ball State community only. / Access to thesis permanently restricted to Ball State community only. / School of Physical Education, Sport, and Exercise Science

We have previously shown that non-specific blockade of the cyclooxygenase (COX) enzymes in skeletal muscle eliminates the normal increase in muscle protein synthesis following resistance exercise. The current study tested the hypothesis that this COX-mediated increase in postexercise muscle protein synthesis is specifically regulated by the COX-2 isoform. Sixteen males (23 ± 1 yr, 177 ± 2 cm, 81.5 ± 3.4 kg) were randomly assigned to one of two groups that received three doses of either a specific COX-2 inhibitor (celecoxib; 200 mg per dose, 600 mg total) or a placebo during the 24 hours following a single bout of resistance exercise with the knee extensors. Skeletal muscle fractional synthesis rate (FSR) was measured at rest and 24 hours postexercise using a primed constant infusion of [2H5]phenylalanine coupled with muscle biopsies of the vastus lateralis. Mixed muscle FSR was increased following exercise to a greater extent (206%, P<0.05) in the COX-2 group (0.052 ± 0.014 %Ih) as compared with the placebo group (0.017 ± 0.007 %Ih). These results suggest that the specific inhibition of the COX-2 isoform in human skeletal muscle causes a compensatory response in muscle protein synthesis. These data also highlight the involvement of the cyclooxygenase pathways in the regulation of muscle protein synthesis following resistance exercise. / School of Physical Education, Sport, and Exercise Science

The purpose of this investigation was to determine the effect of passive and active recovery on the resynthesis of muscle glycogen after high intensity cycle ergometer exercise in untrained subjects. In a cross over design, six college-age males performed three, one min exercise bouts, at 130% V02max with a 4 min rest period between each work bout. Subjects refrained from exercise for two days prior to testing, and consumed a 15% carbohydrate solution (300g sugar in 2000ml of water) the day before each trial to help elevate glycogen concentration. The exercise protocol for each trial was identical, while the recovery following exercise was eitheractive (40-50% VO2max) or passive. The initial muscle glycogen values averaged 144.2 mmol•kg-1 w.w. for the active trial and 158.7 mmol•kg-1 w.w. for the passive trial. Corresponding post-exercise glycogen contents were 97.7 and 106.8 mmol•kg-1 w.w., respectively. These differences were not significant (P>0.05). However, the rate of muscle glycogen resynthesis during passive recovery increased 15 mmol•kg-1 w.w. whereas it decreased 6.27 mmol•kg-1 w.w. following active recovery (P<0.01). Also, the decrease in blood lactate concentration during active recovery was much faster than during passive recovery and significantly different at 10 and 30 min of the recovery period (P<0.01). The major finding of this investigation was that the rate of muscle glycogen resynthesis during passive recovery was significantly greater than that during active recovery. These data suggest that lactate can be used as an endogenous glycogenic precusor in muscle, and that glycogenesis was the prevalent pathway of lactate removal during passive recovery following high intensity cycle ergometer exercise. / Human Performance Laboratory

Collagen content and cross-linking are believed to be major determinants of tendon structural integrity and function. Gender and chronic resistance training have been shown to alter tendon function, and may also alter these key structural features of tendon. Patellar tendon biopsies were taken from untrained men (M, n=8, 25±1 y, 1RM: 53±3 kg), untrained women (W, n=8, 23±2 y, 1RM: 29±2 kg), and resistance-trained (10±1 y trained) men (RTM, n=8, 24±2 y, 1RM: 71 ±6 kg). Biopsies were analyzed for dry mass, collagen content, and collagen cross-linking (hydroxylysylpyridinoline, HP). Tendon dry mass was significantly lower in women than men (M: 376±8, W: 343±5 µg dry mass/mg tendon wet wt, P<0.01), and was not influenced by chronic resistance training (RTM: 364±20 µg dry mass/mg tendon wet wt, P>0.05). The lower tendon dry mass in women reduced (P=0.08) collagen content per tendon wet weight (M: 339±14, W: 306±11 µg collagen/mg tendon wet wt). Collagen content of tendon dry mass was not influenced by gender (P>0.05) or resistance training (P>0.05) (M: 903±38, W: 892±29, RTM: 881±43 !,g collagen/mg tendon dry mass). Similarly, cross-linking of collagen was not impacted by gender (P>0.05) or training (P>0.05) (M: 401±47, W: 418±35, RTM: 424±38 mmol HP/mol collagen). In women, the overall lower amount of collagen per tendon wet weight may explain gender differences in tendon function, while collagen content and cross-linking of the dry mass are remarkably consistent across gender and training status. / School of Physical Education, Sport, and Exercise Science

Age-related bone loss is a serious public health problem affecting 15 to 20 million people in the United States (1). In the last decade, several studies have investigated the effects of repeated bouts of exercise on bone density. Although this increase in bone density is mediated via hormones and/or cellular metabolites few studies have linked the increase in bone density with changes in these hormones or metabolites. Therefore, the purpose of this study was to determine the effect of a single bout of weight bearing exercise on the growth factors that alter bone metabolism. Seven healthy female subjects (age 23 ± 5 yrs.) agreed to participate in this study. A V02 max test was administered to each subject to determine their overall fitness level. A treadmill speed corresponding to 70% of their V02 max was then developed and the subjects ran for 40 minm on the treadmill at that speed. Blood samples were drawn pre and 1, 2, 3, 4, 5, 10, 15, 20, 30, 45, and 60 min post-exercise and assayed for serum growth hormone, calcium, parathyroid hormone, and alkaline phosphatase. No significant change was found in parathyroid hormone, calcium, or alkaline phosphatase serum levels. Growth hormone was found to be significantly decreased 30, 45, and 60 min. post-exercise as compared to pre-exercise levels (7.089, 5.399, 4.728, and 11.28 ng/mL, respectively). While this indicates that exercise may cause a depression in growth hormone levels during recovery, the elevated pre-exercise levels of three of the seven subjects masked the exercise stimulated release of growth hormone. Growth hormone stimulates bone absorption via insulin-like growth factors and the GH data suggests that these hormones may have been released well after our last measurement time point. In conchusion, 40 minutes of running exercise at 70% of V02 max does not produce a change in any of the hormones or metabolic factors directly associated with calcium turnover in the bone, suggesting that acute exercise has no immediate effect on bone metabolism. However, the exercise protocol did stimulate GH release which influences bone growth indirectly by its ability to regulate IGF release. Therefore, even though no acute effects were evident, a single bout of exercise may alter the long term control of bone metabolism. / School of Physical Education

The purpose of this investigation was to comprehensively examine the influence of progressive aerobic exercise training on whole muscle size and function in older women (65-80 yr). Three sedentary, healthy, females (66±1 yrs, 167±2 cm, 70±7 kg) performed 12 weeks of supervised progressive cycle training (42 training sessions 3-4 sessions/week up to 80% HRR). Subjects were tested before and after training for maximum aerobic capacity (VO2max), quadriceps cross sectional area (CSA), whole muscle specific tension, concentric 1-RM, maximum voluntary contraction (MVC), and concentric peak power (wafts). On average, the three subjects improved VO2max (34%), quadriceps CSA (10%), MVC (37%), whole muscle specific tension (25%), and concentric peak power (19%). These positive changes indicate that aerobic exercise may positively influence muscle size and function in the elderly. / School of Physical Education, Sport, and Exercise Science

The aim of this investigation was to compare the acute anabolic and catabolic responses of male and female vastus lateralis (VL) and soleus (SOL) muscles in response to resistance exercise (RE). Muscle biopsies from the VL of 7 males (26±3 y, 75±8 kg) and 7 females (25±3 y, 59±5 kg) were obtained before, and 2 and 6 h after 4 x 7 supine-squat, and 4 x 14 calf-press exercises at maximal effort using inertial ergometry. The mRNA levels of select myogenic (MyoD, myogenin, MRF4), proteolytic (atrogin-1 , MuRF-1), myostatin, and inflammatory (IL-6, -8, -15) genes were quantified using real-time RT-PCR. Male VL vs SOL: The SOL had higher basal mRNA levels of myogenic, proteolytic, and inflammatory genes. After exercise, the myogenic response was similar between the VL and SOL. Both muscles increased MuRF-1 similarly at 2 h, whereas 6 h post-RE proteolytic gene expression (GE) was suppressed in the VL but not in the SOL. The SOL had a reduction in myostatin GE, and a more robust inflammatory response compared to the VL. These findings indicate a more favorable growth response in the VL. Gender comparisons: VL – Basally, the male VL had higher levels of myogenic, proteolytic, myostatin, and inflammatory mRNA compared to the female VL. After exercise, both genders increased myogenic GE similarly. Both genders increased MuRF-1 initially, with females also increasing atrogin-1 and myostatin post-RE. At 6 h, males decreased proteolytic GE to below basal levels. Females also had a greater inflammatory response than males. These findings indicate a greater growth response to RE in the male VL as compared to the female VL. SOL – After exercise, both genders increased myogenic GE in the SOL, but only males increased MyoD expression. Males increased MuRF-1 mRNA but decreased myostatin GE, while females decreased atrogin-1. The inflammatory response was similar between males and females. Despite the modest differences, the net response of the female and male SOL was similar, and indicated a molecular response slightly favorable for growth. / School of Physical Education, Sport, and Exercise Science

Since astronaut time and energy are at a premium, effective countermeasures must be designed to maximize benefits while minimizing time/energy cost. Therefore, our intent was to design and evaluate a low volume, high intensity resistance training program (RTP) on the preservation of knee extensor and plantar flexor size, strength and neuromuscular function in response to unloading. A total of 32 subjects participated. Sixteen men underwent 21 days of unilateral lower limb suspension (ULLS) and were assigned to control (no RTP) (ULLS-CON, n=8) or countermeasures (ULLS-CM, n=8). The remaining subjects were ambulatory for 21 days and were assigned to no RTP (n=8) or countermeasures (n=8). Countermeasure subjects performed RTP every third day during the suspension period (total=6). The RTP consisted of 2 maximal isometric contractions (MVC), 1 set of 10 concentric/eccentric isotonic repetitions, and 1 set to exhaustion, at 80% of 1-repetition maximum (1RM). There was no change in muscle function in ambulatory subjects. Whole muscle cross sectional area (CSA) measured by computed tomography (CT) decreased 7% (thigh) and 7.5% (calf) in ULLS-CON (p<0.05), and was unchanged in ULLS-CM. MVC decreased 16.5% in both quadricep and calf muscles in ULLS-CON (p<0.05) and increased 6% in the quadricep of ULLSCM (p<0.05). Maximal concentric (CNC) and eccentric (ECC) isokinetic strength decreased an average of 18% and 17% in the knee extensors and plantar flexors of ULLS-CON, respectively (p<0.05) and was unchanged in ULLS-CM. 1RM decreased 16% in both quadricep and calf of ULLS-CON (p<0.05) and was unchanged in ULLSCM. Knee extensor work capacity, evaluated during 30 maximal CNC contractions (3.14 rad•sec-'), decreased 18% in ULLS-CON (p<0.05). Neural activation of knee extensors and plantar flexors was measured by electromyography (EMG). Submaximal v.lat, v.med, gast and sol EMG increased in ULLS-CON (p<0.05) and was unaltered in ULLSCM. Maximal EMG decreased 20% and 26% in v.1at and v.med, respectively in ULLSCON (p<0.05). ULLS-CM showed a 15% and 28% increase in v.med and gast maximal EMG (p<0.05). These data suggest knee extensor and plantar flexor muscle size, strength and neuromuscular function were preserved during unloading using a low volume, high intensity RTP performed every third day. / School of Physical Education

No description available.

[Truncated abstract] It is well established that fish, amphibians and reptiles recovering from physical activity of near maximal intensity can replenish completely their muscle glycogen stores in the absence of food. In contrast, the extent to which these stores are replenished under these conditions in humans has been reported in all but one study to be partial. This implies that a few consecutive bouts of intense exercise might eventually lead to the sustained depletion of the muscle glycogen stores in humans if food is unavailable, thus limiting their capacity to engage in fight or flight behaviors unless mechanisms exist to protect muscle glycogen against sustained depletion. The objective of Study 1 was to test this prediction. Eight participants performed three intense exercise bouts each separated by a recovery period of 75 minutes. Although only 53% of muscle glycogen was replenished after the first exercise bout (postexercise and post-recovery glycogen levels of 246 ± 25 and 320 ± 36 mmol.kg-1 dry mass, respectively), all the glycogen mobilised during the second and third bouts was completely replenished during the respective recovery periods, with glycogen reaching levels of 319 ± 29 mmol.kg-1 dry mass after recovery from the third bout. These findings show that humans are not different from other vertebrate species in that there are conditions where humans have the ability to completely replenish without food intake the muscle glycogen mobilised during exercise. The results of our first study raise the intriguing possibility that humans have pre-set muscle glycogen levels that are protected against sustained depletion, with the extent to which muscle glycogen stores are replenished after exercise being dependent on the amount of glycogen required to attain those protected levels. ... During recovery, glycogen levels in the NORM group increased by more than ~50% and reached levels close to those alleged to be protected (189 ± 21 mmol.kg-1 dry mass), whereas no glycogen was deposited in the HCHO group. The sustained post-exercise activation of glycogen synthase, the transient fall in whole body carbohydrate oxidation rate, the increased mobilisation of body proteins, and the prolonged elevation in NEFA levels most probably played important roles in enabling glycogen synthesis in the NORM group. In conclusion, this thesis shows for the first time that there are some conditions (e.g. low pre-exercise muscle glycogen levels) where humans recovering from intense exercise have the capacity, like other species, to replenish completely their muscle glycogen stores from endogenous carbon sources. This study also suggests that humans protect preset levels of muscle glycogen against sustained depletion and at levels high enough to support at least one maximal sprint effort to exhaustion. Evidence is also provided for the existence of a feedback mechanism whereby glycogen below their protected levels mediate the activation of glycogen synthase to restore the depleted muscle glycogen stores back to their protected levels. Our findings, however, leave us with a number of novel unanswered questions which clearly show that the regulation of glycogen metabolism is far from the simple process generally depicted in most textbooks of biochemistry.