Effects of short term dietary nitrate supplementation on energy metabolism during isokinetic knee muscle contractions

textThe purpose of this study was to investigate whether 3 days of dietary nitrate supplementation has positive effects on exercise performance and energy metabolism at rest and during strenuous knee exercise, and exercise recovery. The experimental protocol was a double blind, placebo-controlled, two-period, and within-subjects design. Fourteen healthy nonsmoking males (22.71 ± 0.72yr, 72.93 ± 2.35kg, and 47.67 ± 1.56 ml/kg/min VO2max) participated in the study. Two supplements (nitrate lozenge; NO-L or placebo; PLA) were orally administrated randomly at 48 and 24 hours before each trial day and again 40 minutes before each exercise trial. Total work, peak torque, and respiratory gases were automatically collected during repeated knee extensions/flexions (isokinetic concentric contractions with dominant leg; 4 sets of 28 repetitions at 180°/sec with 30 sec rest intervals) and recovery (6 contractions of 1 repetition maximum with 120 vii sec between contractions). For these results, peak torque, rate of fatigue, work efficiency, and rate of recovery were calculated. Blood specimens were collected at rest before and after the treatment, post exercise, and end of recovery to track the changes in blood glucose and lactate concentrations. There was a significant inverse correlation for total work during knee extension exercise and oxygen consumption (PLA: r = -.560 and NO-L: r = -.546; p < .01, respectively). During the exercise, RER was significantly higher for PLA compared with NO-L (PLA: 1.42 ± 0.02 vs. NO-L: 1.38 ± 0.02: p = .03). Work within each set and total work performed were higher for NO-L, but these differences were not significant. However, NO-L enhanced exercise efficiency by 3.3% when compared with PLA (PLA: 2497.5 ± 134.56 ft-lb/L/min vs. NO-L: 2578.7 ± 132.24 ftlb/L/min; p = .05). Extensor peak torque recovery rate slope was not significant, but meaningfully faster for NO-L (PLA: 2.39 ± 0.52% vs. NO-L: 3.06 ± 0.54%; p = .09) and significant interaction effect (p = .02) was found during recovery contractions, especially from contractions 2 to 3 (p = .03). It is also worth noting that differences in time to peak torque during knee extension exercise for NO-L and PLA approached significances (PLA: 0.213 ± 0.01 sec vs. NO-L: 0.200 ± 0.01 sec; p = .08). The results suggest that 3 days of dietary nitrate supplementation improves rate of exercise recovery and enhances work efficiency during vigorous resistance exercise.Kinesiology and Health EducationMaterials Science and Engineerin

Impact of Heat Therapy on Skeletal Muscle Structure and Function

Skeletal muscle occupies approximately 40 to 50 percent of body mass and is responsible for respiration, postural control, and locomotion and plays a pivotal role in regulating glucose, lipid, and protein metabolism. Acute muscle trauma and chronic disease conditions such as muscular dystrophies are associated with structural abnormalities, enhanced fatigability and impaired metabolism and consequently lead to exercise intolerance and poor quality of life. Despite the clinical importance and a number of studies on the treatment of muscle damage, few modalities have shown to elicit beneficial effects. Heat treatment has been used for a long time to treat soft tissue injuries in the field of physical therapy and sports medicine. However, the underlying mechanisms by which heat treatment accelerates muscle recovery following injury are not clear. The primary aim of my dissertation studies was to determine the impact of heat therapy on skeletal muscle structure and function in humans and animals. In Chapter 2, we report that a single session of local heat treatment promotes the expression of angiogenic and myogeneic mediators including vascular endothelial growth factor (VEGF) and angiopoietin 1(ANGPT1) in healthy human skeletal muscle. In Chapter 3, we report repeated exposure to heat therapy stimulates factors involved in muscle repair process and accelerates functional recovery from exercise-induced muscle damage. In Chapter 4, we show that 8 weeks of local heat therapy improves muscle strength of knee extensor and increases skeletal muscle capillarization in type II muscle fibers. In Chapter 5, we describe the effects of heat therapy in a mouse model of ischemia induced-muscle damage. Animals that were exposed to heat therapy at 39°C had improved maximal absolute force and relative muscle mass in the soleus muscle. These observations reveal that the beneficial effects of heat therapy are muscle fiber type specific and dependent on the treatment temperature. In Chapter 6, we review and summarize the outcomes described in Chapters 2-5 and provide a general conclusion as well the clinical implications of our findings

Skeletal Muscle Mitochondrial Dysfunction and Oxidative Stress in Peripheral Arterial Disease: A Unifying Mechanism and Therapeutic Target

Peripheral artery disease (PAD) is caused by atherosclerosis in the lower extremities, which leads to a spectrum of life-altering symptomatology, including claudication, ischemic rest pain, and gangrene requiring limb amputation. Current treatments for PAD are focused primarily on re-establishing blood flow to the ischemic tissue, implying that blood flow is the decisive factor that determines whether or not the tissue survives. Unfortunately, failure rates of endovascular and revascularization procedures remain unacceptably high and numerous cell- and gene-based vascular therapies have failed to demonstrate efficacy in clinical trials. The low success of vascular-focused therapies implies that non-vascular tissues, such as skeletal muscle and oxidative stress, may substantially contribute to PAD pathobiology. Clues toward the importance of skeletal muscle in PAD pathobiology stem from clinical observations that muscle function is a strong predictor of mortality. Mitochondrial impairments in muscle have been documented in PAD patients, although its potential role in clinical pathology is incompletely understood. In this review, we discuss the underlying mechanisms causing mitochondrial dysfunction in ischemic skeletal muscle, including causal evidence in rodent studies, and highlight emerging mitochondrial-targeted therapies that have potential to improve PAD outcomes. Particularly, we will analyze literature data on reactive oxygen species production and potential counteracting endogenous and exogenous antioxidants