Near-infrared spectroscopy estimation of combined skeletal muscle oxidative capacity and O2 diffusion capacity in humans

The final steps of the O2 cascade during exercise depend on the product of the microvascular-tointramyocyte PO2 difference and muscle O2 diffusing capacity (DmO2). Non-invasive methods to determine DmO2 in humans are currently unavailable. Muscle oxygen uptake (mVO2) recovery rate constant (k), measured by near-infrared spectroscopy (NIRS) using intermittent arterial occlusions, is associated with muscle oxidative capacity in vivo. We reasoned that k would be limited by DmO2 when muscle oxygenation is low (kLOW), and hypothesized that: i) k in well-oxygenated muscle (kHIGH) is associated with maximal O2 flux in fiber bundles; and ii) Δk (kHIGH-kLOW) is associated with capillary density (CD). Vastus lateralis k was measured in 12 participants using NIRS after moderate exercise. The timing and duration of arterial occlusions were manipulated to maintain tissue saturation index (TSI) within a 10% range either below (LOW) or above (HIGH) half-maximal desaturation, assessed during sustained arterial occlusion. Maximal O2 flux in phosphorylating state was 37.7±10.6 pmol·s−1·mg−1 (~5.8 ml·min−1·100g−1). CD ranged 348 to 586 mm-2. kHIGH was greater than kLOW (3.15±0.45 vs 1.56±0.79 min-1, p\u3c0.001). Maximal O2 flux was correlated with kHIGH (r=0.80, p=0.002) but not kLOW (r=-0.10, p=0.755). Δk ranged -0.26 to -2.55 min-1, and correlated with CD (r=- 0.68, p=0.015). mVO2 k reflects muscle oxidative capacity only in well-oxygenated muscle. Δk, the difference in k between well- and poorly-oxygenated muscle, was associated with CD, a mediator of DmO2. Assessment of muscle k and Δk using NIRS provides a non-invasive window on muscle oxidative and O2 diffusing capacity

Effects of a 24-week same-session combined endurance and strength training program on physical performance and serum hormone levels in recreational endurance runners

Combining endurance (E) and strength (S) loadings into the same training session might be an efficient time-saving strategy for endurance runners that want further develop performance thanks to the benefits obtained by adding strength training. However, performing strength training repeatedly after prolonged runs may generate a superior degree of stress on both neuromuscular and endocrine systems that, especially at high training frequencies, may compromise long-term strength training adaptations. This, in turn, might have important implications on endurance running performance. This study investigated the longitudinal changes in the acute responses to a same-session combined endurance and strength training and their influence on the long-term physical performance and serum hormone levels in recreational endurance runners. Eleven male recreational endurance runners (32±5 years) completed a 24-week periodized combined training program consisting in 2 combined endurance and strength training sessions (E+S) and 3-4 endurance-only training sessions per week. Basal measurements of endurance performance (Vpeak, blood lactate at submaximal running speed), neuromuscular performance (MVC, 1RM, F500ms, CMJ) and endocrine function (testosterone, cortisol, GH, TSH and SHBG) were performed in the first week of training (week 0), after 12 weeks (week 12) and at the end of the training period (week 24) under controlled conditions. Acute neuromuscular and hormonal response to the combined training session and early recovery phase were also assessed in the same weeks of basal measurements with a specifically-designed training session, before E (PRE), after E (MID), after E+S (POST) and after 24 and 48 h of recovery. The combined training session lead to significant (p<0.05) decreases at POST in neuromuscular performance (MVC, F500ms and CMJ) both at week 0 and 24 but not in power capacity (F500ms, CMJ) at week 12. Significant (p<0.05) increases occurred in testosterone, cortisol, GH at MID at week 0, 12 and 24, however, a longitudinal reduction was observed in the acute cortisol and TSH response at POST during the intervention period. Whereas MVC, F500ms and CMJ were recovered at 24 h, cortisol and TSH remained (although not always significantly) depressed at 24 and 48 h at week 0, 12 and 24. No long-term improvements in neuromuscular performance were detected during the study period. Significant increases in Vpeak (p<0.01) and blood lactate at 15 km h-1 (p<0.05) occurred in the last 12 weeks of training. Significant correlations were observed between F500ms at MID and Vpeak (r=0.663, p<0.05) and F500ms at MID and blood lactate at 15 km h-1 (r=-0.673, p<0.05) but only at week 12. The present study confirmed that, training strength always after endurance may lead to an augmented stress to the endocrine system that may take several days to recover. Despite minor adaptations, this training design may impede strength and power development, counteracting the benefits of strength training on endurance performance

Effects of different high-intensity interval training prescription models on physiological response and performance in trained distance runners

158 p.Esta tesis aborda varias preguntas abiertas sobre los efectos de los diferentes modelos de prescripción de entrenamiento en intervalos de alta intensidad (HIIT) con la respuesta fisiológica y el rendimiento en corredores de fondo entrenados. La prescripción de entrenamiento de HIIT generalmente se realiza usando un enfoque empírico común y estandarizado, en el que los corredores de un nivel similar entrenan juntos usando el mismo esquema HIIT. Sin embargo, estudios previos mostraron que es posible enfocarse en algunas adaptaciones fisiológicas individualizando las prescripciones de HIIT acorde con las características fisiológicas de los corredores y sus respuestas al ejercicio. Esto puede estar relacionado al mayor tiempo pasado en (o cerca del) V̇ O2max y, por lo tanto, al estímulo cardiorrespiratorio más fuerte que se produce con este modelo de prescripción de entrenamiento. Dado que, en el enfoque estandarizado, en el que la velocidad es la misma para todos, los corredores que caen fuera del rango de intensidad deseado pueden producirse menores ganancias (o nulas) en la aptitud cardiorrespiratoria, se puede observar un efecto promedio de grupo más pequeño junto con una mayor heterogeneidad del efecto de entrenamiento

Differences in acute physiological response and chronic adaptations according to the type of intensity setting

This is the pre-registration of the experimental study entitled "Differences in acute physiological response and chronic adaptations according to the type of intensity setting", which aims to test several hypotheses on the effects of using two different methods (heart rate and speed) to control exercise intensity on acute physiological response and chronic adaptations in healthy adults

Myths and methodologies: The use of equivalence and non-inferiority tests for interventional studies in exercise physiology and sport science

Exercise physiology and sport science have traditionally made use of the null hypothesis of no difference to make decisions about experimental interventions. In this article, we aim to review current statistical approaches typically used by exercise physiologists and sport scientists for the design and analysis of experimental interventions and to highlight the importance of including equivalence and non-inferiority studies, which address different research questions from deciding whether an effect is present. Initially, we briefly describe the most common approaches, along with their rationale, to investigate the effects of different interventions. We then discuss the main steps involved in the design and analysis of equivalence and non-inferiority studies, commonly performed in other research fields, with worked examples from exercise physiology and sport science scenarios. Finally, we provide recommendations to exercise physiologists and sport scientists who would like to apply the different approaches in future research. We hope this work will promote the correct use of equivalence and non-inferiority designs in exercise physiology and sport science whenever the research context, conditions, applications, researchers’ interests or reasonable beliefs justify these approaches

Effects of endurance training only versus same-session combined endurance and strenth training on physical performance and serum hormone concentrations in recreational endurance runners

This study investigated the effects of endurance training only (E, n = 14) and same-session combined training, when strength training is repeatedly preceded by endurance loading (endurance and strength training (E+S), n = 13) on endurance (1000-m running time during incremental field test) and strength performance (1-repetition maximum (1RM) in dynamic leg press), basal serum hormone concentrations, and endurance loading-induced force and hormone responses in recreationally endurance-trained men. E was identical in the 2 groups and consisted of steady-state and interval running, 4–6 times per week for 24 weeks. E+S performed additional mixed-maximal and explosive-strength training (2 times per week) immediately following an incremental running session (35–45 min, 65%–85% maximal heart rate). E and E+S decreased running time at week 12 (–8% ± 5%, p = 0.001 and –7% ± 3%, p < 0.001) and 24 (–13% ± 5%, p < 0.001 and –9% ± 5%, p = 0.001). Strength performance decreased in E at week 24 (–5% ± 5%, p = 0.014) but was maintained in E+S (between-groups at week 12 and 24, p = 0.014 and 0.011, respectively). Basal serum testosterone and cortisol concentrations remained unaltered in E and E+S but testosterone/sex hormone binding globulin ratio decreased in E+S at week 12 (–19% ± 26%, p = 0.006). At week 0 and 24, endurance loading-induced acute force (–5% to –9%, p = 0.032 to 0.001) and testosterone and cortisol responses (18%–47%, p = 0.013 to p < 0.001) were similar between E and E+S. This study showed no endurance performance benefits when strength training was performed repeatedly after endurance training compared with endurance training only. This was supported by similar acute responses in force and hormonal measures immediately post-endurance loading after the training with sustained 1RM strength in E+S

Near‐infrared spectroscopy estimation of combined skeletal muscle oxidative capacity and O2 diffusion capacity in humans

The final steps of the O2 cascade during exercise depend on the product of the microvascular-to-intramyocyte PO2${P}_{{{\rm{O}}}_{\rm{2}}}$ difference and muscle O2 diffusing capacity ( DmO2$D{{\rm{m}}}_{{{\rm{O}}}_2}$ ). Non-invasive methods to determine DmO2$D{{\rm{m}}}_{{{\rm{O}}}_2}$ in humans are currently unavailable. Muscle oxygen uptake (m V̇O2${\dot{V}}_{{{\rm{O}}}_{\rm{2}}}$ ) recovery rate constant (k), measured by near-infrared spectroscopy (NIRS) using intermittent arterial occlusions, is associated with muscle oxidative capacity in vivo. We reasoned that k would be limited by DmO2$D{{\rm{m}}}_{{{\rm{O}}}_2}$ when muscle oxygenation is low (kLOW ), and hypothesized that: (i) k in well oxygenated muscle (kHIGH ) is associated with maximal O2 flux in fibre bundles; and (ii) ∆k (kHIGH &nbsp;-&nbsp;kLOW ) is associated with capillary density (CD). Vastus lateralis k was measured in 12 participants using NIRS after moderate exercise. The timing and duration of arterial occlusions were manipulated to maintain tissue saturation index within a 10% range either below (LOW) or above (HIGH) half-maximal desaturation, assessed during sustained arterial occlusion. Maximal O2 flux in phosphorylating state was 37.7&nbsp;±&nbsp;10.6 pmol&nbsp;s-1 &nbsp;mg-1 (∼5.8&nbsp;ml&nbsp;min-1 &nbsp;100&nbsp;g-1 ). CD ranged 348 to 586&nbsp;mm-2 . kHIGH was greater than kLOW (3.15&nbsp;±&nbsp;0.45 vs. 1.56&nbsp;±&nbsp;0.79&nbsp;min-1 , P &lt; 0.001). Maximal O2 flux was correlated with kHIGH (r&nbsp;=&nbsp;0.80, P&nbsp;=&nbsp;0.002) but not kLOW (r&nbsp;=&nbsp;-0.10, P&nbsp;=&nbsp;0.755). Δk ranged -0.26 to -2.55&nbsp;min-1 , and correlated with CD (r&nbsp;=&nbsp;-0.68, P&nbsp;=&nbsp;0.015). m V̇O2${\dot{V}}_{{{\rm{O}}}_{\rm{2}}}$ k reflects muscle oxidative capacity only in well oxygenated muscle. ∆k, the difference in k between well and poorly oxygenated muscle, was associated with CD, a mediator of DmO2$D{{\rm{m}}}_{{{\rm{O}}}_2}$ . Assessment of muscle k and ∆k using NIRS provides a non-invasive window on muscle oxidative and O2 diffusing capacity. KEY POINTS: We determined post-exercise recovery kinetics of quadriceps muscle oxygen uptake (m V̇O2${\dot{V}}_{{{\rm{O}}}_{\rm{2}}}$ ) measured by near-infrared spectroscopy (NIRS) in humans under conditions of both non-limiting (HIGH) and limiting (LOW) O2 availability, for comparison with biopsy variables. The m V̇O2${\dot{V}}_{{{\rm{O}}}_{\rm{2}}}$ recovery rate constant in HIGH O2 availability was hypothesized to reflect muscle oxidative capacity (kHIGH ) and the difference in k between HIGH and LOW O2 availability (∆k) was hypothesized to reflect muscle O2 diffusing capacity. kHIGH was correlated with phosphorylating oxidative capacity of permeabilized muscle fibre bundles (r&nbsp;=&nbsp;0.80). ∆k was negatively correlated with capillary density (r&nbsp;=&nbsp;-0.68) of biopsy samples. NIRS provides non-invasive means of assessing both muscle oxidative and oxygen diffusing capacity in vivo

Altered leukocyte response to CXCL12 in patients with Warts Hypogammaglobulinemia, Infections, Myelokathexis (WHIM) syndrome

The chemokine receptor CXCR4 and its functional ligand, CXCL12, are essential regulators of development and homeostasis of hematopoietic and lymphoid organs. Heterozygous truncating mutations in the CXCR4 intracellular tail cause a rare genetic disease known as WHIM syndrome (warts, hypogammaglobulinemia, infections, myelokathexis), whose pathophysiology remains unclear. We report CXCR4 function in 3 patients with WHIM syndrome carrying heterozygous truncating mutations of CXCR4. We show that CXCR4 gene mutations in WHIM patients do not affect cell surface expression of the chemokine receptor and its internalization upon stimulation with CXCL12. Moreover, no significant differences in calcium mobilization in response to CXCL12 are found. However, the chemotactic response of both polymorphonuclear cells and T lymphocytes in response to CXCL12 is increased. Furthermore, immunophenotypic analysis of circulating T and B lymphocytes reveals a decreased number of memory B cells and of naive T cells and an accumulation of effector memory T cells associated with a restricted T-cell repertoire. Based on our results, we suggest that the altered leukocyte response to CXCL12 may account for the pathologic retention of mature polymorphonuclear cells in the bone marrow (myelokathexis) and for an altered lymphocyte trafficking, which may cause the immunophenotyping abnormalities observed in WHIM patients

Altered leukocyte response to CXCL12 in patients with warts hypogammaglobulinemia, infections, myelokathexis (WHIM) syndrome

AbstractThe chemokine receptor CXCR4 and its functional ligand, CXCL12, are essential regulators of development and homeostasis of hematopoietic and lymphoid organs. Heterozygous truncating mutations in the CXCR4 intracellular tail cause a rare genetic disease known as WHIM syndrome (warts, hypogammaglobulinemia, infections, myelokathexis), whose pathophysiology remains unclear. We report CXCR4 function in 3 patients with WHIM syndrome carrying heterozygous truncating mutations of CXCR4. We show that CXCR4 gene mutations in WHIM patients do not affect cell surface expression of the chemokine receptor and its internalization upon stimulation with CXCL12. Moreover, no significant differences in calcium mobilization in response to CXCL12 are found. However, the chemotactic response of both polymorphonuclear cells and T lymphocytes in response to CXCL12 is increased. Furthermore, immunophenotypic analysis of circulating T and B lymphocytes reveals a decreased number of memory B cells and of naive T cells and an accumulation of effector memory T cells associated with a restricted T-cell repertoire. Based on our results, we suggest that the altered leukocyte response to CXCL12 may account for the pathologic retention of mature polymorphonuclear cells in the bone marrow (myelokathexis) and for an altered lymphocyte trafficking, which may cause the immunophenotyping abnormalities observed in WHIM patients. (Blood. 2004;104:444-452