Characterization of inflammatory responses to eccentric exercise in humans.

Detaljert om betennelser og immunceller etter hard trening, relatert til DOMS.

http://www.ncbi.nlm.nih.gov/pubmed/16385845

http://www.medizin.uni-tuebingen.de/transfusionsmedizin/institut/eir/content/2005/64/article.pdf

Abstract

Eccentric exercise commonly results in muscle damage. The primary sequence of events leading to exercise-induced muscle damage is believed to involve initial mechanical disruption of sarcomeres, followed by impaired excitation-contraction coupling and calcium signaling, and finally, activation of calcium-sensitive degradation pathways. Muscle damage is characterized by ultrastructural changes to muscle architecture, increased muscleproteins and enzymes in the bloodstream, loss of muscular strength and range of motion and muscle soreness. The inflammatory response to exercise-induced muscle damage is characterized by leukocyte infiltration and production of pro-inflammatory cytokines within damaged muscle tissue, systemic release of leukocytes and cytokines, in addition to alterations in leukocyte receptor expression and functional activity. Current evidence suggests that inflammatory responses to muscle damage are dependent on the type of eccentric exercise, previous eccentric loading (repeated bouts), age and gender. Circulating neutrophil counts and systemic cytokine responses are greater after eccentric exercise using a large muscle mass (e.g. downhill running, eccentric cycling) than after other types of eccentric exercise involving a smaller muscle mass. After an initial bout of eccentric exercise, circulating leukocyte counts and cell surface receptor expression are attenuated. Leukocyte and cytokine responses to eccentric exercise are impaired in elderly individuals, while cellular infiltration into skeletal muscle is greater in human females than males after eccentric exercise. Whether alterations in intracellular calcium homeostasis influence inflammatory responses to muscle damage is uncertain. Furthermore, the effects of antioxidant supplements are variable, and the limited data available indicates that anti-inflammatory drugs largely have no influence on inflammatory responses to eccentric exercise. In this review, we compare local versus systemic inflammatory responses, and discuss some of the possible mechanisms regulating the inflammatory responses to exercise-induced muscle damage in humans.

Delayed onset muscle soreness : treatment strategies and performance factors.

Denne inneholder alt om DOMS. Nevner 6 foreslåtte årsaker, og at det sannsynligvis er en blanding av flere av dem hver gang: melkesyre, muskelkrampe, vevskade, muskelskade, betennelse og enzymeffluks teorier.

http://www.ncbi.nlm.nih.gov/pubmed/12617692

ftp://192.195.81.82/AiDisk_b1/MCD%20E-BOOKS/Personal%20Interest/WORKOUT/Delayed%20Onset%20Muscle%20Soreness.pdf

Abstract

Delayed onset muscle soreness (DOMS) is a familiar experience for the elite or novice athlete. Symptoms can range from muscle tenderness to severe debilitating pain. The mechanisms, treatment strategies, and impact on athletic performance remain uncertain, despite the high incidence of DOMS. DOMS is most prevalent at the beginning of the sporting season when athletes are returning to training following a period of reduced activity. DOMS is also common when athletes are first introduced to certain types of activities regardless of the time of year. Eccentric activities induce micro-injury at a greater frequency and severity than other types of muscle actions. The intensity and duration of exercise are also important factors in DOMS onset. Up to six hypothesised theories have been proposed for the mechanism of DOMS, namely: lactic acid, muscle spasm, connective tissue damage,muscle damage, inflammation and the enzyme efflux theories. However, an integration of two or more theories is likely to explain muscle soreness. DOMS can affect athletic performance by causing a reduction in joint range of motion, shock attenuation and peak torque. Alterations in muscle sequencing and recruitment patterns may also occur, causing unaccustomed stress to be placed on muscle ligaments and tendons. These compensatory mechanisms may increase the risk of further injury if a premature return to sport is attempted.A number of treatment strategies have been introduced to help alleviate the severity of DOMS and to restore the maximal function of the muscles as rapidly as possible. Nonsteroidal anti-inflammatory drugs have demonstrated dosage-dependent effects that may also be influenced by the time of administration. Similarly, massage has shown varying results that may be attributed to the time of massage application and the type of massage technique used. Cryotherapy, stretching, homeopathy, ultrasound and electrical current modalities have demonstrated no effect on the alleviation of muscle soreness or other DOMS symptoms. Exercise is the most effective means of alleviating pain during DOMS, however the analgesic effect is also temporary. Athletes who must train on a daily basis should be encouraged to reduce the intensity and duration of exercise for 1-2 days following intense DOMS-inducing exercise. Alternatively, exercises targeting less affected body parts should be encouraged in order to allow the most affected muscle groups to recover. Eccentric exercises or novel activities should be introduced progressively over a period of 1 or 2 weeks at the beginning of, or during, the sporting season in order to reduce the level of physical impairment and/or training disruption. There are still many unanswered questions relating to DOMS, and many potential areas for future research.

Treating Diabetes with Exercise – Focus on the Microvasculature

Veldig viktig studie som nevner at det ikke finnes glatt muskulatur i kapillærene, så det er arteriolene som avgjør blodsirkulasjonen i kapillærene. His blodsirkulasjonen i en arteriole blir dårlig stopper sirkulasjonen opp i et område av muskelen som serveres av kapillærene.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4000229

Abstract

The rising incidence of diabetes and the associated metabolic diseases including obesity, cardiovascular disease and hypertension have led to investigation of a number of drugs to treat these diseases. However, lifestyle interventions including diet and exercise remain the first line of defense. The benefits of exercise are typically presented in terms of weight loss, improved body composition and reduced fat mass, but exercise can have many other beneficial effects. Acute effects of exercise include major changes in blood flow through active muscle, an active hyperemia that increases the delivery of oxygen to the working muscle fibers. Longer term exercise training can affect the vasculature, improving endothelial health and possibly basal metabolic rates. Further, insulin sensitivity is improved both acutely after a single bout of exercise and shows chronic effects with exercise training, effectively reducing diabetes risk. Exercise-mediated improvements in endothelial function may also reduce complications associated with both diabetes and other metabolic disease. Thus, while drugs to improve microvascular function in diabetes continue to be investigated, exercise can also provide many similar benefits on endothelial function and should remain the first prescription when treating insulin resistance and diabetes. This review will investigate the effects of exercise on the blood vessel and the potential benefits of exercise on cardiovascular disease and diabetes.

At rest, a low proportion of capillaries are exposed to blood flow at one time, with a rapid increase in the number of perfused capillaries after exercise [31], thus increasing functional capillary density.

Vascular smooth muscle cells are located around the arterioles and some venules, and can constrict to change blood flow patterns, while capillaries do not typically contribute to blood flow changes [30] (Figure 1). Blood flow through capillaries is controlled upstream by small arterioles at rest, and the rapid recruitment of unperfused capillaries by exercise could suggest that nerves are responsible for this action [34]. The sympathetic nervous system is mainly responsible for the vasoconstrictor responses, and as the arterioles and larger vessels are innervated [38] the majority of sympathetic nervous system activity is localized to that area of the vascular tree. Physical exercise can enhance sympathetic nerve activity [39] to maintain arterial pressure, and may be involved in maintaining exercise tolerance, as reviewed by Thomas and Segal [38].

Structural differences between artery, arteriole and capillary. No vascular smooth muscle is located on the capillary; therefore flow through capillaires is modified by pre-capillary arterioles. Cessation of flow through arterioles will prevent flow through a portion of the muscle.

Insulin relies on endothelium-dependent vasodilation to enhance perfusion, thus endothelial dysfunction reduces insulin-mediated increases in muscle perfusion, which can contribute to the metabolic deficit in diabetes. As exercise-mediated changes in perfusion are typically endothelium-independent, exercise is still able to recruit capillaries and thus increase muscle perfusion in obesity and type 2 diabetes, even in the face of endothelial dysfunction. Numerous studies have now shown that while insulin’s vascular effects may be blocked in diabetes, exercise still maintains its ability to increase the distribution of blood flow through muscle [42].

Nitric oxide (NO) is the main vasodilator from the endothelium specifically involved in blood flow and blood distribution, and while reduction in nitric oxide synthesis lowered total blood flow, exercise-mediated capillary recruitment was not affected [46]. In fact, inhibition of NO formation enhances both resting and exercise-mediated muscle oxygen uptake [47]; despite a reduction in total flow, microvascular flow was not affected, suggesting that NO is not involved in the vascular response to exercise.

The distribution of blood through muscle increases the capacity for nutrient exchange. In exercise the primary purpose of functional hyperemiais for oxygen delivery, as the oxygen required by exercising muscle is much higher than resting muscle (reviewed in [37]). Recruitment of capillaries can decrease the velocity of blood flow by increasing the cross-sectional area of the capillary bed and the time available for exchange. Recruitment also increases surface area for exchange and decreases perfusion distances to promote oxygen delivery to tissues with exercise [34] (Figure 2). While in exercise the main metabolite required at the working muscle is oxygen, distribution of other nutrients can also be affected, including glucose, fats, other hormones and cytokines. Muscle metabolism can therefore be altered by perfusion of the tissue [48,49]. While there can be regulated transport of certain larger hormones across the vasculature [50,51], smaller molecules can diffuse across the endothelium easily, possibly making muscle perfusion a more important player in the delivery of glucose and oxygen to the tissue.

Vasodilation affects delivery, and thus metabolism. The rate of transfer across the endothelium is dependent on surface area, permeability of the endothelium, diffusion distance, and concentration difference (Fick’s first law of diffusion). Vasodilation increases surface area in arterioles for exchange, but will also recruit downstream capillaries, which will reduce diffusion distance and increase surface area for exchange. Working muscle increases oxygen utilization, increasing the concentration difference from the blood vessel to the tissue.

Mitochondrial dysfunction has been proposed to be both a cause [72] and a consequence [73] of insulin resistance, and may contribute to endothelial dysfunction [74]. If oxygen delivery is a component of mitochondrial health and biogenesis, it is possible that impaired perfusion may contribute to fiber type switching, where an oxidative fiber, which is typically highly vascularized and contains mitochondria, switches to a glycolytic fiber with less vascularity and mitochondria. As exercise can improve oxidative capacity, increase mitochondria content [75], and also increase muscle perfusion [31,32,34,45,76], the relationship between muscle perfusion, fiber type and mitochondrial function needs to be clarified.

The vascular component of exercise may well be linked to the reduction of diabetic complication such as retinopathy, peripheral neuropathy and nephropathy, as there is a vascular basis to many of these complications. The endothelium has been implicated in diabetic nephropathy [88], and the blood vessels formed in response to reduced perfusion in retinopathy show abnormal structure and function [89].

Microvascular Perfusion Changes in the Contralateral Gastrocnemius Following Unilateral Eccentric Exercise

Spennende studie som nevner at blodsirkulasjonen øker i området som har stølhet. Og den økte blodsirkulasjonen vedvarer i mer enn 48 timer etter treningen. I dette tilfellet i leggen som ble trent. De mener det er pga økt betennelse i muskelen.

http://omicsgroup.org/journals/microvascular-perfusion-changes-in-the-contralateral-gastrocnemius-following-unilateral-eccentric-exercise-2165-7025-3-163.php?aid=16679

 

There was a significant main effect for time for blood volume (p=0.023) and blood flow (p=0.010), with no significant difference in blood flow velocity (p=0.316). There were significant increases in blood volume (p=0.001) and blood flow (p<0.001) immediately postexercise (9.77 ± 3.19 dB and 3.53 ± 0.86 dB/sec), respectfully in the contralateral limb compared to baseline (6.18 ± 2.05 dB and 2.40 ± 0.69), with no change in blood flow velocity (p=0.487). The effect size for blood volume was 1.34 (0.09, 2.60) and blood flow was 1.41 (0.15, 2.68). The increases in contra lateral blood volume (p=0.002) and blood flow (p=0.003) were maintained at 48 hours (9.41 ± 1.90 dB and 3.51 ± 0.47 dB/sec) compared to baseline, with again no change in blood flow velocity (p=0.411). The effect size for blood volume was 1.62 (0.32, 2.92) and blood flow was 1.86 (0.51, 3.22). There were no changes in blood volume (p=0.814), blood flow (p=0.962), or blood flow velocity (p=0.493) between post-exercise and 48 hours for the contra lateral limb.

Following eccentric exercise to a single limb, the contralateral limb resulted in increased blood volume and blood flow immediately after exercise and at 48 hours post exercise. From previous research in our lab [12] immediately after eccentric exercise, blood volume and blood flow increased in the exercise leg by 42% and 80%, respectfully. From this study, the contra lateral leg increased 17% and 35% for blood volume and blood flow, respectfully. This finding supports earlier work by Seals [7] and Taylor et al. [8] that identified vasodilatation of the contra lateral limb after exercise initiation. Blood flow velocity did not change in the contra lateral limb after exercise and at 48 hours. Since this limb was not exercised, recruitment of capillaries is not necessary, as would be in exercised muscle [14].

Eccentric exercise increased microvascular perfusion immediately after exercise in the contralateral limb, which had not been examined before. The increased perfusion was maintained over 48 hours, so the prolonged increased in perfusion of the contralateral limb may have been due to an inflammatory response or the extra demands placed on the contralateral limb for support during walking.

Differential blood flow responses to CO2 in human internal and external carotid and vertebral arteries

Denne viser hvordan CO2-responsen er litt forskjellige i forskjellige blodkar. Den er sterkere i blodkar inni hjernen enn i blodkar i kraniet, ansiktet og ryggraden. Blodkar i ryggraden har større respons enn blodkar i ansiktet, men mindre respons enn blodkar i hjernen.

http://jp.physoc.org/content/590/14/3277.long

Because of methodological limitations, almost all previous studies have evaluated the response of mean blood flow velocity (Vmean) in the middle cerebral artery (MCA) to changes in CO2 as a measure of CO2 reactivity across the whole brain (Aaslid et al. 1989Ainslie & Duffin, 2009Ainslie & Ogoh, 2009).

 

ICA, VA and BA CO2 reactivity was significantly higher during hypercapnia than during hypocapnia (ICA, P < 0.01; VA, P < 0.05; BA, P < 0.05), but ECA and MCA were not significantly different.

The major finding from the present study was that cerebral CO2 reactivity was significantly lower in the VA and its distal artery (BA) than in the ICA and its distal artery (MCA). These findings indicate that vertebro-basilar circulation has lower CO2 reactivity than internal carotid circulation. Our second major finding was that ECA blood flow was unresponsive to hypocapnia and hypercapnia, suggesting that CO2 reactivity of the external carotid circulation is markedly diminished compared to that of the cerebral circulation. These findings suggest that different CO2 reactivity may explain differences in CBF responses to physiological conditions (i.e. dynamic exercise and orthostatic stress) across areas in the brain and/or head.

Hypercapnic cerebral CO2 reactivity in global CBF was greater than the hypocapnic reactivity (Ide et al. 2003) (Table 3). The mechanisms underlying this greater reactivity to hypercapnia compared with hypocapnia may be related to a greater influence of vasodilator mediators on intracranial vascular tone compared with vasoconstrictive mediators (Toda & Okamura, 1998Ainslie & Duffin, 2009). In humans, Peebles et al.(2008) recently reported that, during hypercapnia, there is a large release of nitric oxide (NO) from the brain, whereas this response was absent during hypocapnia.

The difference in CO2 reactivity between vertebro-basilar territories (VA and BA) and the cerebral cortex (ICA and MCA) may be due to diverse characteristics of vasculature, e.g. regional microvascular density (Sato et al. 1984), basal vascular tone (Ackerman, 1973Haubrich et al. 2004Reinhard et al. 2008), autonomic innervation (Edvinsson et al. 1976Hamel et al. 1988) and regional heterogeneity in ion channels or production of NO (Iadecola & Zhang, 1994Gotoh et al. 2001).

Interestingly, the response of the ECA to changes in CO2 may be similar to other peripheral arteries. It has long been appreciated that the vasodilatory effect of hypercapnia is much more profound in cerebral than in peripheral vasculature, particularly leg (Lennox & Gibbs, 1932Ainslie et al. 2005) and brachial arteries (Miyazaki, 1973). These findings suggest that control of CO2 is particularly important in the cerebral circulation. The high resting metabolic requirements of the brain, compared with that of other vasculature, might be one reason why this circulatory arrangement is desirable (Ainslie et al. 2005). Specifically, high CO2 reactivity may be a way for the brain to match metabolism with flow (Ainslie et al. 2005).

Lower CO2reactivity in the vertebro-basilar system may be important for maintaining central respiratory function because Graphic in central chemoreceptors is regulated by Graphic and blood flow to maintain breathing stability.

In summary, our study shows that cerebral CO2 reactivity in the vertebro-basilar circulation is lower than that in the internal carotid circulation, while CO2 reactivity in the external carotid circulation is much lower compared with two other cerebral arteries. These findings indicate a difference in cerebral CO2 reactivity between different circulatory areas in the brain and head, which may explain different CBF responses to physiological stress. Lower CO2 reactivity in the vertebro-basilar system may be beneficial for preserving blood flow to the medulla oblongata to maintain vital systemic functions, while higher CO2 reactivity in the internal carotid system may imply a larger tolerance for varied blood flow in the cerebral cortex.

Preventing overtraining in athletes in high-intensity sports and stress/recovery monitoring

Nevner de fleste faktorene rundt restitusjon. Og legger vekt på at idrettsutøvere er under-restituert heller enn over-trent. Beskriver spørreskjemaet RESTQ-Sport som kan brukes til å følge med på restitusjonseffekten hos en idrettsutøver.

http://onlinelibrary.wiley.com/doi/10.1111/j.1600-0838.2010.01192.x/full

The key defining features are

  • Recovery is a process in time and is dependent on the type of and duration of stress.
  • Recovery depends on a reduction of stress, a change of stress, or a break from stress.
  • Recovery is specific to the individual and depends on individual appraisal.
  • Recovery can be passive, active, or pro-active.
  • Recovery is closely tied to situational conditions.

Furthermore, Kellmann und Kallus (2001) defined recovery as

an inter-individual and intra-individual multi-level (e.g., psychological, physiological, social) process in time for the re-establishment of performance abilities. Recovery includes an action-oriented component, and those self-initiated activities (proactive recovery) can be systematically used to optimize situational conditions and to build up and refill personal resources and buffers (p. 22).

This definition also demonstrates the complexity of recovery, as discussed in more detail by Kellmann (2002a), and highlights the need to individually tailor recovery activities.

The RESTQ-Sport consists of 77 items (19 scales with four items each plus one warm-up item), which the participants answer retrospectively. A Likert-type scale is used with values ranging from 0 (never) to 6 (always) indicating how often the respondent participated in various activities during the past 3 days/nights. High scores in the stress-associated activity scales reflect intense subjective stress, whereas high scores in the recovery-oriented scales indicate good recovery activities.

The RESTQ-Sport consists of seven general stress scales (General Stress, Emotional Stress, Social Stress, Conflicts/Pressure, Fatigue, Lack of Energy, Physical Complaints), five general recovery scales (Success, Social Recovery, Physical Recovery, General Well-being, Sleep Quality), three sport-specific stress scales (Disturbed Breaks, Emotional Exhaustion, Injury), and four sport-specific recovery scales (Being in Shape, Personal Accomplishment, Self-Efficacy, Self-Regulation). Examples of items would be: “In the past (3) days/nights … my body felt strong” (for the scale Being in Shape) or “In the past (3) days/nights … I had a satisfying sleep” (for the scale Sleep Quality).

When talking to coaches, it appears easier to frame the current topic as underrecovery rather than overtraining. It is the coaches’ job to train athletes at the optimal level (which is often at the limit); however, they should also avoid overtraining. Coaches may be much more receptive to working with the concept of underrecovery because it acknowledges that underrecovery can also be due to factors, which are outside of their control. The diagnosis of overtraining and underrecovery, should be determined only by an interdisciplinary team that is able and willing to share the data to allow for a comprehensive assessment of the athlete. To optimize this process, the consultation of athletes should be conducted in consultation with coaches, sport physicians, and sport psychologists. Consequently, all physiological and psychological data, as well as training and performance data should be shared on an interdisciplinary basis (Kellmann, 2002a; Smith & Norris, 2002). Assessment should include a complete training documentation, the assessment of subjective and objective physiological and psychological data, and the integration of an athletes’ perspective. It is important that psychological testing like lactate testing, also be part of the regular training routine. Furthermore, research in sport psychology should systematically focus on psychological interventions, which help to optimize the recovery process, ideally in combination with physiological interventions.

Is recovery driven by central or peripheral factors? A role for the brain in recovery following intermittent-sprint exercise

Nevner svært mye spennende om stølhet (DOMS). Spesielt om hvor mye central sensitering har å si, og mye om hydrering (vann). Samt alt om betennelser og andre faktorer knyttet til DOMS. Sier bl.a. at glucogenlagre normaliseres etter 24 timer uavhengig av hva man spiser, men glykogen omsetningen i kroppen er begrenset i 2-3 dager etter. Nevner også at det er alle de perifere faktorene, sammen med de sentrale, som tilsammen skaper DOMS tilstanden.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3909945/

Abstract

Prolonged intermittent-sprint exercise (i.e., team sports) induce disturbances in skeletal muscle structure and function that are associated with reduced contractile function, a cascade of inflammatory responses, perceptual soreness, and a delayed return to optimal physical performance. In this context, recovery from exercise-induced fatigue is traditionally treated from a peripheral viewpoint, with the regeneration of muscle physiology and other peripheral factors the target of recovery strategies. The direction of this research narrative on post-exercise recovery differs to the increasing emphasis on the complex interaction between both central and peripheral factors regulating exercise intensity during exercise performance. Given the role of the central nervous system (CNS) in motor-unit recruitment during exercise, it too may have an integral role in post-exercise recovery. Indeed, this hypothesis is indirectly supported by an apparent disconnect in time-course changes in physiological and biochemical markers resultant from exercise and the ensuing recovery of exercise performance. Equally, improvements in perceptual recovery, even withstanding the physiological state of recovery, may interact with both feed-forward/feed-back mechanisms to influence subsequent efforts. Considering the research interest afforded to recovery methodologies designed to hasten the return of homeostasis within the muscle, the limited focus on contributors to post-exercise recovery from CNS origins is somewhat surprising. Based on this context, the current review aims to outline the potential contributions of the brain to performance recovery after strenuous exercise.

recovery strategies might be broadly differentiated as being either physiological (e.g., cryotherapy, hydrotherapy, massage, compression, sleep), pharmacological (e.g., non-steroidal anti-inflammatory medications) or nutritional (e.g., dietary supplements), all mean to limit continued post-exercise disturbances and inflammatory events within the exercised muscle cells. This peripheral focus emphasizes the importance of an accelerated return of structural integrity and functional capacity from below the neuromuscular junction.

Conceptually, if the brain is held as central to the process of performance declines (i.e., fatigue), it stands to reason that it would also have some role in post-exercise recovery (De Pauw et al., 2013).

Classically defined as an exercise-induced reduction in force generating capacity of the muscle, fatigue may be attributed to peripheral contractile failure, sub-optimal motor cortical output (supraspinal fatigue) and/or altered afferent inputs (spinal fatigue) innervating the active musculature (Gandevia, 2001).

Alternatively, concepts of residual fatigue remain predominately within the domain of peripherally driven mechanisms, such as blood flow, muscle glycogen repletion and clearance of metabolic wastes (Bangsbo et al., 2006).

The physical and biochemical changes observed during intermittent-sprint exercise have traditionally been interpreted in terms of metabolic capacity (Glaister, 2005). Indeed, lowered phosphocreatine concentrations (Dawson et al., 1997), reduced glycolytic regeneration of ATP (Gaitanos et al., 1993) and increasing H+ accumulation (Bishop et al., 2003) have all been associated with declining intermittent-sprint performance.

While reductions in muscle excitability after intermittent-sprint exercise have also been observed (Bishop, 2012), metabolic perturbations are rapidly recovered within minutes (Glaister, 2005).

The ultimate indicator of post-exercise recovery is the ability of the muscle to produce force i.e., performance outcomes.

Reductions in skeletal muscle function after intermittent-sprint exercise are often proposed to be caused by a range of peripherally-induced factors, including: intra-muscular glycogen depletion; increased muscle and blood metabolites concentrations; altered Ca++ or Na+-K+ pump function; increased skeletal muscle damage; excessive increases in endogenous muscle and core temperatures; and the reduction in circulatory function via reduced blood volume and hypohydration (Duffield and Coutts, 2011; Bishop, 2012; Nédélec et al., 2012).

Conversely, Krustrup et al. (2006) reported declines in intramuscular glycogen of 42 ± 6% in soccer players, with depleted or almost depleted glycogen stores in ~55% of type I fibers and ~25–45% of type II fibers reasoned to explain acute declines in sprint speed post-match. Importantly, muscle glycogen resynthesis after team sport activity is slow and may remain attenuated for 2–3 days (Nédélec et al., 2012). Such findings highlight the importance of nutrition in post-exercise recovery (Burke et al., 2006); yet it is noteworthy that muscle glycogen stores remain impaired 24 h after a soccer match, irrespective of carbohydrate intake and should be recognized as a factor in sustained post-match suppression of force (Bangsbo et al., 2006; Krustrup et al., 2011).

Mechanical disruptions to the muscle fiber are task dependant, though likely relate to the volume of acceleration, deceleration, directional change and inter-player contact completed (i.e., tackling or collisions) (McLellan et al., 2011; Duffield et al., 2012). Importantly, EIMD manifests in reduced voluntary force production that has been associated with the elevated expression of intracellular proteins (e.g., creatine kinase and C-reactive protein), swelling, restricted range of motion and muscle soreness (Cheung et al., 2003). Whilst it is generally accepted that lowering blood-based muscle damage profiles may hasten athletic recovery, mechanisms explaining the return of skeletal muscle function are somewhat ambiguous (Howatson and Van Someren, 2008).

Interestingly, markers of EIMD are also not closely associated with muscle soreness (Nosaka et al., 2002; Prasartwuth et al., 2005), though perceptual recovery is reportedly related with the recovery of maximal sprint speed (Cook and Beaven, 2013). While this raises questions in terms of the physiological underpinnings of muscle soreness, weaker relationships between EIMD and neuromuscular performance may suggest the potential for other drivers of recovery outside of peripheral (muscle damage or metabolic) factors alone.

Finally, while the relationship between hydration status and intermittent-sprint performance remains contentious (Edwards and Noakes, 2009), fluid deficits of 2–4% are common following team-sport exercise (Duffield and Coutts, 2011). Mild hypohydration reportedly demonstrates limited effects on anaerobic power and vertical jump performance (Hoffman et al., 1995; Cheuvront et al., 2006); however, some caution is required in interpreting these data as these testing protocols reflect only select components of team sport performance.

Nevertheless, the role of hydration in recovery should not be overlooked as changes in extracellular osmolarity are suggested to influence glucose and leucine kinetics (Keller et al., 2003). Further, the negative psychological associations (conscious or otherwise) derived from a greater perceptual effort incurred in a hypohydrated state may impact mental fatigue (Devlin et al., 2001; Mohr et al., 2010).

Rather, that the integrative regulation of whole body disturbances based on these peripheral factors, alongside central regulation may be relevant.

Physical activity, by enhancing parasympathetic tone and activating the cholinergic anti-inflammatory pathway, is a therapeutic strategy to restrain chronic inflammation and prevent many chronic diseases.

Beskriver hvordan trening aktiverer vagus og demper betennelser.

http://www.ncbi.nlm.nih.gov/pubmed/23395411 

Chronic diseases are the leading cause of death in the world and chronic inflammation is a key contributor to many chronic diseases. Accordingly, interventions that reduce inflammation may be effective in treating multiple adverse chronic conditions. In this context, physical activity is documented to reduce systemic low-grade inflammation and is acknowledged as an anti-inflammatory intervention. Furthermore, physically active individuals are at a lower risk of developing chronic diseases. However the mechanisms mediating this anti-inflammatory phenotype and range of health benefits are unknown. We hypothesize that the «cholinergic anti-inflammatory pathway» (CAP) mediates the anti-inflammatory phenotype and range of health benefits associated with physical activity. The CAP is an endogenous, physiological mechanism by which acetylcholine from the vagus nerve, interacts with the innate immune system to modulate and restrain the inflammatory cascade. Importantly, higher levels of physical activity are associated with enhanced parasympathetic (vagal) tone and lower levels of C-reactive protein, a marker of low-grade inflammation. Accordingly, physical activity, by enhancing parasympathetic tone and activating the CAP, may be a therapeutic strategy to restrain chronic inflammation and prevent many chronic diseases.

Slow Breathing Increases Arterial Baroreflex Sensitivity in Patients With Chronic Heart Failure

Nevner at 6 pust i minuttet gir beste respons på HRV og vagusnerven. I tillegg til å dempe blodtrykk markant. Studien ga disse resultatene med en bare 4 minutters pustesession.

http://circ.ahajournals.org/content/105/2/143.full

Background It is well established that a depressed baroreflex sensitivity may adversely influence the prognosis in patients with chronic heart failure (CHF) and in those with previous myocardial infarction.

Methods and Results We tested whether a slow breathing rate (6 breaths/min) could modify the baroreflex sensitivity in 81 patients with stable (2 weeks) CHF (age, 58±1 years; NYHA classes I [6 patients], II [33], III [27], and IV [15]) and in 21 controls. Slow breathing induced highly significant increases in baroreflex sensitivity, both in controls (from 9.4±0.7 to 13.8±1.0 ms/mm Hg, P<0.0025) and in CHF patients (from 5.0±0.3 to 6.1±0.5 ms/mm Hg, P<0.0025), which correlated with the value obtained during spontaneous breathing (r=+0.202, P=0.047). In addition, systolic and diastolic blood pressure decreased in CHF patients (systolic, from 117±3 to 110±4 mm Hg, P=0.009; diastolic, from 62±1 to 59±1 mm Hg, P=0.02).

Conclusions These data suggest that in patients with CHF, slow breathing, in addition to improving oxygen saturation and exercise tolerance as has been previously shown, may be beneficial by increasing baroreflex sensitivity.

Breathing at 6 breaths/min, compared with spontaneous breathing, slightly increased overall spontaneous fluctuations in RR interval, reduced fluctuations in blood pressure, and significantly increased the baroreflex sensitivity in both CHF patients (from 5.0±0.3 to 6.1±0.5 ms/mm Hg, P<0.0025) and controls (from 9.4±0.7 to 13.8±1.0 ms/mm Hg, P<0.0025) (Figure 1).

The slow breathing rate in the CHF group also produced an increase in mean RR interval of 20 ms and a decrease in both systolic and diastolic blood pressure (systolic, from 117±3 to 110±4 mm Hg, P=0.009; diastolic, from 62±1 to 59±1 mm Hg, P=0.02) (Figure 2).