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Regular, moderate exercise boosts makes neutrophils busier for longer

PainSci » bibliography » Syu et al 2011
Tags: exercise, chronic pain, inflammation, etiology, biology, fun, self-treatment, treatment, pain problems, pro

One article on PainSci cites Syu 2011: Why Does Pain Hurt?

PainSci commentary on Syu 2011: ?This page is one of thousands in the bibliography. It is not a general article: it is focused on a single scientific paper, and it may provide only just enough context for the summary to make sense. Links to other papers and more general information are provided wherever possible.

As nicely summarized by Alex Hutchinson, this research shows that, “Regular, moderate exercise boosts the ability of the neutrophils to get to infection sites quickly (chemotaxis) and attack the bad guys (phagocytosis),” and they live longer too. Busier, longer-lasting neutrophils: sounds great!

But a “boost” to immune function isn’t as simple as it sounds or all good news, and the counterintuitive price of better infection-fighting could be vulnerability to repetitive strain injury, slower healing, and pain chronicity. We know from McDonald et al that neutrophils are active even when they shouldn’t be, responding overprotectively to aseptic (internal) cell trauma even when there is no possibility of pathogens. They go nuts anyway, attracted to exposed mitochondria (because mitochondria are technically, biologically “foreign,” a legacy of evolution and symbiosis). And this inappropriate immune response is a likely partial explanation for one of the great catch-22s of the human condition: exercise is good for you, but it often hurts.

For more about this, see my detailed article: Why Does Pain Hurt? (section: “It gets worse! Exercise makes neutrophils more feisty.”)

~ Paul Ingraham

original abstract Abstracts here may not perfectly match originals, for a variety of technical and practical reasons. Some abstacts are truncated for my purposes here, if they are particularly long-winded and unhelpful. I occasionally add clarifying notes. And I make some minor corrections.

Exercise effects on immunity are highly dependent on exercise intensity, duration and frequency.

PURPOSE: Since neutrophils play an essential role in innate immunity, we investigated whether acute severe exercise (ASE) and chronic moderate exercise (CME) differentially regulate human neutrophil functions.

METHODS: Thirteen sedentary young males underwent an initial ASE (pedaling on a bicycle ergometer with increasing loads until exhaustion), and they were subsequently divided into exercise (n = 8) and control groups (n = 5). The exercise group underwent 2 months of CME (pedaling on the ergometer at moderate intensity for 30 min each day) followed by 2 months of detraining. The control group was abstained from regular exercise during these 4 months. Additional ASE paradigms were performed every month (in the exercise group) or every 2 months (in the control group). Neutrophils were isolated from blood specimens drawn at rest and immediately after each ASE for assaying chemotaxis, phagocytosis, citrate synthase activity and mitochondria membrane potential (ΔΨm). Additional blood specimens were drawn from the exercise group before and immediately after the 1 bout of CME to determine the acute moderate exercise (AME) effects on neutrophil functions.

RESULTS: 1) The initial ASE enhanced chemotaxis and induced ΔΨm depolarization. 2) AME did not influence any measured parameter in neutrophils. 3) CME increased chemotaxis, phagocytosis, citrate synthase activity and ΔΨm. 4) The CME effects remained after detraining except phagocytosis. 5) The ASE effects disappeared after CME and partially restored after detraining.

CONCLUSIONS: ASE and CME differentially affected neutrophil functions, while AME was ineffective. Moreover, the fact that CME improves neutrophil functions may partially explain why physically-active subjects have low risk of infection.

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