Dr. Sara Campbell returns to discuss her lab's cutting-edge research on the bidirectional relationship between exercise and the gut microbiome — including why consumer gut tests oversimplify a complex ecosystem, how antibiotics devastate exercise capacity in animal models, and why single-microbe probiotics miss the bigger picture of functional guilds. She also shares new findings on short-chain fatty acids, amino acid metabolomics after antibiotic treatment, and the emerging neuromuscular junction hypothesis.
In this episode of the Flex Diet Podcast, I sit down with Dr. Sara Campbell, Ph.D., Associate Professor at Rutgers University, for a conversation about the bidirectional relationship between exercise and the gut microbiome.
Dr. Sara Campbell returns to discuss her lab's cutting-edge research on the bidirectional relationship between exercise and the gut microbiome — including why consumer gut tests oversimplify a complex ecosystem, how antibiotics devastate exercise capacity in animal models, and why single-microbe probiotics miss the bigger picture of functional guilds. She also shares new findings on short-chain fatty acids, amino acid metabolomics after antibiotic treatment, and the emerging neuromuscular junction hypothesis.
In this episode you'll learn:
Find Sara here:
Rutgers Faculty Page
Google Scholar: Sara Chelland Campbell
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Dr. Mike T. Nelson: [00:00:00] Welcome back to the Flex Diet Podcast. This is your host, Dr. Mike T. Nelson. On this podcast, we talk about all things to increase performance, increase muscle, improve body composition, do all of it within a flexible framework without destroying your health. Today, we've got Dr. Sarah Campbell. She's back on the podcast once again, discussing some really cool science related to exercise and also gut bugs.
Uh, she did a really cool study about antibiotics that we'll talk about, and some other great stuff. We'll link to her previous episode here also, and we even talked to her about gut testing and many other things. Uh, so she is a professor at Rutgers University, has been doing research for quite some time, and I really enjoy her intersection of exercise and nutrition, and looking at how exercise in and of itself can change, uh, the [00:01:00] gut microbiome.
So check out all of her information, uh, down below. If you want more from me, you can hop onto my free newsletter down below also, and enjoy this podcast with Dr. Sarah Campbell
Dr. Sara Campbell: Welcome back to the program. How are you today? I'm good.
How are you today? Yeah. I know it's been, uh... might even be a couple years since you were last on here, I think, so we'll, we'll make sure to link to the episode. Yeah, yeah. No worries. Sounds good. Thank you for having me back. I really appreciate it. It's always fun to talk to you. Yeah. And one of the things I wanted to ask you about, because I'm- you're the expert on, you know, gut health, and especially the relationship to exercise, and your lab does a ton of actual legitimate, like, testing.
Dr. Mike T. Nelson: What do you think about a lot of the gut testing you can purchase on the market now? And again, I don't think it's companies are trying to be ill-intentioned. I usually don't have as problem with the companies as much as I have an issue with [00:02:00] the proponents of certain labs, I think, overexplaining the significance of some of these tests.
Because it seems like the- everybody wants the key and the lock. Like, "Oh, we tested for X critter. Ooh, X critter bad. You need X probiotic to solve all your issues. And boom, look, we're... This is great." But I, it just doesn't seem to be remotely close to that simple yet. Right. I, I would agree, and it's really interesting you ask me that question, 'cause I was just talking with a PhD student who, um...
Dr. Sara Campbell: or I should say my PhD student, who was mentioning that, um, their friend had went and got this done, and was, "Can, can we explain some of this in, in terms that they'll understand?" And so on and so forth. And I think that's a very good first point to mention, is you get all of this data back and it's hard to know what to [00:03:00] do with all of that data.
Yeah, for sure. You know, does, is this bug really good or is it bad? Is this, you know, um, metabolite productive or not productive, right? And so it comes back, but with a complete lack to, lack of context, right? So you, you really feel like you need to explain this i, in a way that makes it seem, you know, at least palatable so that they can understand that it's, one, not as easy as it's being made out to be, and two, you know- Moderately helpful if you potentially see some things that tend to maybe go together, right?
So I always use, and I really do, Akkermansia muciniphila as the, the, you know, the one microbe, um, that is getting a lot of attention. And, um, and I'm also seeing it get a lot of attention 'cause I'm in that whole menopausal kind of thing going on right now. And, and we know Akkermansia seems to be linked to good metabolic health, and healthy body weights, and so [00:04:00] on and so forth.
So they're like, "Hey, for you, you know, estrogen deficient folks-" "... when you know you gain weight, take some Akkermansia. It'll fix everything." You know, and then the flip side to that is Akkermansia is also really, really high in inflammatory bowel diseases. 'Cause estrogen- Oh, interesting ... it loves your mucus lining.
Ah. And it degrades the mucus lining, making that thinner, and making pathogenic bacteria have easier access to your, you know, your e- epithelial lining and your tissue So it really depends on the context of that microbe and who it's working with, which is a lot of times why, not a lot of times, but why our lab ascribes to the, um, idea of what we say functional guilds or co-abundance groups, which are groups of microbes that, yes, may s- have some foundational species that are really important, but that tend to work together for a specific outcome, right?
So are we going to believe that the one microbe [00:05:00] in the 10 to the 12 trillions that are in your gut is going to make that profound of a difference in the grand scheme of how these microbes are, should be working together for that specific outcome, right? And I think that that's the crux of what you're getting at, is- Yeah
how do we, you know, how do we know that that microbe is doing what it's supposed to be doing, right? Has it been thoroughly tested, you know, in, one, the human model? Has it then been taken from the human and conventionalized into a germ-free animal, and you've completely mimicked the phenotype you hope to see in the human, right?
So you kind of do have to go back and forth, and I would say that the microbiome is, is one area where you really do need the human-animal aspect of looking at things, um, for those kinds of reasons. I mean, we are noticing with exercise things like muribaculum and dysbacter [00:06:00] welbionis being really abundant in our exercise studies.
We have tried to culture both, and it is almost impossible to get some of these microbes alone to come in culture. And the reality is, yes, because they probably rely on some of their friends to be in abundance and to work properly, so when you try to isolate them down, it, it becomes a challenge. And so that's why you get this really interesting, you know, disconnect sometimes in translation between take this probiotic or these probiotics, it should help to work this way, when, you know, is it so easy to put them in other environments and manifest the phenotype you want, or see it in culture to truly test its, its physiology and even confirm its genomes, right?
And so I, I think that the theory behind the testing to provide information to [00:07:00] individuals is really important. I think there's still a long way to go with using that information beneficially based on sound science. Yeah, and it seems like everybody wants the simple reductionist answer of, you know, you're either missing this one or this one's too high or this is good or bad, and then if we just supplement or just take this one that's missing, then, hey, we fixed all your issues.
Dr. Mike T. Nelson: But I... correct me if I'm wrong, but I think we have a hard time even knowing what a normal, air quote, microbiome is, and there's probably a wide range of normals, like you said, for which person, what type of exercise, where do you live, and all those types of things too. So it's hard to equate to, okay, even if we find that this is in a high population, well, what as a human we're, we're talking about?
Maybe for one group it's good, maybe for one group it's not so [00:08:00] good, and just the complexity gets really challenging very fast. Right. A- and I totally agree. I mean, I think the general rule of thumb is, you know, we share maybe one-third microbiome maybe between us as humans, and two-third is typically gonna be unique to that individual, right?
Dr. Sara Campbell: So, you know, the hope is defining it, you know, comes down to, you know, again, what maybe some of those co-abundance groups or those links of microbes and how they're acting to promote that health aspect that you're looking for is, is becoming important. And again, why we don't necessarily look for the singular microbe, but those groups that tend to be working together.
And, and are those groups more abundant in your one treatment compared to another? That way you at least have a group of microbes that you know can be working. And, and to us, that's, that's more important than saying it's just this one that's doing that one thing that's gonna fix that [00:09:00] one problem. And, you know, given that it's an ecosystem, right?
I mean, you think of ecosystems like in, in nature and outside, and we... you know, you respect that it's the trees and the birds and the insects and the water and the grass and all of those things that combine to make that ecosystem unique. It's like if you take one of those out, it might change the ecosystem, right?
But, you know, there's still other parts of it. The gut has to be the same way if you think of it as an ecosystem. You know, there's your ones that are, you know, um, es- related to estrogen and re- related to lactate and, you know, butyrate producers and our propionate producers and acetate producers. And it's like, you know, um, and it's not just usually one, it's a group of them that are working to do this and a group of them.
So, you know, envisioning taking one part of that ecosystem out and saying that's the only thing that matters- I, I think is, um, probably difficult to swallow. Yeah. Yeah. So you're saying if I did a microbiome test, I won't say the name of the company, but... And it comes back and it says I should definitely not eat asparagus, cauliflower, and broccoli, that that's not accurate?
Um- 'Cause someone literally sent me this[00:10:00]
Dr. Mike T. Nelson: one a couple- Well, for sure I would not avoid your cruciferous- ... couple months ago I would not avoid- And they said, "Here's a list of vegetables I need to avoid." I'm like, "How did you come up..." "Well, I did this, this microbiome test." And I'm like, "There's no way we're at that level yet." Right. Yeah. I mean, I definitely would not say to avoid those fibrous, cruciferous vegetables.
Dr. Sara Campbell: I mean, that fiber is what provides the microbes an environment to thrive in. Yeah. Right? And so, and, and that fiber then gets fermented to the short-chain fatty acids, which are a huge part of why we think the microbiome is so beneficial to- Mm-hmm ... both humans and animals, you know, what those short-chain ch- short-chain fatty acids can do, so.
Dr. Mike T. Nelson: Can we just supplement the short-chain fatty acids then since that's the intermediate [00:11:00] part? Right. I know someone's thinking that. Right. So, you know, um, again, this is where the microbiome is interesting where you can do those translational studies, right? You know- Mm-hmm ... not really hard, but, you know, feeding somebody a whole bunch of things that you hope produces butyrate, right?
Dr. Sara Campbell: Whereas, like, in an animal we can kind of infuse, you know, butyrate and acetate- Yep ... and/or propionate, particularly as it relates to exercise. And depending on the study, butyrate seems best. And depending on the study, you know, propionate seems best. And depending on this other study, it's like, well, acetate seemed to do this, but not the other two, right?
Which I think when you see research that kind of highlights all three, it supports, you know, a lot of what we've been saying, is that there's probably these groups of microbes that are working together for a variety of outcomes that then make all of exercise work, right? You know, so y- research is fairly consistent that exercise manifests butyrate [00:12:00] producers.
If you take a look at the, you know, the Scheiman paper from, you know, quite some time back, they linked propionate to lactate pr- you know, um, metabolism and how that seemed to enhance the, the marathon runners. And then, you know, there was the other study about acetate. So I think the reality is, you know, exercise is a complex...
Or I should say exercise is not complex. Exercise is, you know, just engaging in what you do, but it manifests- Right ... the number of- The physiology of it Yes, physiological adaptations- Which you would be likely hard-pressed to link that to one or two particular microbes that, that seem to be driving that exercise, right?
Dr. Mike T. Nelson: What's gonna impact maybe heart is not gonna be the same that impacts m- lactate or this or that, right? Chances are that there's a number of those co-abundance groups that are linked to those physiological and/or metabolic outcomes. Yeah. 'Cause I'm starting to see more probiotics now for flat-out exercise [00:13:00] performance, which seems like a new category.
And I haven't checked into it all that much since I knew you were gonna be on the podcast, but- Right ... um, what are your thoughts on that? And then the follow-up question is, d- are probiotics actually doing what we think they're, they're doing? Right. Um, so good question. To be honest with you, I also... I'm never afraid to say I don't know.
Dr. Sara Campbell: I have not- Yeah, yeah. No, that's fine ... I definitely have not, you know, PubMed-ed or Googled the latest, you know, exercise-related probiotics, right? Um, but now that you've perked my interest- ... I will do that 'cause I'm, I'm curious. Um, but as someone, I guess, who hasn't really looked into those but knows the literature around exercise and gut microbiota, I would say that there may be a consensus over a handful of microbes that seem to consistently come up, but what they do, you know, and, and where they are, and I [00:14:00] hate to say, but the bidirectional relationship- Mm
right, where exercise manifests those microbes. Yeah. There seem to be association studies is what I've seen. Right. We, we looked at exercisers with the marathon or whatever and, oh, look, they had more of these little bugs. And it seems like the, the jump- Right ... from the supplement industry is, oh, look at this study.
Dr. Mike T. Nelson: This study said, hey, they got more of these little bugs, so we'll, we'll just give you the bug and woo-hoo. Right. Right. And I think that's what we're, you know, especially the, the one, you know, the villainella atypica, you know- Mm-hmm ... manifested as one. And, you know, um, early on, you know, we've shown and then, you know, Jeff Woods and, and Jacob Allen and, and that whole crew has shown like faecalibacterium prausnitzii tends to be a really big one.
Dr. Sara Campbell: And then we've shown in a couple of other studies that muribaculum intestinale YL 27 seems to be a really big one. So there do seem to be bugs that manifest as a result of exercise training, but whether or not supplementing those means it will further exacerbate exercise performance or if you can take a completely sedentary person, give them that [00:15:00] bug, and expect exercise adaptations without engaging in exercise- No, yeah, yeah, especially if you remove the stimulus altogether.
Right. Right. And so, um- Yeah, so I, I think that that's, um, from a, from a research perspective, right? That, you know, those are out there. They probably, you know, have been developed based on some of the, the studies that have come out, but maybe not as rigorously tested to see where they fit in in the whole training, training adaptation, untrained versus, you know, acutely trained versus chronically trained.
I mean, there are so many questions, and there's so many questions about, you know, um, exercise thresholds for a variety of diseases- Oh, yeah ... let alone knowing exactly what microbes to give somebody to make them exercise more, right? I mean, that's, that's also a motivation thing, right? Maybe not necessarily just a straight exercise, but, like, what is gonna motivate someone to exercise, and there are, [00:16:00] are there specific bugs that are associated with that that might be completely independent of the ones that change as a result of exercise training, right?
So it's like, you know, there's all these, I think, parts to that equation that get left out by saying that you can reduce it to just take this exercise probiotic or take this probiotic, right? I think that there, from the, you know, metabolomics types of studies that have been coming out and that, that will be coming out, um, there are probably other metabolites that are really- Yeah
important, right, for, for this that, you know, may or may not even be linked to the gut I mean, we're still trying to figure out new compounds that muscle is releasing, period, into the bloodstream. Like, I don't think we've identified all of them. I, I would be hard-pressed... We know some of them, but it just seems like it...
Dr. Mike T. Nelson: And that's, I don't wanna say a more simple [00:17:00] system, but it's something we've studied longer. It appears to be more simple, and I don't think we're even close to getting that figured out. Right, which is why there's MotorPAC from the NIH, right? The molecular transducers. And, and, you know, if that molecular transducer is released from muscle, if it's also released from adipose tissue, does it even carry out- Yeah, what does it do?
Dr. Sara Campbell: yeah, the same function? Is there some sort of interaction? How do they communicate with one another, right? And so you have to think about that aspect, again, in that ecosystem of the gut. Those bugs are using quorum sensing to talk to one another and find out like, "Hey, if you're gonna be here, I'll be here," and doing, you know, these types of activities.
So I think, you know, as, as you're kind of asking that to just take a probiotic or just, you know, with- without recognizing all of the facets that go into trying to understand how helpful it is or by which mechanism it [00:18:00] works, I think, you know, has yet to be really elucidated. So you really sometimes can't answer those questions fully.
Dr. Mike T. Nelson: Yeah. And related to probiotics, do you- How do probiotics work? Like, because I think the assumption in the general audience is that, oh, I take X little bugger and it goes into my gut and I assimilate it in there, and if I was low in this population, now I can air quote supplement, and it becomes kind of part of my microbiome and I'm good to go.
But it doesn't appear to work that way at all, and there's some data we're even taking... You know, the, the dead bugs have signaling effects and promote other things going on, and they don't even have to all be alive. But in some cases they probably need to be alive, and it just seems to be pretty, not as clear cut again as what...
as the story we've been sold, I guess. Right. Right. I think, you know, for a long time there, and I'd have to look, although I think those kind of announcements have [00:19:00] expired, but the NIH was proactively putting out calls for research to understand how probiotics worked. Mm. Because they were kind of like, "Oh, okay, but w- what's the mechanism?
Dr. Sara Campbell: How does it, how does it work?" Right. Right? And I think it goes back to this, you know, question that we were talking about earlier. Do we really believe that only the most commonly sold probiotics, which is typically what a lactobacillus and a bifidobacterium, right? Are those the only bugs in your system that really matter, right?
Or, you know, um... And even more importantly, if you believe in this, like I said, this gut as an ecosystem and that these bugs kind of work together for an outcome and, you know, push and pull on one another, which we, you know, um, which we call a, an interaction group, right? Um, and the probiotics definitely are part of an interaction group, and when they do t- tend to be abundant, some of the more pathogenic ones aren't.
[00:20:00] Um, but those probiotic bugs aren't the only one in that group, right? And they're not just in this group. They, you know, some are scattered here, um, some are missing here. But then those might be some of the ones that you see abundant with exercise and/or this type of food or that type of food, right? So I think- Assuming that they're just going to go in and make this immediate impact in the grand scheme of this ecosystem, um, again, I don't know that there's the research out there that to support that they're efficacious in all circumstances.
That's not to say they aren't efficacious in, in other circumstances, right? Yeah. When you're going through, you know, heavy antibiotic, you know, um, prescriptions and/or so forth, and we know those are gonna get rid of bugs. Yeah, the probiotic bugs do tend to be important enough that you wanna maintain those, right?
So taking those k- types of things to avoid [00:21:00] losing all of that community, um, is helpful. But the reality is the community still takes a couple of weeks to recover, which means- Mm-hmm ... that probiotic is helping certain things, but certainly not the entire community, right? So I think that there's still a lot to, um, unpack with, with probiotics in, in truly understanding if and how they impact that ecosystem.
I know for exercise, they don't appear to be ergogenic in any- Hmm ... you know, they may help with things like immunity and/or gut barrier. Um, gut barrier, we could have a whole separate conversation. But, um, you know, but not necessarily that they're ergogenic and performance promoting, but just that they may keep or help be a part of what keeps an athlete healthier and, you know, training.
Dr. Mike T. Nelson: Awesome. Any update on [00:22:00] antibiotics? I know you've done some work with- Yeah ... uh, effect of antibiotics, and maybe recap a little bit of what we covered last time you were on here. Yeah, yeah. So, um- Last time we were on, um, we talked about a study that had come out in Medicine & Science in Sport & Exercise, and that was probably one of the really big ones that came out where we showed that exercise really reduced...
Dr. Sara Campbell: Um, sorry. We're providing the antibiotics to basically get rid of the, the microbiome, right? So you can... I guess let's take a step back. So you can... There are two ways to test kind of the, um, the implication of the microbiome in an outcome, right? You can have a germ-free animal, which is basically the mouse in a bubble, as I call it, right?
It has no microbiome. Unless you put known microbes in there, you know, you just kind of test it. And, you know, those are really, really expensive, um, mice. And to be honest, when you're like the researcher on the budget, [00:23:00] which, let's see, we're all researchers on a budget, right? That's pretty much everybody now.
Dr. Mike T. Nelson: Pretty much everybody now, right? You t- we tend to use a cocktail of antibiotics, you know, and, um, to knock out the gut microbes, or at least upwards of 90% of them, which is about what we get when we knock out our gut microbiotas. Um, and so, you know, what we found is there's a reduction in exercise capacity, which by the way had been shown as early as 2015 that these germ-free mice don't r- really exercise as well as mice who have one microbe versus a full set of microbes.
Dr. Sara Campbell: And so that was good. But what we tried to do is we looked at mice who were training, right? So they were treadmill running five days a week for 45 to 60 minutes and, and so forth. And so what we did was we looked at hind limb blood flow and then their, their skeletal muscle. So what did their, you know, mitochondria in particular we were [00:24:00] interested in, in looking at.
And what we found is there were significantly lower, um, proteins related to mitochondrial oxidative phosphorylation. If you're not having ox phos going on, you're not having mitochondrial biogenesis, right? So the increase in the size and number of mitochondria that you'd like to see with endur- endurance training.
And so we kind of had our conceptual model that, you know, there was this reduction in nitric oxide, citrate synthase, complex IV. So, you know, changes in nitric oxide could be linked to the reduced hind limb blood flow, but those, you know, proteins of oxidative phosphorylation then reduce SIRT2 and 1, and PGC1 alpha, and AMPK.
And so we're like, "Okay, well, if there's not a lot of that going on-" With, um, there's not a lot going on with exercise. And so, you know, that's kind of what we put out then. Since then we did one, two, three studies, two [00:25:00] animal studies and a, and a human antibiotic study actually then that, um, we're getting some results back for.
The, the first animal study was to look at, um, what we called the RGS-14. It was basically a super mouse. It really, really loved to exercise. In fact, at baseline it exercised twice as much as a kind of like your normal what you'd call wild type mouse. Yeah. And the- These are the ones that were actually bred for the...
Dr. Mike T. Nelson: I think it was partially just the desire to exercise, right? If you left them in their cage- So- ... they would do more voluntary exercise. Is that correct? Right. So along those lines, right? That, um, you know, that mouse strain came out quite some time ago, and I'll be damned, I will email you the name of it. It is not- No, that's all right.
I, I- ... tipping my mind at the moment ... I'm not a mouse researcher, so I get them mixed up. Right. So but... No, no, no. But the, uh, the idea is, you know, similar, right? So, um, so what was uncovered about this mouse is it, is it [00:26:00] mostly got, um, its exercise phenotype from increased brown adipose tissue and skeletal muscle metabolism.
Dr. Sara Campbell: Hmm. So first the Navy was interested, 'cause they were interested in understanding what kind of microbes may activate metabolic tissue. So we got into all of that, and that's when we came up... You know, we did the antibiotic thing to say, okay, how much of it is involved? And, you know, we just... Actually two months ago it just came out in European Journal of Applied Phys, and we, we found that, um, consistently, like the animals could not exercise once you gave them the antibiotics.
The difference between this study and the one from MSSE, as I mentioned, that was a six-week training study. So they were exercising every day, and we saw all these changes. This, they were just interested in, in, you know, does it work or does it not work? So you give the, the animals antibiotic on day one, right?
Uh, or test them, I should [00:27:00] say. What's their exercise capacity look like, so on and so forth. You give them that weak cocktail that we had published about, and you retest them a week later. So when you retested them, exercise again completely, um, you know, significantly decreased. We didn't notice the changes to their skeletal muscle.
Like we did- Hmm ... in the previous study. So we're like, "Okay, this is really interesting." That's kind of odd. You would've expected changes, correct? I would have expected changes, right? That would be my guess. Same, because we assumed since we saw it last time, right? So what's the one big difference? Well, they're not really training per se, right?
Mm. It's just like before and after a week. So was there no, you know, um, there was no stimulus to maybe increase mitochondrial proteins. But, you know, then you go back to the other study, it was like, well, okay, they were training for that entire time, and the entire week they got antibiotics, and they still saw these big [00:28:00] decrements.
So what does a good researcher do? Try and replicate their results. So, um, and then at the time the only animals available to us in that study were male. So we're like, uh, this, um, that's not acceptable to me as a female in science, so- Sure ... woman in science I should say. So we did a sex differences study.
So where- Oh, nice ... sim- similar thing. It was male and female mice. You know, do baseline testing, start them on antibiotics for a week, and, um, test them one week later. Well, male and females both respond to antibiotics in a similar way, both huge decreases in exercise. Same muscle findings, though. Really?
Dr. Mike T. Nelson: Interesting. Yes. So we're like- No exercise, correct? No exercise, right. Okay. So we're like, okay, this is, this is starting to get really cool and really interesting because one of the big questions that we have, um, [00:29:00] is we did notice, and a, an amazing collaborator of mine at Newark, Nathan Wages, um, has these really cool research lines where he looks at like neuromuscular junction and like communication and sarcopenia and dynapenia-type patients.
Dr. Sara Campbell: And I sent him this data set, and I was just like, "Hey, do you see anything interesting?" So he divided our animals up into quartiles based on, you know, how, you know, fit they were, right? You have your top quartile as your strongest athle- you know, athletes, and you have your bottom as like kind of your weakest animals.
We noticed that the antibiotics, you know, impacts the weaker animals to a much greater extent than some of your stronger ones. Wow. I was like, okay, this is really interesting. And almost to the tune of like, you know, there's a change in critical power that's significant with antibiotics regardless, you know?
But of like 22% to like 58% change. Oh, so that's a big [00:30:00] difference. Huge difference, right? So I was like, so I'm like, okay, this is cool. We're putting this in the EJAT paper, and it is going out 'cause it's... It'll answer a couple of the questions that some of the reviewers h- were asking us about like, are you sure about this?
How... You know, how can you...? And I'm like, "Okay, here's how we re-ran the data and looked at it in this way, way." And they were like, "Oh, yeah, this is really cool." And then we were like, "Yay." So, um, but then we start thinking. So the next text I sent him, and I was like- Well, antibiotics by virtue of the lack of microbiome, does that interfere with neuromuscular junction firing?
Like, is there some- Hmm ... type of miscommunication going on between the neuron and the muscle that, like, is blunted when the microbiome isn't there, 'cause maybe it's not sending a signal or something? And so from that has been born the idea to kind of look at, you know, that aspect of things, as well as the time course, right?
Because antibiotics seems [00:31:00] to universally... And I shouldn't say antibiotics, because the idea is antibiotics and the lack of a gut microbiome, and there, you know, may or may not be, um... I'm just gonna stop there. Um. But it's not the an- it's not the antibiotics causing it. It is the lack of the microbiome- Hmm
that's causing it. Um, and so the reality is, you know, the, the microbiome or the lack thereof, um, eliminates exercise capacity. I mean, significantly reduces it in our wild-type animals, in our two models of enhanced exercise aging, whether it's a male animal, whether it's a female animal. And I mean, this is, like, five studies now that we've, you know, looked at this and consistently find this.
And it's like, okay, well, we see the reduction in exercise capacity, and this kind of like, you know, untrained acute antibiotics, you know, that one week versus the [00:32:00] six to seven weeks of, like, the trained chronic response, the big difference is the, you know, muscle proteins that we're seeing. So then you start thinking, okay, well, if they can't exercise, they can't stimulate mitochondrial oxidative phosphorylation to a great extent, and hence the mitochondrial biogenesis proteins, and then you get this kind of cycle of your inability to exercise without a microbiome.
And so we're trying to figure out, okay, is that for sure how it works? Does that come first, right? The lack of a gut microbiome means less exercise and, and so forth, right? Data out of Woods Lab says, well, that doesn't necessarily mean they can't adapt, they just won't ever exercise as much. But they can adapt to that response.
Hmm. So, you know, we're stuck with this question of, well, what order does this happen in and why does this begin to happen, right? [00:33:00] Does... You know, if you take it, all the microbes away, and they have this exercise problem, if they start to, say, naturally reseed themselves and, um, get the microbes back, will the microbes needed for exercise appear first, or will they begin to exercise and then the microbes appear, and then you get your increased ability to exercise and so forth?
So that's kind of the question we're looking at and, and hoping to get answered, because I think that's the big thing that's come from this data set, is that there might be an, an order of where, how and when this happens. And so that's, that's some of the new animal stuff that, that- Yeah ... we're doing. Um, and then we did finish, finish, um, and my, uh, senior PhD student is analyzing and finishing analyzing some of that data right now.
Um, and we're still awaiting the microbiome, so I don't actually have the bugs yet, so we can, you know, catch up. [00:34:00] But we do have all of the performance data and actually some metabolomic data back already. And we took, you know, pretty recreationally active, based on the protocol, probably a little more than recreationally active, but they definitely had to meet the 150 minutes a week of, of exercise, um, moderate to vigorous physical activity.
Um, and then healthy, because most of the antibiotic, you know, literature in humans is usually confounded by being sick, right? And so we all know that being sick could just make you not wanna exercise, and not the antibiotics. So we were, um, testing basically a Z-Pak. Yeah. And seeing- Azithromycin. Yeah. And so basically seeing if that does anything to their, um, exercise capacity, running economy, you know, time to crossover point, and a whole bunch of other things.
A long story short, it doesn't seem to to, to have that effect- [00:35:00] Oh, interesting ... in trained humans. You know, but again, I go back to, we were talking about earlier, like the translational, right? As- Yep ... you found these couple of microbes that seem to be abundant with exercise, you try to culture them, it's very difficult to get them in culture, right?
Um, one of the other reasons that, you know, I feel like you need animal models in microbiome research is 'cause I'm ethically not going to give a human enough antibiotics- Yeah. ... to destroy their microbiome and see if they don't run, because- Probably let's be real, if I gave someone enough, mm, antibiotics to wipe out their microbiome, they're probably not going to exercise.
Yeah. Right? I, I mean, I don't know that that's a big stretch to hypothesize that, right? So a Z-Pak will only get rid of certain bugs. Mm-hmm. So it's not quite translatable. Um- But it's also very commonly prescribed too, so you could argue- It's- ... it's much more of a real world application. And that's why we [00:36:00] figured it's kind of like a win-win situation to run this study, right?
Yeah. You see, okay, the most commonly prescribed or one of the most commonly prescribed antibiotics to athletes doesn't appear to impact their performance, right? Um, so maybe it's the fact that they're sick that is impacting their- Yeah ... right? So it's like, okay, well, you probably need a day or two just to get well, not because the antibiotics are not making you wanna exercise.
Um, and so we figured it that way is good, or we, we could have found that it did impact your performance, and then so clinicians are gonna have to seriously think about what kind of antibiotics they're going to, to, um, prescribe. But w- we did notice some interesting... So unlike animals, we can't, and at Rutgers unfortunately we don't have the capability to do a muscle biopsy, which would be amazing, but the next best thing is you can think about some metabolomics at least in the serum, like what's showing up or not showing up.
And there were some, you know, really big [00:37:00] changes in, um, amino acids- Hmm ... serum after one week of antibiotics. Interesting. Again, didn't impact performance, but it seems like their serum metabolome was, was quite different, impacting, you know, s- some pathways, and we're still trying to work out, um, you know, to what extent those are changed.
You know, if they're, if the pathways are significantly altered, you know, we have to factor in false discovery rates and, you know, put all these parameters in place. But there does seem to be this interesting set of, um, amino acid related metabolites that are significantly lower after antibiotic treatment.
Hmm. So. Any theories as to what that may impact? Well, um, we were able to do metabolomics in our animal skeletal muscle tissue. Oh, nice. And the pathways are nearly identical. [00:38:00] Hmm. Interesting So AKA these pathways seem to be really abundant pre-antibiotics in the skeletal muscle, and then are not any longer After antibiotics.
Hmm. That's all in the EJAT paper that we just put out. Um, and so it's really interesting that in the serum these metabolites are much lower, you know, which would mean less potential availability, especially if you're talking things like essential amino acids, which- Right ... has hepatic portal circulation, and suppose, you know, gotta go right to the skeletal muscle to be oxidized.
Used as help, you know, for intermediates in the Krebs cycle, which would be, you know, all of the things that you think of when you think of complex four and cer- citrate synthase, and how that could be lower, right? So you start to get kind of excited to make some of these, these leaps. Um, you know, whether or not any of the leaps are, you know, relevant yet, we're just, like I said, getting some of our data back and, [00:39:00] and really have to then start looking at these pathways.
But it does seem to be really, um, interesting in, in terms of, of looking at some of your animal data, especially related to metabolomics and, and how that might link to what you're seeing in the humans. Do you think there might be any change in, like, muscle protein synthesis at all possibly? So I do, and I...
Oh, God, I'd have to go back. Um, but Taylor, uh, Valentino out of John McCarthy's lab actually published in JAP the paper. Um, and I do believe they were showing there were less type 1 muscle fibers in the, the female animals they used after antibiotic treatment. Oh, interesting. Oh, yeah. So there does- Huh
seem to be some of those impacts. That's... And, you know, and so... And that's kind of, like, why we're thinking about this. Is there some sort of, you know, something going on at the m- neuromuscular junction, right? That [00:40:00] there's a change in the firing rate. I don't, you know, I don't know if any of that sounds ridiculous, but there ha- there's...
You know, you start to then work your way back up the chain, right? Right. So you start to see changes in muscle. Okay, calcium handling, right? You start going through all of these things to, to hopefully start looking at and then answering as you go up the, the cycle of events that leads to contraction. So that's kind of- Yeah
that's, I mean, maybe that's not a lot, but that's what we've- No, no, that's good. I, in my head, I'm just trying to think about how that would change things in the neuromuscular junction, and that's definitely not my area of expertise, but it's super interesting. Yeah. Yeah, and I'm not sure. I think, you know, I think it's just one thing to either say yes or no, does or doesn't.
For sure, yeah. Right? And the, you know, 'cause the only way to know it is to test it, right? Yeah. And so if it doesn't come out, then you work an alternative hypothesis based on whatever that data tells us. [00:41:00] So that's, that's kind of the route we're taking, you know, in trying to uncover, you know, how- Or I should say why this lack of a gut microbiota so consistently...
And it's not just our lab. I mean, there are a number of labs now that have shown that n- no microbiome means no exercise tolerance. Um, so it's a very real finding that the microbiome is clearly involved in your ability to exercise. And vice versa. When you exercise, you have a much better microbiome, which is why- Yeah, yeah
kind of, you know, coined the bidirectional relationship kind of thing. So they're, they're heavily involved. So trying to understand, as I was mentioning earlier, like which comes first? Does the exercise have to change the microbes which then feeds back to the exercise? Or, you know, do you have to have certain microbes there to generate the exerci- you know, or...
And so we're just kind of trying to look at the data and, and make the [00:42:00] connections and see what we can test. Yeah. That, that's super interesting. And was part of that model, you said, the willingness of the animal to exercise, or were they kind of forced to exercise, or was it a combination of both just in different studies?
Right, it is a combination of both, 'cause we were, you know, yep, curious. So we've, you know, looked at some running wheel stuff. We've looked at some treadmill stuff, and so yeah, it does seem to be, um, a combination. 'Cause they're, you know... Forced is the whole treadmill thing, although the- Right ... typically like to run regardless, you know?
Um, but the running wheel is really an indicator of how much they wanna get on there and just kind of be happy and, you know, be in their little wheel, as, you know, the- Yeah. I think that was, like, one of the simple studies where they, they put them in a little cage, and they put a wheel in there, and they literally just measure off, and they get on the wheel and do exercise.
Dr. Mike T. Nelson: Yep. Yeah, and as, uh, i- in our early studies, that's what we, that's what we did. We did, you know, a lot of the running wheel stuff. And then when we start, you know, started becoming, [00:43:00] okay, well, how does this translate to performance, like you kind of move to the treadmill just because you can measure VO2 that way.
Dr. Sara Campbell: Sure. And a lot of those, you know, respiratory exchange ratios, VO2, VCO2. Um, and, and so to collect the other metabolic aspects of the data set, you know, we wanted to, to look into that, and we can only do that really... Not, hate to say it's the only way, but the treadmill is seems to be the best way to be able to do that in the animals.
Dr. Mike T. Nelson: And I'm just visualizing in my head, you don't put a little, uh, a little mask on the little animals? Is it in a controlled, like, environmental cage, I'm guessing, and you just measure- Yeah ... air in and out then? Is that right? Yeah, yeah. So it's, um- ... it could actually be up to six lane, you know, I shouldn't say six lanes to train them, but yeah.
Dr. Sara Campbell: To do the, the m- the metabolic aspects and the VO2 and the VCO2, it's kind of like a, almost like, yeah, um, um, a metabolic treadmill cage, for lack of a better term. Yeah, yeah. Where they do all of that, and you get all the expired gases and so forth. [00:44:00] Oh, that's super cool. Yeah. It is a lot of fun. And like I said, I think the microbiome is an area where, you know, um, having that translation is good because you can't, like we said earlier, you can't give a human enough antibiotics to knock some, you know, knock it out, particularly if they're healthy, right?
If, I mean, for some reason they're on a cocktail of antibiotics because they're sick, that's one thing, right? But we can't ethically do that, and I mean, you wouldn't want to, right? So you kinda do have to go back and forth. But you can, what we call, humanize a germ-free animal, right? You can notice, say, a group of microbes that seem to be abundant in, um, a human phenotype and, and, you know, FMT, fecal microbiota transplant- Mm-hmm
that into a germ-free mouse. Hmm. Um, it becomes then gnotobiotic because then you know, you know, um, which microbes are, are in there, and then see how that manifests the phenotype, and does it match your human phenotype? [00:45:00] Oh, super cool That's how you can go back and forth, yeah And are fecal transplants still kind of a thing?
Dr. Mike T. Nelson: I know I heard of someone talking about this initially at, God, I was at a conference maybe 12, 13 years ago, and the first time someone explained this to me I was like, "What?" Yeah. But it, there's... I mean, I haven't looked at the data for quite some time, but the early data was pretty positive, showing some pretty impressive changes.
Dr. Sara Campbell: Yeah. So I- FMTs are a thing. I think they are, like, FDA approved for, like, C. diff, Clostridium difficile. Mm. Like, you know, one of the big- Yeah ... things. Some of the, the data is as you probably, you know, would expect, um That you, you have to do it, like, a couple of times. Like, I, I consider the microbiome a training response, one, because the literature has suggested it's so, right?
So you have to kind of exercise to keep those beneficial changes to the microbiome, just like you have to exercise to keep your mitochondria [00:46:00] abundant or your, you know, cardiac output, or I should say your stroke volume, more abundant than when before, right? Um, so you know, and the microbiome can be kind of resilient.
AKA, if you stop doing something, it'll just be like, "Okay, let's go back to the standard quo," right? Or the status quo. So you know, the reality is some microbiomes are gonna be more resilient in, in people and, and more resistant to change. So you know, it would be kind of like an over time kinda... You know, you would have to do it once and then do it again and, you know, potentially do it again, again to make sure it ingrafts to the host.
It, it kind of does what it's supposed to do. You get your community structure, you know, away from the C. diff profile and towards the healthier one, so. But yeah, I still think it's... I- To my knowledge, I haven't seen that it's been, you know, taken back by the FDA or that it's not a, a treatment option. Yeah.
Dr. Mike T. Nelson: Um, one other [00:47:00] myth that comes up a lot or you hear a lot is that, oh, well, your neurotransmitters are made in your, your gut, and therefore we want more of these other little bugs or no bugs. But correct me if I'm wrong, but I think, like, serotonin, I don't think it makes it across the blood-brain barrier though, does it?
Dr. Sara Campbell: Um, good question. It, is it that or is it metabolites like tryptophan and things like that that- Yeah ... act as precursors that the gut, you know, the microbes could produce that cross? Yeah, that makes more sense to me, 'cause I'm, I'm pretty sure those do cross as far as I'm aware. But- Yeah ... again, back to sometimes the simple stories just don't always pan out so direct in physiology.
Dr. Mike T. Nelson: 'Cause otherwise you would have huge pharmaceutical companies, like, trying to figure out, how do we modify these things for the next, you know, antidepressant or whatever? Right. We, we can argue about if it's a serotonin issue or not. That's a separate discussion, but. Right. Right. [00:48:00] No, and I think, like, you know, you...
Dr. Sara Campbell: I mean, you're in the metabolic flexibility field, and you probably have to ex- explain to folks all the time, well, m- metabolism is a little more complicated than- Yeah. ... this good, this bad, you know? Yeah. Same thing with the microbiome, like, it's a little more complicated. I mean, you know, I think currently we're still estimating how much of microbial-derived metabolites are in system.
Mm-hmm. You know, I don't know that there's been any very specific- You know, study that's, for example, labeled something, had someone or even an animal eat it, and then determine how much of that makes it- Yeah, I'm trying to... That's what I was like. I'm like, where did these numbers come from and how did you get them?
Dr. Mike T. Nelson: They just, it just sounds too clean. Right. It, it is an estimate. And, and I know because I've had many a conversations with my good friends over at Research Diet to be like, "Okay, how do we do this?" But [00:49:00] then the reality is, right, you only label one substrate, not all of them. Sure. So you'd have to label a protein of some sort, a fat of some sort, a, a carbohydrate of some sort, a fiber, a this or that.
Dr. Sara Campbell: You know, um, not that fibers aren't carbohydrates, but you know, you'd have a- Right. They do different things ... fructose versus an inulin, right, kind of thing. Yep. And so you have that. And so to truly get a number where you do estimate that, I, I, you know, and where it, you know, you actually eat it, so it starts in the mouth and then- Mm-hmm
goes through the whole process, right? And how much, you know, shows up in your fecal sample versus how much is in your blood versus how much is exhale- exhaled, you know, as, you know, with your CO2, right? So I, to my knowledge, those kinds of studies have not been done. To get- Yeah ... like those accurate estimates.
Dr. Mike T. Nelson: Yeah. I, if I were to go back and do stuff all over again, like the two areas I probably would've looked at more would be, [00:50:00] the one area would probably be just the, the tracer isotope areas and... 'Cause to me it's fascinating how you can, you know, air quote, kinda label something or, or tweak it a little bit and then kinda trace it around the body to see where it goes.
And there's a, you know, people do those studies. There's a lot of estimates and stuff that go in there, but it's also kind of a, a super cool way to get at actual mechanisms and to, air quote, trace where things go and see where they end up. Because a lot of times our assumptions are not always correct, and that's just one way to get some data to see what's really going on.
Dr. Sara Campbell: Right. Yeah. I know, you know, a lot of those tracer studies were orig- originally done by, you know, Brooks, and many of his students have, you know, kind of used that knowledge of tracers and kind of made it their own in other areas. So, um, you know, if you find some of his students, you probably could find, um, someone who could [00:51:00] do that.
I know Greg Henderson is at Purdue, and just because he was at Rutgers, you know, getting some of those- Mm ... studies done, so he still does a, a lot of that, um, and came out of, uh, Brooks's lab, so. Oh, very cool. Yeah, yeah. So there are definitely people around you could, you know, have a fun conversation with.
Dr. Mike T. Nelson: Yeah. And those, I even think of, like, uh, talking to, um, people at Maastricht from Dr. Luc Van Loenen's lab where they did the, they got the, the r- air quote, "radioactive tracer" into the food that they gave the cows. The cows made the milk. They took the milk and they made whey, and then eventually I think later they made casein, also protein.
Dr. Sara Campbell: Right. And they use the casein first, 'cause that's, you know, not as expensive. And then they actually got IRB approval to give it to human subjects to actually trace to see where they went. They did, like, the overnight feeding studies and he's like, "Yeah, and we woke them up at, like, 2:00 in the morning with a muscle biopsy," and, you know, just to see, like, how [00:52:00] much of it actually ends up in muscle tissue is just- fascinating.
Dr. Mike T. Nelson: But he said that whole process, I think, took them, like, six years or something like that to the tune of hundreds of thousands of dollars to do. Right. No, for sure. And I think, you know, that's a, a big limiting factor is to really- Oh, yeah ... concretely answer some of these types of questions takes willing participants, right?
Dr. Sara Campbell: Um, lots of money in, you know, ingenuity. And so I think that, you know, that whole lots of money and sometimes willing participants is, you know, a limiting factor. Yeah. Definitely. Studies done. G- but it would be exciting to, to do those studies, 'cause it would be great to know truthfully how much of what the microbiota, you know, derives as metabolites ends up actually in serum making that difference that we hypothesize it does.
Dr. Mike T. Nelson: [00:53:00] Yeah. So. Any other new and cool data? I know that's a ton of super new stuff, so it's kind of a high expectation to meet. Oh, no. Um, not, not too much. You know, we just also... I think you and I have talked. I mean, a whole separate aspect of, of what the lab does is we look at things like environmental toxicants.
Dr. Sara Campbell: Yeah. Um, I think, uh, my previous PhD student, who's now a post-doc just in toxicology, um, is preparing a paper on ozone. So, like- Oh, interesting. Yeah, yeah, yeah. So ozone and how that affects, you know, the gut microbiome and, you know, we always get weird looks. We're like, how can something you inhale affect your gut?
I'm like, "Well, it does, and a lot." Um, and- Does it kill off a bunch of things? Because ozone itself can be pretty toxic to a lot of stuff. Yeah. In, in both a... This is not really a good or bad way, right? I, I had bought an industrial ozone thing [00:54:00] I stick on my cold water, you know, freezer in the garage to basically try to kill everything that's in there.
Right. Yeah, no. I, I mean, I think ozone is like, you know, we more kind of... When you think about it, um, from a- Different aspect. I mean, it's just like the whole air pollution kind of- Sure ... aspect of things. But, um, no, we definitely w- see it both in acute and a chronic response. It, it significantly altering the microbial composition.
Hmm. Some of the, you know, um, gap, you know, tight junction related proteins, and for sure, um, you know, goblet cell counts and the type of mucus, mucin you see there in terms of, um, acidity. Uh, and, and so that's been really interesting. And- Are those changes, are they going up or down, or what kind of changes do you see?
Um, typically not the good kind. Yeah, I was gonna say. You can imagine. [00:55:00] Um, and then, you know, the other study we, we just got w- got finished, and I, I, you know, I'm hoping to get some funding for there's a grant in review right now to look at, um, ingested micro/nanoplastics. Oh, interesting. I was gonna say, I tho- thought that might, like, perk your- Yeah, yeah
huge thing right now. Yeah. So we've got, you know, fecal samples. We took tissues, like heart, skeletal muscle, brain, you know, a- a- all the types, and we're gonna try and, you know, profile the plastic accumulation in all the tissues, in the, the fecal sample, then run some microbiome and, and, um, intestinal health related, um, markers on that.
Hmm. You know, the things we look at are the tight junctions, the cadherins. We look at antimicrobial proteins, inflammatory proteins, um, and then, you know, what those mucins are doing and, and how the acidity of the mucins [00:56:00] change with the way the microbiome kind of moves around. So, so hopefully sh- that my, my one PhD student will be looking at that late this summer.
Dr. Mike T. Nelson: Oh, fascinating. Yeah. Do you, do you know if there's a good consumer test for microplastics? It seems like every time I turn around I hear someone promoting that as a thing. And then my question is, is there a way to get rid of them? I've heard sauna, I've heard all sorts of stuff, but it, it still seems like this area where people agree that it's an issue, but nobody can agree how much of an issue or when you should kinda be more worried about it.
It's kind of a black box from what I've seen so far. Yeah. So the government just resu- uh, issued an ARPA to try and answer those questions. Oh, interesting. Yeah. So the hope would be that, you know, folks will be, you know, um, getting some of that money to look at- How it accumulates, why it accumulates, [00:57:00] mechanisms of, of its accumulation, and hopefully then ex- you know, does it get excreted?
Dr. Sara Campbell: How much of it? Where does it go and so forth. So, um, yeah, so I think they're, as you said, they're trying to actively answer those types of questions here in the next couple of years. Yeah. 'Cause I've had a few people just on inquiries are like, "Oh, I wanna do a microplastics test. What do I do?" And I'm like, "I, I can send you to some people that claim to do it," but again, I, I always get nervous about What kind of tissue are you collecting?
Dr. Mike T. Nelson: Is it just blood? Is it urine? Is it... Because all those are completely different pathways, you know. You're obviously, in a consumer thing, you're limited what tissues you can probably collect, and sample size, and does that transfer to other tissues? If you look at blood, are you just looking at blood? Are you looking at the red blood cell?
Does that transfer to other components? And it just, it just, again, back to it's just not as simple without a fair amount of [00:58:00] investigative data. Like, I think of, like, like omega-3 testing, which I've used for a long time, and just the amount of time and data it went in to have a representative blood value, have a representative RBC value.
It's- Right ... those are... There's many, many years, and many, many studies that went in just to get that base of knowledge. Right. Right. And again, you know, it's one of those where you need both the human and animal stuff going on, right? For sure. Because we ingest nanoplastics, you know, just because we're living, right?
Dr. Sara Campbell: Yep. But like you said, understanding how it might accumulate in all of those tissues, you know, is not something you can easily do in a human, right? And so then you have to sort out ways to, well, okay, if it's accumulating here in the animal, how do we figure out how to look at that in a human? Is it only through a biopsy?
Is there some sort of scan you need? Is there a dye to then go with that scan so it highlights the plast- you know? So- Yeah ... lots of, I think, steps to, to look at that. But it's definitely been an [00:59:00] interesting, you know, area to kind of get ourselves into. So I'm ex- I'm excited to see where that data set goes.
Dr. Mike T. Nelson: Yeah, and since... This is kind of a tangent question, but you're looking at environmental pollutants. The one thing I've noticed lately the last couple years is on my little weather guide, I've had more days that show up with the air part- I think it's just looking at air particles, than- Air quality ... ever before from forest fires, from who knows what.
Yeah. And my brief look at the literature, which again is a very brief scan and definitely not my expertise area, is I was kinda horrified that there's a lot of pretty decent data that air quality, at least looking at particles and things like that, it, it's not good. Yeah. Yes. So that was another one of those big kind of like government-funded things and, and there are two or three folks at Rutgers who have one of them.
Dr. Sara Campbell: Oh, okay. So [01:00:00] that data will probably be coming out soon. I haven't heard much about that at all. But the... I, I agree with you, the air quality has been, um- Not great. I mean, I'm someone who more recently suffers from asthma and, you know, I can- Oh, okay ... tell you immediately- Hmm ... when the air quality is off. I don't even need the app.
Like, I'm like, "Ugh, I definitely need my extra inhaler today." Hmm. And you can feel it, and it is more days than not un- recently. So, so yeah, so that, that is definitely an area that, that Rutgers is, is looking into, I can tell you for sure. So, hmm. Awesome. Just, uh, again, we always talk, so we'll have to connect when I start to see- Yeah, for sure
Dr. Mike T. Nelson: data come out from some of my colleagues, so. Yeah. 'Cause I think it's a, it's an area that y- dealing with environmental stuff, it, it kind of fascinates me in a negative way how [01:01:00] we're so worried about unknowns, but we have some pretty good data on knowns that are already affecting people, and we still seem to be very inadequately equipped to do anything about the dangers we already know.
And it's this sort of never-ending discussion of, well, this next thing could be worse, and this could be bad, and that could be bad, and which are all true. Like, yeah, we, we should study those things for sure, but we have some good data to show that these are definitely bad, so maybe we should start keep researching the other stuff, but focus on what we can do about this- Right
now in the meantime. It doesn't have to be this either/or, and I'm sure there's- Right. Is there a- ... political reasons to- ... countermeasure for something, right? Yeah. Is there a way to- To confiscate it, to make it confusing ... right, to, you know, mediate the impacts and so forth. And so, you know, and I think a lot of that comes down to, again, money, and unfortunately I think a lot of those money pools are not as quite, you know, they're not as [01:02:00] deep as they used to be.
Dr. Sara Campbell: So- Oh, for sure ... unfortunately I think that's, you know, one of the big ways that science has really been impacted, particularly the last two years is, is certain things that were on a roll are, you know, have come to a pretty abrupt halt. Yeah, this administration definitely seems to be the see no evil, hear no evil.
Dr. Mike T. Nelson: We'll just, we'll gut the EPA, we'll cut all the science out, and therefore nobody can tell us any of these things are gonna be bad. Right. And just like that, uh, politics aside, that is just not gonna end well. No. And, and you think about the recovery time that some fields are going to experience. Long. Long.
Dr. Sara Campbell: Right? Well past when I feel like you and I will be kind of moved on from the science, which is unfortunate and- Yeah ... to put it- Especially with some people I have in environmental sciences, like the... I think people forget, like the, it's not only certain agencies are [01:03:00] losing current research, it's like some of them have been gutted so bad that they're actually losing the care of samples that have been around for many, many years, that y- you're not gonna be able to get that data back maybe ever, or if not very long protracted time.
Dr. Mike T. Nelson: So you're not just losing out on the current research and, and solving questions, you're losing historical data to allow you to do things in the future, and that's the thing that scares me the most. Yeah. Yeah, and it's not just... It's, it's m- it's across most of the federal agency, funding agencies. Yes.
Dr. Sara Campbell: Right? It's not... I mean, I gripe because NIH and NSF have been cut, but you're, you're exactly right. NOAA and the EPA and a number of the scientific organizations with, you know, um, focus on supporting that kind of research have been, you know, gutted. So- Yeah ... crossing my- Any, any positive news we can end on?
No. W- [01:04:00] my oldest son just finished his first semester, first year in college. Oh, that's cool. That's awesome. So, and, yeah, and he did really good. And, um, no, I mean, it'll be a productive summer. Looking forward to, you know, attending conferences and talking more science with people and, um, you know, hopefully finishing up one of my PhD students this summer.
To see them graduate will be great. And so, you know, lots of positive things. We, you know, we have to, while, you know, certain things are upsetting, you know, having some hope and, and leaning on some of those more positive things can, can really make a difference. And exercise is still really good for us. Yes.
Exercise is still really good for us. Yeah. Which, I mean, just the... It's fascinating that, I mean, you could argue about when exercise as a field really started. Maybe it's AV Hill in the early, what, 1914, 1917, whatever. But just a little bit over 100 years we've been s- you know, actively studying this to some degree, [01:05:00] and there's so much that we have no idea on the mechanistic side.
Dr. Mike T. Nelson: But on the flip side, there's so much, all the data we accumulate keeps showing us time and time again via multiple mechanisms that exercise is probably one of the most beneficial things you can do as a human. Right. Yeah. And, you know, I enjoy when I teach being on that kind of soapbox and just telling the students the important, the importance of that and, you know, and across the lifespan and how the types of exercise might differ as you age and what becomes really important, the things you really need to think about.
Dr. Sara Campbell: And, and, and then, you know- Linking that with, you know, good dietary practices and- For sure ... yeah, it's, it's exercise is, is still good for you. I still love that we can say that message, for sure. Yeah. Awesome. And then with your lab, are you looking for any more graduate students or anything? Um, I, I'm always [01:06:00] looking, so don't- Okay.
Cool ... you know, anybody who's interested in the kind of stuff we do, you can just look me up and shoot me an email. So yeah, we're always looking for motivated, you know, kids to come into the lab and, and contribute and ask crazy questions and see where they go. Yeah. That's great. Awesome. And where can people find out more about you?
Dr. Mike T. Nelson: I know you publish a fair amount of research that'll be out coming up, and new stuff- Yeah ... will be out very soon. Yeah. Well, I'm at Kinesiology and Health in, at Rutgers University. So if you, you know, if you Google Campbell, kines, Rutgers, I probably will pop right up. You just look for the red-headed bun with the glasses.
Awesome. Well, thank you so much for all your time, and thank you so much for all the great research and everything you're doing. It's super nice and easy for me just to sit in my chair and ask you about all the studies and all the stuff you've done, because it takes many, many, many hours and approval and paperwork and running the studies.
Even animal studies, all that stuff takes... I think [01:07:00] people who haven't done it underestimate how much time and effort and just will it takes to, to do that. So thank you for doing all that work. It's super interesting. Yeah. Thanks. Well, we love it, and we're not gonna stop, so. Awesome. Thank you so much.
Dr. Sara Campbell: Thanks.
Dr. Mike T. Nelson: Thank you so much for listening to the podcast today. Really appreciate it. Huge thanks to Dr. Sarah Campbell for coming back on the podcast again, discussing all of the really cool, uh, science and everything she's doing there, and the testing, and how you can apply that to your life. And again, it also underscores the importance of how exercise is changing multiple, multiple different things within our physiology to make us better.
So huge thanks to her. If you want more information from me, check out the Fitness Insider newsletter. You can go to the link down below, [01:08:00] miketnelson.com/newsletter. Have all the information there for you. As always, thank you so much for listening to the podcast. Really, really appreciate it. You have time, give us the old likes up, down...
Likes up. Likes, downloads, subscribe, whatever the heck all the AI algorithms and everyone is trying to get us to do now with podcasts. You can actually leave a human review. That helps us a long way also getting better distribution of the podcast. So thank you so much. We really appreciate it, and stay tuned for more great episodes coming up.
And then also, we've got... Well, I'll leave it as a special guest. We've got many special guests coming up, and I'll leave it as a surprise, uh, so stay tuned for that. As always, thank you so much for listening. We'll talk to you next week. See ya.
Oh, a great little actress. Yep, and getting smaller all the [01:09:00] time.
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