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[159.112.244.44]) by mx.google.com with UTF8SMTPS id d75a77b69052e-50b36ec6dcdsi93629971cf.294.2026.03.21.05.24.25 for (version=TLS1_2 cipher=ECDHE-ECDSA-AES128-GCM-SHA256 bits=128/128); Sat, 21 Mar 2026 05:24:26 -0700 (PDT) Received-SPF: pass (google.com: domain of bounce+91e48a.63af5d-tjphuhs=gmail.com@mg-d0.substack.com designates 159.112.244.44 as permitted sender) client-ip=159.112.244.44; Authentication-Results: mx.google.com; dkim=pass header.i=@mg-d0.substack.com header.s=mailo header.b="uUZIC/tf"; dkim=pass header.i=@mailgun.org header.s=mg header.b=r8l2arqB; spf=pass (google.com: domain of bounce+91e48a.63af5d-tjphuhs=gmail.com@mg-d0.substack.com designates 159.112.244.44 as permitted sender) smtp.mailfrom="bounce+91e48a.63af5d-tjphuhs=gmail.com@mg-d0.substack.com"; dmarc=pass (p=REJECT sp=REJECT dis=NONE) header.from=substack.com DKIM-Signature: a=rsa-sha256; v=1; c=relaxed/relaxed; d=mg-d0.substack.com; q=dns/txt; s=mailo; t=1774095864; x=1774103064; h=List-Unsubscribe-Post: List-Unsubscribe: List-Post: List-Id: List-Archive: List-Owner: Reply-To: In-Reply-To: References: Sender: Sender: Date: Message-Id: To: To: From: From: Subject: Subject: Content-Type: Mime-Version: X-Feedback-Id; bh=UE6rStLAQqUuw8TLyAzAEJM2HefiPQmVML0jXXH6opI=; b=uUZIC/tfgTK0cMFFO7F+K6fZgfH5BvZho0uPiResasbCZgvvpPCeMxKvTjcD7T6KPeUmC8mjxEQo8MdjZDYZTXPswCKMTiEKP5Fh3BqWRTfsc90fy3rHAZiB9g8ZHobNhSIm45F+oFzRI93Hrk1vSRwRYWQ3hkvjA1XXEkXQhqM= DKIM-Signature: a=rsa-sha256; v=1; c=relaxed/relaxed; d=mailgun.org; q=dns/txt; s=mg; t=1774095864; x=1774103064; h=List-Unsubscribe-Post: List-Unsubscribe: List-Post: List-Id: List-Archive: List-Owner: Reply-To: In-Reply-To: References: Sender: Sender: Date: Message-Id: To: To: From: From: Subject: Subject: Content-Type: Mime-Version: X-Feedback-Id; bh=UE6rStLAQqUuw8TLyAzAEJM2HefiPQmVML0jXXH6opI=; b=r8l2arqBV4KuRa1D4etmpermjGJmoJD+JnxOuSnj13/7n9UtcbaybKeisp17XG5Fx05+SWF1wPUCa+yz2mUJSi6qfUNlkjhMgASXTlQqVTJxBA7W9yBhc38nnMcMAz1tat9hSy1UnBGSugdSAXEvsEcRegjgeQYWPyKKbwmDOBA= X-Mailgun-Sid: WyJkZWU4NyIsInRqcGh1aHNAZ21haWwuY29tIiwiNjNhZjVkIl0= X-Feedback-Id: postmaster@mg-d0.substack.com:post:6148c7d8a45790427cda307f:mailgun Received: by 70260a2fffe178094d157540384641f22c2ac7b0f22ef5ba2e28cffbfe5e42d5 with HTTP id 69be8df8277fbf794a2b0514; Sat, 21 Mar 2026 12:24:24 GMT X-Mailgun-Sending-Ip: 159.112.244.44 Mime-Version: 1.0 Content-Type: multipart/alternative; boundary="7672c1ee2c80cdeea31744f9614c74448394d48c9c116042cf3d35e81027" Subject: =?UTF-8?q?MOTS-c_&_Morning_Workout_Timing_=E2=80=94_A_Beginner-Friendly_B?= =?UTF-8?q?reakdown?= From: Derek from Peptide Price To: tjphuhs@gmail.com X-Mailgun-Tag: post X-Mailgun-Track-Clicks: false Message-Id: <20260321122420.3.3d75d9e37d583de7@mg-d0.substack.com> Date: Sat, 21 Mar 2026 12:24:20 +0000 Feedback-Id: post-191667996:cat-post:pub-3365367:substack Sender: Derek from Peptide Price References: In-Reply-To: Reply-To: Derek from Peptide Price List-Owner: List-Url: List-Archive: List-Id: List-Post: List-Unsubscribe: List-Unsubscribe-Post: List-Unsubscribe=One-Click X-Mailgun-Variables: {"category": "post", "email_generated_at": "1774095864556", "is_freemail": "true", "post_audience": "everyone", "post_id": "191667996", "post_type": "newsletter", "pub_community_enabled": "true", "publication_id": "3365367", "subdomain": "derekpruski", "user_id": "273622398"} --7672c1ee2c80cdeea31744f9614c74448394d48c9c116042cf3d35e81027 Content-Type: text/plain; charset="utf-8" Content-Transfer-Encoding: quoted-printable View this post on the web at https://derekpruski.substack.com/p/mots-c-and-= morning-workout-timing Not medical advice, not personal advice. For educational purposes only. All= use cases discussed are strictly research use only. If a researcher is using MOTS-c and also hitting the gym in the morning, ti= ming matters. Here=E2=80=99s why =E2=80=94 broken down in plain language. First, What Is MOTS-c? MOTS-c is a small peptide encoded in mitochondrial DNA, which makes it uniq= ue among peptides. Most peptides are encoded in the cell=E2=80=99s nucleus.= Mitochondria are the energy-producing organelles inside your cells =E2=80= =94 often called the =E2=80=9Cpowerhouse of the cell.=E2=80=9D MOTS-c is es= sentially a signal that mitochondria send out to communicate with the rest = of the body about energy status. In research, it has shown strong effects on metabolism, insulin sensitivity= , fat utilization, and cellular energy regulation. Two Pathways You Need to Understand To understand why timing matters, a researcher needs to understand two oppo= sing biological pathways. Think of them like two switches in the body that = generally can=E2=80=99t both be fully on at the same time. AMPK =E2=80=94 The Low Fuel Switch AMPK stands for adenosine monophosphate-activated protein kinase. Just thin= k of it as the body=E2=80=99s low-energy alarm system. When cellular energy= is running low =E2=80=94 during fasting, cardio, or caloric restriction = =E2=80=94 AMPK activates. Once on, it tells the body to: Burn fat for fuel Improve how cells use glucose Build new mitochondria Conserve energy by slowing down expensive biological processes =E2=80=94 in= cluding building new muscle tissue MOTS-c is a potent AMPK activator. That=E2=80=99s largely where its metabol= ic benefits originate. mTOR =E2=80=94 The Build and Grow Switch mTOR stands for mechanistic target of rapamycin. Think of this as the body= =E2=80=99s anabolic =E2=80=94 or growth =E2=80=94 signal. When mTOR is acti= vated, the body ramps up muscle protein synthesis, drives hypertrophy (musc= le growth), and invests resources into repair and building. Resistance training is one of the most powerful ways to stimulate mTOR. Eat= ing adequate protein and carbohydrates after training also helps keep it el= evated. Why They Conflict Here=E2=80=99s the key point: AMPK and mTOR are opposing signals. When AMPK= is highly active, it puts the brakes on mTOR. Biologically this makes sens= e =E2=80=94 the body doesn=E2=80=99t want to be building expensive new musc= le tissue when it thinks it=E2=80=99s in an energy-deficient state. These t= wo pathways actively suppress each other, which is why administering a pote= nt AMPK activator right before resistance training creates a potential conf= lict worth thinking about. The Important Nuance Before getting into scenarios, this needs to be stated clearly because it g= ets misunderstood constantly. Activating AMPK does not completely shut off mTOR. It does not eliminate mu= scle growth. The relationship between these two pathways is nuanced =E2=80=94 it depends= on how strongly each is activated, the researcher=E2=80=99s nutrition stat= us, training intensity, recovery, and a range of other factors. A research = subject is not going to lose all their gains because MOTS-c was administere= d before a workout. The effect is more of a partial dampening under certain= conditions, not a complete block. There=E2=80=99s also a compelling wrinkle specific to MOTS-c: research has = shown it can suppress myostatin. Myostatin is a protein the body produces t= hat actively limits how much muscle can grow =E2=80=94 it functions as a bi= ological brake on muscle development. Lower myostatin means that brake is l= oosened, which can support greater skeletal muscle growth potential. Whether this effect is enough to fully offset any mTOR dampening from AMPK = activation is still an open research question =E2=80=94 but it makes the pi= cture considerably more complex than simply writing off MOTS-c as counterpr= oductive to muscle growth. Scenario 1 =E2=80=94 The Optimal Approach (If Schedule Allows) This is the approach that theoretically extracts the most from both MOTS-c = and resistance training by keeping the two signals separated. Step 1 =E2=80=94 Administer MOTS-c fasted, first thing in the morning. Step 2 =E2=80=94 Follow with low-to-moderate intensity movement. A walk, st= eady state cardio, a light bike ride. Not resistance training. In a fasted = state with low-intensity activity, AMPK is heavily biased and substrate ava= ilability is low =E2=80=94 the body is primed to respond to MOTS-c=E2=80=99= s metabolic signals. This is the environment where its effects on mitochond= rial function, fat oxidation, glucose metabolism, and metabolic flexibility= are operating at full capacity with no interference. Step 3 =E2=80=94 Remain in a fasted or semi-fasted state for roughly 2=E2= =80=934 hours. This gives the acute AMPK signaling window time to normalize= =2E Step 4 =E2=80=94 Break the fast with a solid meal. Protein, carbohydrates, = adequate calories. This refuels glycogen stores, raises circulating amino a= cid availability, and shifts the hormonal environment toward anabolism. Step 5 =E2=80=94 Train. With MOTS-c out of the acute signaling window and t= he body adequately refueled, resistance training can potently stimulate mTO= R without meaningful AMPK interference. The anabolic response to training i= s uncompromised. The end result is two clean, well-supported signaling environments =E2=80= =94 one optimized for metabolic and mitochondrial adaptation in the morning= , one optimized for muscle growth later in the day. Both get their moment. Scenario 2 =E2=80=94 Morning Administration Before Resistance Training Not every researcher has the schedule flexibility for Scenario 1, and that= =E2=80=99s completely fine. For a researcher who can only train in the morning: administer MOTS-c, trai= n, and don=E2=80=99t overthink it. The mechanistic concern around AMPK and mTOR is real, but it is not catastr= ophic in a practical context. The research subject is still going to produc= e a meaningful training stimulus, still going to drive muscle protein synth= esis, and still going to see adaptation over time. The myostatin suppressio= n effect from MOTS-c also adds a layer that may partially compensate for an= y attenuation of mTOR signaling. Compared to Scenario 1, outcomes on the muscle growth side may be marginall= y less optimal =E2=80=94 but results are still being produced on both front= s. This is not a failure mode. It is a practical, workable approach for res= earchers whose schedules demand it. The Simple Version Maximum benefit: Administer MOTS-c fasted in the morning, do light cardio, = eat a solid meal a few hours later, then train. Constrained schedule: Administer MOTS-c and train in the morning anyway. St= ill worth it. For research use only, not for human consumption. This is not medical advic= e or personal advice =E2=80=94 strictly educational. I want to give a huge shoutout to Coach Cam because he provided a lot of di= fferent perspectives on this through his research as well. =20 Questions or thoughts? Drop them in the comments. Unsubscribe https://substack.com/redirect/2/eyJlIjoiaHR0cHM6Ly9kZXJla3BydXN= raS5zdWJzdGFjay5jb20vYWN0aW9uL2Rpc2FibGVfZW1haWw_dG9rZW49ZXlKMWMyVnlYMmxrSW= pveU56TTJNakl6T1Rnc0luQnZjM1JmYVdRaU9qRTVNVFkyTnprNU5pd2lhV0YwSWpveE56YzBNR= GsxT0RZMExDSmxlSEFpT2pFNE1EVTJNekU0TmpRc0ltbHpjeUk2SW5CMVlpMHpNelkxTXpZM0lp= d2ljM1ZpSWpvaVpHbHpZV0pzWlY5bGJXRnBiQ0o5LmpUS3FtbU1hSzdSTzJjX3lkbFZRRGxBck1= QT0FJMmc3cDRMcnNhek45ZDAiLCJwIjoxOTE2Njc5OTYsInMiOjMzNjUzNjcsImYiOnRydWUsIn= UiOjI3MzYyMjM5OCwiaWF0IjoxNzc0MDk1ODY0LCJleHAiOjIwODk2NzE4NjQsImlzcyI6InB1Y= i0wIiwic3ViIjoibGluay1yZWRpcmVjdCJ9.N55ia8ELyP8tsTopBG51S9CSlvFIU9AlSKljWM_= t-Co? --7672c1ee2c80cdeea31744f9614c74448394d48c9c116042cf3d35e81027 Content-Type: text/html; charset="utf-8" Content-Transfer-Encoding: quoted-printable MOTS-c & Morning Wor= kout Timing — A Beginner-Friendly Breakdown3D""
Not medical advice, not personal advice.
͏     = 73;͏     ­͏     ­͏   &#= 8199; ­͏     ­͏     ­͏ =     ­͏     ­͏     = 3;͏     ­͏     ­͏   = 199; ­͏     ­͏     ­͏ &= nbsp;   ­͏     ­͏     ­= ;͏     ­͏     ­͏   Q= 99; ­͏     ­͏     ­͏ &n= bsp;   ­͏     ­͏     ­= ͏     ­͏     ­͏   ̳= 9; ­͏     ­͏     ­͏ &nb= sp;   ­͏     ­͏     ­&= #847;     ­͏     ­͏    = ; ­͏     ­͏     ­͏ &nbs= p;   ­͏     ­͏     ­&#= 847;     ­͏     ­͏    = ­͏     ­͏     ­͏  = ;   ­͏     ­͏     ­= 47;     ­͏     ­͏     = ­͏     ­͏     ­͏  =   ­͏     ­͏     ­T= 7;     ­͏     ­͏     &= #173;͏     ­͏     ­͏   =   ­͏     ­͏     ­͏= ;     ­͏     ­͏     &#= 173;͏     ­͏     ­͏   &= #8199; ­͏     ­͏     ­͏=     ­͏     ­͏     = 73;͏     ­͏     ­͏   &#= 8199; ­͏     ­͏     ­͏ =     ­͏     ­͏     = 3;͏     ­͏     ­͏   = 199; ­͏     ­͏     ­͏ &= nbsp;   ­͏     ­͏     ­= ;͏     ­͏     ­͏   Q= 99; ­͏     ­͏     ­͏ &n= bsp;   ­͏     ­͏     ­= ͏     ­͏     ­͏   ̳= 9; ­͏     ­͏     ­͏ &nb= sp;   ­͏     ­͏     ­&= #847;     ­͏     ­͏    = ; ­͏     ­͏     ­͏ &nbs= p;   ­͏     ­͏     ­&#= 847;     ­͏     ­͏    = ­͏     ­͏     ­͏  = ;   ­͏     ­͏     ­= 47;     ­͏     ­͏     = ­͏     ­͏     ­͏  =   ­͏     ­͏     ­T= 7;     ­͏     ­͏     &= #173;͏     ­͏     ­͏   =   ­͏     ­͏     ­͏= ;     ­͏     ­͏     &#= 173;͏     ­͏     ­͏   &= #8199; ­͏     ­͏     ­͏=     ­͏     ­͏     = 73;͏     ­͏     ­͏   &#= 8199; ­͏     ­͏     ­͏ =     ­͏     ­͏     = 3;͏     ­͏     ­͏   = 199; ­͏     ­͏     ­͏ &= nbsp;   ­͏     ­͏     ­= ;͏     ­͏     ­͏   Q= 99; ­͏     ­͏     ­͏ &n= bsp;   ­͏     ­͏     ­= ͏     ­͏     ­͏   ̳= 9; ­͏     ­͏     ­͏ &nb= sp;   ­͏     ­͏     ­&= #847;     ­͏     ­͏    = ; ­͏     ­͏     ­͏ &nbs= p;   ­͏     ­͏     ­&#= 847;     ­͏     ­͏    = ­͏     ­͏     ­͏  = ;   ­͏     ­͏     ­= 47;     ­

MOTS-c & Morning Workout Timing — A Beginner-Friendl= y Breakdown

Forwarded t= his email? Subscribe here for = more
=

Not medical advice, not perso= nal advice. For educational purposes only. All use cases discussed are stri= ctly research use only.

If a researcher is using MOTS-c = and also hitting the gym in the morning, timing matters. Here’s why &= #8212; broken down in plain language.

Derek
 
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<= tbody>
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=
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First, What Is MOTS-c?

MOTS-c is= a small peptide encoded in mitochondrial DNA, which makes it unique among = peptides. Most peptides are encoded in the cell’s nucleus. Mitochondr= ia are the energy-producing organelles inside your cells — often call= ed the “powerhouse of the cell.” MOTS-c is essentially a signal= that mitochondria send out to communicate with the rest of the body about = energy status.

In research, it has shown strong effects on = metabolism, insulin sensitivity, fat utilization, and cellular energy regul= ation.

Two Pathways You Need to Understand

To understand why timing matters, a researcher needs to understand two opp= osing biological pathways. Think of them like two switches in the body that= generally can’t both be fully on at the same time.

AMPK — The Low Fuel Switch

AMPK stands for adenosin= e monophosphate-activated protein kinase. Just think of it as the body̵= 7;s low-energy alarm system. When cellular energy is running low — du= ring fasting, cardio, or caloric restriction — AMPK activates. Once o= n, it tells the body to:

  • Burn fat for fuel

  • Improve how cells use glucose

  • Build new mitochon= dria

  • Conserve ene= rgy by slowing down expensive biological processes — including buildi= ng new muscle tissue

MOTS-c is a potent AMPK acti= vator. That’s largely where its metabolic benefits originate.

mTOR — The Build and Grow Switch

mTOR sta= nds for mechanistic target of rapamycin. Think of this as the body’s = anabolic — or growth — signal. When mTOR is activated, the body= ramps up muscle protein synthesis, drives hypertrophy (muscle growth), and= invests resources into repair and building.

Resistance tra= ining is one of the most powerful ways to stimulate mTOR. Eating adequate p= rotein and carbohydrates after training also helps keep it elevated.

Why They Conflict

Here’s the key point: = AMPK and mTOR are opposing signals. When AMPK is highly active, it puts the= brakes on mTOR. Biologically this makes sense — the body doesn’= ;t want to be building expensive new muscle tissue when it thinks it’= s in an energy-deficient state. These two pathways actively suppress each o= ther, which is why administering a potent AMPK activator right before resis= tance training creates a potential conflict worth thinking about.

The Important Nuance

Before getting into scenarios,= this needs to be stated clearly because it gets misunderstood constantly.<= /p>

Activating AMPK does not completely shut off mTOR. = It does not eliminate muscle growth.

The relations= hip between these two pathways is nuanced — it depends on how strongl= y each is activated, the researcher’s nutrition status, training inte= nsity, recovery, and a range of other factors. A research subject is not go= ing to lose all their gains because MOTS-c was administered before a workou= t. The effect is more of a partial dampening under certain conditions, not = a complete block.

There’s also a compelling wrinkle s= pecific to MOTS-c: research has shown it can suppress myostatin. Myostatin = is a protein the body produces that actively limits how much muscle can gro= w — it functions as a biological brake on muscle development. Lower m= yostatin means that brake is loosened, which can support greater skeletal m= uscle growth potential.

Whether this effect is enough to fu= lly offset any mTOR dampening from AMPK activation is still an open researc= h question — but it makes the picture considerably more complex than = simply writing off MOTS-c as counterproductive to muscle growth.

Scenario 1 — The Optimal Approach (If Schedule Allows)

This is the approach that theoretically extracts the most from bot= h MOTS-c and resistance training by keeping the two signals separated.

<= p style=3D"margin: 0 0 20px 0;color: rgb(54,55,55);line-height: 26px;font-s= ize: 16px;">Step 1 — Administer MOTS-c fasted,= first thing in the morning.

Step 2= — Follow with low-to-moderate intensity movement. A walk, stea= dy state cardio, a light bike ride. Not resistance training. In a fasted st= ate with low-intensity activity, AMPK is heavily biased and substrate avail= ability is low — the body is primed to respond to MOTS-c’s meta= bolic signals. This is the environment where its effects on mitochondrial f= unction, fat oxidation, glucose metabolism, and metabolic flexibility are o= perating at full capacity with no interference.

Step 3 — Remain in a fasted or semi-fasted state f= or roughly 2–4 hours. This gives the acute AMPK signaling window time= to normalize.

Step 4 —= Break the fast with a solid meal. Protein, carbohydrates, adequate calorie= s. This refuels glycogen stores, raises circulating amino acid availability= , and shifts the hormonal environment toward anabolism.

Step 5 — Train. With MOTS-c out of the ac= ute signaling window and the body adequately refueled, resistance training = can potently stimulate mTOR without meaningful AMPK interference. The anabo= lic response to training is uncompromised.

The end r= esult is two clean, well-supported signaling environments — one optim= ized for metabolic and mitochondrial adaptation in the morning, one optimiz= ed for muscle growth later in the day. Both get their moment.

Scenario 2 — Morning Administration Before Resistance Training

Not every researcher has the schedule flexibility for Scenari= o 1, and that’s completely fine.

For a researcher who= can only train in the morning: administer MOTS-c, train, and don’t o= verthink it.

The mechanistic concern around AMPK and mTOR i= s real, but it is not catastrophic in a practical context. The research sub= ject is still going to produce a meaningful training stimulus, still going = to drive muscle protein synthesis, and still going to see adaptation over t= ime. The myostatin suppression effect from MOTS-c also adds a layer that ma= y partially compensate for any attenuation of mTOR signaling.

Compared to Scenario 1, outcomes on the muscle growth side may be marg= inally less optimal — but results are still being produced on both fr= onts. This is not a failure mode. It is a practical, workable approach for = researchers whose schedules demand it.

The Simple Version

Maximum benefit: Administer MOTS-c f= asted in the morning, do light cardio, eat a solid meal a few hours later, = then train.

Constrained schedule: Administer MOTS-c and train in the morning anyway. Still worth it.

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For research use only, not for human consumption. Thi= s is not medical advice or personal advice — strictly educational.

I want to give a huge shoutout to Coach Cam because he p= rovided a lot of different perspectives on this through his research as wel= l.

Questions or thoughts? Drop them in the comments.<= /em>

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You're currently a = free subscriber to Peptide Pri= ce. For the full experience, upgrade your subscription.=

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548 Market Street PMB 72296, San Francisco, CA 94104
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